Gliclazide is not the preferred initial treatment for type 2 diabetes. Due to the patient’s inability to tolerate metformin and a QRISK score of >10, there is now a higher likelihood of cardiovascular disease.

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.

The primary treatment for hypercalcaemia is IV fluid therapy.

Managing Hypercalcaemia

Hypercalcaemia is a condition where there is an excess of calcium in the blood. The initial management of hypercalcaemia involves rehydration with normal saline, typically 3-4 litres per day. This helps to flush out the excess calcium from the body. Once rehydration is achieved, bisphosphonates may be used to further lower the calcium levels. These drugs take 2-3 days to work, with maximal effect being seen at 7 days.

Calcitonin is another option for managing hypercalcaemia. It works quicker than bisphosphonates but is less commonly used due to its short duration of action. Steroids may be used in sarcoidosis, a condition that can cause hypercalcaemia.

Loop diuretics such as furosemide may also be used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.

In summary, the management of hypercalcaemia involves rehydration with normal saline followed by the use of bisphosphonates or other medications depending on the underlying cause of the condition. It is important to monitor electrolyte levels and adjust treatment accordingly to prevent complications.

Diagnosing Cranial Diabetes Insipidus: A Pituitary Tumour as the Likely Cause

Cranial diabetes insipidus (DI) is a condition where the kidneys are unable to reabsorb free water, resulting in excessive water loss. The most likely cause of this condition is reduced antidiuretic hormone (ADH) secretion, which can be caused by a pituitary tumour. In this case, the patient’s low urine osmolality and reduced response to the water deprivation test confirm the presence of cranial DI.

Chronic renal disease and lithium therapy can also cause nephrogenic DI, but the patient’s response to desmopressin im excludes these as potential causes. Diabetes mellitus may cause polydipsia and polyuria, but it also presents with glycosuria and hyperglycaemia. Primary polydipsia, characterized by a compulsive desire to drink, can cause low urine osmolality, but the patient’s ability to concentrate urine to some extent excludes this as a likely cause.

In conclusion, a pituitary tumour is the most likely cause of the patient’s cranial DI, as confirmed by the water deprivation test and response to desmopressin im.

The patient is suffering from Cushing’s syndrome, which is characterized by an excess of cortisol. This can be caused by exogenous glucocorticoid therapy, autonomous overproduction by the adrenal glands, or increased production of adrenocorticotrophic hormone. High levels of cortisol can mimic the effects of aldosterone, leading to increased sodium and water retention and increased potassium excretion, resulting in hypokalemia. The increased resorption of bicarbonate in the tubules due to potassium depletion causes metabolic alkalosis. Hyperkalemic metabolic acidosis is not expected because cortisol’s effect on the mineralocorticoid receptor causes a loss of potassium. Hyperkalemic respiratory alkalosis is also not expected because cortisol’s effect on the mineralocorticoid receptor leads to potassium excretion. Additionally, any acid-base disturbance in Cushing’s syndrome is likely to be metabolically mediated rather than respiratory. Hypokalemic metabolic acidosis is not expected because the concomitant loss of potassium and reabsorption of bicarbonate causes metabolic alkalosis.

Investigations for Cushing’s Syndrome

Cushing’s syndrome is a condition caused by excessive cortisol production in the body. There are various causes of Cushing’s syndrome, including iatrogenic, ACTH-dependent, and ACTH-independent causes. To diagnose Cushing’s syndrome, doctors typically perform tests to confirm the condition and determine its underlying cause.

General lab findings consistent with Cushing’s syndrome include hypokalaemic metabolic alkalosis and impaired glucose tolerance. Ectopic ACTH secretion, which is often associated with small cell lung cancer, is characterized by very low potassium levels.

The two most commonly used tests to confirm Cushing’s syndrome are the overnight dexamethasone suppression test and the 24-hour urinary free cortisol test. The overnight dexamethasone suppression test is the most sensitive test and is used first-line to test for Cushing’s syndrome. Patients with Cushing’s syndrome do not have their morning cortisol spike suppressed. The 24-hour urinary free cortisol test measures the amount of cortisol in the urine over a 24-hour period.

