Primary Care Guidelines

The video version of this podcast can be found here:

·      https://youtu.be/z7eZ1MLItGw

The previous episode on first line treatment of T2DM can be found here:

·      https://youtu.be/32Lf5UlyTOA

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The links to the NICE guideline can be found below.

In today’s episode, we are focusing on treatment options if further interventions are needed after first line treatment. If you haven’t already, I recommend that you check the previous episode on the first line drug management of type 2 diabetes.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In this episode, we’ll go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The link to it is in the episode description.

In today’s episode, we are focusing on glucose lowering treatment options if further interventions are needed after first line treatment.

If you haven’t already, I recommend that you check the previous episode on the first line drug management of type 2 diabetes.

Right, let’s jump into it.

So we are going to look at treatment options if further intervention is needed—basically, what to do after first-line treatment.

But first, let’s talk about reviewing drug treatments and when we will need to add an SGLT2 inhibitor at any point after starting first-line therapy.

For adults with type 2 diabetes, no matter where they are in their treatment journey, if they have or develop chronic heart failure, established atherosclerotic cardiovascular disease, or become high risk for cardiovascular disease, if they are not already on it, we should offer an SGLT2 inhibitor that has proven cardiovascular benefits. This can be added on to their current treatment or used to replace an existing medication.

And let’s remember that this is because there is strong evidence in large randomised controlled trials, that has shown that SGLT2 inhibitors not only improve blood glucose control but also reduce the risk of hospitalisation for heart failure, and in some cases lower cardiovascular mortality. These benefits are seen even in patients without diabetes, which highlights their role in protecting the cardiovascular system as well as the kidneys.

Right, now, before we look into how to intensify treatment, let’s quickly cover what NICE says about monitoring and targets.

Regarding diabetes monitoring, NICE recommends measuring HbA1c every 3 to 6 months until it’s stable on unchanging treatment. After that, once HbA1c is fully stable, measuring every 6 months is usually enough.

When it comes to HbA1c targets, we should discuss and agree on an individual goal with each patient. The aim is to help them reach and maintain that target—unless trying to do so causes problems like hypoglycaemia or lowers their quality of life.

Generally speaking, for those managing their diabetes with lifestyle changes or a single drug that doesn’t cause hypoglycaemia, the target is around 48 mmol/mol, or 6.5%. For patients on medications that do carry a risk of hypoglycaemia, the target is a bit higher, around 53 mmol/mol, or 7.0%.

If an adult’s HbA1c isn’t controlled by a single drug and rises to 58 mmol/mol, or 7.5%, or above, then we need to review and reinforce their current treatment and after that, we usually move to intensify drug treatment by adding a second medication.

Now let’s look at treatment options when further intervention is needed.

For adults with type 2 diabetes, if monotherapy isn’t enough to keep HbA1c below their individual target, we can consider adding one of the following:

·      a DPP-4 inhibitor,

·      pioglitazone,

·      a sulfonylurea,

·      or an SGLT2 inhibitor.

If dual therapy—usually metformin plus another oral drug—still isn’t controlling HbA1c below the agreed threshold, then we have two main options. We can either:

·      move to triple therapy by adding a DPP-4 inhibitor, pioglitazone, a sulfonylurea, or an SGLT2 inhibitor,

·      or we can consider starting insulin.

In adults with type 2 diabetes, if metformin is contraindicated or not tolerated, and dual therapy with two oral drugs still isn’t keeping HbA1c below the agreed threshold, then insulin should be considered. This essentially means that triple therapy is only recommended by NICE when one of those three drugs is metformin, not otherwise

If triple therapy with metformin and two other oral drugs isn’t effective, isn’t tolerated, or is contraindicated, we may consider switching one of those drugs for a GLP-1 mimetic—but according to NICE, this is only for adults who:

• Have a BMI of 35 or higher (with adjustments for people from Black, Asian, and other minority ethnic groups by reducing the BMI by 2.5 to 32.5) and who also have specific psychological or medical problems linked to obesity, or
• Have a BMI under 35 but for whom insulin would have significant occupational impacts, or where weight loss would help other serious obesity-related health issues.

GLP-1 mimetic therapy should only be continued if the patient shows a clear benefit, that is, a drop in HbA1c of at least 11 mmol/mol (or 1%) and a weight loss of at least 3% of their starting body weight within six months.

Also, we need to be aware that combining a GLP-1 mimetic with insulin should only be done under specialist care and advice.

So, as we’ve just seen, NICE recommends using GLP-1 mimetics mainly for people with type 2 diabetes who have a higher BMI or specific obesity-related problems. They also set clear criteria for continuing treatment, based on how well the patient responds metabolically and whether they lose enough weight.

Now, we should also point out that other guidelines, like those from the ADA and EASD, take a fairly different approach. They suggest considering GLP-1 receptor agonists earlier in the treatment journey—especially for patients who already have cardiovascular disease or are at high risk of developing it, no matter their BMI. These guidelines focus more on the cardiovascular benefits of GLP-1 therapies, in addition to blood sugar control.

So, while NICE tends to emphasize weight and BMI, the ADA and EASD put more weight on cardiovascular risk when they recommend GLP-1 receptor agonists.

This is because research has shown that GLP-1 receptor agonists can reduce the risk of major cardiovascular events in people with type 2 diabetes who either have established cardiovascular disease or are at high risk.

For example, the LEADER trial looked at liraglutide, and the SUSTAIN-6 trial studied semaglutide. Both showed significant reductions in cardiovascular events compared to placebo.

Next, let’s move on to insulin-based treatments for adults with type 2 diabetes.

When starting insulin therapy, we are likely to continue offering metformin—provided there are no contraindications or intolerance. At the same time, we should review whether other blood glucose-lowering medications are still needed.

For insulin options, we have several choices. The first line option for NICE is NPH insulin, which can be given once or twice daily, depending on the person’s needs.

A quick note about NPH insulin: it’s an intermediate-acting insulin with an onset of action around 1 to 2 hours after injection. Its peak effect usually occurs between 4 to 8 hours, and it lasts for about 12 to 16 hours. Because of this profile, it’s useful for covering blood sugar levels between meals and overnight.

We should consider starting both NPH and short‑acting insulin particularly if the person's HbA1c is 75 mmol/mol [9.0%] or higher. This can be administered either:

• separately or
• as a pre-mixed (or biphasic) human insulin preparation.

However, NICE also suggests we can consider using insulin detemir or insulin glargine as alternatives to NPH insulin in certain situations. For example:

• If the person needs help with injections,
• If they experience recurrent symptomatic hypoglycaemia, or
• If they would otherwise need twice-daily NPH insulin injections along with other medications.

And now a quick note on insulin detemir and glargine:

Insulin glargine is a long-acting basal insulin that provides a steady release over about 24 hours with no pronounced peak, which helps maintain more stable blood sugar levels throughout the day and night.

Insulin detemir is also a long-acting insulin but usually has a slightly shorter duration, lasting around 16 to 20 hours. It tends to have a mild peak and may require twice-daily dosing in some people to maintain adequate coverage.

Both glargine and detemir offer a more predictable action profile than NPH insulin, which can help reduce the risk of hypoglycaemia and improve blood glucose control.

When it comes to pre-mixed, or biphasic, insulin preparations, NICE recommends considering short-acting insulin analogues rather than short-acting human insulin—particularly if:

• The person prefers injecting insulin just before a meal,
• Hypoglycaemia is a concern, or
• Their blood glucose levels spike significantly after eating.

This is because short-acting analogue insulins are rapid-acting insulins designed to manage the blood sugar spikes that happen around meal times.

They start working fast—usually within 10 to 20 minutes—peak around 1 to 3 hours, and their effects last for about 3 to 5 hours. Because of this quick action and shorter duration, they can be injected right before or just after eating, offering more flexibility.

Common examples include insulin lispro, insulin aspart, and insulin glulisine.

One key advantage of these analogues over regular human insulin is a lower risk of hypoglycaemia, especially overnight or between meals. Their rapid onset and shorter duration mean insulin levels drop off sooner, reducing the chance of blood sugar dipping too low when it’s not needed.

Finally, if someone is already on NPH insulin, we should also consider switching from NPH insulin to a long-acting analogue like insulin detemir or insulin glargine if:

• They experience significant hypoglycaemia while using NPH insulin,
• They are unable to use the device required for NPH, or
• They need help with injections, and switching to a long-acting insulin analogue could reduce the number of daily injections needed.

We will need to monitor patients on a basal insulin regimen—whether that’s NPH, detemir, or glargine—for the possible need to add short-acting insulin before meals, or to switch to a pre-mixed, biphasic insulin preparation.

Similarly, adults on pre-mixed insulin should be regularly assessed to see if they need an additional injection of short-acting insulin before meals or if their blood glucose control would benefit from moving to a basal-bolus regimen with NPH, detemir, or glargine.

This ongoing review helps ensure insulin therapy is tailored to achieve the best possible blood sugar control for each patient.

So that is it, a review of the treatment options in type 2 diabetes if further interventions are needed after first line treatment.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/32Lf5UlyTOA

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The links to the NICE guideline can be found below.

In today’s episode, we are focusing on the first line drug management. In the next episode, we will cover treatment options if further interventions are needed.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In this episode, we’ll go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The link to it is in the episode description.

In today’s episode, we are focusing on the first line glucose-lowering drugs. In the next episode, we will cover treatment options if further interventions are needed.

Right, let’s jump into it.

And before we look at regular glucose-lowering drugs, we first need to check whether rescue therapy is required, remembering that it can be necessary at any stage of treatment.

If the patient has symptoms of hyperglycaemia, we’ll consider starting insulin or a sulfonylurea, then review the treatment once blood glucose control is achieved. In symptomatic patients, the priority is to bring glucose levels down quickly to prevent complications and improve wellbeing. Because insulin and sulfonylureas lower blood glucose faster than most other diabetes medications, we’ll use these first, and once control is restored, switch to more suitable long-term treatment.

After that, we’ll move on to first-line regular drug treatment. The usual starting point is standard-release metformin. After starting a low dose, we will increase the dose gradually over several weeks to reduce the risk of gastrointestinal side effects, and if those occur, we can switch to a trial of modified-release metformin.

