Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty five patients were examined in order to evaluate the usefulness of glucagon and insulin as a therapy of fulminant hepatitis. Thirty patients were treated with simultaneous infusion of glucagon and insulin, whereas prednisolone was given at a daily dose of 60 to 90 mg in 15 cases. In the former group, 1 mg of glucagon and 10 units of regular insulin were infused over a period of 2 to 6 hours. Two such treatments were given per day in the early critical period of fulminant hepatitis. The therapeutic effect of glucagon and insulin was evaluated in comparison with that of prednisolone, and additionally, with a combination therapy of either blood exchange or plasmapheresis in both groups. The survival rate was superior in the group treated with glucagon and insulin (46%) and in the one with combined infusion of these hormones plus plasmapheresis (33%).
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PMID:Clinical evaluation of glucagon and insulin in therapy of fulminant hepatitis. 331 19

To estimate the number of adults medically eligible to donate blood, the percent of the general population over the age of 16 deferrable by 13 current American Red Cross donor guidelines was calculated using the best available United States data. Categories examined included age, weight, hematocrit, pregnancy, blood pressure, heart disease, diabetes requiring insulin, male homosexual activity since 1977, intravenous drug use, sexual partner of high-risk group member, recent transfusion, history of cancer, and other (medical, surgical, travel history). Sex-specific total eligibility rates were estimated by serial multiplication of individual eligibility rates (1.0 minus deferral rates) to account for the proportionate overlap of independent categories, with corrections for expected associations between categories. The resultant eligibility rates for women (57%) and men (70%) indicate fewer eligible donors than commonly stated. Surrogate testing (ALT, anti-HBc) for non-A, non-B hepatitis would further reduce the percent of eligible donors to 55 and 67%, respectively. Based on the actual numbers of women and men in the population, these calculations indicate that an equal number of women and men are medically eligible to donate.
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PMID:An estimate of blood donor eligibility in the general population. 337 67

It is suggested that the important drugs rifampicin and halothane and the raised glucose levels in diabetes mellitus exert injurous effects on cells through a lysosomal mechanism. Further evidence is given of by time rifampicin induction of beta-glucuronidase and beta-N acetylglucosaminidase and its possible relation to hepatitis and pancreatitis. On the basis of preliminary data halothane may cause hepatitis connected to lysosomal enzyme release in the presence of other aggravating factors common to the perioperative period. The onset of diabetic vascular complications may be related to the similar raised levels of lysosomal enzymes found in insulin, drug and diet controlled disease. Release of these enzymes into plasma may be a marker of important changes in the lysosome, whether due to enzyme induction or damage, and could be a primary mechanism of many disease processes including some thought to be mainly autoimmune in character. Routine estimation in the clinical laboratory along with existing cytoplasmic and microsomally derived enzymes in the chemical screen would be a useful way of surveying lysosomal changes in the wide spectrum of disease in a general hospital.
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PMID:Rifampicin, halothane and glucose as mediators of lysosomal enzyme release and tissue damage. 341 3

Acute fulminant hepatitis was induced in 55 healthy adult male rabbits with the potent hepatotoxin galactosamine hydrochloride (3.75 mmoles per kg i.v.). Control rabbits (n = 27) were divided into three groups: Group I (n = 10) underwent sham surgery for placement of an indwelling central venous catheter; Group II (n = 9) received 5% dextrose and water via an indwelling central venous catheter, and Group III (n = 8) received daily intramuscular injections of 0.9% sodium chloride. Treated rabbits (n = 28) also consisted of three groups: Group IV (n = 9) received 12-hr intravenous infusions of insulin (0.029 units per kg per hr) and glucagon (2.86 micrograms per kg per hr) daily; Group V (n = 10) received a continuous infusion of parenteral amino acids (Travasol), and Group VI (n = 9) received daily intramuscular methylprednisolone (0.69 mg per kg). In each case, treatment was initiated 16 hr following galactosamine injection. Serum aminotransferase activity was determined on Days 0, 1, 4 and 10 of the 10-day study. Liver histology was obtained immediately after death and graded under code on a scale of 1 to 4 for severity of hepatitis. Rabbits surviving 10 days were sacrificed on Day 10 for histologic examination. The extent of galactosamine-induced hepatic injury was similar in all six groups as manifest by peak mean SGPT (range: 2,662 to 3,568 IU per liter), SGOT (range: 4,435 to 5,625 IU per liter) levels and hepatic histologic findings. The overall survival rate in controls was 6/27 (22%); in insulin/glucagon-treated animals 2/9 (22%), and in the amino acid-treated group 2/10 (20%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparative study of the effects of insulin/glucagon infusions, parenteral amino acids and high dose corticosteroids on survival in a rabbit model of acute fulminant hepatitis. 351 Sep 52

