Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 inhibitory effect of calcitonin on human pancreatic secretion was evaluated to examine whether the different results reported earlier between humans, cats and dogs can be ascribed to the different sensitivity of these species to calcitonin, as suggested by some investigators. Pancreatic juice was obtained by endoscopic cannulation of the pancreatic duct from 11 patients with relapsing pancreatitis during intravenous infusion of secretin (1 U/kg/h) plus caerulein (0.04 microgram/kg/h). After steady secretion was attained 20 min after the beginning of collection, five 2-min fractions were obtained before, and ten 2-min fractions were obtained after intravenous infusion of calcitonin (1 IU/kg/h). The pre- and post-calcitonin fractions from each patient were compared by Student's t-test. Calcitonin inhibited the secretory volume (26.8 to 65.6%) and bicarbonate secretion (21.4 to 62.0%) in 8 patients, and amylase (48.4 to 89.5%) and lipase secretion (47.4 to 90.5%) in all patients. The present studies reconfirmed that prominent inhibition of enzyme secretion occurs in humans. A new finding was that significant inhibition of the secretory volume and bicarbonate secretion occurs in humans. The inhibitory effects of calcitonin in humans did not appear to differ from those in cats and dogs, when evaluated similarly with the use of pure pancreatic juice.
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PMID:Inhibitory effect of calcitonin on pure human pancreatic secretion. 276 66

Severely acute necrotizing pancreatitis (degrees II and III) requires good teamwork between surgery and intensive care from the very beginning. Treatment was successful in 10 of 12 of our cases (83.4%); laparotomy and subsequent endoscopic necrosectomy were performed using a mediastinoscope, supplemented by optimal perioperative intensive therapy (long-term respiration with PEEP, infusion therapy, calcitonin, antibiotics, etc.). Before 1981, lethality amounted to 70%. No relaparotomies were necessary and organ failures (kidney and lung) were avoided.
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PMID:[Perioperative interdisciplinary management of acute necrotizing pancreatitis]. 409 Dec 47

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

While pancreatitis may provide the clue to the diagnosis of hyperparathyroidism preoperatively, the occurrence of pancreatitis following parathyroidectomy is not generally recognized. In this study preoperative and postoperative serum amylase estimations, together with a clinical assessment, were performed on 86 patients undergoing neck exploration for hyperparathyroidism. It was found that postoperative hyperamylasaemia occurred in 35% of the total group, while clinically significant pancreatitis was found in 9% of cases. Pancreatitis was significantly more common when thyroidectomy was performed at the time of parathyroidectomy, occurring in 23% of this group of patients, and may be due to the blunted C-cell response of calcitonin secretion to the induced hypercalcaemia associated with operative manipulation. Careful attention should be paid to postoperative abdominal symptoms, for they may indicate pancreatitis.
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PMID:Pancreatitis following parathyroid surgery. 617 21

Frequently a causal relationship between hyperparathyroidism (HPT) and pancreatitis has been defended. Bess et al. queried the existence of any causality. A series of 686 patients with surgically confirmed primary hyperparathyroidism (PHPT) was analysed with a coincidence of pancreatitis of 1.5% (n = 10). Three patients had an attack immediately after exploration of the neck, which is more than one would expect after a non-related operation. Although these data are not conclusive, a causal relationship cannot be excluded. It is uncertain whether a parathyrotoxic crisis due to surgical manipulation plays a part. In 27 patients a partial or total thyroidectomy was performed at the time of the parathyroidectomy. None of these patients had a postoperative pancreatitis, which means that in this series the recently postulated protective role of calcitonin cannot be confirmed.
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PMID:Primary hyperparathyroidism and pancreatitis. 672 28

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 innervation of the sphincter of Oddi (SO) has been extensively studied experimentally, but human studies have not been published, which is why this study was undertaken. Biopsies, taken by gastroscopy-biopsy forceps from duodenal epithelium of the papilla of Vater and from ampullary epithelium after sphincterotomy, did not demonstrate nerves and could not be used for studying SO innervation. Therefore SO specimens were obtained from brain-dead organ donors (N = 5) and from autopsies (N = 14). By staining with a myelin marker S-100, a rich network of nerves was demonstrated in SO. The occurrence of vasoactive intestinal polypeptide (VIP), peptide histidine-isoleucine (PHI) (or its immunologically similar human equivalent peptide histidine methioninamide, PHM), neuropeptide Y, calcitonin gene-related peptide (CGRP), galanin, substance P, enkephalin, bombesin, and somatostatin were studied by immunohistochemical technique. SO demonstrated immunoreactivity for VIP, PHI (PHM), neuropeptide Y, CGRP, galanin, somatostatin, substance P, and enkephalin, but no immunoreactivity was observed for bombesin. The SO immunoreactivity was similar in specimens from organ donors and from autopsies of victims of violence without pancreatobiliary diseases (N = 3) when the specimens were taken within 48 hr of death. Autopsy specimens of SO from subjects with gallstone disease (N = 5), recurrent pancreatitis (N = 3) or periampullary carcinoma (N = 3) also demonstrated similar immunoreactivity. We conclude that VIP-, PHI- (PHM-), neuropeptide Y-, CGRP-, galanin-, substance P-, somatostatin-, and enkephalin-like immunoreactivity occur in human SO. These neuropeptides may have role in the neural control of human SO function.
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PMID:Peptidergic innervation of human sphincter of Oddi. 831 11

The mortality rate in acute pancreatitis (AP) is significantly lower in patients hospitalized directly at the intensive care unit than in patients admitted to hospital in 2 weeks after the assessment of diagnosis, prophylactic administration of low-molecular protease inhibitor reduces the occurrence of post ERCP pancreatitis a well a coincident complications. Despite rational considerations concerning the significance of pryphylactic administration of antibodies (ATB) in severe AP, there still not enough convincing data which could be recommended a standard therapy. One of the concepts of causal therapy of AP. Suggest that inhibition of exocrine pancreatic enzymatic secretion reduces autodigestion of the gland (setting the gland at rest). The reports on success of secretin-inhibiting substances a glucagon, calcitonin, atropine and somatostatin require confirmation in randomized or accurately defined comparable groups. The initial studies on the therapeutic significance of lexipanphate-antagonist of platelet activating factor (PAF) in acute pancreatitis is promising. A long-term lavage had reduced the mortality.
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PMID:[Therapy of acute pancreatitis]. 972 66

Procalcitonin (PCT), the precursor protein of the hormone calcitonin, appears to be an early marker of the presence of severe systemic infection. High serum concentrations are associated with severe systemic bacterial, parasitic or fungal infections. In contrast, PCT is generally not induced by severe viral infections or inflammatory reactions of non-infectious origin. Hence, PCT can be used for differential diagnosis of bacterial and viral meningitis. PCT may be helpful in the differentiation between infectious and non-infectious origin of systemic inflammatory response syndrome (SIRS) and acute respiratory distress syndrome (ARDS), pancreatitis, cardiogenic shock and acute rejection of organ transplants. PCT monitoring may be useful in patients with high risk of bacterial infection (major surgery, trauma, immunocompromised patients). PCT is a very stable molecule in vitro, and its measurement requires only 20 ml of plasma or serum and can be done within 2 hours.
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PMID:[Procalcitonin, a new marker for bacterial infections]. 1067 14


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