Metformin is recommended first because it’s been shown in large clinical trials to lower blood glucose with a low risk of hypoglycaemia, and it doesn’t promote weight gain. The UK Prospective Diabetes Study — or UKPDS — found that in people with type 2 diabetes who were overweight, metformin not only improved blood glucose control, but also reduced the risk of diabetes-related complications. Importantly, it also lowered their cardiovascular risk and overall mortality. These benefits, together with its long track record of safety, make metformin the preferred first-line treatment for most patients.

At the same time that we start metformin, we’ll assess the patient’s cardiovascular status and risk. The goal is to determine whether they have chronic heart failure, established atherosclerotic cardiovascular disease, or are at high risk of developing it.

We need to remember that established atherosclerotic cardiovascular disease includes conditions such as coronary heart disease, acute coronary syndrome, previous myocardial infarction, stable angina, ischaemic stroke or TIA, and peripheral arterial disease.

We also need to be aware that a high cardiovascular risk means a QRISK score above 10% in anyone aged 40 or over, or, for those under 40, having any one of these factors: hypertension, dyslipidaemia, smoking, obesity, or a family history in a first-degree relative of premature cardiovascular disease.

If the patient has chronic heart failure, established atherosclerotic cardiovascular disease, or is at high risk of developing cardiovascular disease, we’ll offer an SGLT2 inhibitor in addition to metformin — and we’ll do this regardless of their HbA1c level.

This approach is supported by strong evidence. Large randomised controlled trials, have shown that SGLT2 inhibitors not only improve blood glucose control but also reduce the risk of hospitalisation for heart failure, and in some cases lower cardiovascular mortality. These benefits are seen even in patients without diabetes, which highlights their role in protecting the cardiovascular system as well as the kidneys.

Now, when starting dual therapy with metformin and an SGLT2 inhibitor as first-line treatment, we’ll introduce the drugs sequentially. We will start with metformin first, then check tolerability, and then add the SGLT2 inhibitor as soon as metformin is confirmed to be well tolerated.

If metformin is contraindicated or not tolerated, our approach will also depend on the patient’s cardiovascular history and risk.

If they have chronic heart failure, established atherosclerotic cardiovascular disease, or are at high risk of developing it, we’ll offer an SGLT2 inhibitor as monotherapy. We do this because of the SGLT2 inhibitors cardiovascular benefits.

If the patient is not in any of these higher-risk groups, we can consider any other glucose-lowering treatments. Options include:

• a DPP-4 inhibitor
• pioglitazone
• a sulfonylurea
• or an SGLT2 inhibitor.

In order to make the right choice of drug, it may be a good idea here to give a comparative overview based on their effect on weight, hypoglycaemia risk etc.

And let’s start with weight. Although metformin was once thought to cause weight loss, NICE now describes it as weight neutral. DPP-4 inhibitors, or gliptins, are also generally weight neutral, meaning they usually don’t cause significant weight gain or loss. In contrast, SGLT2 inhibitors—also called flozins—tend to promote weight loss, which can be especially helpful for patients who are overweight or need to lower their cardiovascular risk. On the other hand, both Pioglitazone and Sulfonylureas are linked with weight gain, something to watch out for, particularly in patients where added weight could worsen insulin resistance or raise cardiovascular risk.

In terms of hypoglycaemia risk. Metformin, DPP-4 inhibitors, Pioglitazone, and SGLT2 inhibitors all carry a low risk of hypoglycaemia. However, Sulfonylureas stand out here with a much higher risk, especially in older adults or those with irregular meal patterns.

All these oral medications are contraindicated in diabetic ketoacidosis but SGLT2 inhibitors, in particular, carry a significant risk of ketoacidosis, including the unusual euglycemic form, so patients on these drugs need careful monitoring. Pioglitazone is also contraindicated in patients with current or past heart failure, as well as those with a history of bladder cancer or unexplained haematuria.

Renal function is another key factor. Most of these drugs need dose adjustments or close monitoring when kidney function is reduced. Metformin, for example, requires dose reduction or may need to be avoided depending on the patient’s eGFR. Most clinicians will reduce the dose of metformin to half if the eGFR is between 30 and 45 and metformin is stopped completely if eGFR falls below 30. Pioglitazone generally doesn’t require dose changes for kidney impairment, but it should still be used with caution.

Finally, liver impairment can affect how we prescribe these medications. Many require caution or should be avoided depending on the severity of liver disease. I won’t cover every detail here, but we should always consult the BNF before prescribing.

Because of what we said earlier about the increased risk of ketoacidosis, before starting someone on an SGLT2 inhibitor, we need to check if they might be at higher risk of diabetic ketoacidosis. This includes people who have had a previous episode of DKA, those who are currently unwell with an illness, or anyone following a very low carbohydrate or ketogenic diet.

And because of the risk that SGLT2 inhibitors carry in this respect, we will want to address any modifiable risks before starting them. For example, if someone is on a very low carb or ketogenic diet, they may need to delay treatment until they’ve stopped it. We will also advise them not to restart that kind of diet without talking to their healthcare team first, as they might need to stop the SGLT2 inhibitor if they do.

I will not go through all other possible side effects of SGLT2 inhibitors, but it’s important to know that SGLT2 inhibitors have been linked to a rare but serious infection called Fournier’s gangrene. This is a rapidly progressing infection of the genital and perineal area. It happens because SGLT2 inhibitors increase glucose in the urine, which can create an environment where bacteria grow more easily.

Patients at higher risk include those who are immunocompromised, have poor hygiene, or have other infections.

If Fournier’s gangrene develops, it can cause severe tissue damage and can quickly become life-threatening if not treated promptly. That’s why patients should be warned to look out for symptoms like redness, swelling, pain, or tenderness around the genital area, along with fever or feeling generally unwell.

If any of these symptoms appear, they should seek urgent medical care immediately, because early treatment is critical to prevent serious complications or the need for surgery.

And well, that brings us to the end of the first-line drug treatment section for type 2 diabetes.

There’s a separate part of the diabetes guideline that focuses on people with type 2 diabetes and chronic kidney disease, because they have some specific recommendations when it comes to SGLT2 inhibitors.

This section essentially says that, for patients with both CKD and type 2 diabetes, we start by giving an ACE inhibitor or an ARB, titrated up to the highest tolerated licensed dose if their albumin-to-creatinine ratio, or ACR, is 3 mg/mmol or higher.

Once they’re on this medication, we then add an SGLT2 inhibitor—on top of the ACEI or ARB—if their ACR is above 3 mg/mmol, especially if it’s over 30, and if they meet the appropriate eGFR thresholds for each particular SGLT2 inhibitor.

We also need to remember that not all SGLT2 inhibitors are licensed specifically for CKD. NICE has produced specific technology appraisals for dapagliflozin and empagliflozin for adults with chronic kidney disease. These two drugs can be given to CKD patients without type 2 diabetes specifically for their CKD management.

So that is it, a review of the first line drug management in type 2 diabetes. In the next episode, we will cover treatment options if further interventions are needed.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/t8U8-isTieM

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through recommendations on the diagnosis and monitoring of type 2 diabetes, which includes guidance by NICE. The links to the NICE guideline is in the episode description.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll go through recommendations on the diagnosis and monitoring of type 2 diabetes using HbA1c, focusing on what is relevant in primary care only. This information includes guidance by NICE contained in the NICE guideline on Type 2 diabetes. The link to it is in the episode description.

Right, let’s jump into it.

Let’s start with the diabetic diagnostic thresholds. They could be:

• An HbA1c of 48 mmol/mol or 6.5% or more or
• A Fasting plasma glucose level of 7.0 mmol/L or more or
• A Random plasma glucose of 11.1 mmol/L or more in the presence of symptoms or signs of diabetes.

Why have these thresholds been chosen?

These thresholds are based on the evidence of glucose levels at which the risk of diabetes-related complications—particularly retinopathy—increases significantly.

They have been agreed in order to strike a balance between diagnostic accuracy and early intervention, helping to catch diabetes at a point where treatment can prevent progression and complications.

And let’s also remember that if the person has symptoms of diabetes, a single abnormal HbA1c or fasting plasma glucose level can be used, although repeat testing is always advisable to confirm the diagnosis.

However, If the person is asymptomatic, we should not diagnose diabetes on the basis of a single abnormal HbA1c or plasma glucose result. Instead, we should arrange repeat testing, preferably with the same test, to confirm the diagnosis. If the repeat test result is normal, we will monitor the person for the development of diabetes, and the frequency of such monitoring will depend on our clinical judgement.

This guidance to not diagnose diabetes in an asymptomatic person based on a single abnormal result is based on principles of biological variability, and the importance of avoiding misdiagnosis.

This is because Glucose levels and HbA1c can fluctuate due to a variety of reasons and a single abnormal result may not reflect the person's usual glycaemic status. Repeating the test helps rule out false positives due to possible transient factors or a lab artefact or error.

Can we use HbA1c and plasma glucose interchangeably to diagnose type 2 diabetes?

Well, in general, yes, but there are times when HbA1c should not be used to diagnose diabetes. This is the case for:

• Children and young people under the age of 18. 
• Pregnant women or women within 2 months postpartum. 
• People with symptoms of diabetes for less than 2 months. 
• People at high diabetes risk who are acutely ill.
• People taking medication that may cause hyperglycaemia (for example, long-term corticosteroids). 
• People with acute pancreatic damage, including pancreatic surgery.
• And People with end-stage renal disease (ESRD).

Additionally, HbA1c should be interpreted with caution in people with abnormal red blood cell turnover or abnormal haemoglobin type, like: 

• Abnormal haemoglobin, such as haemoglobinopathy, including sickle cell trait.
• Severe anaemia (of any cause).
• Altered red cell lifespan (for example, in post-splenectomy). 
• And a recent blood transfusion.

Why do we need caution in these situations?

Well, HbA1c reflects the percentage of haemoglobin that has glucose attached to it—essentially giving us an average of blood glucose over the past 2 to 3 months, which is the typical lifespan of a red blood cell. However, anything that alters red blood cell turnover or haemoglobin structure can affect the accuracy of this measurement. For example:

• In conditions like haemoglobinopathies (e.g. sickle cell trait or thalassaemia), the structure of haemoglobin is different, which can interfere with how HbA1c is measured or how glycation occurs.
• In severe anaemia or increased red cell turnover, red blood cells are cleared from the circulation more quickly, so there’s less time for glucose to attach—leading to falsely low HbA1c.
• Conversely, if red cells live longer than normal (such as after splenectomy), HbA1c may be falsely high because glucose has more time to accumulate.
• And finally, after a recent blood transfusion, the donor’s red blood cells—often with a different glycaemic history—can distort the result.

