Carbimazole is the preferred initial treatment for Graves’ disease, especially in elderly patients or those with underlying cardiovascular disease and significant thyrotoxicosis, as evidenced by this patient’s symptoms and peripheral signs of Graves’ disease such as ophthalmopathy. Radioiodine treatment is not recommended as first-line therapy in these cases due to the increased risk of Graves’ ophthalmopathy. Adrenalectomy is the primary treatment for pheochromocytoma, while ketoconazole is used to manage excess cortisol production in conditions like Cushing’s. Hydrocortisone is part of the treatment plan for Addison’s Disease.

Management of Graves’ Disease

Despite numerous attempts, there is no clear consensus on the best way to manage Graves’ disease. The available treatment options include anti-thyroid drugs (ATDs), radioiodine treatment, and surgery. In recent years, ATDs have become the most popular first-line therapy for Graves’ disease. This is particularly true for patients who have significant symptoms of thyrotoxicosis or those who are at a high risk of hyperthyroid complications, such as elderly patients or those with cardiovascular disease.

To control symptoms, propranolol is often used to block the adrenergic effects. NICE Clinical Knowledge Summaries recommend that patients with Graves’ disease be referred to secondary care for ongoing treatment. If a patient’s symptoms are not controlled with propranolol, carbimazole should be considered in primary care.

ATD therapy involves starting carbimazole at 40mg and gradually reducing it to maintain euthyroidism. This treatment is typically continued for 12-18 months. The major complication of carbimazole therapy is agranulocytosis. An alternative regime, known as block-and-replace, involves starting carbimazole at 40mg and adding thyroxine when the patient is euthyroid. This treatment typically lasts for 6-9 months. Patients following an ATD titration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime.

Radioiodine treatment is often used in patients who relapse following ATD therapy or are resistant to primary ATD treatment. However, it is contraindicated in pregnancy (should be avoided for 4-6 months following treatment) and in patients under the age of 16. Thyroid eye disease is a relative contraindication, as it may worsen the condition. The proportion of patients who become hypothyroid depends on the dose given, but as a rule, the majority of patients will require thyroxine supplementation after 5 years.

It is common for elderly patients who are unwell to have abnormal thyroid function tests, known as sick euthyroid. This is likely the case for the woman in question, as she has no history of thyroid disease and is not taking levothyroxine. It may be reasonable to consider starting levothyroxine, but it would be preferable to wait until her current illness has resolved. Discontinuing her antibiotics before completing her course is not appropriate, as they are unlikely to be causing the abnormal TFTs and she is currently asymptomatic. It is also unnecessary to perform a radio-isotope scan, as there is no suspicion of malignancy. Her thyroid function tests tomorrow are expected to be similar.

Understanding Sick Euthyroid Syndrome

Sick euthyroid syndrome, also known as non-thyroidal illness, is a condition where the levels of TSH, thyroxine, and T3 are low. However, it is important to note that in most cases, the TSH level is within the normal range, which is considered inappropriate given the low levels of thyroxine and T3. This condition is reversible and typically resolves upon recovery from the underlying systemic illness. As such, treatment is usually not necessary.

In summary, sick euthyroid syndrome is a condition where the thyroid hormone levels are low, but the TSH level is within the normal range. It is a reversible condition that typically resolves upon recovery from the underlying illness. No treatment is usually required for this condition.

Interpreting Glucose Tolerance Test Results in Insulin-Dependent Diabetes

Glucose tolerance tests are commonly used to diagnose and monitor diabetes. In insulin-dependent diabetes, the results of these tests can provide valuable information about the patient’s glucose metabolism. Here are some key points to consider when interpreting glucose tolerance test results in insulin-dependent diabetes:

– A peak of plasma glucose occurring between 1 and 2 hours that stays high: In insulin-dependent diabetes, the plasma glucose remains elevated throughout the 4 hours of the test. This is in contrast to normal individuals, who typically have a sharper and earlier peak that returns to basal levels.
– An ‘overshoot’ in the decline of plasma glucose at 3.5 hours: This phenomenon is seen in normal individuals but not in insulin-dependent diabetics.
– A plasma glucose level of 4 mmol/l at zero time: This is unlikely in diabetic patients, who typically have high basal glucose levels.
– A glucose concentration of 5.2 mmol/l at 4 hours: In insulin-dependent diabetes, the plasma glucose remains elevated throughout the 4 hours of the test.
– A low haemoglobin A1c (HbA1c): If the patient has been suffering from diabetes for some time without treatment, the HbA1c would likely be elevated rather than low.

