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Primary hyperparathyroidism and malignancy account for around 90% of all cases of hypercalcemia in primary care. https://www.medscape.com/viewarticle/... -- TRANSCRIPT -- In this podcast, I’m going to talk about the interpretation and management of hypercalcemia, or high calcium levels, in primary care. So, let’s start with some grassroots, simple calcium physiology. Most of the calcium in our bodies is stored in bone. Calcium has a key role in skeletal mineralization. However, in addition to this role, calcium is involved in many pathways throughout the body, including enzyme pathways, muscle contraction, blood clotting, and maintaining a regular heart rhythm. Hence the wide range of symptoms and signs associated with abnormal calcium levels, which I’ll cover shortly. Normal calcium range is around 2.15 to 2.60 mmol/L, but reference ranges and units will vary globally. We also often get a corrected calcium level reported to us in primary care. What’s the relevance of this? In the blood, around 40% of calcium is bound to proteins such as albumin. Abnormal albumin levels can make total calcium levels appear too high or low. Corrected calcium levels are a better indicator of the amount of calcium that is free in the blood for its physiologic functions. So, corrected calcium levels are recommended in particular for people with hypoalbuminemia, or low albumin levels. Next, parathyroid hormone, or PTH, is the main regulator of calcium homeostasis and is secreted by the parathyroid glands in response to low calcium levels. PTH increases calcium reabsorption in the kidneys and stimulates conversion of vitamin D, which in turn promotes calcium uptake in the bowel. PTH also stimulates osteoclast activity to release calcium from bone. The overall effect of this is to increase blood calcium levels. Finally, calcitonin is released by the thyroid C cells in response to increased calcium levels. Calcitonin stimulates osteoclasts to deposit calcium in the bone and inhibits the renal reabsorption of calcium, therefore increasing urinary calcium excretion. Calcitonin also reduces calcium uptake in the bowel. And the overall effect of this is to reduce blood calcium levels. Calcitonin levels are not something we routinely check in primary care. Calcitonin levels are primarily checked to diagnose and monitor medullary thyroid cancer, particularly in those individuals with MEN, multiple endocrine neoplasia type 2, where screening is recommended. Now let’s talk about hypercalcemia, or high calcium levels, which is a common finding in primary care. Calcium levels less than 3 mmol/L are usually asymptomatic and do not require urgent intervention by us in primary care. Levels above 3 mmol/L typically do cause symptoms but may be well tolerated if levels have risen slowly over time. However, we should consider hospital admission if calcium levels rise above 3.5 mmol/L or in the presence of severe symptoms due to the high risk for cardiac arrhythmias. Furthermore, at these levels of calcium, there is often an underlying malignancy driving the hypercalcemia. So, what are the symptoms of hypercalcemia? I still remember the adage from medical school: bones, stones, moans, and abdominal groans, which summarizes the classic signs and symptoms of hypercalcemia. First, bones: Hypercalcemia can cause vague muscle, bone, and joint pains or, rarely, fractures associated with underlying bone disorders. Next, stones: Hypercalcemia can cause kidney stones, polyuria, and polydipsia. Next, moans: Hypercalcemia can cause fatigue, low mood, muscle weakness, confusion, ataxia, and coma in severe cases. And finally, abdominal groans: Hypercalcemia can cause constipation, dyspepsia, nausea and vomiting, and pancreatitis. Transcript in its entirety can be found by clicking here: https://www.medscape.com/viewarticle/...