In hospital practice, hypocalcaemia is most commonly seen in subjects with dietary vitamin D deficiency or as a transient event after total thyroidectomy. Hypoparathyroidism is most commonly due to surgical removal but may also be caused by autoimmunity, infiltration by amyloid or heavy metals eg iron in haemochromatosis or thalassaemia, or copper in Wilson's disease.
Hypocalcaemia can occur in acute pancreatitis, largely as a result of the release of pancreatic lipase into retroperitoneal space and peritoneal cavity, where it saponifies, releasing free fatty acids which bind calcium. Hypocalaemia in pancreatitis is associated with a poor prognosis. The fall in calcium is usually gradual and investigation for the cause should be delayed until the pancreatitis has settled. This is to ensure that any changes in PTH are not secondary to the plasma calcium. Treatment for hypocalcaemia is probably only necessary if symptoms eg cramps or parasthesiae occur. The mechanisms for hypocalcaemia in endotoxic shock are currently unknown.
Hyperventilation causes an acute respiratory alkalosis and this affects calcium binding to circulating proteins. The result is tetany with normal total but reduced ionised calcium since the calcium has no competition for protein binding sites and is functionally removed. The hyperventilation may be due to hysteria, head injury etc.
Abnormally low plasma concentrations of magnesium, phosphate and potassium are frequently (20-30%) detected in association with hypocalcaemia and these abnormalities should be corrected; as they may be the primary cause or, at least, an exacerbating factor of the hypocalcaemia due to their effects on renal tubular function and, in the case of magnesium, on the inhibition of PTH synthesis and secretion.
- Bushinsky DA, Monk RD. Calcium. Lancet 1998;352:306-311.