Mechanisms of hypocalcemia in acute hemorrhagic pancreatitis.
Thyrocalcitonin release mediated by glucagon secreted from the acutely inflamed pancreas has been postulated as a possible mechanism for hypocalcemia in acute pancreatitis. To test this hypothesis, hemorrhagic pancreatitis was induced in a group of thyroidectomized pigs. No source of thyrocalcitonin other than the thyroid has been described in the pig. Their subsequent serum calcium concentrations were compared with those in a group of thyroid intact pigs also given hemorrhagic pancreatitis. The results indicate that the hypocalcemia observed during the first 24 hours following induction of pancreatitis is not related to the presence of an intact thyroid. Differences observed in the degree of hypocalcemia between the two groups 30 to 48 hours after pancreatitis developed may be of significance but could be explained by dilutional differences alone. Thyrocalcitonin apparently has little if any role in the hypocalcemia observed during the course of acute pancreatitis.
D000208:Acute Disease; D000818:Animals; D002116:Calcitonin / Q000378:metabolism; D004195:Disease Models, Animal; D006470:Hemorrhage / Q000150:complications* / Q000378:metabolism; D006996:Hypocalcemia / Q000209:etiology* / Q000378:metabolism; D010195:Pancreatitis / Q000150:complications* / Q000378:metabolism; D013552:Swine
D002116:Calcitonin