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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcitonin was measured in four patients with acute pancreatitis with hypocalcemia. A marked elevation of this hormone was noted in each case and persisted over several days. The peak level of calcitonin preceded the maximum fall in calcium. Among the various factors affecting calcium balance in pancreatitis, calcitonin probably plays an important role.
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PMID:Hypercalcitoninemia in acute pancreatitis. 112 85

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.
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PMID:The hypocalcemia of acute pancreatitis. 114 52

Serum calcium changes in severe pancreatitis were studied in 23 dogs. Twelve dogs underwent duodenotomy and served as controls. Pancreatitis was induced in the other 11 by autologous bile injection (1 ml/kg) into the pancreatic duct. Serum amylase, total calcium, ionized calcium, albumin, magnesium, chloride, phosphorous, parathyroid hormone (PTH), and calcitonin were measured at 0, 1/2, 1, 3, 6, 24, 48, and 72 hours after duodenotomy or bile injection. Serum amylase levels became significantly elevated in all dogs with pancreatitis at 30 minutes (p less than 0.01) and remained so throughout the entire experiment. Total calcium levels dropped significantly 30 minutes after pancreatitis was induced from 10.0 +/- 0.3 mg/dl compared with 8.8 +/- 0.4 mg/dl in control dogs (p less than 0.05) and remained statistically lower for as long as 1 hour. Ionized calcium levels were significantly lower than were those of control dogs at 1/2, 1, 3, and 6 hours (p less than 0.05). Serum magnesium and chloride levels showed no significant changes between both groups. The only significant difference in phosphorus values was at 6 hours when they were higher in dogs with pancreatitis than in controls (6.2 +/- 0.3 mg/dl versus 4.8 +/- 0.4 mg/dl; p less than 0.05). Serum albumin levels remained unchanged throughout the study except for 48 hours when they were significantly lower in animals with pancreatitis (p less than 0.02). PTH levels were significantly greater in dogs with pancreatitis than in controls at 1, 3, 6, and 24 hours (p less than 0.05). There was no significant difference in calcitonin levels between both groups. Ionized calcium is a more reliable indicator of calcium fluxes in acute experimental pancreatitis since it remains depressed longer than total serum calcium. The time course of PTH elevation indicates a reaction to hypocalcemia, and failure of PTH secretion is not the cause of hypocalcemia in pancreatitis. This study does not support elevation of calcitonin as a cause of hypocalcemia in acute pancreatitis.
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PMID:Serum calcium metabolism in acute experimental pancreatitis. 241 69

The comparative analysis of the influence on the glucose metabolism of rats in acute pancreatitis of synthetic analogues was made: somatostatin, calcitonin, leu-enkefalin-dalargin. It was shown that dalargin has the maximum normalizing effect as a result of its antistress qualities. Physiological reaction of beta-cells is preserved in infusion of somatostatin. However, infusion of calcitonin results in the distortion of counterregulatory action of insulin and glucagon.
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PMID:[The effect of regulator peptides on pancreatic endocrine function in experimental acute pancreatitis]. 257 73

The influence of regulatory peptides (somatostatin, calcitonin, and dalargin) on xanthine oxidase activity and lipid peroxidation level in pancreatic tissues as well as on the release of pancreatic enzymes (alpha-amylase, trypsin, lipase, and transamidinase) into blood was studied in 205 rats with experimental acute pancreatitis. Somatostatin and dalargin were shown to have obvious antioxidant effect seen by reduced xanthine oxidase activity and MDA level. All studied peptides stimulate reduced release of pancreatic enzymes. Particularly, reduction of dalargin and somatostatin is caused by inhibition of their synthesis as well as by pancreas protective effect of the peptides. Release of enzymes reduced by calcitonin is probably associated only with inhibition of secretory activity of the pancreas.
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PMID:[Effects of several regulatory peptides on the functional activity of the pancreas in acute experimental pancreatitis]. 259 53

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

In the course of acute pancreatitis an edematous and a hemorrhagic necrotizing pattern have to be discerned. Clinical symptoms are upper abdominal pain, shock, and metabolic derangements. Only subtle diagnostic procedures are appropriate as for instance x-ray of the chest and x-ray of the abdomen. Laboratory exams are of little value. For conservative treatment atropin, glucagon, calcitonin and antibiotics are being used nowadays, where as the efficacy of aprotinin is controversial. In the Department of Surgery of the Freiburg University Medical School an attempt at early surgery is made. In edematous pancreatitis the bursa omentalis is drained; in addition a T-drain has to be entered into the ductus choledochus. Seqmental necrosis of the pancreas may require resection of the left part of the pancreas. Necrotic areas of the head of the pancreas have to be removed by ablation. If there is total necrosis only drainage with an irrigation-suction pattern is possible.
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PMID:[Diagnosis and therapy of acute pancreatitis (author's transl)]. 615 55

Animal experiments demonstrate that the intracerebro-ventricular administration of calcitonin induces analgesia. During the treatment of such diseases as osteitis deformans Paget and acute pancreatitis with calcitonin no spectacular pain-relieving effect was evident, but the application of calcitonin in hypercalcemic patients with bone tumors led to considerable pain relief. Recent double-blind studies document the analgesic effectiveness of calcitonin in malignant diseases, but also against postoperative pains in nontumor patients. Calcitonin as an analgesic drug deserves further investigation.
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PMID:Calcitonin: analgesic effects. 636 72

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.
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PMID:Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction. 701 27

The role of calcitonin (CT) in the regulation of the calcium homeostasis in humans is doubtful, while the therapeutic use in various bone diseases gains increasing interest. Numerous investigations during the last eight years have indicated that CT affects a variety of gastrointestinal organs when CT is administered in pharmacological high doses: CT inhibits gastric acid and pepsin secretion, gastrin release, pancreatic enzyme secretion as well as the hormonally stimulated contraction of the lower esophageal sphincter and of the gallbladder. CT increases intestinal secretion. The therapeutic use of CT in gastric hypersecretory states appears to be inferior and less practicable compared to the histamine-H2-receptor antagonists. The benefit of CT in the clinical course of acute pancreatitis was observed in two controlled double blind studies but CT did not lower the mortality rate. CT does not influence increases in serum-amylase and -lipase occurring after ERCP.
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PMID:Pharmacological actions of calcitonin on the gastrointestinal tract and their therapeutical implications. 702 34


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