So, in these cases, HbA1c may not accurately reflect the patient’s glycaemic control, and alternative measures like fasting glucose or an oral glucose tolerance test may be more reliable.

What about diabetic monitoring?

NICE recommends that we should measure HbA1c levels in adults with type 2 diabetes:

• Every 3 to 6 months until HbA1c is stable on unchanging therapy or
• Every 6 months once the HbA1c and diabetic therapy are stable. 

If HbA1c monitoring is invalid because of disturbed erythrocyte turnover or abnormal haemoglobin type, we will need to estimate trends in blood glucose control using one of the following:

• quality-controlled plasma glucose profiles
• total glycated haemoglobin estimation (if there are abnormal haemoglobins) or
• fructosamine. 

What do these alternative forms of monitoring involve?

Well:

• Quality-controlled plasma glucose profiles involve measuring fasting and postprandial glucose at regular intervals, giving a day-to-day picture of control, although they don’t reflect long-term trends as well as HbA1c.
• Total glycated haemoglobin measures all forms of glycated haemoglobin (not just HbA1c), and may be more accurate when variant haemoglobins interfere with standard HbA1c assays.
• And finally, fructosamine reflects glycation of serum proteins (mainly albumin) rather than haemoglobin, giving an average of blood glucose over the past 2–3 weeks. As we have said, it's useful in cases where red blood cell lifespan is abnormal, but also in pregnancy, or when rapid changes in glucose control are occurring.

Each of these methods has limitations, but they can give a more reliable picture than HbA1c when red cell-related interference is present.

What about HbA1c targets?

NICE advises that we should discuss and agree an individual HbA1c target with patients, encouraging them to reach and maintain it, unless any resulting adverse effects (including hypoglycaemia), or their efforts to achieve their target impair their quality of life.

However, from a general perspective, for those managed either by lifestyle and diet alone, or combined with a single drug not associated with hypoglycaemia, we should aim for an HbA1c target of 48 mmol/mol (6.5%). For those on a drug associated with hypoglycaemia, we will aim for an HbA1c target of 53 mmol/mol (7.0%). 

In adults, if HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher:

• we will review and reinforce their current treatment and
• then proceed to intensify drug treatment, generally by adding a second drug.

These thresholds are heavily influenced by the results of clinical trials such as the UKPDS (or United Kingdom Prospective Diabetes Study), which is still one of the most influential long-term RCTs on glycaemic control in type 2 diabetes.

It showed that intensive blood glucose control (targeting HbA1c around 53 or ~7.0%) significantly reduced:

• Microvascular complications (like retinopathy, nephropathy, and neuropathy).
• And additionally, long-term benefits for macrovascular outcomes emerged in extended follow-up giving rise to the so-called “legacy effect”

What is exactly the legacy effect?

Well, it describes the fact that participants in the UKPDS randomised controlled trial were followed for 10 years after the trial ended. Although the differences in HbA1c between intensive and conventional groups disappeared within a year, the intensive group still had significantly lower rates of both micro and macrovascular complications as well as all-cause mortality. In a way, this showed that early good control leaves a "metabolic imprint" that protects patients long term, even if later control becomes less strict.

However, although tight control can be beneficial, we will consider relaxing the target HbA1c on a case-by-case, with particular consideration for people who are older or frailer, if:

• they are unlikely to achieve longer-term risk-reduction benefits, for example, people with a reduced life expectancy
• if tight blood glucose control would put them at high risk if they developed hypoglycaemia, for example, if they are at risk of falling, they have impaired hypoglycaemia awareness, or they drive or operate machinery as part of their job
• or if intensive management would not be appropriate, for example if they have significant comorbidities. 

This is because there is strong evidence that in older or frail adults, sometimes the risks of hypoglycaemia may outweigh the benefits of strict control. In particular, the ACCORD Trial found that intensive glucose lowering (with a target HbA1c of less than <6.0%) increased all-cause mortality in people with type 2 diabetes at high cardiovascular risk. In fact, the trial had to be stopped early due to this excess mortality. Our take home message is that tight control is not always safe, especially in older, comorbid populations.

On the other hand, if the HbA1c level is lower than their target and they are not experiencing hypoglycaemia, we will encourage them to maintain it, being aware that there are other possible reasons for a low HbA1c level, for example deteriorating renal function or sudden weight loss. 

So that is it, a review of the diagnosis and monitoring of type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/j5z0Qv35dWE

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in July 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for July 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-07-01&to=2025-07-31&ndt=Guidance&ndt=Quality+standard

The updated quality standard Cardiovascular risk assessment and lipid modification [QS100]  can be found here:

·      https://www.nice.org.uk/guidance/qs100

The new technology appraisal Dapagliflozin for treating chronic kidney disease [TA1075] can be found here:

·      https://www.nice.org.uk/guidance/ta1075

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in July 2025, focusing on what is relevant in Primary Care only.

Today we just have two clinical areas to discuss, the updated quality standard on cardiovascular risk assessment and a new technology appraisal on Dapagliflozin for CKD.

Right, let’s jump into it.

There are only 5 updated quality standard on cardiovascular risk assessment and lipid modification, so let’s have a look at them:  

Quality statement 1 refers to the identification of adults who are likely to be at high CV risk.

What does the new statement say?

It says that General practices should systematically search their patient records to identify people who are likely to be at high risk of CVD. Using routinely collected data, practices can estimate someone's 10-year risk of CVD ideally using the QRISK3 tool.

What’s different from the old guideline?

Previously, the guidance said that If a person between 25–84 was flagged as having an increased CVD risk, we would offer them a formal QRISK3 assessment.

Now, the focus is to use a proactive, structured search of patient records to find those likely to be at risk. So instead of waiting for risk to be flagged, we now go looking for it.

However, we have to be cautious and use clinical judgment, especially in groups which may have missing or incomplete data in their records, which can lead to their risk being underestimated.

Let’s now look at Quality Statement 2, which covers Diet and lifestyle advice for primary prevention.

What does the new guideline say?

Someone with a CVD risk of 10% or more, should be given lifestyle advice and this should happen within 3 months of their risk score being recorded.

What’s different from the older guidelines?

The previous (now obsolete) standards said that:

• People should be assessed for secondary causes before being offered statins and that
• They should get lifestyle advice before being offered statins.

So, this update simplifies and strengthens this advice. Everyone with a ≥10% CVD risk should get lifestyle advice within 3 months. It's no longer just a “before statins” step. It’s a core part of primary prevention.

Let’s move on to Quality Statement 3, on Lipid-lowering treatment for primary prevention.

What does the new guideline say?

People with a 10-year CVD risk of 10% or more should be prescribed a high-intensity statin unless it's not suitable for them. If they can’t tolerate statins or have a medical reason not to take them, then an alternative lipid-lowering treatment should be offered.

The recommended statin here is atorvastatin 20 mg, which is proven to be effective.

What’s different?

Under the obsolete standards we were first advised to try lifestyle changes, and only if those changes were ineffective or unsuitable, would a discussion about statin therapy take place

Now, the emphasis is on timely treatment. If a person has a 10-year CVD risk of 10% or more, and they choose to start treatment, they should be prescribed a high-intensity statin straightaway, usually atorvastatin 20 mg. There is no longer a requirement to try lifestyle changes first. While lifestyle advice remains important, it’s not a prerequisite to offering statins. This change reflects stronger evidence that earlier intervention with statins in high-risk people can significantly reduce the risk of CVD events.

But let’s remember other key considerations:

• For those close to the 10% threshold, we will need to use our clinical judgement.
• For Trans people we need to be aware that QRISK3 needs the biological sex, which may not reflect an individual’s gender identity, so adjustment may be necessary.
• And for people aged 85 and over: Atorvastatin 20 mg may still be appropriate, but we should consider factors like frailty, comorbidities, polypharmacy, etc.

Quality statement 4 refers to Assessing response to lipid-lowering treatment. This one focuses on how we monitor people after starting or changing lipid-lowering treatment, such as statins.

The obsolete guidance recommended that adults on a high-intensity statin should have a repeat lipid profile and liver transaminase levels measured after 2 to 3 months.

What’s changed?

The new quality statement broadens this. It now applies to all adults starting or changing any lipid-lowering treatment, not just those on high-intensity statins.

This change recognises that monitoring response and safety is important for everyone, not just high-intensity statin users.

And let’s remember that Fasting is not required for a full lipid profile, which should include

• Total cholesterol
• HDL cholesterol and
• Triglycerides
• And that, from these, non-HDL and LDL cholesterol are calculated

Let’s now look at the final quality statement, Quality statement 5 which focuses on Secondary prevention of cardiovascular disease

The previous (now obsolete) guidance said that people newly diagnosed with CVD should be offered atorvastatin 80 mg and that, if someone developed side effects, they should be offered a lower dose or a different statin.

What’s changed?

The new guidance shifts the focus from prescribing a specific drug or dose to achieving a specific cholesterol target. It says that people with CVD should have either:

• An LDL cholesterol which is 2 or below (≤ 2.0 mmol/L),
• Or a non-HDL cholesterol which is 2.6 or below (≤ 2.6 mmol/L)

This is a move toward outcome-focused care, rather than just prescribing a medication and assuming it's effective.

So, instead of asking:

"Did we prescribe atorvastatin 80 mg?"

We now ask:

"Has this person’s cholesterol actually reached a level that protects them?"

Besides, using non-HDL cholesterol as an alternative to LDL is helpful when LDL hasn't been specifically measured or calculated. Let’s remember that, for example,  LDL may not be calculated in people with very high triglycerides.

Let’s now take a few minutes to go through the updated NICE guidance on dapagliflozin for chronic kidney disease. This updated recommendation replaces earlier guidance and reflects both new evidence and a broader treatment scope for patients with CKD.

So, what’s changed?

Under the previous guidance dapagliflozin was only recommended for people with CKD, with or without type 2 diabetes, but only if their eGFR was between 25 and 75.

