Baldini G G, Zaina A, Della Ventura G, Giacomini V, Muzio F
Divisione Medicina Generale II, USSL 67-Regione Lombardia, Ospedale Santa Corona, Garbagnate Milanese, Milano.
Minerva Gastroenterol Dietol. 1995 Jun;41(2):157-62.
AIMS. 1) To evaluate the nutritional status of a group of alcohol abusers, relatively to their liver function and morphology, and 2) to compare these data with those of a previous study carried out by out team ten years ago. According to their body weight, 135 alcohol abusers were divided into three groups: normal-weight, over-weight and under-weight. The severity of their hepatopathy was defined as: 1. slight hepatopathy; 2. alcohol-induced hepatitis; 3. alcohol-induced hepatitis plus cirrhosis; 4 child A cirrhosis; 5. child B cirrhosis. RESULTS. 1. The overweight group was homogeneously distributed among the several degrees of compensated hepatopathy. 2. There was a marked reactivity to skin tests (Multitest) in patients with alcohol hepatitis without cirrhosis, independently of nutritional disorders. 3. Only decompensated cirrhosis may cause caloric-protein malnutrition; consequently, nutritional disorders due to alcohol abuse appear late and they are unlikely to play a leading role in the pathogenesis of liver disease due to alcohol abuse. Obesity, on the other hand, may facilitate the onset of liver steatosis.
目的。1）评估一组酗酒者的营养状况，及其与肝功能和形态的关系；2）将这些数据与我们团队十年前进行的一项先前研究的数据进行比较。根据体重，135名酗酒者被分为三组：正常体重、超重和体重过轻。他们肝病的严重程度定义为：1. 轻度肝病；2. 酒精性肝炎；3. 酒精性肝炎加肝硬化；4. 儿童A期肝硬化；5. 儿童B期肝硬化。结果。1. 超重组在代偿性肝病的几个程度中分布均匀。2. 无肝硬化的酒精性肝炎患者对皮肤试验（多项试验）有明显反应，与营养紊乱无关。3. 只有失代偿性肝硬化可能导致热量 - 蛋白质营养不良；因此，酗酒引起的营养紊乱出现较晚，且不太可能在酗酒所致肝病的发病机制中起主导作用。另一方面，肥胖可能促进肝脂肪变性的发生。
