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isonicotinic acid/hepatitis

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9 結果

Anti-tubercular treatment in patients with hepatitis.

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Sixty seven patients with coexistent tuberculosis and hepatitis were given a 3 drug regimen of streptomycin (SM), isonicotinic acid hydrazide (INH) and ethambutol (ETB) and observed for a period of 15 days. Total bilirubin as well as SGPT were repeated weekly and these showed a significant drop in a

Lymphocyte-mediated cytotoxicity in isoniazid-associated hepatitis.

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The release of lymphotoxin (LT) from peripheral blood lymphocytes of patients with isoniazid (INH)-induced hepatitis was studied, using L929 fibroblast target cells, as was the cytotoxic effect of these lymphocytes on murine hepatoma cells (L1469) and L929 fibroblasts, using a 3H-proline

Paradoxical attenuation of autoimmune hepatitis by oral isoniazid in wild-type and N-acetyltransferase-deficient mice.

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Isoniazid (INH) treatment can cause serious liver injury and autoimmunity. There are now several lines of evidence that INH-induced liver injury is immune mediated, but this type of liver injury has not been reproduced in animals, possibly because immune tolerance is the dominant response of the
The effect of daily administration of rifampin on the direct conversion of isoniazid to isonicotinic acid and hydrazine by isoniazid hydrolase was investigated in 6 slow and 8 rapid acetylators of isoniazid. The proportion of isoniazid metabolized through this direct pathway during the first 6 h was

Evaluation of isoniazid-associated hepatitis by immunological tests.

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In a retrospective study of patients developing hepatitis or persistent serum glutamic oxaloacetic transaminase (SGOT) elevations while receiving isoniazid, it was found that the lymphocyte transformation test (LTT) was positive in nineteen cases (95%) in response to stimulation by isoniazid,

The predictive value of the lymphocyte transformation test in isoniazid-associated hepatitis.

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Sixty-one patients receiving isoniazid (INH) for chemotherapy or chemoprophylaxis were assessed by the lymphocyte-transformation test (LTT) shortly after starting treatment. Thirty-eight per cent exhibited stimulation with INH, isonicotinic acid (INA) or human-serum albumin conjugates of these

[Drug prophylaxis of liver lesions induced by isoniazid and its metabolites].

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The results of the experiments with use of isoniazid and its metabolites showed that in the liver of rats isoniazid induced albuminous degeneration with stroma inflammation and hepatocyte necrosis, monoacetylhydrazine induced fatty hepatosis, acetylisoniazid induced fatty hepatosis with stroma

Histologically proven isoniazid hepatoxicity in complicated tuberculous salpingitis.

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Isoniazid (INH) hepatic injury is histologically indistinguishable from viral hepatitis and is related to individual susceptibility of patients who hydrolyze the drug to isonicotinic acid at different rates. We here present a case initially involving a complaint of lower abdominal pain, which was

Isoniazid liver injury: clinical spectrum, pathology, and probable pathogenesis.

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The clinical spectrum of isoniazid-induced liver injury seems to be clinically, biochemically, and histologically indistinguishable from viral hepatitis, except that the injury occurs primarily in persons older than 35 years. A possible relation between susceptibility of patients to isoniazid liver
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