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)

A 76-year-old man presented with hypoglycemic coma associated with metastatic liver disease. Serum immunoreactive insulin excluded insulinoma as a cause of hypoglycemia. Negative glucose responses to glucagon and epinephrine testing indicated failure of compensatory glycogenolysis. The patient's increased glucose requirements of 500 g per 24 hr were reduced to normal only after shrinkage of the liver tumor bulk was accomplished with chemotherapy. Hepatic hypoglycemia is discussed and the literature is reviewed.
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PMID:Hypoglycemia secondary to metastases to the liver. A case report and review of the literature. 83 May 86

Fifty-nine patients with chronic pancreatitis were studied in retrospect. The incidence of overt diabetes was high, 36/59. Half of the diabetics were insulin-dependent, and among these labile diabetes with hyperglycemia and high amounts of glucose in the urine was not uncommon. Hypoglycemic episodes were noted in 14 of the 18 insulin-treated patients, and in 3 patients severe hypoglycemia was believed to be the cause of death. Mechanisms leading to such disastrous hypoglycemia are discussed, and a hypothesis regarding lack of glucagon as the cause of severe hypoglycemic attacks was experimentally tested by measuring pancreatic glucagon in plasma in two patients with pancreatic diabetes and severe brain damage following hypoglycemic coma. Low basal glucagon values were found, and the normal rise upon insulin-induced hypoglycemia was not seen. From these results it may be justified to suggest, firstly that glucagon should be used in the management of severe hypoglycemia in chronic pancreatitis, and secondly that a certain degree of hyperglycemia should be allowed in the treatment of diabetes in these patients.
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PMID:Diabetes and hypoglycemia in chronic pancreatitis. 86 1

Fasting hypoglycemia is frequently observed in patients with Multiple Sclerosis (S.M.) showing orthostatic hypotension and defective thermoregulation, although they never complicate in hypoglycemic coma. The aim of this study was to evaluate glucose homeostasis in S.M. patients. Both insular and counter-insular regulating mechanisms were investigated by determination of glucose, insulin, C-peptide and cortisol plasmatic levels during OGTT, and subsequently by evaluating glucagon plasmatic levels after arginine administration (30 g., i.v.). Our results suggest that the increased susceptibility of S.M. patients to undergo fasting hypoglycemia could be related to some alterations in counter-insular mechanisms, generally included among neurovegetative modifications in S.M. patients and probably due to orthosympathetic function impairment.
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PMID:[Insulin counter-regulation in multiple sclerosis]. 229 33

Hypoglycaemia remains a serious and much feared complication of insulin therapy. In this study, patients attending an accident and emergency department in hypoglycaemic coma were randomized to treatment with either intravenous dextrose (25g) or intramuscular glucagon (1mg), administered into the right thigh. Restoration of normal conscious level was slower after glucagon than dextrose (9.0 vs 3.0 min, P less than 0.01), although the average duration of hypoglycaemic coma was 120 min. Two patients in the glucagon-treated group, who failed to show satisfactory recovery after 15 min, required additional treatment with intravenous dextrose. On questioning following recovery, all except two patients reported loss of awareness of the onset of hypoglycaemia Intramuscular glucagon is valuable in the treatment of severe hypoglycaemia outwith hospital and, although the slightly slower and less predictable recovery may appear to make it a less attractive option than intravenous dextrose in the accident and emergency department, this must be balanced against the advantages of ease of administration and a lower incidence of serious adverse effects.
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PMID:Comparison of intramuscular glucagon and intravenous dextrose in the treatment of hypoglycaemic coma in an accident and emergency department. 239 Jan 57

Profound hypoglycaemia is a rare event which has been described in seven cases of anorexia nervosa. A further case is reported here and the literature regarding this complication is reviewed. The major risk factors identified are body weight below 30 kg, a period of fasting and intercurrent infection. Excessive exercise may also play a role. The precise pathogenesis has not been elucidated but several mechanisms, including depletion of liver glycogen, defective gluconeogenesis or failure of glucagon secretion have been proposed. Although hypoglycaemic coma frequently results in death, prompt treatment may result in full recovery as occurred in the case described here.
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PMID:Hypoglycaemic coma associated with anorexia nervosa. 307 24

Hypoglycemia is a serious problem in insulin-treated diabetic patients. In this study the efficacy of intravenous glucagon (1 mg) was compared with that of intravenous dextrose (25 g) in the treatment of hypoglycemia in insulin-treated patients attending an accident and emergency department. In addition, the prevailing glycemic control of these patients was compared with patients routinely attending a diabetic outpatient clinic. Both intravenous glucagon and dextrose were effective in the treatment of hypoglycemic coma. There was a difference in the glycemic profile after intravenous glucagon compared with intravenous dextrose, and recovery of a normal level of consciousness after glucagon was slower than after dextrose (6.5 vs. 4.0 min, respectively; P less than .001), although the average duration of hypoglycemic coma was 1.4 h. The glucagon- and dextrose-treated groups had significantly lower HbA1 than comparable patients routinely attending the clinic (9.5 +/- 0.8 vs. 12.0 +/- 3.8%, respectively; P less than .001). In view of the ease of administration and the small risk of vascular and extravascular complications, intravenous glucagon appears to be a useful alternative to intravenous dextrose in the treatment of severe hypoglycemia.
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PMID:Comparison of intravenous glucagon and dextrose in treatment of severe hypoglycemia in an accident and emergency department. 342 48