To localize the cause of Cushing’s syndrome, doctors may perform additional tests such as high-dose dexamethasone suppression test, CRH stimulation, and petrosal sinus sampling of ACTH. An insulin stress test may also be used to differentiate between true Cushing’s and pseudo-Cushing’s. Overall, a combination of these tests can help diagnose Cushing’s syndrome and determine its underlying cause.

Subacute (De Quervain’s) thyroiditis is the likely diagnosis for this woman who presents with hyperthyroidism and a tender goitre following an upper respiratory tract infection. This condition is characterized by high ESR and painful thyroid gland. Graves’ disease, Hashimoto’s thyroiditis, and thyroid cancer are less likely causes as they do not present with these specific symptoms.

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.

In the case of a patient with Addison’s disease who develops an additional illness, it is recommended to increase the dose of glucocorticoids while maintaining the same dose of fludrocortisone.

Addison’s disease is a condition that requires patients to undergo both glucocorticoid and mineralocorticoid replacement therapy. This treatment usually involves taking a combination of hydrocortisone and fludrocortisone. Hydrocortisone is typically given in 2 or 3 divided doses, with patients requiring 20-30 mg per day, mostly in the first half of the day. Patient education is crucial, and it is essential to emphasize the importance of not missing glucocorticoid doses. Additionally, patients should consider wearing MedicAlert bracelets and steroid cards, and they should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis.

During an intercurrent illness, it is crucial to manage the glucocorticoid dose properly. In simple terms, the glucocorticoid dose should be doubled, while the fludrocortisone dose should remain the same. The Addison’s Clinical Advisory Panel has produced guidelines that detail specific scenarios, and patients should refer to these guidelines for more information. It is essential to discuss how to adjust the glucocorticoid dose during an intercurrent illness with a healthcare professional. Proper management of Addison’s disease is crucial to ensure that patients can lead healthy and fulfilling lives.

Medical Conditions and Differential Diagnosis

Addisonian Crisis: A condition caused by adrenal insufficiency, often due to autoimmune disease, TB, metastases, or adrenal haemorrhage. Symptoms include vague complaints such as depression, anorexia, and GI upset, as well as tanned skin and pigmented palmar creases. Diagnosis is confirmed through a short ACTH stimulation test. Emergency treatment involves IV hydrocortisone and fluids, while long-term treatment involves oral cortisol and mineralocorticoid.

Other Differential Diagnoses: Meningococcal septicaemia, insulin overdose, paracetamol overdose, and salicylate overdose. However, the clinical features described in the scenario are not suggestive of these conditions.

The patient’s symptoms of hypertension, hypokalaemia, and hypernatraemia suggest a diagnosis of hyperaldosteronism, which is characterized by increased water and sodium reabsorption in the kidneys and potassium loss due to high aldosterone levels. While muscle weakness and lethargy are common symptoms, they are only present in 40% of cases. Metabolic alkalosis is another common finding. Primary hyperaldosteronism is often caused by bilateral idiopathic adrenal hyperplasia, rather than an adrenal adenoma. To diagnose hyperaldosteronism, a plasma aldosterone/renin ratio is recommended as the first-line investigation, followed by a high-resolution CT scan of the abdomen and adrenal vein sampling to differentiate between unilateral and bilateral sources of aldosterone excess. While an overnight dexamethasone suppression test is useful for diagnosing Cushing syndrome, it is not relevant in this case. Urine dipstick and formal urinalysis would be helpful in identifying renal causes of secondary hypertension, but are not necessary in this case.

The patient is suffering from primary hyperaldosteronism, which is caused by bilateral adrenal gland hyperplasia. This condition leads to elevated aldosterone levels, resulting in increased sodium retention and negative feedback to renin release. The most common cause of primary hyperaldosteronism is bilateral adrenal hyperplasia, which can be treated with spironolactone, an aldosterone receptor antagonist, for four weeks. Adrenalectomy is only recommended for unilateral adrenal adenoma, which is not the case for this patient. Fludrocortisone and hydrocortisone are not appropriate treatments for hyperaldosteronism as they act on mineralocorticoid receptors, exacerbating the condition. Reassurance and discharge are not recommended as untreated primary hyperaldosteronism can lead to chronic elevation of blood pressure, increasing the risk of cardiovascular disease, stroke, and kidney damage.