This meant that certain patients were excluded — for example:

• Those with mild CKD and an eGFR above 75
• Those with an eGFR between 25 and 45 with normal levels of albumin in their urine
• And notably, those without diabetes and without significant proteinuria

At the time, these restrictions were based mostly on the inclusion criteria of the DAPA-CKD trial, and also concerns that the size of the eligible population might have been overestimated.

Now, with this update, things have shifted significantly.

The new guidance states that dapagliflozin can be used more widely, in people with an eGFR between 20 and 90 as long as certain conditions are met.

For people with an eGFR between 20 and 45, no additional criteria are required.

But for those with an eGFR between 45 and 90, they must also either:

• Have type 2 diabetes, or
• Have a urine albumin-to-creatinine ratio or ACR of 22.6 milligrams per millimole or more

So, this new recommendation includes a much broader group of patients, especially those with early-stage CKD and diabetes, or those with elevated proteinuria but better preserved kidney function.

Why has it changed?

The change is due to new evidence, including meta-analyses and indirect treatment comparisons between dapagliflozin and empagliflozin. While the two haven’t been directly compared in a clinical trial, the available data suggest that they are similarly effective and safe for people with CKD.

Also, the costs of dapagliflozin and empagliflozin are comparable, so there’s no financial reason to prefer one over the other.

As a result, NICE has aligned the eligible population for dapagliflozin with that of empagliflozin creating a consistent and flexible approach to SGLT2 inhibitor use in CKD.

It also reflects a more inclusive and practical approach, one that gives patients better access to effective treatment and gives clinicians greater flexibility when choosing between dapagliflozin and empagliflozin.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/sUlAwcaUrB0

The first episode can be found here:

·      https://youtu.be/nguVbiQc5Ww

This episode makes reference to guidelines produced by the European Association of Urology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the recommendations by the European Association of Urology (EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The links to the guideline is in the episode description.

Today’s episode covers the clinical presentation, interpretation of test results, and a brief overview of the management.

The previous episode focused on the definition, classification, causes, and clinical associations of male hypogonadism.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The EAU sexual and reproductive health full guideline can be found here:

·      https://uroweb.org/guidelines/sexual-and-reproductive-health/chapter/male-hypogonadism

The EAU pocket guideline can be found here:

·      https://d56bochluxqnz.cloudfront.net/documents/pocket-guidelines/EAU-Pocket-on-Sexual-Reproductive-Health-2025.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the recommendations by the European Association of Urology (or EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The link to the guideline is in the episode description.

In today’s episode, we’ll focus on late-onset hypogonadism, its presentation, interpretation of test results, and a brief overview of the general management.

If you haven’t already, I recommend that you check the previous episode where we cover the definition, classification, causes, and clinical associations of male hypogonadism.

Right, let’s jump into it.

The diagnosis of functional hypogonadism is based on the exclusion of an organic or structural cause. The main causes suggested for functional hypogonadism are obesity, comorbidities and ageing, with the first two accounting for most cases. This is because the evidence shows that chronic comorbidities can interfere with the HP testicular axis leading to functional hypogonadism. In fact, the role of ageing in hypogonadism up to age 80 years seems relatively small.

Late onset hypogonadism is a term that is used, frequently incorrectly to describe the declining testosterone production due to ageing or simply the detection of hypogonadism in adults.

However, the truth is that late onset hypogonadism is in fact a broad clinical entity including adult-onset forms which can have an organic or functional origin and can be primary or secondary. Late onset hypogonadism is frequently diagnosed in the absence of an identifiable organic cause, and it becomes more prevalent with age. By definition LOH must comprise both persistent specific symptoms and biochemical evidence of testosterone deficiency.

The mainstay of LOH diagnosis includes signs and symptoms consistent with hypogonadism coupled with biochemical evidence of low morning total testosterone levels on two or more occasions, measured in fasting conditions.

In the history, we will take note of specific symptoms associated with hypogonadism. Symptoms can be grouped into three main categories: sexual, physical, and psychological.

Examples of sexual Symptoms include:

• Reduced libido
• Erectile dysfunction
• Fewer spontaneous erections
• Less frequent sexual activity or masturbation and
• Delayed ejaculation

Examples of Physical Symptoms are

• Reduced ability to perform vigorous activities
• Difficulty walking more than 1 kilometre
• Hot flushes
• Lower energy levels and
• Reduced physical strength

And finally, examples of Psychological Symptoms include

• Low mood
• Loss of motivation
• General fatigue
• Difficulty concentrating and
• sleep disturbances

As we can see, some of these symptoms are non-specific and need to be taken in context with the clinical and biochemical state. Also, headache and/or visual disturbance may indicate a pituitary related disorder.

As part of the physical examination, BMI and the measurement of waist circumference are strongly recommended for everyone. This is because of the strong association between hypogonadism and obesity. Testicular and penile size, as well the presence of sexual secondary characteristics can also provide useful information regarding the overall androgen status. Finally, digital rectal examination (DRE) should be performed before testosterone therapy or to support suspicion of hypogonadism where we would normally expect reduced prostatic volume.

How should we investigate male hypogonadism? The main initial test is obviously serum testosterone.

Testosterone levels are produced in a circadian variation, which may persist in ageing men. Testosterone levels are also potentially influenced by food intake therefore, serum total testosterone should be measured in fasting conditions and in the morning, usually between 07.00 and 11.00 o’clock. A confirmatory measurement should always be undertaken in the case of an abnormal value.

A testosterone of 12 nmol/L should be considered as a possible threshold for starting testosterone therapy in the presence of typical symptoms.

If abnormal total testosterone levels are found, we should check LH and FSH along with prolactin (PRL) in order to investigate possible underlying conditions and exclude possible organic causes. Let’s look at these tests individually:

FSH and LH levels can help differentiate between the diagnosis of primary or secondary hypogonadism. In primary hypogonadism, testosterone will be low and gonadotropins will be high, In secondary hypogonadism, testosterone will be low and gonadotropins will be low or inappropriately normal.

Due to its negative influence on libido, PRL should also be considered as a first-line screening test in patients with reduced sexual desire.

In addition, contrast-enhanced pituitary MRI scanning, as well as other pituitary hormone evaluations, is required in the presence of specific symptoms such as visual disturbances, headache and when hyperprolactinemia is confirmed.

We also need to be aware that total testosterone values may change as a function of circulating SHBG levels.

Let’s now look at the factors that may affect SHBG concentrations:

Common Conditions That Increase SHBG include:

• Certain drugs, like anticonvulsants, oestrogens, and thyroid hormone
• Hyperthyroidism
• Liver disease
• Ageing
• Smoking and
• HIV or AIDS

A high SHBG can lead to lower free testosterone, even if total testosterone looks normal.

Conversely, and although not connected to hypogonadism, Conditions That Decrease SHBG levels include:

• Drugs like glucocorticoids, testosterone, or anabolic steroids
• Hypothyroidism
• Obesity
• Cushing’s syndrome
• Insulin resistance, as seen in metabolic syndrome or type 2 diabetes and
• Non-alcoholic fatty liver disease (NAFLD) and related conditions

A low SHBG can lead to higher free testosterone, and it may be a sign of underlying metabolic issues.

Therefore, Understanding SHBG levels is important because it helps us interpret total testosterone results more accurately, especially in men with metabolic or endocrine disorders.

In clinical conditions that may affect SHBG levels, checking free testosterone can be considered. However, there is currently no consensus on threshold values, so this remains an area of uncertainty.

Having considered all this, let’s look at a Step-by-Step Approach to Evaluating Male Hypogonadism.

Firstly, we will Start with a clinical suspicion, so if a man presents with symptoms like fatigue, low libido, erectile dysfunction, or reduced muscle mass, we should consider hypogonadism.

As initial lab test for hypogonadism, we will check total testosterone, ideally in a morning fasting sample (between 7–11 AM).

If the result:

• Is low or borderline, we will repeat the testosterone to confirm it and add LH, FSH, prolactin and possibly SHBG and free testosterone depending on our clinical judgement.
• However, if the result Is normal, then hypogonadism is unlikely. However, if symptoms are strong and highly suspicious, we could consider repeating the test and checking other tests, including free testosterone.

If the repeat sample confirms low testosterone then we will need to differentiate the type of hypogonadism by looking at the gonadotropins:

• If testosterone is low and LH/FSH is high, we are looking at Primary hypogonadism (which in principle would be a testicular problem)
• However, if testosterone is low and LH / FSH is low or normal, then we are looking at Secondary hypogonadism (which would refer to a hypothalamic or pituitary problem)

Depending on the type, we will take the following Next steps:

• For primary hypogonadism:
• We can consider karyotyping (like e.g. Klinefelter syndrome) and
• We will refer to Urology to fully assess testicular function
• For secondary hypogonadism:
• We should consider referral and further imaging such as a pituitary MRI scan to exclude pituitary tumours and
• We should also assess for chronic illness, obesity, metabolic disorders and medications that could interfere with the hypothalamic pituitary axis

Additionally, if SHBG is abnormal (e.g. in obesity, ageing, or liver disease), we could also consider, if not already done, checking free testosterone, as this may give a better diagnostic clarity.

In terms of management, I will not say much because the treatment will be guided by secondary care. I will just mention that, generally, Patients with symptomatic hypogonadism (usually with a total testosterone < 12 nmol/L) without specific contraindications are given testosterone therapy.

Absolute contraindications for testosterone therapy are untreated breast and prostate cancer (PCa) and conditions such as cardiovascular events, a Haematocrit ≥ 54% and poorly controlled congestive heart failure.

There are a range of relative contraindications and cautions, which will need to be considered by secondary care.

Finally, we will need to Check the patient’s fertility needs. If the patient wants to maintain fertility, we should avoid testosterone therapy in secondary hypogonadism and consider alternatives like gonadotropins instead. This is because Testosterone therapy suppresses gonadotropin and endogenous testosterone secretion as well as spermatogenesis, reducing fertility as a result.

So that is it, a review of late-onset hypogonadism, its presentation, interpretation of test results, and a brief overview of management.

Remember to check the previous episode where we covered the definition, classification, causes, and clinical associations of male hypogonadism.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/OcxWFhMAbPQ

This episode makes reference to guidelines produced by the European Association of Urology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the recommendations by the European Association of Urology (EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The links to the guideline is in the episode description.

Today’s episode covers the definition, classification, causes, and clinical associations of male hypogonadism.

