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Kunze KD, Porst H, Lohmann J, et al. Leberschäden durch Dihydralazin und Propranolol. [Liver lesions induced by dihydralazine and propranolol]. Zentralbl Allg Pathol. 1985;130(1):19-29
Kunze, K. D., Porst, H., Lohmann, J., & Tschöpel, L. (1985). Leberschäden durch Dihydralazin und Propranolol. [Liver lesions induced by dihydralazine and propranolol]. Zentralblatt fur allgemeine Pathologie u. pathologische Anatomie, 130(1), 19-29.
Kunze, K D, et al. "Leberschäden durch Dihydralazin und Propranolol." [Liver lesions induced by dihydralazine and propranolol]. Zentralblatt fur allgemeine Pathologie u. pathologische Anatomie vol. 130,1 (1985): 19-29.
Kunze KD, Porst H, Lohmann J, Tschöpel L. Leberschäden durch Dihydralazin und Propranolol. [Liver lesions induced by dihydralazine and propranolol]. Zentralbl Allg Pathol. 1985;130(1):19-29. German. PMID: 3984541.
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Zentralbl Allg Pathol. 1985;130(1):19-29.

[Liver lesions induced by dihydralazine and propranolol].

Zentralblatt fur allgemeine Pathologie u. pathologische Anatomie

[Article in German]
K D Kunze, H Porst, J Lohmann, L Tschöpel

PMID: 3984541

Abstract

The antihypertensive drugs dihydralazine and propranolol can produce identical liver injuries which must be distinguished clinically and morphologically from acute viral hepatitis. In 19 cases selected from our biopsy file during the last two years, clinical and morphological findings suggested that the liver injury diagnosed by light microscopy had been caused by an adverse reaction to dihydralazine and/or propranolol. In order to establish a causal relation the lymphocyte proliferation test (LPT) was performed with dihydralazine in 11 cases. Positive results were observed in 9 cases, demonstrating an etiologic role for dihydralazine in liver injury in these cases. The dihydralazine and/or propranolol induced liver injury consisted mainly of drug-induced hepatitis with confluent (bridging) necrosis. Different findings were observed in three cases: In two of these drug-induced hepatitis with confluent necrosis was observed together with eosinophilic cholangio-cholangiolitis. In one other case the histologic changes corresponded to drug hepatitis resembling viral hepatitis. Each of the three cases showed conspicuous centrolobular cholestasis, a feature which is unusual in drug-induced hepatitis with confluent necrosis irrespective of serum bilirubin levels. In one third of our cases we found morphological features of hypersensitivity reactions in the liver biopsies. Considered together with the results of LPT these features emphasize the role of cell mediated immune reaction in the mechanism of liver injury caused by dihydralazine and/or propranolol.

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