Overall, glucose tolerance tests can provide valuable insights into the glucose metabolism of insulin-dependent diabetics. By understanding the nuances of these test results, healthcare providers can better diagnose and manage this chronic condition.

The most probable diagnosis in this case is primary hyperparathyroidism, which is caused by parathyroid adenoma or hyperplasia. The typical biochemical markers are low phosphate and high serum calcium levels. However, the parathyroid hormone level may be high or inappropriately normal. On the other hand, secondary hyperparathyroidism is caused by chronic hypocalcemia, such as in chronic kidney disease, where serum calcium levels are low or normal, but parathyroid hormone levels are high. Tertiary hyperparathyroidism is a result of autonomous parathyroid production and usually occurs in patients with end-stage renal disease. Sarcoidosis and type 1 renal tubular acidosis are rare causes of hypercalcemia.

Understanding Primary Hyperparathyroidism

Primary hyperparathyroidism is a condition commonly seen in elderly females, characterized by an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level. It is usually caused by a solitary adenoma, with hyperplasia, multiple adenoma, and carcinoma being less common causes. While around 80% of patients are asymptomatic, those who do experience symptoms may have polydipsia, polyuria, depression, anorexia, nausea, constipation, peptic ulceration, pancreatitis, bone pain/fracture, renal stones, and hypertension. Primary hyperparathyroidism is also associated with multiple endocrine neoplasia (MEN I and II).

To diagnose primary hyperparathyroidism, doctors may look for raised calcium levels and low phosphate levels, as well as perform a technetium-MIBI subtraction scan. A characteristic X-ray finding of hyperparathyroidism is the pepperpot skull. Treatment options include total parathyroidectomy, conservative management, and the use of calcimimetics like cinacalcet. Calcimimetics mimic the action of calcium on tissues by allosteric activation of the calcium-sensing receptor.

In summary, primary hyperparathyroidism is a condition that can be asymptomatic or present with a range of symptoms. It is most commonly caused by a solitary adenoma and is associated with multiple endocrine neoplasia. Diagnosis involves blood tests and imaging, while treatment options include surgery and medication.

Differential Diagnosis of Endocrine Disorders: Symptoms and Treatment Options

Hypothyroidism, adrenal insufficiency, Cushing syndrome, primary hypoparathyroidism, and secondary hypoparathyroidism are all endocrine disorders that can present with various symptoms. Hypothyroidism may cause cerebellar ataxia, myxoedema, and congestive cardiac failure, and is treated with replacement of thyroid hormone. Adrenal insufficiency may cause tiredness, weakness, and postural hypotension, among other symptoms. Cushing syndrome may present with central obesity, skin and muscle atrophy, and osteoporosis. Primary hypoparathyroidism may cause hypocalcaemia symptoms, while secondary hypoparathyroidism may also present with hypocalcaemia symptoms. Treatment options vary depending on the specific disorder.

Choosing the Right Treatment for Hypoglycaemic Episodes in Type 2 Diabetes

When metformin alone is not enough to control HbA1c in type 2 diabetes, NICE recommends adding a sulfonylurea, pioglitazone, or a DPP-4 inhibitor. However, if the patient experiences hypoglycaemic episodes, it is important to reassess the treatment plan.

Stopping gliclazide, a sulfonylurea, is necessary as it is likely causing the hypoglycaemic episodes. Pioglitazone is contraindicated in patients with heart failure, so a DPP-4 inhibitor like sitagliptin is the appropriate next step.

Initiating insulin is not recommended as it can be dangerous, and should only be considered after other options have failed. Reducing metformin is unlikely to prevent hypoglycaemic episodes as it does not typically cause them on its own.

In summary, choosing the right treatment for hypoglycaemic episodes in type 2 diabetes involves careful consideration of the patient’s medical history and NICE guidelines.

The most common cause of hypothyroidism is autoimmune thyroiditis, specifically Hashimoto’s thyroiditis, which is often associated with other autoimmune diseases. This is indicated by a presentation and blood test showing hypothyroidism with a raised TSH, suggesting a failure of the thyroid gland to respond to pituitary stimulation or a primary hypothyroidism. While iodine deficiency is the main cause of hypothyroidism worldwide, it is rare in the UK. Papillary thyroid cancer does not affect thyroid function, as the cancer cells do not secrete thyroxine. Although De Quervain’s can cause a primary hypothyroidism with similar symptoms, it is much less common than Hashimoto’s and therefore an incorrect answer.