The next episode will focus on the clinical presentation, interpretation of test results, and a brief overview of the management.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The EAU sexual and reproductive health full guideline can be found here:

·      https://uroweb.org/guidelines/sexual-and-reproductive-health/chapter/male-hypogonadism

The EAU pocket guideline can be found here:

·      https://d56bochluxqnz.cloudfront.net/documents/pocket-guidelines/EAU-Pocket-on-Sexual-Reproductive-Health-2025.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the recommendations by the European Association of Urology (or EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The link to the guideline is in the episode description.

In today’s episode, we’ll cover the definition, classification, causes, and clinical associations of male hypogonadism.

In the next episode, we’ll focus on the clinical presentation, interpretation of test results, and a brief overview of the management.

Right, let’s jump into it.

Male hypogonadism is a clinical condition characterised by symptoms (with or without physical signs) and confirmed by low testosterone levels. Hypogonadism is linked to reduced testicular function, leading to decreased production of androgens (such as testosterone) and/or impaired sperm production.

This may result from a primary problem within the testes (that is, primary hypogonadism) or from insufficient stimulation by the hypothalamic–pituitary axis (or secondary hypogonadism). In rare cases, it may be due to reduced cellular response to testosterone.

Hypogonadism can negatively affect various organ systems and overall quality of life. This episode focuses on the management of adult male hypogonadism, also known as late-onset hypogonadism (LOH), although it may include some comments on congenital or pre-pubertal forms of the condition.

The prevalence of LOH increases with age, with the major causes being obesity, other co-morbidities (e.g., diabetes) and overall poor health. Ageing accounts for a low percentage of hypogonadism, as there is only a small gradual decline in testosterone, up to the age of 80 years, in healthy ageing men.

There is a high prevalence of LOH within specific populations, including patients with obesity, type 2 diabetes (T2DM), metabolic syndrome (MetS), cardiovascular disease (CVD), chronic obstructive pulmonary disease (COPD), renal disease and cancer. In particular low testosterone levels are relatively common in men with T2DM and in those with metabolic abnormalities.

Klinefelter syndrome, a trisomy associated with a 47,XXY karyotype, is the most prevalent genetic cause of primary hypogonadism, with a global prevalence of 1/500-1,000 live male births. However, < 50% of individuals with Klinefelter syndrome are diagnosed during their lifetime.

Male hypogonadism can be classified according to the cause into primary hypogonadism or secondary hypogonadism. A compensated or subclinical form of hypogonadism, characterised by normal testosterone and a high LH, has also been reported but the clinical significance of this condition is unclear.

The classification of hypogonadism has also been divided into two broad categories: ‘Classical or Organic’ and ‘Functional’.

Classical hypogonadism includes: congenital or acquired diseases causing structural and/or irreversible impairment of the pituitary and/or testes.

Functional hypogonadism is diagnosed in the absence of any recognised organic abnormality and it is mainly a consequence of co-morbidities. It should be treated first by improving the underlying condition (e.g., anorexia in a younger male).

Late onset hypogonadism represents an even broader clinical entity including adult-onset forms which can have an organic or functional origin and can be primary or secondary. Late onset hypogonadism is in the majority of cases diagnosed in the absence of an identifiable organic cause. By definition LOH must comprise both persistent specific symptoms and biochemical evidence of testosterone deficiency.

Finally, as we said earlier, in rare cases, it may be due to reduced cellular response to testosterone and its metabolites.

The European association of urology guideline maintains a classification of Primary and Secondary Hypogonadism, with special reference to LOH.

Classifying hypogonadism by its underlying cause will also help guide treatment options. For example, in secondary hypogonadism, both fertility and testosterone levels can potentially be restored with proper therapy. In contrast, primary hypogonadism usually requires testosterone replacement, which can impair fertility by suppressing the hypothalamic–pituitary–testicular (HPT) axis.

We need to remember that when hypogonadism develops after puberty—especially as men age—its symptoms may be mild and often mistaken for normal ageing.

Let’s now look at some common causes for the three main categories of male hypogonadism. Please note that this list is not exhaustive.

In Primary Hypogonadism we can have congenital and acquired causes.

Common congenital causes of primary hypogonadism include:

• Klinefelter syndrome – the most common
• Other chromosomal disorders, like Down syndrome
• And also, conditions like sickle cell disease, amongst others

Acquired causes of primary hypogonadism include:

• Drug-related like, for example, in
• Chemotherapy drugs and
• Testosterone synthesis blockers like ketoconazole
• Direct testicular damage, like, for example:
• Bilateral orchidectomy or testicular trauma
• Radiation to the testes and
• Infective or autoimmune orchitis
• And finally systemic diseases that affect the testes, like for example:
• Chronic illnesses
• Cushing’s syndrome
• HIV and
• Cancers like lymphoma or testicular cancer

In Secondary Hypogonadism we also have congenital and acquired causes.

Congenital causes of secondary hypogonadism include:

• Haemochromatosis and
• Other genetic or idiopathic causes

Acquired causes of secondary hypogonadism include:

• Drugs that suppress the hypothalamus or pituitary, like for example:
• Oestrogens and progestogens
• Testosterone or anabolic steroids
• Drugs that increase prolactin
• Opiates and
• Corticosteroids
• Local problems in the brain, like, for example:
• Head trauma
• Tumours in the pituitary or hypothalamus
• Surgery or radiation to the pituitary gland and
• Infections or inflammation in the brain
• And finally systemic conditions that affect brain hormone control, such as, for example:
• Type 2 diabetes and metabolic syndrome
• Chronic organ failure
• HIV
• Rheumatoid arthritis and other chronic inflammatory diseases
• Cushing’s syndrome and
• Eating disorders

I will only touch briefly on the Androgen Resistance or Reduced Testosterone Activity type, where testosterone levels may be normal, but the body can't respond properly to it.

Causes include:

• Genetic conditions affecting androgen receptors
• Drugs that interfere with testosterone function
• High levels of SHBG (sex hormone-binding globulin), which reduces free testosterone and
• Conditions like coeliac disease, which can also interfere with hormone action

Let’s now look in more detail into comorbidities associated with male hypogonadism

And the first one is obesity. Low testosterone levels are common in obese men. Male hypogonadism is associated with a greater percentage of fat mass and low testosterone levels are strongly associated with increased visceral adiposity, lipid deposition in the liver and muscle and atherosclerosis.

The second one is Metabolic Syndrome (MetS) and Type 2 Diabetes (T2DM), given that male hypogonadism is commonly associated with Metabolic Syndrome and its individual components, including:

• Central obesity
• Hyperglycaemia
• Insulin resistance
• Dyslipidaemia and
• hypertension

Additionally, several randomised controlled trials (RCTs) have shown that testosterone therapy can:

• Improve insulin resistance
• Reduce blood glucose levels
• Lower total cholesterol and LDL cholesterol

Some studies suggest that testosterone therapy in men with MetS and low testosterone may be associated with reduced mortality compared to those who are untreated, although the results are not conclusive.

Erectile dysfunction is very common in men with MetS and T2DM. Additionally, although ED is multifactorial, up to 30% of men with ED also have testosterone deficiency. This means that

• Men presenting with ED should be screened for Metabolic Syndrome and diabetes but also that
• Those with ED should also have their testosterone levels measured to screen for possible hypogonadism, especially if they have diabetes or metabolic syndrome.

I will also just finally mention that data suggest that low testosterone levels are more frequently associated with worse clinical outcomes in men with COVID-19 although the link and the exact implications are still under investigation.

So that is it, a review of the definition, causes and clinical associations of male hypogonadism.

Remember that in the next episode I will cover late onset hypogonadism in more detail including the clinical presentation, laboratory testing and its interpretation and a brief overview of the general management.  

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/nguVbiQc5Ww

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE" and Public Health England. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the recommendations on H Pylori testing and treatment, focusing on what is relevant in Primary Care only. It is based on the NICE guideline on Gastro-oesophageal reflux disease and dyspepsia in adults (CG184) and the quick reference guide on the subject by Public Health England. The links to them are in the episode description.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

Eradication regimens:

First-line treatment

Offer people who test positive for H pylori a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      amoxicillin and

·      either clarithromycin or metronidazole.

Choose the treatment regimen with the lowest acquisition cost, and take into account previous exposure to clarithromycin or metronidazole. 

Offer people who are allergic to penicillin a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      clarithromycin and

·      metronidazole. 

Offer people who are allergic to penicillin and who have had previous exposure to clarithromycin a 7‑day course of treatment with:

·      a PPI and

·      bismuth and

·      metronidazole and

·      tetracycline.

Second-line treatment

Offer people who still have symptoms after first-line eradication treatment a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      amoxicillin and

·      either clarithromycin or metronidazole (whichever was not used first line). 

Offer people who have had previous exposure to clarithromycin and metronidazole a 7‑day course of treatment with:

·      a PPI and

·      amoxicillin and

·      tetracycline (or, if a tetracycline cannot be used, levofloxacin).

Offer people who are allergic to penicillin (and who have not had previous exposure to a fluoroquinolone antibiotic) a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      metronidazole and

·      levofloxacin.

Offer people who are allergic to penicillin and who have had previous exposure to a fluoroquinolone antibiotic a 7‑day course of:

·      a PPI and

·      bismuth and

·      metronidazole and

·      tetracycline.

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on Gastro-oesophageal reflux disease and dyspepsia in adults (CG184) can be found here:

·      https://www.nice.org.uk/guidance/cg184

The NICE recommendations organised by site of cancer on the guideline Suspected cancer: recognition and referral can be found here:

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#upper-gastrointestinal-tract-cancers

The Public Health quick reference guide on Helicobacter pylori in dyspepsia: test and treat can be found here:

·      https://www.gov.uk/government/publications/helicobacter-pylori-diagnosis-and-treatment

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the recommendations on H Pylori testing and treatment, focusing on what is relevant in Primary Care only. It is based on the NICE guideline on Gastro-oesophageal reflux disease and dyspepsia and the quick reference guide on the subject by Public Health England. The links to them are in the episode description.

Right, let’s jump into it.

What is helicobacter pylori and why is it relevant?

Helicobacter pylori (also commonly referred to as simply H. pylori) is a gram-negative bacterium that colonises the human gastric mucosa. It’s usually acquired in childhood and persists unless treated.