Understanding Primary Hyperaldosteronism

Primary hyperaldosteronism is a medical condition that was previously believed to be caused by an adrenal adenoma, also known as Conn’s syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases. It is important to differentiate between the two as this determines the appropriate treatment. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism.

The common features of primary hyperaldosteronism include hypertension, hypokalaemia, and alkalosis. Hypokalaemia can cause muscle weakness, but this is seen in only 10-40% of patients. To diagnose primary hyperaldosteronism, the 2016 Endocrine Society recommends a plasma aldosterone/renin ratio as the first-line investigation. This should show high aldosterone levels alongside low renin levels due to negative feedback from sodium retention caused by aldosterone.

If the plasma aldosterone/renin ratio is high, a high-resolution CT abdomen and adrenal vein sampling are used to differentiate between unilateral and bilateral sources of aldosterone excess. If the CT is normal, adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia. The management of primary hyperaldosteronism depends on the underlying cause. Adrenal adenoma is treated with surgery, while bilateral adrenocortical hyperplasia is treated with an aldosterone antagonist such as spironolactone.

In summary, primary hyperaldosteronism is a medical condition that can be caused by adrenal adenoma, bilateral idiopathic adrenal hyperplasia, or adrenal carcinoma. It is characterized by hypertension, hypokalaemia, and alkalosis. Diagnosis involves a plasma aldosterone/renin ratio, high-resolution CT abdomen, and adrenal vein sampling. Treatment depends on the underlying cause and may involve surgery or medication.

Medical Conditions Associated with 21-Hydroxylase Deficiency

21-hydroxylase deficiency is a medical condition that results in decreased cortisol synthesis and commonly reduces aldosterone synthesis. This condition can lead to adrenal insufficiency, causing salt wasting and hypoglycemia. However, it is not associated with diabetes insipidus, which is characterized by low ADH levels. Patients with 21-hydroxylase deficiency may also experience stunted growth and elevated androgens, but hypogonadism is not a feature. Treatment may involve the use of gonadotrophin-releasing hormone (GnRH).

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.

In addition to metformin, an SGLT-2 inhibitor (such as empagliflozin) should be prescribed for this patient who has a history of cardiovascular disease.

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.

The guidelines of NICE have been revised, stating that women who are at risk of gestational diabetes should undergo an oral glucose tolerance test immediately after booking, instead of waiting until 16-18 weeks as previously recommended.

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.

Thyroid Cancer Types and their Association with Multiple Endocrine Neoplasia Type 2 (MEN2)

Thyroid cancer can be classified into different types based on their histology and clinical features. Among these types, medullary thyroid cancer is associated with multiple endocrine neoplasia type 2 (MEN2), a genetic disorder that predisposes individuals to develop tumors in various endocrine glands. MEN2 has three subtypes, and medullary thyroid cancer is a hallmark feature of MEN2a and MEN2b. Other associated neoplasms include phaeochromocytoma and parathyroid tumors in MEN2a, and marfanoid habitus/mucosal neuromas in MEN2b.

Anaplastic thyroid cancer, on the other hand, is not associated with MEN2 and has a poor prognosis. It is more common in older women and is characterized by rapid growth and aggressiveness. Follicular thyroid cancer is also not associated with MEN2 and is more prevalent in women over 50 years old. Lymphoma and papillary thyroid cancer are also not associated with MEN2, with the latter having an excellent prognosis and primarily affecting young women.

Fluid retention may be caused by pioglitazone.

Thiazolidinediones: A Class of Diabetes Medications

Thiazolidinediones are a type of medication used to treat type 2 diabetes. They work by activating the PPAR-gamma receptor, which reduces insulin resistance in the body. However, one medication in this class, rosiglitazone, was withdrawn in 2010 due to concerns about its cardiovascular side effects.