Understanding Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis is a chronic autoimmune disorder that affects the thyroid gland. It is more common in women and is typically associated with hypothyroidism, although there may be a temporary period of thyrotoxicosis during the acute phase. The condition is characterized by features of hypothyroidism, such as a firm, non-tender goitre, and the presence of anti-thyroid peroxidase (TPO) and anti-thyroglobulin (Tg) antibodies.

Hashimoto’s thyroiditis is often associated with other autoimmune conditions, including coeliac disease, type 1 diabetes mellitus, and vitiligo. Additionally, there is an increased risk of developing MALT lymphoma with this condition. It is important to note that many causes of hypothyroidism may have an initial thyrotoxic phase, as shown in the Venn diagram. Understanding the features and associations of Hashimoto’s thyroiditis can aid in its diagnosis and management.

If a patient with TD2M is already taking two drugs and their HbA1c is above 58 mmol/mol, they should be offered a third drug or insulin therapy. However, insulin therapy should be avoided if possible for patients who are afraid of needles. In this case, the best option is to add sitagliptin to the patient’s current medication regimen of metformin and gliclazide. SGLT-2 inhibitors should be avoided due to the patient’s history of recurrent urinary tract infections, and pioglitazone is rarely prescribed. Exenatide is not appropriate for this patient as it is a GLP-1 mimetic and should only be added if the patient cannot tolerate triple therapy and has a BMI greater than 35. It is not recommended to stop any current medications and substitute them with sitagliptin, as the drugs should work synergistically together.

NICE updated its guidance on the management of type 2 diabetes mellitus (T2DM) in 2022, reflecting advances in drug therapy and improved evidence regarding newer therapies such as SGLT-2 inhibitors. The first-line drug of choice remains metformin, which should be titrated up slowly to minimize gastrointestinal upset. HbA1c targets should be agreed upon with patients and checked every 3-6 months until stable, with consideration for relaxing targets on a case-by-case basis. Dietary advice includes encouraging high fiber, low glycemic index sources of carbohydrates and controlling intake of foods containing saturated fats and trans fatty acids. Blood pressure targets are the same as for patients without type 2 diabetes, and antiplatelets should not be offered unless a patient has existing cardiovascular disease. Only patients with a 10-year cardiovascular risk > 10% should be offered a statin, with atorvastatin 20mg as the first-line choice.

Differentiating Pituitary Disorders: Causes and Symptoms

Pituitary disorders can present with a variety of symptoms, making it important to differentiate between them for proper diagnosis and treatment. Here are some common causes and symptoms of pituitary disorders:

Prolactinoma: This is the most common functional pituitary tumor, which can cause headaches, visual field defects, and suppression of the normal hypothalamus-pituitary-gonadal axis, leading to loss of libido and gonadotrophin levels.

Craniopharyngioma: More common in children and adolescents, this tumor can lead to hypopituitarism, growth hormone deficiency, and visual changes. It can sometimes cause increased serum prolactin.

Idiopathic panhypopituitarism: This condition manifests with decreases in all anterior pituitary hormones, including prolactin.

Isolated LH deficiency: This can explain loss of libido and decreased plasma levels of LH and testosterone, but not the increase in prolactin or bitemporal hemianopia.

Pituitary infarction: This can occur in women who hemorrhage excessively during parturition, leading to varying degrees of hypopituitarism, but not hyperprolactinemia.

By understanding the specific causes and symptoms of pituitary disorders, healthcare professionals can provide appropriate treatment and improve patient outcomes.

Understanding the Different Causes of Cushing Syndrome

Cushing syndrome is a condition that occurs when the body is exposed to high levels of cortisol for an extended period. There are several different causes of Cushing syndrome, including iatrogenic, pituitary-dependent, ectopic ACTH secretion, primary adrenal disorder, and pseudo-Cushing’s syndrome.

The most common cause of Cushing syndrome is iatrogenic, which is related to the use of corticosteroid medication. This risk is higher in people who take oral corticosteroids, but it can also affect those who misuse inhaled or topical corticosteroids.

Pituitary-dependent Cushing’s disease is a much rarer cause of Cushing syndrome that arises from a pituitary tumour. Ectopic ACTH secretion is a very rare cause of Cushing syndrome that arises due to ACTH secretion from a carcinoid tumour.

