Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

16 patients suffering from acute pancreatitis were treated by intramuscular or intravenous administration of glucagon, with control of the amylasemia and amylasuria values at the start of treatment, the 12th hour and the 36th hour. By the 12th hour from the start of therapy they already observed a reduction in amylasemia and amylasuria to normal values, with disappearance of the symptomatology (pains, vomiting, shock) and complete cure of the patients in 94% of cases. On the basis of their own and others' experience, the Authors therefore believe that glucagon can advantageously be used in this disease, which is characterised by much higher mortality if treated with the traditional therapeutic means.
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PMID:[Glucagon in the treatment of acute pancreatitis (clinical contribution)]. 100 41

All 78 patients with acute pancreatitis admitted to one hospital in a 2-year period were included in a prospective survey of conservative management. The overall mortality rate was 11.5 per cent, being 46 per cent for 11 patients subjected to early laparotomy and only 6 per cent for patients managed without operation. Twenty-six patients were considered to have severe acute pancreatitis and all 9 deaths occurred in this group. Biliary disease was present in 51 per cent of patients, and the majority of those with biliary disease were over 60 years old. Alcohol-related acute pancreatitis occurred in 26 per cent of the total patients, and none of this group was over 60 years old. Acute pancreatitis was considered idiopathic in origin in only 13 per cent of the patients. Elective biliary surgery in 30 patients resulted in freedom from recurrent attacks of acute pancreatitis for the follow-up period (12-30 months). The results compare favourably with those in which glucagon and high dosage aprotinin (Trasylol) have been utilized in the management of acute pancreatitis.
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PMID:A prospective study of acute pancreatitis. 108 65

Seventy patients admitted to Waikato Hospital between 1964-74 with acute pancreatitis have been reviewed. Biliary tract disease and alcohol are the most common aetiological agents. The disease is most common in middle age. Europeans and Polynesians have similar incidence rates. The diagnosis is frequently not made at admission and most admissions are in the afternoon or early evening. Radiology is helpful in the diagnosis although nonspecific. Abnormal biochemistry is discussed and related to mortality. Additional tests, serum catalase/methaemalbumin are promoted to assist in the diagnosis and indicating the severity of the disease. Glucagon and Trasylol are discussed as being beneficial in this disease and combination therapy is suggested. The role of surgery is discussed.
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PMID:Acute pancreatitis ten years experience in the Waikato district. 108 Dec 8

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

Personal experience with glucagon in 15 cases of acute pancreatitis is reported. Complete remission of pain within 2-3 hr after infusion of the drug was noted in 85% of the series, together with normalisation of blood amylase within 48-72 hr. Glucagon inhibits pancreatic secretio&n. Vairous theories concerning its mechanism of action are examined.
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PMID:[Use of glucagon in the treatment of acute pancreatitis]. 114 73

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

Thyrocalcitonin release mediated by glucagon secreted from the acutely inflamed pancreas has been postulated as a possible mechanism for hypocalcemia in acute pancreatitis. To test this hypothesis, hemorrhagic pancreatitis was induced in a group of thyroidectomized pigs. No source of thyrocalcitonin other than the thyroid has been described in the pig. Their subsequent serum calcium concentrations were compared with those in a group of thyroid intact pigs also given hemorrhagic pancreatitis. The results indicate that the hypocalcemia observed during the first 24 hours following induction of pancreatitis is not related to the presence of an intact thyroid. Differences observed in the degree of hypocalcemia between the two groups 30 to 48 hours after pancreatitis developed may be of significance but could be explained by dilutional differences alone. Thyrocalcitonin apparently has little if any role in the hypocalcemia observed during the course of acute pancreatitis.
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PMID:Mechanisms of hypocalcemia in acute hemorrhagic pancreatitis. 119 6

Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.
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PMID:Glucagon secretion in acute and chronic pancreatitis. 120 May 23

CFY male rats anaesthetized with pentobarbital were used in different groups for inducing acute pancreatitis by the retrograde injection either of 1 mg elastase, 5 mg trypsin, 4 mg lysolecithin, 10 mg Na-taurocholate in 0.2 ml volume or of 0.3 m. sunflower oil. In each group laparatomized animals served for control. The animals with pancreatitis were treated either with 15 mug/b.w.kg/hour glucagon or with physiological saline for 72 hours. Twenty-four and 72 hours after inducing pancreatitis glucagon did not influence the significant fall in blood pressure elicited by the intraductal injection of trypsin or elastase or in the plasma calcium level in pancreatitis induced by trypsin or sunflower oil. Neither did glucagon affect the significant increase of plasma lipase activity in pancreatitis induced by trypsin or taurocholate. It also failed to reduce the 24-hour mortality rate and the extension of fat tissue necrosis in the abdominal cavity of pancreatitic animals. In contrast, glucagon treatment significantly reduced the amount of abdominal exudate associated with bile salt induced pancreatitis and, probably due to its pancreatic blood flow increasing effect, seemed to moderate the degree of tissue damage elicited in the pancreas by detergents such as taurocholate or lysolecithin.
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PMID:Glucagon treatment of experimental acute pancreatitis. 123 17


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