Now, in terms of prevalence, we see big differences between developed and developing countries:

·      In developing countries, prevalence can exceed 70–80% in adults, largely due to poor sanitation, crowded living conditions, and limited access to clean water.

·      In contrast, in developed countries, the prevalence is much lower—usually around 20–40%—and continues to decline. Better hygiene, sanitation, and widespread antibiotic use are key reasons for this.

Overall, socioeconomic status, living conditions, and age are the main factors influencing prevalence.

So why is H. pylori important?

H Pylori plays a key role in the development of chronic gastritis and peptic ulcer disease and is a major risk factor for gastric adenocarcinoma and MALT lymphoma.

Here’s how it works: H. pylori infection reduces mucosal defences and increases gastric acid secretion, which together lead to ulcer formation, particularly in the stomach and duodenum. On top of that, the ongoing presence of the bacteria triggers a chronic inflammatory response that causes chronic gastritis. Chronic gastritis, over time, can progress to atrophic gastritis, then intestinal metaplasia, then dysplasia—and eventually, adenocarcinoma.

Now, let’s look at MALT lymphoma—MALT stands for mucosa-associated lymphoid tissue—H. pylori infection stimulates the development of this tissue in the stomach, which isn’t normally there. The chronic stimulation by the bacteria drives B-cell proliferation and can eventually lead to malignant transformation into low-grade B-cell lymphoma. Interestingly, in early-stage MALT lymphoma, H. pylori eradication alone can lead to regression of the lymphoma. That really highlights how central the bacterium is in the disease process.

So, how do we test for H. pylori?

The main options are the urea breath test and stool antigen test. There's also serology, though we are advised against using that routinely.

The urea breath test is the most accurate, but it needs a prescription and staff time to carry out—so it’s not always practical in primary care. In most cases, we’ll use a stool antigen test instead.

We need to remember that recent or ongoing PPI use can reduce the bacterial load and increase the chance of a false-negative result—particularly with breath and stool tests. So, if the patient has been on a PPI, we should stop it and leave a two-week washout period before testing.

The H Pylori serology test has a low cost but also a lower accuracy so it is not recommended for most patients, and positive results should be confirmed by a second test such as a Urea Breath Test, or biopsy. H Pylori serology has very good negative predictive value in low prevalence developed countries and it is most useful in patients with acute gastrointestinal bleed, to confirm a negative urea breath test or stool antigen test when there is a possibility that blood and PPI use would make those test results unreliable. Serology testing detects IgG antibodies, so it does not differentiate active from past infection. Near patient H Pylori serology testing is not recommended and only locally validated laboratory-based serology are acceptable. Additionally, Public Health England states that we should not use serology testing post eradication therapy or in children and the elderly.

What does NICE say about when to test?

H. pylori testing is addressed in two areas of the NICE guideline:

– Uninvestigated and functional dyspepsia and

– Peptic ulcer disease

Let’s look at dyspepsia first.

And to clarify, the term dyspepsia is used broadly in primary care—it includes recurrent epigastric pain, heartburn or acid reflux, with or without bloating, nausea, or vomiting.

For these patients—if there are no alarm symptoms—we follow a ‘test and treat’ approach for H. pylori.

But before we go further, let’s remind ourselves of the alarm symptoms and what to do if they’re present.

If someone presents with significant acute GI bleeding, we will refer them immediately to A&E.

We will also refer under the suspected cancer pathway to exclude oesophageal or stomach cancer if they have:

– Dysphagia,

– Or if they’re aged 55 or over, have weight loss, and also have either upper abdominal pain, reflux, dyspepsia, or a mass suggesting stomach cancer.

We should also consider direct access upper GI endoscopy in:

People of any age with a history of haematemesis or

In people aged 55 and over with:

– Treatment-resistant dyspepsia or

– Upper abdominal pain with low haemoglobin or

– Raised platelets with any upper GI symptoms, like nausea, vomiting, weight loss, reflux, dyspepsia or upper abdominal pain or

– Or nausea or vomiting with either weight loss, reflux, dyspepsia or upper abdominal pain

Now, let’s go back to dyspepsia without alarm features.

In these cases, we’ll test for H. pylori. If the patient has already been prescribed a PPI, we’ll stop it and wait at least two weeks before testing, because—as we have already said—PPIs can interfere with the test result.

Once testing is done, we will offer a four-week course of a full-dose PPI for dyspepsia. If H. pylori is detected and eradication treatment given, we will not routinely re-test in cases of functional dyspepsia. This is because 64% of patients with functional dyspepsia will have persistent recurrent symptoms, so re-testing after eradication is not recommended.

However, things are different in peptic ulcer disease.

Here, we test for H. pylori and, if positive, we will treat it. But unlike with functional dyspepsia, we will re-test after eradication therapy—usually 6 to 8 weeks after starting treatment, depending on the size of the lesion.

And while we usually do the initial test with a stool antigen test, when it comes to re-testing, we should use the urea breath test instead. That’s because there isn’t enough evidence to support using the stool test to confirm successful eradication.

So, in summary, NICE recommends testing for H Pylori in uninvestigated dyspepsia and in peptic ulcer disease. Additionally, Public Health England adds that we could also test in other scenarios, like patients before taking NSAIDs, if they have a prior history of gastro-duodenal ulcers/bleeds, as well as patient with unexplained iron-deficiency anaemia, after negative endoscopic investigation has excluded gastric and colonic malignancy, and investigations have excluded all other potential causes.

Now that we know when to test for H Pylori, are there cases where we shouldn’t routinely test?

And the answer is yes. NICE doesn’t recommend routine H. pylori testing in patients with proven oesophagitis or with predominant symptoms of gastro-oesophageal reflux disease. Public Health also advises against testing children with functional dyspepsia. In these cases, if further assessment is needed, we should refer them to secondary care.

So, what do we do with the test results?

If the result is negative, we can reassure the patient. The negative predictive value of all tests is over 95%, especially in low-prevalence settings like the UK.

If the result is positive, we will offer eradication therapy. That means a 7-day, twice-daily course of a PPI plus two antibiotics.

NICE recommends the following PPI doses twice a day for eradication therapy:

– Esomeprazole or rabeprazole: 20 mg

– Omeprazole: 20 or 40 mg

– Lansoprazole: 30 mg

– Pantoprazole: 40 mg

For first-line treatment, we combine the PPI with amoxicillin and either clarithromycin or metronidazole. If the patient is allergic to penicillin, we will use both clarithromycin and metronidazole.

There are other regimens depending on whether the patient has had previous exposure to clarithromycin or metronidazole, whether they have penicillin allergy or not and whether we are looking at first line or second line treatment. I will not go through all the different possible regimens, as you can look at all the different possibilities in the NICE guideline on dyspepsia. I have also put all the recommended regimens in the episode description.

If eradication therapy is not successful with second-line treatment we will seek advice from a gastroenterologist. 

So that is it, a review of the assessment and management of cluster headache.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/GelDVWruIlA

The link to the video on updated migraine management can be found here:

·      https://youtu.be/LumBxN-yFmI

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the updated NICE recommendations on the diagnosis and management of cluster headaches, focusing on those that are relevant to Primary Care only. It is based on the clinical guideline on headaches in over 12s: diagnosis and management [CG150].

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The updated clinical guideline Headaches in over 12s: diagnosis and management [CG150] can be found here:

·      https://www.nice.org.uk/guidance/cg150

The MHRA advice on the use of topiramate can be found here:

·      https://www.gov.uk/drug-safety-update/topiramate-topamax-introduction-of-new-safety-measures-including-a-pregnancy-prevention-programme

The NICE recommendations organised by site of cancer on the guideline Suspected cancer: recognition and referral can be found here:

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#brain-and-central-nervous-system-cancers 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the updated NICE recommendations on the diagnosis and management of cluster headache, focusing on what is relevant in Primary Care only. It is based on the NICE guideline on headaches or CG150 and the link to it is in the episode description.

Right, let’s jump into it.

Cluster headaches are a primary headache disorder. Let’s remember that we classify headache disorders as either primary or secondary. The cause of primary headaches isn’t well understood, so we group them by clinical pattern. The most common primary headache disorders are tension-type headache, migraine, and cluster headache.

By the way, if you are interested in the updated management of migraines, check the corresponding episode on this channel. The link to it is in the episode description.

Secondary headaches are due to underlying disorders including medication overuse headache, giant cell arteritis, raised intracranial pressure, and infection.

Headaches are very common and there’s often concern about possible underlying causes from both patients and healthcare professionals.

So, firstly, let’s look at when we need to consider further investigations or referral.

The NICE cancer guideline says that we should suspect a brain or a central nervous system malignancy in

·      adults if there is progressive, sub‑acute loss of central neurological function. We will refer them urgently for direct access, MRI scan of the brain to be done within 2 weeks. Alternatively, we can refer for a CT scan if MRI is contraindicated

·      In children and young people with newly abnormal central neurological function, we will arrange instead a very urgent specialist referral, that is, an appointment within 48 hours. 

There are some headache features that should also instigate further investigations or referral. The list is long and it includes symptoms such as:

• worsening headache with fever
• sudden‑onset headache reaching maximum intensity within 5 minutes
• new‑onset neurological or cognitive dysfunction
• head trauma within the past 3 months
• headache triggered by cough, sneeze or exercise or an
• orthostatic headache, that is, a headache that changes with posture

Additionally, we will consider further investigations or referral for people who present with new‑onset headache and:

• compromised immunity,
• a history of malignancy or
• vomiting without other obvious cause.

Once secondary causes of headaches have been excluded, then we’ll know that we are dealing with a primary headache. But, how do we differentiate cluster headache from other primary headaches such as migraine or tension-type headache?

Well, we will diagnose it according to the headache clinical features. So, let’s have a look at these features, and compare them with what we would expect in migraine and tension-type headache.

Let’s look at the pain location first. In cluster headache the pain location is unilateral, usually around the eye, above the eye and along the side of the head or face. In migraine it can be unilateral or bilateral and in tension-type headache it is usually bilateral.

The pain quality in cluster headache is variable. It can be sharp, boring, burning, throbbing or tightening. In migraine the pain is usually pulsating, although in young people it can also be throbbing or banging and in tension-type headache it is pressing or tightening and generally non‑pulsating.

The pain intensity in cluster headache is severe or very severe whereas in migraine it is moderate or severe and in tension-type headache it is mild or moderate.