Primary adrenal disorder is an unusual cause of Cushing syndrome that arises from primary hypercortisolism. Finally, pseudo-Cushing’s syndrome describes hypercortisolism arising as a result of a separate condition, such as malnutrition or chronic alcoholism, resulting in the same phenotype and biochemical abnormalities of Cushing syndrome.

Understanding the different causes of Cushing syndrome is important for proper diagnosis and treatment.

Subacute Thyroiditis: A Self-Limiting Condition with Four Phases

Subacute thyroiditis, also known as De Quervain’s thyroiditis or subacute granulomatous thyroiditis, is a condition that is believed to occur after a viral infection. It is characterized by hyperthyroidism, a painful goitre, and raised ESR during the first phase, which lasts for 3-6 weeks. The second phase, which lasts for 1-3 weeks, is characterized by euthyroidism. The third phase, which can last for weeks to months, is characterized by hypothyroidism. Finally, in the fourth phase, the thyroid structure and function return to normal.

To diagnose subacute thyroiditis, thyroid scintigraphy is used to show a globally reduced uptake of iodine-131. However, most patients do not require treatment as the condition is self-limiting. Thyroid pain may respond to aspirin or other NSAIDs, but in more severe cases, steroids may be used, particularly if hypothyroidism develops.

It is important to note that subacute thyroiditis is just one of the many causes of thyroid dysfunction. A Venn diagram can be used to show how different causes of thyroid dysfunction may manifest. It is interesting to note that many causes of hypothyroidism may have an initial thyrotoxic phase. Proper diagnosis and management of thyroid dysfunction are crucial to ensure optimal patient outcomes.

Common Medications for Adrenal Disorders

Adrenal disorders such as Addison’s disease and Cushing’s syndrome require specific medications for treatment. Here are some commonly used drugs and their indications:

Hydrocortisone and Fludrocortisone: These are the mainstays of treatment for Addison’s disease, as they replace the deficient glucocorticosteroids and mineralocorticoids.

Phenoxybenzamine: This medication is used to treat phaeochromocytoma before surgery.

Metyrapone: It can be used to diagnose or treat Cushing’s syndrome by reducing the amount of aldosterone and cortisol in the body.

Prednisolone and Levothyroxine: Prednisolone can be used instead of hydrocortisone in Addison’s disease to avoid peaks and troughs. However, levothyroxine is not used to treat Addison’s disease, but it’s important to check for concurrent thyroid disease.

Spironolactone: It’s used to treat Conn’s disease, which causes hyperaldosteronism. It’s not appropriate for Addison’s disease treatment, as both can cause hyperkalaemia.

Thyroid storm is a medical emergency that can occur in patients with hyperthyroidism, such as those with Graves’ disease. It is characterized by symptoms such as high fever, rapid heartbeat, jaundice, and altered mental status. In such cases, IV beta-blockers, such as propranolol, are the first-line treatment to inhibit the peripheral adrenergic effects of excess thyroid hormone. However, propranolol should not be used in patients with asthma or reversible COPD, and caution should be exercised in patients with heart failure. Lugol’s solution can also be used to inhibit the release of stored thyroid hormone, but it is usually delayed until after antithyroid therapy has been initiated. Therapeutic plasma exchange may be considered for patients who do not respond to medical therapy. In this case, the patient’s jaundice is likely due to her hyperthyroid crisis, and there is no evidence of biliary disease or cholecystitis. Therefore, IV co-amoxiclav, which is the first-line antibiotic for community-acquired pneumonia, would be appropriate for this patient. If propranolol is contraindicated, a cardiac-specific beta-blocker or calcium-channel blocker may be used instead. However, in this patient, IV propranolol should be used as the first-line treatment.

Understanding Thyroid Storm

Thyroid storm is a rare but serious complication of thyrotoxicosis, which is characterized by an overactive thyroid gland. It is usually seen in patients who already have thyrotoxicosis and is not typically the first symptom. It is important to note that an excess of thyroxine caused by medication does not usually lead to thyroid storm.

There are several events that can trigger thyroid storm, including surgery, trauma, infection, and exposure to iodine, such as through CT contrast media. The clinical features of thyroid storm include fever, tachycardia, confusion, nausea, vomiting, hypertension, heart failure, and abnormal liver function tests.

The management of thyroid storm involves treating the underlying cause and providing symptomatic relief. This may include medications such as beta-blockers, anti-thyroid drugs, Lugol’s iodine, and dexamethasone. Paracetamol may also be used to manage fever.