Since the development of radioimmunoassay for insulin, the diagnosis of insulinoma has been made easily. However, it has been assumed that insulinoma is heterogenous in the histological structure as well as in clinical findings. Therefore, the present study was performed to investigate the insulin response to various stimuli and to evaluate the various insulin response tests in 19 patients with insulinoma. The fasting blood glucose was 19 to 90 mg/100 ml in insulinoma and 81 +/- 5 (mean +/- S.D.) mg/100 ml in normal controls. Plasma insulin (IRI) in insulinoma ranged from 10 to 255 microU/ml, while in the control it was 14 +/- 9 microU/ml. However, insulin/blood glucose ratio increased in insulinoma (0.2-11.2) compared with the normal control (0.18 +/- 0.11). In oral glucose tolerance tests, plasma IRI increased and reached peak levels of 48-244 microU/ml, remaining elevated in most cases. In the intravenous tolbutamide test, plasma IRI increased conspicuously to 82-1,330 microU/ml and hypoglycemic coma was provoked in 54%. Plasma IRI was elevated in the intravenous glucagon test and reached the peak levels of 85-400 microU/ml, which exceeded those of the control group. Plasma IRI increased to more than 100 microU/ml after arginine infusion and formed bizarre curves. There were no correlations between plasma IRI response to various stimuli and malignancy, type of B-granule or insulin content of insulinoma tumors. It is concluded that fasting plasma IRI, insulin/glucose ratio, tolbutamide test and glucagon test are highly valuable for the diagnosis of insulinoma.
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PMID:Plasma insulin response to various secretagogues in insulinoma. 628 49

Thirteen patients with pancreatic diabetes caused by calcifying pancreatitis were divided into 2 groups; 5 with diabetic autonomic neuropathy [AN(+) group] and 8 without [AN(-) group]. They were subjected to an insulin-induced hypoglycemic stress test to evaluate their blood pancreatic glucagon, adrenalin, and cortisol responses. When a blood glucose level below 45 mg/100 ml was defined to be hypoglycemia, all the patients in the AN(-) group exhibited peripheral adrenalin responses, with a significant increase (mean, 19.0 times the basal level) in the blood adrenalin level. Among the AN(+) group, on the other hand, central nervous symptoms became evident rather than the peripheral adrenalin response (the blood adrenalin level hardly exceeded the basal level). With the exception of a single patient, none exhibited responses in the blood pancreatic glucagon levels. Only one patient showed a minimal cortisol response but the remaining 12 reacted normally in the cortisol release. The findings are summarized as follows: in pancreatic diabetes, insulin-induced hypoglycemia causes little change in pancreatic glucagon secretion; when the condition is complicated with autonomic neuropathy, central nervous symptoms develop while the blood adrenalin level hardly increases. These findings indicated that patients with pancreatic diabetes complicated with diabetic autonomic neuropathy have a risk of lapsing into an acute hypoglycemic coma and difficulty in recovering from the hypoglycemic state.
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PMID:Decreased counterregulatory hormone responses to insulin-induced hypoglycemia in patients with pancreatic diabetes having autonomic neuropathy. 773 13

Insulin has been in therapeutic use for around 70 years, and the range of adverse effects associated with its use is very limited. Insulin allergy and other local cutaneous reactions, which were common with the early insulins, are now rarely seen with highly purified and biosynthetic preparations. By far the most important complication of exogenous insulin is hypoglycaemia, which affects almost all insulin-treated patients and is largely a manifestation of nonphysiological insulin regimens and routes of administration. The problem of hypoglycaemia unawareness is now being increasingly recognised, with onset of severe neuroglycopenia and coma which is not preceded by the characteristic warning symptoms associated with autonomic activation. This can occur with excessively tight glycaemic control, and this situation is usually reversible. More commonly, however, hypoglycaemia unawareness is a chronic problem which is predominantly a feature of long duration of diabetes. Although individual episodes of hypoglycaemic coma can usually be effectively treated with parenteral dextrose or glucagon, management of patients with chronic hypoglycaemia unawareness is a difficult clinical challenge, with limited therapeutic options. In the past few years, there has been concern that the use of human insulin preparations may predispose to hypoglycaemia unawareness. The evidence for and against this is discussed, although at present it is difficult to draw any absolutely firm conclusions.
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PMID:Adverse effects of exogenous insulin. Clinical features, management and prevention. 832 48

Hypoglycemia is often associated with typical, but not specific symptoms. A differentiation is made between neuroglucopenic symptoms (e.g., confusion, somnolence) on the one hand, and those that arise as a result of the counterregulatory response of the sympathetic nervous system (e.g., tremor, sweating), on the other. The diagnosis of hypoglycemia can cause considerable problems, in particular when only isolated single symptoms present (e.g., confusion, psychosis, seizures, coma). For the elective clarification of recurrent hypoglycemia, further diagnostic examinations (e.g., fasting with determination of hormones, measurement of insulin) are employed in addition to the patient's history. For differential diagnostic considerations not only organic causes, but also adverse drug reactions and a factitious genesis must be excluded. In the event of an emergency (e.g., hypoglycemic coma) the usual form of treatment is the administration of glucoses or glucagon.
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PMID:[Hypoglycemia. Symptoms, differential diagnosis, therapy]. 917 11


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