The PPAR-gamma receptor is a nuclear receptor found inside cells. It is naturally activated by free fatty acids and is involved in regulating the differentiation and function of adipocytes (fat cells).

While thiazolidinediones can be effective in treating diabetes, they can also have adverse effects. Patients may experience weight gain, liver impairment (which requires monitoring of liver function tests), and fluid retention. Thiazolidinediones are contraindicated in patients with heart failure due to the increased risk of fluid retention, especially if the patient is also taking insulin. Recent studies have also shown an increased risk of fractures and bladder cancer in patients taking pioglitazone, another medication in this class.

Abdominal pain can be an initial symptom of DKA, which stands for diabetic ketoacidosis. In this particular case, a young man is showing signs of DKA, such as dehydration, Kussmaul respiration, and a significantly elevated capillary glucose level. DKA patients lose around 5-8 liters of fluids, which require immediate correction. The diagnostic criteria for DKA include a pH level of less than 7.3 and/or bicarbonate level of less than 15mmol/L, blood glucose level of over 11mmol/L or known diabetes mellitus, and ketonaemia level of over 3mmol/L or significant ketonuria ++ on urine dipstick. Alcoholic ketoacidosis is not the correct diagnosis as it usually presents with low or normal glucose levels and occurs due to starvation. Hyperosmolar hyperglycaemic state is also incorrect as it typically presents with marked hyperglycemia without ketoacidosis. Opioid overdose is not the correct diagnosis either as it usually presents with respiratory depression, pinpoint pupils, and a lowered GCS, while this patient has a raised respiratory rate and abnormal respirations consistent with Kussmaul respirations.

Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes mellitus, accounting for around 6% of cases. It can also occur in rare cases of extreme stress in patients with type 2 diabetes mellitus. However, mortality rates have decreased from 8% to under 1% in the past 20 years. DKA is caused by uncontrolled lipolysis, resulting in an excess of free fatty acids that are ultimately converted to ketone bodies. The most common precipitating factors of DKA are infection, missed insulin doses, and myocardial infarction. Symptoms include abdominal pain, polyuria, polydipsia, dehydration, Kussmaul respiration, and acetone-smelling breath. Diagnostic criteria include glucose levels above 13.8 mmol/l, pH below 7.30, serum bicarbonate below 18 mmol/l, anion gap above 10, and ketonaemia.

Management of DKA involves fluid replacement, insulin, and correction of electrolyte disturbance. Most patients with DKA are depleted around 5-8 litres, and isotonic saline is used initially, even if the patient is severely acidotic. Insulin is administered through an intravenous infusion, and correction of electrolyte disturbance is necessary. Long-acting insulin should be continued, while short-acting insulin should be stopped. DKA resolution is defined as pH above 7.3, blood ketones below 0.6 mmol/L, and bicarbonate above 15.0mmol/L. Complications may occur from DKA itself or the treatment, such as gastric stasis, thromboembolism, arrhythmias, acute respiratory distress syndrome, acute kidney injury, and cerebral oedema. Children and young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations.

Associations of Acromegaly with Various Medical Conditions

Acromegaly is a medical condition caused by hypersecretion of growth hormone, which can lead to various health problems. One of the associated conditions is diabetes mellitus, as acromegaly is often linked with insulin resistance. Another condition is acanthosis nigricans, which involves hyperpigmentation of the skin. However, there is no general pigmentation associated with acromegaly. Cardiovascular disease is also a common association, which can increase the risk of atrial fibrillation. Left ventricular hypertrophy is another condition that can occur with acromegaly. Finally, ulnar nerve entrapment is not directly associated with acromegaly, but carpal tunnel syndrome affecting the median nerve is a common association.

The patient is experiencing Cushing’s disease, which is caused by excessive secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, often due to a pituitary adenoma. Addison’s disease and acromegaly can be ruled out based on the patient’s symptoms. It is important to differentiate between Cushing’s triad, which includes irregular breathing, bradycardia, and systolic hypertension caused by increased intracranial pressure, and Cushing’s syndrome, a collection of symptoms resulting from prolonged exposure to cortisol. Cushing’s disease is a specific type of Cushing’s syndrome characterized by increased ACTH production due to a pituitary adenoma or excess production of hypothalamus CRH.