Chronic contamination of rats with heliotrin causing the development of hepatitis or hepatocirrhosis and partial hepatectomy to decrease the amount of liver cellular elements resulted in intolerance to glucose, a decrease in the sensitivity of the body to insulin, hyperinsulinemia after a glucose-tolerance test. The content of glycogen in the liver of the heliotrin contaminated rats was much lower than that in the controls and after glucose-tolerance an absolute increment of glycogen in the controls was 8.8-fold higher than in the heliotrin-contaminated rats. It was concluded that a decrease in glucose-tolerance and hyperinsulinemia in patients with chronic hepatitis and hepatocirrhosis were determined by a decrease in the amount of functionally active liver cellular elements and the development of insulin resistance.
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PMID:[Causes of hyperinsulinemia and decreased sensitivity to insulin in liver damage]. 352 17

Sixty-five patients with histologically proven chronic active hepatitis of unknown cause but associated with the antiliver/kidney microsome antibody type 1, confirmed by immunofluorescence and immunoprecipitation, were selected as forming a special entity. This disease was found to be rare with a prevalence of 5/1,000,000. The female to male ratio was 8:1. The condition occurred at all ages but was most common between the ages of 2 and 14 years. In 22 of the 65 cases, the hepatitis was associated with an autoimmune disease, most commonly insulin-dependent diabetes, autoimmune thyroid disease and vitiligo. The same autoimmune diseases were present in first-degree relatives from seven families. In 36 cases, the onset of disease resembled acute viral hepatitis. Serum biochemical tests showed marked elevation in aminotransaminases and hypergammaglobulinemia. Paradoxically, serum and salivary IgA levels were often normal or low. Histologic findings were multifocal hepatic necrosis with bridging in the acute stage, and aggressive hepatitis with mononuclear cell infiltration or macronodular cirrhosis in the late stages. Serologically, apart from the presence of antiliver/kidney microsome antibody type 1, the disease was characterized by the absence of antiactin, antimitochondria and antinucleus antibodies; however, organ-specific autoantibodies were often present. The clinical course was usually severe: six patients in the acute stage presented with fulminant hepatitis, and all, except two, other patients progressed to cirrhosis. Prolonged treatment with corticosteroids and immunosuppressants was usually effective in rendering the cirrhosis inactive. The cumulative survival rate was 51% at 14 years. We propose to call this entity "anti-LKM1 chronic active hepatitis" or "autoimmune hepatitis type II" to differentiate it from classical "lupoid hepatitis" or autoimmune hepatitis type I.
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PMID:Chronic active hepatitis associated with antiliver/kidney microsome antibody type 1: a second type of "autoimmune" hepatitis. 367 93

Serum markers for hepatitis B virus (HBV) were studied in 395 healthy control subjects and in 100 diabetic patients. Of the patients, 28 had type I diabetes, 31 had type II diabetes requiring insulin, and 41 had type II diabetes treated with oral agents or diet alone. None gave history of previous icterus or other signs of hepatitis, had received blood transfusions, or had been on hemodialysis. There was a significant difference in the prevalence of HBV markers (mainly HB surface antibody) between the diabetic group and the controls (51% versus 25%, P less than 0.001). The control subjects included hospital personnel and, hence, their risk of HBV exposure was already relatively high. The increased occurrence of HBV markers did not seem to be related to diabetes duration, patient age, intake of insulin injections, or presence of microvascular complications. This study reveals a high degree of exposure to HBV in a moderately controlled diabetic group and possibly a high degree of proneness to subclinical hepatitis B.
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PMID:Hepatitis B virus markers in diabetes mellitus. 400 59