When it comes to the effect on activities, there is restlessness or agitation in cluster headache. In migraine it is aggravated by, or causes avoidance of, routine daily activities whereas tension type headache is not normally aggravated by routine activities.

And finally, the duration of cluster headache is usually 15 minutes to 3 hours whereas in migraine it is usually 4 to 72 hours in adults, but sometimes shorter, from about 1 hour in young people. In tension-type headache it is usually anything from 30 minutes to continuous.

Cluster headache also usually presents with associated symptoms and we can consider them to help with the diagnosis.

For example, in cluster headache, on the same side as the headache we can find:

• a red or watery eye
• a swollen and or drooping eyelid
• a constricted pupil
• nasal congestion or a runny nose
• and forehead and facial sweating

On the other hand, common associated symptoms in migraine are unusual sensitivity to light or sound as well as nausea and vomiting. Additional, migraine can also have symptoms of aura, which can occur with or without headache.

Typical aura symptoms include speech disturbance, visual symptoms such as flickering lights, spots or lines and partial loss of vision; and also, sensory symptoms such as numbness or pins and needles.

 Generally, aura symptoms:

• are fully reversible
• develop over at least 5 minutes
• and last 5 to 60 minutes

However, we need to remember that tension type headache usually does not have any other associated symptoms.

If we look at the frequency of the headache, we can classify cluster headache in either episodic or chronic.

Episodic cluster headache has a frequency from once every other day to 8 times a day with a pain-free period of more than 1 month and

Chronic cluster headache is the same, that is, from once every other day to 8 times a day but with a continuous pain-free period of less than 1 month in a 12-month period.

And let’s remember that both migraine and tension-type headache can also be episodic when it happens fewer than 15 days per month or chronic when it is 15 or more days per month for more than 3 months.

Let’s now look at the management of cluster headache

And first of all, for people with a first bout of cluster headache we should consider neuroimaging, discussing with or referring to a specialist if necessary.

As the actual treatment for acute cluster headache, we will offer oxygen and/or a subcutaneous or nasal triptan. Currently, nasal triptans are unlicensed for this and the subcutaneous route is also unlicensed in under 18s.

When using oxygen for the acute treatment of cluster headache:

• we will use 100% oxygen at a flow rate of at least 12 litres per minute with a non‑rebreathing mask and a reservoir bag and
• we will arrange provision of home and ambulatory oxygen. 

When using a subcutaneous or nasal triptan, we will prescribe a sufficient number of doses, bearing in mind that the attacks may be multiple and frequent, so the quantity needed may also be significant.

We will not offer paracetamol, anti-inflammatory painkillers, opioids, ergots or oral triptans for the acute treatment of cluster headache.

What is the position in respect of prophylactic treatment for cluster headache?

NICE does not actually specify exactly when prophylactic treatment should be initiated. But in general, we should consider prophylaxis if:

• The patient has chronic cluster headache
• If attacks are frequent, severe, or disabling
• If there’s a need to reduce acute medication use
• And sometimes in episodic cluster headache, we can initiate prophylaxis early in a cluster period, ideally at the onset of symptoms, because, even if the bout is expected to last only a few weeks, prophylaxis can reduce frequency, severity, and duration of the attacks.

NICE recommends verapamil as the only option for prophylactic treatment during a bout of cluster headache. This is at the moment an off-label use of verapamil and, if we are unfamiliar with its use for cluster headache, we should seek specialist advice, including advice on ECG monitoring. The BNF actually says that it should be initiated under specialist supervision.

For cluster headache that does not respond to verapamil or during pregnancy, we should refer to a specialist

So that is it, a review of the assessment and management of cluster headache.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/LumBxN-yFmI

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in June 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for June 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-06-01&to=2025-06-30&ndt=Guidance&ndt=Quality+standard

The updated clinical guideline Headaches in over 12s: diagnosis and management  [CG150] can be found here:

·      https://www.nice.org.uk/guidance/cg150

The MHRA advice on the use of topiramate can be found here:

·      https://www.gov.uk/drug-safety-update/topiramate-topamax-introduction-of-new-safety-measures-including-a-pregnancy-prevention-programme

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in June 2025, focusing on what is relevant in Primary Care only.

We’ve got another short episode today, as there is just one updated clinical guideline relevant to us, the guideline on headaches in people over 12.

Right, let’s jump into it.

The update to the guideline makes only a very small change. NICE has changed the strength of recommendations on migraine prevention. Now, topiramate and propranolol are ‘consider’ options, alongside amitriptyline, whereas previously, only amitriptyline was a ‘consider’ option, and the other two were actively ‘offered’. This change better reflects the balance between benefits and harms with these three medicines.

And that is it. Given how straightforward this update is, let’s take the opportunity to review the overall management of migraine.

And we will start by saying that Headaches are among the most common neurological problems seen by GPs. They’re debilitating, and a major cause of time off work or school. They also represent a substantial burden on society.

We classify headache disorders as either primary or secondary. The cause of primary headaches isn’t well understood, so we group them by clinical pattern. The most common primary headache disorders are tension-type headache, migraine, and cluster headache.

Secondary headaches are due to underlying disorders. Examples include medication overuse headache, giant cell arteritis, raised intracranial pressure, and infection. Medication overuse headache often occurs in people already taking medication for a primary headache disorder.

The greatest health and social burden of headaches is caused by primary headaches and medication overuse headache.

Many people with headache don’t have an accurate diagnosis. Diagnosis can be difficult, and there’s often concern about possible underlying causes from both patients and healthcare professionals. By improving recognition of primary headache disorders, we’ll manage headaches better, improve quality of life, and reduce unnecessary investigations.

Now, let’s review the acute treatment of migraine with or without aura.

For this, we should offer combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol depending on our clinical judgement.

For young people aged 12 to 17, we’ll consider a nasal triptan instead of an oral one. Currently, this is off-label in under-18s, except for nasal sumatriptan.

If someone prefers to take only one medicine, we’ll consider monotherapy with an oral triptan, NSAID, aspirin at 900 mg, or paracetamol, depending on their circumstances. And again, for 12 to 17-year-olds, we’ll consider a nasal triptan.

Because of the link with Reye’s syndrome, we should not offer aspirin to under-16s.

When prescribing a triptan, we’ll start with the lowest-cost option, and try alternatives if it’s not effective.

We should consider using an antiemetic alongside other acute migraine treatments, even if the person doesn’t have nausea or vomiting.

If oral preparations, or nasal preparations in young people, are ineffective or not tolerated, we’ll consider non-oral metoclopramide or prochlorperazine. If we do use one of these, and a non-oral NSAID or triptan hasn’t been tried, we’ll consider adding one.

We need to be aware of special warnings and precautions for metoclopramide and prochlorperazine as per the BNF, and we should discuss the benefits and risks with the patient.

At present, only buccal prochlorperazine is licensed for migraine. Other preparations are only licensed for nausea and vomiting.

Rimegepant (an oral calcitonin gene-related peptide [CGRP] inhibitor placed on or under the tongue) is recommended as an option for the acute treatment of migraine with or without aura in adults, only if:

• at least 2 triptans were tried and they did not work well enough or
• triptans were contraindicated or not tolerated, and NSAIDs and paracetamol were tried but did not work well enough.

We should not offer ergots or opioids for acute migraine treatment.

Now let’s turn to prophylactic treatment.

We will consider propranolol, topiramate, or amitriptyline to prevent migraine. This decision should follow a full discussion of benefits, risks, and suitability.

We will take into account the following factors:

• People with depression and migraine could be at an increased risk of using propranolol for self-harm so we should use caution when prescribing it.

·      We’ll follow MHRA guidance on topiramate: it should not be used for migraine prophylaxis in pregnancy or in women of childbearing potential unless the Pregnancy Prevention Programme conditions are fulfilled. That includes using highly effective contraception. The link to the MHRA advice is in the episode description.

·      For amitriptyline, we need to follow guidance on the prescribing of antidepressants and the management of medicines associated with dependence or withdrawal symptoms.

·      Currently, topiramate and amitriptyline are unlicensed for migraine in children and young people.

If the first prophylactic treatment doesn’t work or isn’t tolerated, we should discuss trying another. If necessary, we move on to the third option, unless there are safety concerns.

We will not offer gabapentin for migraine prevention.

If all three options, propranolol, topiramate, and amitriptyline, are ineffective, not tolerated, or unsuitable, we’ll consider a course of up to ten acupuncture sessions over five to eight weeks.

We can advise that the food supplement riboflavin 400 mg daily may help reduce migraine frequency and intensity for some people.

Calcitonin gene-related peptide (CGRP) inhibitors are recommended for preventing episodic or chronic migraine in adults with at least four migraine days per month, but only if at least three other preventive medicines haven’t worked, aren’t tolerated, or are unsuitable due to safety concerns. Of these agents, only atogepant is oral—the others are injectables.

Rimegepant is another Calcitonin gene-related peptide (CGRP) inhibitor which is placed on the tongue or under the tongue and which is recommended for preventing episodic migraine in adults who have between four and fourteen migraine attacks per month, but only if at least three preventive treatments haven’t worked or are unsuitable. It’s not recommended for chronic migraine.

Let’s remember that episodic migraine means fewer than 15 headache days per month, and chronic migraine means 15 or more headache days per month for more than 3 months.

And in summary, atogepant can be used as prophylaxis for both episodic and chronic migraine, whereas Rimegepant only for episodic migraine

Once prophylaxis has been given, we’ll review the need for ongoing treatment three to six months after starting it.

We’ll stop CGRP inhibitors after twelve weeks if the number of migraines hasn’t reduced by at least 50% in episodic migraine—or 30% in chronic migraine.

We need to remember that we will not offer combined hormonal contraception to women and girls with migraine with aura and, for predictable menstrual-related migraine that doesn’t respond to standard acute treatment, we’ll consider frovatriptan 2.5 mg twice daily or zolmitriptan 2.5 mg twice or three times daily, on days when migraine is expected. These are currently off-label uses.

During pregnancy, we’ll offer paracetamol for acute migraine. We can consider a triptan or NSAID, but only after discussing the need and the associated risks.

If prophylaxis is needed in pregnancy, we will seek specialist advice.

