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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood concentration of pituitary hormones (corticotropin, somatotropin, thyrotropin and prolactin) was studied in 145 male patients with aggravation of chronic pancreatitis and in 15 healthy male subjects. The pre-treatment concentration of corticotropin, somatotropin and thyrotropin was markedly increased and the level of prolactin had a tendency to decrease. By the end of treatment the level of thyrotropin and prolactin was fully normalized, the content of corticotropin had a tendency to decrease and the concentration of somatotropin somewhat decreased but did not reach the normal values. Changes in the blood level of pituitary hormones were more pronounced in the severe course of the disease and also when the level of pancreatic enzymes and hormones in the blood was high.
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PMID:[Functional status of the hypophysis in patients with chronic pancreatitis]. 274 65

The present investigation defined the pattern of pancreatic, pituitary and adrenal responses after insulin-induced hypoglycemia in chronic calcific pancreatitis (CCP) related to alcohol abuse, and assessed the role of some of these hormones in the counterregulation of blood glucose. We studied 6 Black men with recently diagnosed CCP, all showing radiological evidence of pancreatic calcification and normal glucose tolerance, as well as 7 matched nonobese male controls. After a standard iv insulin tolerance test inducing marked hypoglycemia, patients with CCP showed significantly impaired mean plasma pancreatic glucagon and pancreatic polypeptide responses compared to the controls. Mean basal plasma somatostatin levels tended to be higher in chronic pancreatitis and remained so throughout the test without altering consistently; in the controls somatostatin peaked significantly at 30 min. Concerning extrapancreatic hormonal changes, plasma growth hormone, prolactin and total catecholamines responded normally in CCP, but plasma cortisol rose to significantly higher levels than controls at 60 and 120 min after the injection of insulin. This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. We conclude that patients with CCP show impaired pancreatic hormone release after insulin hypoglycemia with the exception of somatostatin; there is also an excessive rise in plasma cortisol, possibly related to the long standing abuse of alcohol in the past.
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PMID:Hormonal profile after insulin-induced hypoglycemia in chronic calcific pancreatitis. Pancreatic, pituitary and adrenal responses. 639 52