In summary, thyroid storm is a serious complication of thyrotoxicosis that requires prompt medical attention. Understanding the triggers and clinical features of thyroid storm can help with early diagnosis and effective management.

Based on the presence of thyrotoxic symptoms, goitre, and anti-thyroid peroxidase antibodies, the likely diagnosis is

Graves’ Disease: Common Features and Unique Signs

Graves’ disease is the most frequent cause of thyrotoxicosis, which is commonly observed in women aged 30-50 years. The condition presents typical features of thyrotoxicosis, such as weight loss, palpitations, and heat intolerance. However, Graves’ disease also exhibits specific signs that are not present in other causes of thyrotoxicosis. These include eye signs, such as exophthalmos and ophthalmoplegia, as well as pretibial myxoedema and thyroid acropachy. The latter is a triad of digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.

Autoantibodies are also present in Graves’ disease, including TSH receptor stimulating antibodies in 90% of patients and anti-thyroid peroxidase antibodies in 75% of patients. Thyroid scintigraphy can also aid in the diagnosis of Graves’ disease, as it shows diffuse, homogenous, and increased uptake of radioactive iodine.

Overall, Graves’ disease presents with both typical and unique features that distinguish it from other causes of thyrotoxicosis. Early diagnosis and treatment are crucial to prevent complications and improve outcomes for patients.

Understanding Carbimazole and Its Mechanism of Action

Carbimazole is a medication used to manage thyrotoxicosis, a condition characterized by an overactive thyroid gland. It is typically administered in high doses for six weeks until the patient becomes euthyroid, or has a normal thyroid function. The drug works by blocking thyroid peroxidase, an enzyme responsible for coupling and iodinating the tyrosine residues on thyroglobulin, which ultimately reduces thyroid hormone production.

In contrast to propylthiouracil, another medication used to treat thyrotoxicosis, carbimazole only has a central mechanism of action. Propylthiouracil, on the other hand, also has a peripheral action by inhibiting 5′-deiodinase, an enzyme that reduces peripheral conversion of T4 to T3.

While carbimazole can be effective in managing thyrotoxicosis, it is not without its adverse effects. One of the most serious side effects is agranulocytosis, a condition characterized by a severe reduction in white blood cells. Additionally, carbimazole can cross the placenta, but may be used in low doses during pregnancy.

Overall, carbimazole is a medication that can be effective in managing thyrotoxicosis, but it is important to be aware of its mechanism of action and potential adverse effects. Patients should always consult with their healthcare provider before starting any new medication.

Management of Phaeochromocytoma: Medications and Interventions

Phaeochromocytoma is a neuroendocrine tumor that secretes adrenaline and noradrenaline, leading to sympathetic stimulation and clinical symptoms such as tachycardia, hypertension, anxiety, diaphoresis, and weight loss. Diagnosis is made through the measurement of catecholamines and metanephrines in plasma or urine. Surgery is required, but patients are at high risk due to potential life-threatening tachycardia and hypertension. The following medications and interventions are used in the management of phaeochromocytoma:

Alpha-adrenergic receptor blockers: Phenoxybenzamine or doxazosin are used to dampen sympathetic stimulation by blocking alpha-adrenoceptors.

Beta-adrenergic receptor blockers: Beta-blockers are used after alpha-blockers to avoid unopposed alpha-receptor stimulation, which can cause a hypertensive crisis.

Calcium channel blockers: These are not commonly used in phaeochromocytoma management but may be used as an antihypertensive in certain populations or as an anti-anginal drug.

Intravenous fluids: IV fluids should be readily available for all surgeries to address potential blood loss and hypotension following surgery.

Low-salt diet and low fluid intake: These interventions are not typically used in phaeochromocytoma management but may be used for chronic hypertension or fluid overload.

Treatment of Diabetic Ketoacidosis: Continuing Long-Acting Insulin and Stopping Short-Acting Insulin

When a patient presents with diabetic ketoacidosis (DKA), it is important to provide prompt treatment. This involves fluid replacement with isotonic saline and an intravenous insulin infusion at 0.1 unit/kg per hour. While this takes place, the patient’s normal long-acting insulin should be continued, but their short-acting insulin should be stopped to avoid hypoglycemia.

In addition to insulin and fluid replacement, correction of electrolyte disturbance is essential. Serum potassium levels may be high on admission, but often fall quickly following treatment with insulin, resulting in hypokalemia. Potassium may need to be added to the replacement fluids, guided by the potassium levels. If the rate of potassium infusion is greater than 20 mmol/hour, cardiac monitoring is required.

