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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of glucagon and aprotinin ('Trasylol') on the death-rate of acute pancreatitis has been studied in a randomised double-blind multicentre trial. The death-rate in 257 patients was 11%. In the doses used neither drug was found to diminish the risk of death.
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PMID:Death from acute pancreatitis. M.R.C. multicentre trial of glucagon and aprotinin. 7 49

Recent data seem to support a tubular defect as the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon has been proposed by some to be an important factor in this phenomenon. To examine the role of glucagon as this "tubular dysfunction factor", we investigated the effect of intravenously infused glucagon on the fractional excretion of amylase and the tubular handling of a low molecular weight protein, beta2 microglobulin, in normal, healthy volunteers. At glucagon levels far in excess of those seen in pancreatitis, the clearance ratio of beta2 microglobulin relative to creatinine increased, whereas the clearance ratio of amylase relative to creatinine did not increase above the normal range. The dissociation between beta2 microglobulin clearance and amylase clearance allows one to question the theory that tubular dysfunction is the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon does not appear to be the sole factor responsible for the elevation of renal clearance of amylase relative to creatinine in acute pancreatitis.
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PMID:Effect of glucagon infusion on the renal clearance of amylase relative to creatinine. 8 90

The authors made a comparative study of the use of glucagon (4 mg/day IV) in 30 dogs with acute pancreatitis. They found that the mortality and amylasemia were significantly lower in the glucagon-treated group than in the control groups (saline and glucose solution 5%). In the glucagon group, the areas of necrosis were smaller (1.5 cm) and rarely found; microscopically, the areas of necrosis and the inflammatory reaction were much smaller than in the other groups. These findings lead to the conclusion that the beneficial action of glucagon is due to another mechanism other than its hyperglycemic effect and that the administration of hypertonic solutions of glucose does not have a beneficial effect in acute pancreatitis.
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PMID:[Treatment of acute pancreatitis by glucagon. Experimental studies in dogs]. 9 32

A questionnaire on the conservative treatment of acute pancreatitis was answered by 312 surgical [n = 139] and medical [n = 173] departments from all over Western Germany and from West-Berlin. Nearly total positive agreement was found about routine administration of parenteral fluids and on the prohibition of oral food and fluids. The application of glucocorticoids, glucagon, heparin in small doses and of a carboanhydrase inhibitor [Diamox] is rejected by most of the departments. Renal failure is treated in 63% by hemodialysis and in 37% by peritoneal dialysis. There is great disagreement between the answers about the administration of atropine, antacids and aprotinin [Trasylol]. Antibiotics are applied routinely by 63% of the surgical and 70% of the medical departments.
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PMID:[The conservative treatment of acute pancreatitis in the Federal Republic of Germany in 1977 (author's transl)]. 10 62

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

Gastric acid secretion by the parietal cell is a single digestive process involving a continuous interplay between nervous and hormonal stimuli. Gastric acid hypersecretion and hypergastrinemia may represent pathologic disturbance of the normal "gastric phase" of acid secretion (excluded antrum syndrome) or abnormal gastrin secretion from a nongastric source as in the Zollinger-Ellison syndrome. Diagnosis of these two syndromes preoperatively is dependent on immunoassay for serum gastrin. A fall in serum gastrin level after the injection of secretin will distinguish the excluded antrum syndrome from the Zollinger-Ellison syndrome. Which hormone or hormones cause the acid hyposecretion of the watery diarrhea hypokalemia achlorhydria syndrome is still uncertain. Potential candidates include secretin, glucagon (alone or combined with gastrin), vasoactive intestinal peptide and gastric inhibitory polypeptide. Secretin has undergone trials as therapy in peptic ulcer whereas glucagon is under investigation for the treatment of acute pancreatitis because of its dual actions as (1) an enterogastrone and (2) an inhibitor of pancreatic secretion.
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PMID:Current concepts on physiological control of gastric acid secretion. Clinical applications. 23 80

Acute pancreatitis may present as the mild edematous type or the more rare and dangerous hemorrhagic form. The effects of the latter are believed to be due to the activation of pancreatic enzymes, notably trypsin. Therefore attempts are being directed towards suppression of pancreatic enzyme activation in the management of the condition. Aprotinin and glucagon are the agents for this purpose that have received most attention. Patients with acute hemorrhagic pancreatitis are subject to respiratory failure, which is not detectable early by clinical evidence, so that early monitoring of pulmonary function by the determination of arterial blood-gas pressures is desirable. This is borne out by the findings in six fatal cases.
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PMID:Symposium on pancreatitis: 1. Conservative management of acute pancreatitis. 30 73

Blood glucagon levels were found to be elevated in patients with acute pancreatitis. The significance of this in the individual patient is obscure, and there was a marked variability from patient to patient.
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PMID:Glucagon levels in acute pancreatitis. 32 21

The results of a double-blind trial of glucagon in 69 patients with acute pancreatitis are reported. In a subgroup of 59 patients statistical analysis showed no significant differences between the glucagon-treated (n = 29; 2 X 5 mg protamine-zinc glucagon intramuscularly per day) and the placebo-treated (n = 30) subjects for the following data: duration of pain left spontaneously and induced by palpation, amounts of analgesics and antispasmodics required by the patients, duration of hospital stay, amylase activities in serum and 24 hour urine collections. Mortality rates did not differ significantly between the glucagon-treated and the placebo-treated subjects in the total group of 69 patients and in the two subgroups of patients who were treated conservatively (n = 59) and those who underwent laparotomy because of severe peritonitis (n = 10). From the results of this study it is concluded that favourable effects of glucagon upon the course of acute pancreatitis--if they do exist--are not significant.
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PMID:Glucagon therapy in acute pancreatitis. Report of a double-blind trial. 34 59

In two prospective studies the effect of proteinase inhibiting agents and glucagon in acute pancreatitis have been studied by a randomised series. Moreover the effect of the basic therapy was examined in additional 103 patients. Symptoms, clinical and laboratory chemical findings correspond to each other in all collectives. The results seem to be the best ones in those patients having been treated by basic therapy only.
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PMID:[Proteinase inhibiting agents and glucagon in acute pancreatitis (author's transl)]. 34 61


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