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Experimental evidence suggests that the relationship between chronic pancreatitis and hyperparathyroidism results from the stimulation of the parathyroid glands by hypersecretion of glucagon. This hypothesis is supported by the observation of elevated circulating levels of glucagon in chronic pancreatitis and in hyperparathyroidism. Conspicuous islet and alpha cell hyperplasia is correlated with marked increases in circulating and pancreatic tissue glucagon. A significant incidence of islet hyperplasia was found in a retrospective review of autopsy material from a series of 15 cases of parathyroid adenoma or carcinoma.
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Edward Paloyan (1967) studied this question.
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