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氰胺相关酒精性肝病:一项连续组织学评估

Cyanamide-associated alcoholic liver disease: a sequential histological evaluation.

作者信息

Yokoyama A, Sato S, Maruyama K, Nakano M, Takahashi H, Okuyama K, Takagi S, Takagi T, Yokoyama T, Hayashida M

机构信息

National Institute on Alcoholism, Kurihama National Hospital, Kanagawa, Japan.

出版信息

Alcohol Clin Exp Res. 1995 Oct;19(5):1307-11. doi: 10.1111/j.1530-0277.1995.tb01616.x.

DOI:10.1111/j.1530-0277.1995.tb01616.x
PMID:8561306
Abstract

This is the first study that we are aware of that followed the histopathological progression of the liver disease that was caused by the combination of both chronic alcohol use and cyanamide, an antidipsotropic agent. Two sequential liver biopsy specimens were obtained on 29 alcoholics who relapsed with varying histories of cyanamide treatment. Cyanamide induced ground-glass inclusions (GGIs) in the hepatocytes. Two groups were identified, depending on whether GGIs proliferated or regressed, which was, in turn, found contingent on the duration of cyanamide treatment and the drug-free period. Group 1 included 14 cases in which GGIs either emerged only in the second biopsy specimen or else were increased in the second specimen as compared in the initial specimen. Group 2 composed of 15 cases in which GGIs were either not observed in either specimen or decreased in the second specimen as compared in the initial specimen. Acidophilic bodies were sequentially increased in five cases (36%) of group 1 and in none of group 2. The severity of portal inflammation worsened in 10 cases (71%) of group 1 but in 2 cases (13%) of group 2, although the changes in fibrotic process did not differ between two groups. These differences could not be explained on the basis of the daily ethanol consumption and the length of relapses of the two groups. Thus, when cyanamide-treated alcoholics relapsed, the combined effect of cyanamide and alcohol produced the development of acidophilic bodies and portal inflammation along with the emergence of GGIs.

摘要

据我们所知,这是第一项追踪由长期饮酒与戒酒硫(一种抗嗜酒剂)联合导致的肝脏疾病组织病理学进展的研究。对29例有不同戒酒硫治疗史且复发的酗酒者获取了两份连续的肝脏活检标本。戒酒硫在肝细胞中诱导产生毛玻璃样包涵体(GGIs)。根据GGIs是增多还是消退确定了两组,而这又取决于戒酒硫治疗的持续时间和停药期。第1组包括14例,其中GGIs要么仅在第二次活检标本中出现,要么在第二次标本中比初始标本增多。第2组由15例组成,其中在两份标本中均未观察到GGIs,或者在第二次标本中比初始标本减少。嗜酸性小体在第1组的5例(36%)中依次增多,而在第2组中无一例增多。第1组10例(71%)门脉炎症严重程度加重,而第2组为2例(13%),尽管两组纤维化进程的变化无差异。这些差异无法根据两组的每日乙醇摄入量和复发时长来解释。因此,接受戒酒硫治疗的酗酒者复发时,戒酒硫和酒精的联合作用会导致嗜酸性小体和门脉炎症的发展以及GGIs的出现。

相似文献

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Cyanamide-associated alcoholic liver disease: a sequential histological evaluation.氰胺相关酒精性肝病:一项连续组织学评估
Alcohol Clin Exp Res. 1995 Oct;19(5):1307-11. doi: 10.1111/j.1530-0277.1995.tb01616.x.
2
Cyanamide-induced liver dysfunction after abstinence in alcoholics: a long-term follow-up study on four cases.
Alcohol Clin Exp Res. 2000 Apr;24(4 Suppl):100S-105S.
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Comparison of cyanamide and disulfiram in effects on liver function.氨基氰和双硫仑对肝功能影响的比较。
Alcohol Clin Exp Res. 2000 Apr;24(4 Suppl):97S-99S.
4
Hepatic disease associated with ground-glass inclusions in hepatocytes after cyanamide therapy.
Arch Pathol Lab Med. 1986 Oct;110(10):906-10.
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Cyanamide-induced liver injury. A predictable lesion.氰胺引起的肝损伤。一种可预测的病变。
Liver. 1983 Aug;3(4):225-30. doi: 10.1111/j.1600-0676.1983.tb00872.x.
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Use of a monoclonal antibody against Lafora bodies for the immunocytochemical study of ground-glass inclusions in hepatocytes due to cyanamide.一种抗拉福拉小体的单克隆抗体在免疫细胞化学研究中用于检测由氨基氰导致的肝细胞毛玻璃样包涵体。
Histopathology. 2001 Jul;39(1):60-5. doi: 10.1046/j.1365-2559.2001.01127.x.
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Cyanamide hepatotoxicity. Incidence and clinico-pathological features.氰胺肝毒性。发病率及临床病理特征。
Liver. 1987 Aug;7(4):216-22.
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Hepatitis induced by drugs used as alcohol aversion therapy.用作酒精厌恶疗法的药物所致肝炎。
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