Fulminating Hepatitis with Recurrent Hypoglycemia and Hemorrhage

Samson, Rohan; Trey, Charles; Timme, A. H.; Saunders, S. J.

doi:10.1016/s0016-5085(19)34237-4

Cited by 53 publications

(13 citation statements)

References 23 publications

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“…Despite extensive study, the factors responsible for the reduction of blood glucose are unknown. Fulminating hepatitis with recurrent hypoglycaemia has been reported [10]. In lymphocyte choriomeningitis virus (LCMV) infection in mice, perturbation of endocrine function resulting in altered synthesis of growth hormone is reported to be responsible for hypoglycaemia [11].…”

Section: Discussionmentioning

confidence: 99%

“…Hypoglycaemia has been reported in few viral infections. Samson et al [10] have reported recurrent hypoglycaemia during viral hepatitis, which is associated with hyperinsulinaemia, while Oldstone et al [11] have observed that lymphocytic choriomeningitis virus perturbs the endocrine functions without any change in serum cortisol, or insulin levels. Hypoglycaemia with hyperinsulinaemia have been reported in Plasmodium falciparum malaria [12,13].…”

Section: Introductionmentioning

confidence: 99%

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Induction of hypoglycaemia in Japanese encephalitis virus infection: the role of T lymphocytes

Khanna¹,

Mathur²,

Bharadwaj³

et al. 1997

Clinical and Experimental Immunology

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SUMMARYWe report here development of hypoglycaemia in the convalescent phase of Japanese encephalitis virus (JEV) infection in mice by the induction of antigen-specific Ly1 ¹ 2 + T cells in the spleen which mediate hypoglycaemia through the generation of soluble T cell hypoglycaemic factor (TCHF). The TCHF acted in a dose-dependent manner and was found to be trypsin-sensitive and thermolabile. It was purified on Superose-12 high performance liquid chromatography (HPLC) gel filtration column and purified protein migrated as a ϳ25-kD band on SDS-PAGE. The JEV-induced hypoglycaemia coincided with an increased circulating glucagon level, without any alterations in blood insulin and growth hormone concentrations. These effects were mimicked by TCHF. These results indicate that JEV-primed T lymphocytes mediate hypoglycaemia through the production of a soluble hypoglycaemic factor.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Induction of hypoglycaemia in Japanese encephalitis virus infection: the role of T lymphocytes

Khanna¹,

Mathur²,

Bharadwaj³

et al. 1997

Clinical and Experimental Immunology

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“…A decrease in insulin degradation by the damaged liver could account for the hyperinsulinism seen in acute hepatitis patients which would thus resemble the case described by Samson, Trey & Timme (1967) in which hyperinsulinism complicated fulminant hepatic failure. However, in their case this resulted in severe hypoglycaemia.…”

Section: Glucose Tolerance In Infectionmentioning

confidence: 72%

Glucose Tolerance and Metabolic Changes in Human Viral Hepatitis

et al. 1973

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1. Glucose tolerance and metabolic changes after intravenous glucose were studied in fifteen patients with acute viral hepatitis and in eight patients after recovery. In the acute stage glucose tolerance was significantly impaired compared with control subjects or with patients after recovery from hepatitis.2. Serum insulin concentrations were significantly higher in fasting acute hepatitis patients than in control subjects and the time-integrated serum insulin concentration in the first 5 min after glucose was inappropriately high for the observed glucose disappearance rate, indicating insulin resistance. Serum growth hormone concentrations in male acute hepatitis patients were significantly higher than controls and suppressed poorly.3. Fasting blood lactate concentrations were significantly elevated and after intravenous glucose there was a variable response. 2-OxoglutarateY glutamate and glutamine concentrations from blood of fasting subjects, were significantly higher in acute hepatitis patients than controls.4. There were no significant differences in blood ketones, glycerol and plasma free fatty acid concentrations from fasting subjects, but plasma triglycerides were significantly increased in the acute hepatitis patients.5. The results indicate that viral hepatitis is associated with glucose intolerance and insulin resistance. After recovery the lactate response after glucose is diminished compared with controls.

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“…In one large series, two of twenty-nine patients with acute hepatocellular failure had blood glucose levels less than 40 mg/100 ml (Jones et al, 1967). Hypoglycaemia may sometimes be very persistent and intractable (Samson, et al, 1967). It is essential that the blood glucose be measured repeatedly in patients with fulminant hepatitis.…”

Section: Hypoglycaemiamentioning

confidence: 99%