Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A multicenter randomized double-blind trial on the use of synthetic salmon calcitonin (SCT) was carried out in 94 patients with acute pancreatitis. In addition to strict standard treatment--without aprotinin, atropine, or antacids--50 patients received daily 3 x 20 micrograms = 300 MRCU SCT intravenously and 44 patients received placebo for 6 days. Mortality rate was not influenced, overall mortality being 5.3%. The number of patients without pain and with normalized serum amylase on a given day was significantly higher in the group treated with SCT. Other parameters such as doses of analgesics, leukocyte count, and normalization of seven defined clinical and laboratory criteria within 6 days showed a positive trend without reaching significance.
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PMID:A double-blind trial of synthetic salmon calcitonin in the treatment of acute pancreatitis. 9 76

We studied nine consecutive hypocalcemic patients with acute pancreatitis to elucidate the mechanism of hypocalcemia. Mean serum ionized calcium, 0.97 mM, was below the normal mean of 1.16 mM (P less than 0.001). Seven of eight patients tested had normal parathyroid hormone levels. All responded to parenteral parathyroid extract by increasing serum ionized calcium and urinary cyclic AMP, indicating parathyroid-hormone-responsive target organs. Calcitonin and glucagon concentrations were increased above normal in some patients, but there was no relation with serum ionized calcium. Parenteral glucagon had no significant effect on serum ionized calcium or calcitonin concentrations. These findings suggest that neither glucagon nor calcitonin was primarily responsible for the hypocalcemia, which did not produce expected increases in serum parathyroid hormone concentrations. Relative parathyroid insufficiency may account for the persistent hypocalcemia frequently observed in patients with acute pancreatitis.
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PMID:Inadequate parathyroid response in acute pancreatitis. 17 71

The inhibitory action of both calcitonin (CT) and glucagon (GK) on human pancreatic secretion has been evaluated in detail. The reduction of enzyme secretion expressed as percentage corresponded to 60--80% of the initial values in response to both CT and GK when the hormones were given as single infusions during background stimulation with secretin or with secretin plus cholecystokinin-pancreozymin (CCK-PZ). After withdrawal of GK-infusion the return to normal values of enzyme secretion was distinctly faster than after CT, thus reflecting a more rapid degradation of circulating GK than of CT. In the presence of stimulation with secretin plus CCK-PZ, the combined administration of CT and GK did not enhance the inhibitory actions of CT and GK. Fluid and bicarbonate secretions were not affected by either CT or GK. The results suggest that CT and GK inhibit human pancreatic enzyme secretion by similar modes of action. Therefore, the combined administration of both CT and GK does not offer a reasonable approach to the treatment of acute pancreatitis.
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PMID:Similar modes of action of calcitonin and glucagon in inhibiting pancreatic enzyme secretion in man. 54

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15

Although calcitonin and somatostatin are polypeptid hormones of entirely different structure, in pharmacological doses they possess a similar effect to secretions of stomach and pancreas. Given intravenously, they generally inhibit the basal secretion of organs, stimulated by pentagastrin or pancreozymin, as well as the contraction of the gallbladder. Orally, calcitonin also suppresses by direct contact the secretion of the stomach. While calcitonin in higher doses shows only very slight and tolerable side effects (nausea, headache), somatostatin acts suppressively on many other hormone-regulated systems. Apart from this, disturbances of blood coagulation in monkeys and man were observed, findings which necessitate very careful application. Therapeutical trials appear reasonable with calcitonin in treating acute pancreatitis, in prophylaxis and treatment of stress ulcers with the danger of bleeding, in intensive care medicine, in preoperative procedure of Zollinger-Ellison syndrome as well as in duodenal ulcers (oral calcitonin). Double blind studies are carried out at present to answer most of these questions (acute pancreatitis, stress ulcers, duodenal ulcers), results of which should definitely be awaited.
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PMID:[Summary of work session 4: Effects of calcitonin and somatostatin on the stomach and pancreas--a possible therapeutic principle]. 82 14