Drug-induced autoimmune diseases have two immunological peculiarities. Firstly, some autoantibodies are present, which are virtually never seen in spontaneous human diseases and may be regarded as specific. This applies to antimitochondria antibody type 3 (anti M3) in the lupus-like syndrome caused by Venocuran, to antimitochondria antibody type 6 (anti M6) in iproniazide-induced hepatitis, to anti-insulin antibody found after treatment with methimazole, and to anti liver/kidney microsome antibody type 2 (anti LKM2) associated with hepatitis induced by tielinic acid. Secondly, a search for other autoantibodies shows that the immune disorder is much more limited than in spontaneous autoimmune diseases. Thus, contrary to myasthenia and idiopathic autoimmune haemolytic anaemia, we never found autoantibodies specifically directed against the thyroid, the stomach or the adrenal gland during treatment with D-penicillamine and alpha-methyldopa. Only some hypotheses may account for these peculiarities. Cross-reaction between drug and autoantigen may occur, but the fact that the antigen-antibody reaction is not inhibited by the drug or its metabolites does not support this explanation. Much more attractive is the "T-cell bypass" theory, according to which autoreacting suppressor T-cells are circumvented by helper T-cells stimulated by the drug-modified autoantigen. In this case, the autoimmune reaction would indicate to which body substance the drug is bound, thus making it immunostimulant, and not a structural similarity between the drug and the autoantigen.
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PMID:[Autoimmunity induced by drugs. Immunological characteristics and etiopathogenic hypotheses]. 624 48

Serological studies were carried out in the time course of insulin-dependent diabetes mellitus in 419 children, among whom paired sera from 66 were studied in the very beginning of diabetes mellitus. By seroconversion in 83% of the children early in the disease, different, frequently mixed virus infections were diagnosed: Coxsackie B2, B3, B4 (46%), rubella (41%), influenza A, B, C (38%), parainfluenza types 1-3 (35%), mumps (23%), adenovirus infection (18%), HB virus infection (4.5%). Acute respiratory diseases preceded or coincided with the onset of diabetes in half of the children with diagnosed acute respiratory and enterovirus infections. No clinical signs of rubella, mumps, or hepatitis immediately before the onset of diabetes or early in the disease were found. A possible role of virus infection diagnosed early in diabetes, in the etiology of chronic insulitis, in provocation of its exacerbation, and manifestation of diabetes mellitus is discussed.
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PMID:[Antibodies to viruses in children with diabetes mellitus]. 631 65

Insulin and C-peptide in venous blood were determined during oral glucose tolerance testing in 59 non-manifest diabetics with histologically established chronic liver disease (fatty degeneration, chronic aggressive hepatitis, cirrhosis). Glucose tolerance was pathologic in 60-80% of patients. When compared to a control group patients with chronic liver disease showed significantly increased values of blood glucose (after glucose intake), of insulin and of C-peptide (fasting and after glucose intake). The C-peptide/insulin ratio, a measure of hepatic insulin degradation, was significantly decreased after glucose uptake. There were no significant differences of blood sugar, insulin and C-peptide among the various liver diseases. In chronic aggressive hepatitis and in cirrhosis the C-peptide/insulin ratio was partly significantly lower than in fatty degeneration. From the increased C-peptide values increased insulin secretion in chronic liver diseases can be deducted. In addition, the decreased C-peptide/insulin ratios show an impairment of insulin degradation in liver cirrhosis and other chronic hepatic diseases. However, in fatty liver degeneration this is clearly less pronounced than in more serious liver diseases.
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PMID:[Insulin and C-peptide in chronic liver diseases during oral glucose tolerance testing]. 636 4


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