Overall, the key to successful treatment of DKA is a careful balance of insulin, fluids, and electrolyte replacement. By continuing long-acting insulin and stopping short-acting insulin, healthcare providers can help ensure the best possible outcome for their patients.

The measurement of insulin-like growth factor 1 (IGF-1) is now the preferred method for screening and monitoring suspected cases of acromegaly, replacing the oral glucose tolerance test (OGTT). IGF-1, also known as somatomedin C, is produced by the liver and plays a crucial role in childhood growth and has anabolic effects in adults. OGTT with growth hormone assay is no longer the first-line investigation for acromegaly diagnosis, but can be used as a second-line test to confirm the diagnosis if IGF-1 levels are elevated. The insulin tolerance test is used to assess pituitary and adrenal function, as well as insulin sensitivity, and is not useful for diagnosing acromegaly. Random growth hormone assay is also not helpful in diagnosing acromegaly due to the pulsatile nature of GH secretion. Elevated serum prolactin levels may also be present in up to 20% of GH-secreting pituitary adenomas, but this is not diagnostic.

For a patient presenting with elevated fasting plasma glucose (6.8 mmol/L), indicating possible gestational diabetes, the recommended initial management is a trial of diet and exercise to control blood glucose without medication. The patient should be advised to consume a high-fibre diet with minimal refined sugars and monitor their blood glucose regularly. If the patient’s blood glucose remains elevated despite lifestyle interventions, insulin should be started if the initial fasting plasma glucose is 7 mmol/L or more. If there is no improvement within 1-2 weeks, metformin may be added, and if still inadequate, insulin may be required. It is important to note that pregnant women should not aim to lose weight and should maintain a balanced diet. Advising the patient to only monitor blood glucose without any interventions is inappropriate as lifestyle changes are necessary to manage gestational diabetes.

Gestational diabetes is a common medical disorder affecting around 4% of pregnancies. Risk factors include a high BMI, previous gestational diabetes, and family history of diabetes. Screening is done through an oral glucose tolerance test, and diagnostic thresholds have recently been updated. Management includes self-monitoring of blood glucose, diet and exercise advice, and medication if necessary. For pre-existing diabetes, weight loss and insulin are recommended, and tight glycemic control is important. Targets for self-monitoring include fasting glucose of 5.3 mmol/l and 1-2 hour post-meal glucose levels.

An HbA1c level ranging from 42-47 mmol/mol suggests the presence of prediabetes. Individuals with this condition should be motivated to enhance their physical activity, shed excess weight, and adopt a healthier diet by consuming more dietary fiber and reducing fat intake. Metformin may be an option for those with prediabetes, but the initial dose should be 500mg once daily. Regular HbA1c monitoring is necessary for individuals diagnosed with prediabetes as they are at a heightened risk of developing diabetes.

Type 2 diabetes mellitus can be diagnosed through a plasma glucose or HbA1c sample. The diagnostic criteria vary depending on whether the patient is experiencing symptoms or not. If the patient is symptomatic, a fasting glucose level of 7.0 mmol/l or higher or a random glucose level of 11.1 mmol/l or higher (or after a 75g oral glucose tolerance test) indicates diabetes. If the patient is asymptomatic, the same criteria apply but must be demonstrated on two separate occasions.

In 2011, the World Health Organization released supplementary guidance on the use of HbA1c for diagnosing diabetes. A HbA1c level of 48 mmol/mol (6.5%) or higher is diagnostic of diabetes mellitus. However, a HbA1c value of less than 48 mmol/mol (6.5%) does not exclude diabetes and may not be as sensitive as fasting samples for detecting diabetes. For patients without symptoms, the test must be repeated to confirm the diagnosis. It is important to note that increased red cell turnover can cause misleading HbA1c results.

There are certain conditions where HbA1c cannot be used for diagnosis, such as haemoglobinopathies, haemolytic anaemia, untreated iron deficiency anaemia, suspected gestational diabetes, children, HIV, chronic kidney disease, and people taking medication that may cause hyperglycaemia (such as corticosteroids).

Impaired fasting glucose (IFG) is defined as a fasting glucose level of 6.1 mmol/l or higher but less than 7.0 mmol/l. Impaired glucose tolerance (IGT) is defined as a fasting plasma glucose level less than 7.0 mmol/l and an OGTT 2-hour value of 7.8 mmol/l or higher but less than 11.1 mmol/l. People with IFG should be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person does not have diabetes but does have IGT.