HEPATIC ZINC CONTENT IN PATIENTS WITH VARIOUS STAGES OF ALCOHOLIC LIVER-DISEASE AND IN PATIENTS WITH CHRONIC ACTIVE AND CHRONIC PERSISTENT HEPATITIS
HEPATIC ZINC CONTENT IN PATIENTS WITH VARIOUS STAGES OF ALCOHOLIC LIVER-DISEASE AND IN PATIENTS WITH CHRONIC ACTIVE AND CHRONIC PERSISTENT HEPATITIS
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DOI：
10.1002/hep.1840080622
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发表时间：
1988-11-01
期刊：
影响因子：
13.5
通讯作者：
BODE, C
中科院分区：
文献类型：
--
作者：
BODE, JC;HANISCH, P;BODE, C
用质子激发X射线发射法测定了酒精性和非酒精性肝病患者肝活检组织中的锌含量。从27例无急性或慢性肝病证据的患者尸检肝脏标本中获得的值作为对照。对照组中锌含量的平均值和范围（75 ± 100）。24 ppm湿重）与文献中报道的那些一致。对照组肝锌含量无明显的年龄和性别依赖性。所有酒精性肝病患者组的平均锌含量均显著降低。在酒精性脂肪肝（-56.7%，n = 12）、轻度酒精性肝炎（-50.5%，n = 6）和酒精性肝硬化（-45.6%，n = 10）患者的活检中，这种下降相当。慢性活动性肝炎（-60.3%，n = 15）和慢性迁延性肝炎（-44.9%，n = 8）肝锌含量也明显降低。对7例酒精性肝硬化患者和6例对照者的尸检标本中肝脏亚细胞组分中锌含量的估计显示，含细胞核和膜的组分以及线粒体组分中锌含量显著降低。在100，000 g上清液中观察到类似的降低;然而，差异未达到统计学差异。对照组中微粒体组分的锌含量低于其他三种细胞组分。两组研究样本的微粒体锌含量无显著差异。这项研究的结果强调了这样一个事实，即肝脏锌缺乏不仅发生在酒精性肝病，而且发生在不太严重的酒精性和非酒精性肝病。
The hepatic zinc content was determined in liver biopsies of patients with alcoholic and nonalcoholic liver disease using proton-induced X-ray emission. The values obtained in postmortem specimens of the liver from 27 patients with no evidence of acute or chronic liver disease served as controls. The mean value and the range of the zinc content in the controls (75 .+-. 24 ppm wet weight) are in good agreement with those reported in the literature. The hepatic zinc content in the control group showed no signifiant age or sex dependence. The mean zinc content was significantly decreased in all groups of patients with alcoholic liver disease. The decrease was comparable in biopsies from patients with alcoholic fatty liver (-56.7%, n = 12), mild alcoholic hepatitis (-50.5%, n = 6) and alcoholic cirrhosis (-45.6%, n = 10). The hepatic zinc content was also distinctly reduced in patients with chronic active hepatitis (-60.3%, n = 15) and in those with chronic persistent hepatitis (-44.9%, n = 8). The estimation of the zinc content in subcellular fract ions of the liver performed in postmortem specimens from seven patients with alcoholic liver cirrhosis and in six controls revealed a significant reduction in the zinc content in the fraction containing cell nuclei and membranes and in the mitochondrial fraction. A similar decrease was seen in the 100,000 g supernatant; however, the difference did not attain statistical difference. The zinc content of the microsomal fraction in the controls was lower than in the other three cell fractions. There was no significant difference in microsomal zinc content between the samples of the two groups studied. The results of this study underline the fact that zinc deficiency in the liver occurs not only in cirrhotics but also in less advanced alcoholic and nonalcoholic liver disease.