So that is it, a review of the NICE updates relevant to primary care, including a review of the treatment of migraines

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

·      https://youtu.be/HQnpwZFnedg

This channel may make reference to guidelines produced by a number of NHS organisations. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the diagnosis and primary care management of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS Health website, North East London ICB and Health Improvement Scotland. The links to this guidance can be found below.

In the previous episode, I covered the initial assessment and investigations of PCOS.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the PCOS information on the NHS Health website can be found here:

·      https://www.nhs.uk/conditions/polycystic-ovary-syndrome-pcos/

The link to the PCOS guideline by Primary Care North East London ICB can be found here:

·      https://primarycare.northeastlondon.icb.nhs.uk/wp-content/uploads/2025/01/Pathway-Polycystic-Ovary-Syndrome-10_2024.pdf

The link to the PCOS information by Right Decisions for Health and Care - Healthcare improvement Scotland can be found here:

·      https://rightdecisions.scot.nhs.uk/ggc-clinical-guidelines/gynaecology/gynaecology-guidelines/guidelines-a-z-all-gynaecology-guidelines/polycystic-ovarian-syndrome-622/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the primary care management of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS website, North East London ICB and Health Improvement Scotland. The links to them are in the episode description.

If you haven’t already, I recommend that you watch the previous episode where I cover the initial assessment and diagnosis.

Right, let’s jump into it.

And let’s start by reminding ourselves of the referral recommendations.

We should consider endocrinology referral if:

• There are severe symptoms such as signs of virilisation or rapidly progressing hirsutism
• When testosterone is significantly elevated, defined as greater than 5 nanomoles per litre or more than twice the upper limit of normal or
• Abnormal levels of DHEA or dehydroepiandrosterone, androstenedione, or 17-hydroxyprogesterone, which could indicate the possibility of alternative diagnoses such as congenital adrenal hyperplasia, Cushing’s syndrome, or androgen-secreting tumours.

Otherwise, the Management of PCOS is symptom-driven, so we should identify the patient's main concern, whether it's menstrual irregularity, hirsutism, fertility, or metabolic risk.

Also, we should not neglect psychological wellbeing given that many women with PCOS are at increased risk of anxiety, depression, and body image issues. We should therefore screen for symptoms of anxiety and depression as well as other mental health conditions, and offer appropriate management if indicated.

For all patients, lifestyle modification is the first-line of treatment, especially in those who are overweight. A weight reduction of even 5 percent can restore ovulation, reduce androgen levels, and improve insulin sensitivity. Women should be counselled that although PCOS is associated with weight gain, it does not inherently make weight loss more difficult. Referral to local weight management services may be appropriate and could be advised.

Cardiovascular disease risk should be assessed by assessing individual risk factors and we should counsel patients on possible long-term complications including T2DM, hypertension, hyperlipidaemia, CVD, obstructive sleep apnoea and endometrial cancer. Screening for type 2 diabetes is recommended, especially if they have a BMI over 25 or additional risk factors such as age over 40, gestational diabetes, or a family history of diabetes.

Although HbA1c is usually preferred for the diagnosis of diabetes for practical reasons, the North East London Primary care guideline recommend testing with OGTT instead.

Let’s stop here for a moment and ask ourselves, why would OGTT be preferred in PCOS?

There are two main reasons:

Firstly, because HbA1c can miss impaired glucose tolerance given that postprandial glucose spikes may occur early in the disease process, even before fasting glucose or HbA1c becomes abnormal.

Also, HbA1c Can Miss Early Glucose Dysregulation, especially in younger women and those with mild or intermittent abnormal glycaemia. So this is why an OGTT may be preferred over HbA1c in these situations.

But let’s go back to the general management. And, as we said earlier, the treatment should be symptoms driven. So, let’s now look at the treatment in specific clinical scenarios.

From a practical perspective, we should check whether the patient is pregnant or trying to get pregnant. If they are, we should:

·      Stop any hormonal treatment

·      Offer preconception counselling (including high dose folic acid 5mg if obese)

·      Refer them to fertility or obstetric services depending on the situation and

·      If pregnant, we should also organise an OGTT

Fertility treatment in secondary care may include ovulation induction with drugs such as clomiphene or letrozole. If these fail, gonadotrophins or laparoscopic ovarian drilling may be considered.

But, if the patient is not pregnant and not planning to get pregnant, we will check which symptom they are most concerned about and treat each patient holistically according to their concerns. This could be:

·      Acne

·      Hirsutism or

·      Oligo or amenorrhoea

Let’s have a look at the management of acne first.

For this we can offer:

·      The combined hormonal contraceptive if appropriate,

·      Any other acne treatment as per dermatology guidelines or

·      We could prescribe spironolactone checking baseline U&Es and considering ongoing monitoring if clinically indicated, for example, if they are >45 or have other relevant comorbidities. Although this is an unlicensed use, the North East Primary care guidelines advocate their use in general practice.

But spironolactone is a potassium sparing diuretic. Why does it work in acne?

There are two ways. By blocking androgen receptors and by reducing androgen production in the ovaries and adrenal glands. Since androgens stimulate oil production in the sebaceous glands, blocking their action leads to less sebum, which reduces the clogged pores and the inflammation that cause acne.

Let’s now look at the treatment options for hirsutism. They are:

·      Hair removal methods e.g. shaving, waxing, and laser

·      The combined hormonal contraceptive, considering dianette, which is a combination of Cyproterone acetate and Ethinylestradiol, a synthetic estrogen

·      Metformin, which should be considered over inositol for hirsutism and central adiposity

·      And finally the BNF also states that, for hirsutism, topically applied eflornithine (Vaniqa®) is of some benefit in reducing facial hair growth and should be used for 3 months prior to referral for laser treatment of hirsutism.

What do we need to know about eflornithine or Vaniqa?

Eflornithine inhibits specific hair follicle enzymes slowing down the rate of hair growth, making facial hair appear finer, lighter, and less noticeable over time.

Key points that we need to about it is that:

• It does not remove existing hair but reduces regrowth speed.
• Effects may take 8 weeks or more to become noticeable.
• It’s often used alongside other hair removal methods like plucking or laser.
• And once treatment is stopped, hair growth usually returns to baseline.

Eflornithine is particularly useful for women with mild-to-moderate facial hirsutism who prefer a non-hormonal, non-systemic option.

But we have also just said that Metformin should be considered over inositol for hirsutism and central adiposity.

But, why? And what are inositols? And how do we prescribe them?

Well, in the UK, inositol is not available as a licensed prescription medicine in the BNF and it is considered a dietary supplement.

Some international PCOS management guidelines note that inositol could be considered for metabolic improvements (like insulin resistance), but evidence for reproductive benefits (such as ovulation or hirsutism) is still limited, and no specific dose or form is recommended. Some private or fertility specialists may support its use given its good safety profile and occasional anecdotal success but it cannot be formally prescribed.

So, if it cannot be prescribed, how are people accessing it in the UK?

At the moment, it can be obtained from Supplement retailers or speciality health stores.

The North East Primary Care guideline does recommend inositols for some aspects of PCOS management, but obviously, it is a grey area where your individual clinical judgement will be the deciding factor.

How does inositol actually work?

Inositols are naturally occurring sugar alcohols that act as second messengers for insulin at intracellular level, improving insulin sensitivity and decreasing androgens.

Why is metformin better than inositol for hirsutism?

There are various reasons.

1. Firstly, there is evidence that metformin reduces central adiposity and insulin resistance more consistently than inositol.

2. Then metformin has a greater effect on Hirsutism. We need to remember that hirsutism is largely driven by hyperandrogenism and that Metformin indirectly lowers androgens by improving insulin sensitivity (which in turn reduces ovarian androgen production). Inositols may reduce androgens too, but the effect is milder and less predictable.

When Might Inositol Still Be Considered? We can recommend them:

• If the patient cannot tolerate metformin.
• In mild PCOS symptoms without central obesity or significant insulin resistance
• If there is a patient preference for over-the-counter non-pharmacological treatments or
• As an adjunct to other therapies.

If the main concern is oligomenorrhoea or amenorrhoea we need to remember that oligo- or amenorrhoea is a risk factor for endometrial hyperplasia and carcinoma and we should aim for a minimum of 4 periods per year to protect the endometrium.

So, in this situation, we should organise a TVUSS to assess endometrial thickness if there has been prolonged amenorrhoea or abnormal vaginal bleeding. An endometrial thickness < 7mm makes hyperplasia unlikely. Referral for biopsy and possible hysteroscopy should be considered if the endometrial thickness is raised.

The treatment options for oligo- or amenorrhoea are:

·      A cyclical progestogen e.g. medroxyprogesterone 10 mg OD for 14/7 every 2-3 months

·      The combined hormonal contraceptive

·      The Levonorgestrel Intrauterine System

·      Metformin, which may be most beneficial in high metabolic risk groups. We need to be aware that Metformin is not licensed for treating PCOS in the UK, but it can be used "off-label" if clinically appropriate. However, The BNF states that Treatment with insulin-sensitising drugs, such as metformin, should NOT be prescribed routinely as first-line therapy and it should only be initiated by a specialist. There is evidence that Metformin improves short-term insulin sensitivity and also reduces androgen concentrations, but there is limited supporting evidence on the long-term benefits in PCOS. So, this is why it should only be prescribed in the context of a specialist endocrine clinic

·      And finally, other options for oligo or amenorrhoea include

o  A Progesterone Only Pill such as Drosperinone for their antiandrogenic effect and

o  Inositol although the evidence is limited.

Before ending, let’s look at COC in a little bit more detail. One of the known benefits of combined hormonal contraception is that it increases SHBG. So, combined oral contraceptives are commonly used in PCOS for the treatment of acne, hirsutism, and menstrual irregularity but again this is an unlicensed indication.

But, why does CHC increase SHBG?

The main reason is the oestrogen component of CHC (normally ethinylestradiol), which has a hepatic effect by increasing synthesis of several proteins, including SHBG. Then, the higher circulating SHBG levels bind to free testosterone, reducing the free androgen index. This leads to reduced clinical signs of hyperandrogenism (e.g., acne, hirsutism, or alopecia).

However, we also have to bear in mind the progesterone side of CHC. Not all progestogens are equal. Some CHCs contain anti-androgenic progestogens (e.g., drospirenone, or cyproterone), whereas others do not. So we should choose the contraceptive wisely.

So that is it, a review of the management of polycystic ovary syndrome.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.