The unpredictable course of acute pancreatitis needs a careful surveyance of the patient in the first days of the acute attack in order to apply therapeutic measures adequate to the severity of the symptoms. The avoidance of food or drink and gastric suction appears to be sufficient to prevent endogenous stimulation of the gland while there is probably no benefit of anticholinergic drugs or carboanhydrase inhibitors. Early adequate substitution of fluids using watery solutions, plasmaexpanders or blood is of decisive importance. For treatment of pains spasmoanalgetics, synthetic opium derivatives or infusion of procain are recommended. Tetracyclines should be given to prevent secondary infections. Trasylol is indicated only, if the benefit of the drug just now proven in one therapeutical trial will be confirmed in another study. The effectiveness of glucagon or calcitonin has not yet been proven. The medical treatment "by all means" is being replaced by elective surgical measures. After recovery etiological factors have to be determined by a number of routine investigations in order to prevent recurrency of the disease.
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PMID:[Therapy of acute pancreatitis]. 82 86

Serum calcitonin (Ct) levels, serum calcium, and urine amylast were analyzed in 29 patients with an acute pancreatitis collected at random. In two of the patients the acute pancreatitis complicated a primary hyperparathyroidism. It was found that the calcitonin levels in serum were usually elevated during the acute phase of the pancreatitis. During this phase of the disease 22 of 27 examined patients had Ct-values above the upper normal limit of 1 mug/ml. The patients with normal Ct-values also had moderately elevated amylast values and a less pronounced pancreatitis. Normal Ct-values were usually found in patients more than 10 days after the onset of symptoms. Serum calcium was mostly within normal limits. However, a slight fall in serum calcium or low values was recorded in six patients with a pronounced disese. One patient with hyperparathyroidism normalized a previously elevated serum calcium during the calcitonin release.
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PMID:Serum calcitonin in acute pancreatitis in man. 83 66

Recently in our laboratory we have demonstrated increased immunoreactive calcitonin (iCT) levels in 4 patients with acute pancreatitis and hypocalcemia. The present study consists of 17 additional patients in whom serial determinations for (iCT) were performed. Furthermore, with the use of 2 different antisera directed against human calcitonin we present evidence for immunochemical heterogeneity of this hormone in acute pancreatitis.
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PMID:Hypercalcitoninemia in pancreatitis--evidence for immunochemical heterogeneity. 86 67

Calcitonin was administered to 4 patients presenting with acute pancreatitis as well as to 6 patients presenting with postoperative pancreatitis. Prophylactic administration was performed in 3 cases consecutive to pancreatic interventions. Following calcitonin all patients showed considerable improvement of clinical course. Although 8 patients recuperated completely 2 patients died from independent complications. After prophylactic administration of calcitonin the postoperative course was uncomplicated without demonstrable increase in serum amylase. It is emphasized that only early case histories are reported; their verification will depend upon the results of a controlled survey presently being performed.
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PMID:[Preliminary observations on the clinical use of calcitonin. Treatment and postoperative prevention of pancreatitis]. 95 24

Plasma calcitonin, glucagon and parathyroid hormone were measured in patients with acute pancreatitis. Plasma calcitonin was not detectable in 6 specimens obtained from the hypocalcaemic patients. Plasma glucagon values were similar in patients with acute pancreatitis and control subjects and were unrelated to hypocalcaemia, which was not even induced by glucagon infusion. High or rising parathyroid hormone levels were noted in association with hypo-and normocalcaemia, suggesting that parathyroid hormone rises and maintains plasma calcium within normal limits. Plasma parathyroid hormone was, however, undetectable in 8 patients with prolonged hypocalcaemia. Deficiency of parathyroid hormone due to its destruction by proteolytic enzymes or because of parathyroid gland exhaustion is suggested as the major factor inducing persistent hypocalcaemia in acute pancreatitis. Administration of parathyroid hormone should, therefore, be considered in patients with acute pancreatitis when hypocalcaemia does not respond to intravenous calcium therapy.
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PMID:The aetiology of hypocalcaemia in acute pancreatitis. 111 72


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