ObjectiveTo investigate the clinical features of male patients with alcoholic liver cirrhosis (ALC) or hepatitis B cirrhosis (HBC) complicated by abnormal glucose metabolism. MethodsA total of 287 patients with liver cirrhosis who were admitted to Guangzhou Panyu Central Hospital from January 2008 to September 2013 were selected. Among these patients, 74 had ALC and were all male, including 54 with abnormal glucose metabolism; the other 213 had HBC, including 97 with abnormal glucose metabolism (69 male patients and 28 female patients). A controlled study was performed for the clinical data of ALC and HBC patients with abnormal glucose metabolism, to investigate the association of patients′ clinical manifestations with the indices for laboratory examination, insulin resistance index, incidence rate of abnormal glucose metabolism, and Child-Pugh class. The t-test was applied for comparison of continuous data between groups, the chi-square test was applied for comparison of categorical data between groups, and the Spearman rank correlation was applied for correlation analysis. ResultsCompared with HBC patients, ALC patients had significantly higher incidence rates of abnormal glucose metabolism (730% vs 32.4%), hepatogenous diabetes (35.1% vs 14.6%), fasting hypoglycemia (27.0% vs 10.3%), and impaired glucose tolerance (31.1% vs 14.1%) (χ2=4.371, 3.274, 4.784, and 1.633, all P<0.05). The Spearman correlation analysis showed that in ALC and HBC patients, the incidence rate of abnormal glucose metabolism was positively correlated with Child-Pugh class (rs=0.41, P<005). Compared with the HBC patients with abnormal glucose metabolism, the ALC patients with abnormal glucose metabolism had a significantly higher incidence rate of Child-Pugh class A (χ2=7.520, P=0.001), and a significantly lower incidence rate of Child-Pugh class C (χ2=6.542, P=0.003). There were significant differences in the incidence rates of dim complexion, telangiectasia of the face, spider angioma, hepatomegaly, hepatorenal syndrome, malnutrition, ascites, jaundice, hepatic encephalopathy, spontaneous bacterial peritonitis, and upper gastrointestinal bleeding between the ALC and HBC patients with abnormal glucose metabolism (χ2=3.785, 2.651, 1974, 3.316, 3.771, 5.843, 7.251, 5.214, 5.778, 2.966, and 6.312, all P<0.05). Compared with the HBC patients with abnormal glucose metabolism, the ALC patients with abnormal glucose metabolism had significantly higher levels of aspartate aminotransferase and total bilirubin, a significantly greater mean corpuscular volume, a significantly higher level of gamma-glutamyl transpeptidase, and a significantly lower level of albumin (t=4.775, 7.887, 5.143, 6.124, and 5.210, all P<0.05). There were significant differences in the fasting blood glucose level, insulin level 2 hours after meal, and insulin resistance index between the ALC and HBC patients with abnormal glucose metabolism (t=2.770, 6.331, and 3.770, all P<0.05). ConclusionThe male patients with ALC or HBC gradually develop abnormal glucose metabolism with the deterioration of liver function, with individual etiology and features of liver cirrhosis, and the manifestations of abnormal glucose metabolism are not obvious. Related examinations should be performed for these male patients with liver cirrhosis of various causes, to confirm the existence of abnormal glucose metabolism.