Understanding the Causes of Cushing’s Syndrome

Cushing’s syndrome is a condition that occurs when the body is exposed to high levels of cortisol for an extended period. While exogenous causes of Cushing’s syndrome, such as glucocorticoid therapy, are more common, endogenous causes can also occur. The causes of Cushing’s syndrome can be divided into two categories: ACTH dependent and ACTH independent.

ACTH dependent causes of Cushing’s syndrome include Cushing’s disease, which is caused by a pituitary tumor secreting ACTH and producing adrenal hyperplasia. Ectopic ACTH production, which is caused by small cell lung cancer, is another ACTH dependent cause. On the other hand, ACTH independent causes of Cushing’s syndrome include iatrogenic causes such as steroid use, adrenal adenoma, adrenal carcinoma, Carney complex, and micronodular adrenal dysplasia.

In addition to these causes, there is also a condition called Pseudo-Cushing’s, which mimics Cushing’s syndrome. This condition is often caused by alcohol excess or severe depression and can cause false positive dexamethasone suppression tests or 24-hour urinary free cortisol tests. To differentiate between Cushing’s syndrome and Pseudo-Cushing’s, an insulin stress test may be used. Understanding the causes of Cushing’s syndrome is crucial in diagnosing and treating this condition.

If blood glucose targets are not achieved through diet and metformin in gestational diabetes, insulin should be added. Pregnant women with GDM should aim to keep their CBGs below specific levels, including fasting at 5.3mmol/L and 1 hour postprandial at 7.8 mmol/L or 2 hours postprandial at 6.4 mmol/L. If these targets are not met, insulin should be offered as an additional therapy. Gliclazide is not recommended, and the use of any sulphonylurea in GDM is an off-license indication. Gliptins are not recommended due to insufficient evidence of their safety in pregnancy. It is not appropriate to continue the same management or de-escalate treatment by stopping metformin if CBG readings are above target levels. Failure to achieve glycaemic control can result in serious risks to both mother and fetus, including pre-eclampsia, pre-term labour, stillbirth, and neonatal hypoglycaemia, even if fetal growth appears normal.

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.

Parathyroid hormone levels serve as a valuable tool in identifying the underlying causes of hypercalcaemia, with malignancy and primary hyperparathyroidism being the most prevalent culprits. If the parathyroid hormone levels are normal or elevated, it indicates the presence of primary hyperparathyroidism.

Understanding the Causes of Hypercalcaemia

Hypercalcaemia is a medical condition characterized by high levels of calcium in the blood. In most cases, two conditions account for 90% of hypercalcaemia cases. The first is primary hyperparathyroidism, which is the most common cause in non-hospitalized patients. The second is malignancy, which is the most common cause in hospitalized patients. Malignancy-related hypercalcaemia may be due to various processes, including PTHrP from the tumor, bone metastases, and myeloma. For this reason, measuring parathyroid hormone levels is crucial when investigating patients with hypercalcaemia.

Other causes of hypercalcaemia include sarcoidosis, tuberculosis, histoplasmosis, vitamin D intoxication, acromegaly, thyrotoxicosis, milk-alkali syndrome, drugs such as thiazides and calcium-containing antacids, dehydration, Addison’s disease, and Paget’s disease of the bone. It is important to note that hypercalcaemia may occur with prolonged immobilization in patients with Paget’s disease of the bone, although this condition is usually normal.

In summary, hypercalcaemia can be caused by various medical conditions, with primary hyperparathyroidism and malignancy being the most common. Measuring parathyroid hormone levels is essential in investigating patients with hypercalcaemia. Other causes of hypercalcaemia include sarcoidosis, tuberculosis, histoplasmosis, vitamin D intoxication, acromegaly, thyrotoxicosis, milk-alkali syndrome, drugs, dehydration, Addison’s disease, and Paget’s disease of the bone.