Irreversible Liver Damage After Azathioprine

Zarday, Zoltan

doi:10.1001/jama.1972.03210060044010

Cited by 50 publications

(6 citation statements)

References 2 publications

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“…On retrospect, it might be better to explain these findings by calling these three cases non-A-non-B-hepatitis instead of azathioprine hepatoxicity. Single cases of fulminant liver cell necrosis have rarely been re ported [7] and its relation to azathioprine remains in doubt. In HbsAG-positive long-term survivors with functioning kidney grafts, it is chronic active hepatitis rather than acute graft rejection which determines the out come.…”

Section: Discussionmentioning

confidence: 99%

Withdrawal of Azathioprine in Renal Transplant Patients with Chronic Active Hepatitis: Is It Wise or Not?

Loertscher¹,

Brunner²,

Harder³

et al. 1983

Nephron

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Withdrawal of azathioprine in renal transplant recipients with chronic active hepatitis and persisting HBs antigenemia was recommended for its beneficial effect on the course of liver disease. We report here three cases in which azathioprine treatment was stopped for this reason. One of these patients lost his graft due to irreversible vascular rejection 6 years after successful transplantation. Decrease of graft function paralleled azathioprine withdrawal in a second patient. Data from other reports indicate that cessation of azathioprine treatment may be followed by decreased graft function or even graft loss. We conclude that the risk of altered graft function is substantial and this is too high a price to pay for a procedure that may not prevent chronic active hepatitis from progressing to cirrhosis.

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Section: Discussionmentioning

confidence: 99%

Withdrawal of Azathioprine in Renal Transplant Patients with Chronic Active Hepatitis: Is It Wise or Not?

Loertscher¹,

Brunner²,

Harder³

et al. 1983

Nephron

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“…Liver disease is a frequent cause of morbidity and mortality in renal transplant recipients [1][2][3][4][5][6][7][8][9][10]. The re ported incidence of this complication varied from 4% [7] to 38% [8], depending on the criteria used for diagnosis.…”

mentioning

confidence: 99%

“…Recent studies also indicate that liver failure is a leading cause of death in the late survivors of renal transplanta tion -i.e., 3-5 years and beyond [11,12]. Viral infections such as hepatitis B [3][4][5][6], non-A non-B [8], herpes sim plex and cytomegalovirus (CMV) [6][7], and drugs used in the posttransplant period such as azathioprine [2], isoniazid [9], and cyclosporin A [10] are believed to be the common causes of liver dysfunction in the graft recipi ents.…”

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confidence: 99%

Hemosiderosis and Hemochromatosis in Renal Transplant Recipients

Rao

Anderson²

1985

Am J Nephrol

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We analyzed the clinical data and liver histology for iron overload in 74 renal allograft recipients. Twenty of the 74 patients had histological evidence of hemosiderosis. Four patients had hemochromatosis. Of the 2 noninvasive diagnostic tests the serum ferritin level was more reliable than percent saturation of transferrin in predicting the histological diagnosis of hemosiderosis. Of the 20 patients with hemosiderosis 14 died either from liver failure or concomitant sepsis. Female patients and those who received long-term dialysis had higher susceptibility for developing hemosiderosis. Of the 6 patients treated with phlebotomies, the response was good in 4 and incomplete in 2. Hemosiderosis and hemochromatosis should be considered in the differential diagnosis of posttransplant liver disease. Intermittent phlebotomies if carried out early may prevent the progression of hemosiderosis to micronodular cirrhosis.

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“…The use of azathioprine in various non-hepatic diseases has occasionally resulted in liver toxicity, manifested by portal fibrosis and cholestasis (Du Vivier, Munro, and Verbov, 1974;Zarday, Veith, Gliedman, and Soberman, 1972). Although difficult to distinguish from the natural course of the disease, this drug is also thought to have a detrimental effect on hepatic function in some patients with chronic active liver disease (Soloway et al, 1972).…”

Section: Discussionmentioning

confidence: 99%

Influence of Azathioprine on Hepatic Reserve in Chronic Active Liver Disease

Rikkers¹,

Sherlock²

Diseases of the Liver and Biliary Tract

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Howard, 1967).Following the demonstration that hepatic uptake of ICG is a saturable process (Hunton, Bollman, and Hoffman, 1961), Paumgartner, Probst, Kraines, and Leevy (1970) utilized classical MichaelisMenten enzyme kinetics to determine the maximal rate of ICG removal (Rmax) from disappearance rates of multiple, submaximal doses. The discovery of a close correlation between regenerating liver mass in the rat and Rmax by Rikkers and Moody (1974a) encouraged the application of this technique to the clinical estimation of hepatic reserve.The purposes of the present investigation are twofold: (1) to determine if hepatic removal of ICG in patients with chronic active liver disease follows saturation kinetics, allowing calculation of Rmax, and (2) to assess the role of azathioprine in the management of these patients by evaluating the influence of this drug on Rmax.

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Irreversible Liver Damage After Azathioprine

Cited by 50 publications

References 2 publications

Withdrawal of Azathioprine in Renal Transplant Patients with Chronic Active Hepatitis: Is It Wise or Not?

Withdrawal of Azathioprine in Renal Transplant Patients with Chronic Active Hepatitis: Is It Wise or Not?

Hemosiderosis and Hemochromatosis in Renal Transplant Recipients

Influence of Azathioprine on Hepatic Reserve in Chronic Active Liver Disease

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