| Objective: Liver is main organ of sex hormones metabolism and conversion, the damage of liver function usually cause abnormality of sex hormone levels. The correlation between sex hormone levels and the degree of liver damage has already been acknowledged, various hormonal patterns of gonadal failure and of the impairment of steroid metabolism and transport, observed in cirrhosis, can be attributed to the degree of liver dysfunction. Domestic and international scholars have common opinions of the decreasion of testosterone, but have various opinions of estradiol., Currently, domestic researchs into estrogen only examined E2 , but did not examine the E1, E3. Clinical features of male cirrhotic subjects are feminization(palmar erythema, spider naevi, gynecomastia) and hypogonadism. The man's feminization is abnormally outstanding manifestations in chronic liver disease, The past researchs thought the feminization was the result of the increase of estrogen, but some studies thought that increased estrogen wasn't consistent with the feminization in the liver disease .To further clarify the relation between serious degree of cirrhosis and sex hormones, explore the changes of sex hormones and severity of liver dysfunction in the male patients with cirrhosis in the stage of decompensation, The correlation between various index signs of the Child-pugh's grade and sex hormones is studied in this paper.. The purposes of our studies, on the one hand, were to learn change of sex hormones and explore their mechanism and clinical significance in patients with decompensated hepatic cirrhosis, on the other hand, were to conform the relation between feminization and estrogen in patients with decompensated cirrhosis.Materials and Methods:Forty-five patients with decompensated hepatic cirrhosis admitted to the first affiliated hospital Zheng Zhou University during the period between January 2004 and June 2OO4.The series consisted of 45 patients (all is 45 men; age range,20-70 years, average 51 years)with decompensated hepatic cirrhosis. All cases were definitely diagnosed to decompensated hepatic cirrhosis according to disease history,clinical sign, biochemistry examination and Bultrasonography ,computerized tomography ,and electronic gastric mirror. All patients hadn't heart disease, lung disease and kidney disease, and didn't take medicines which possibly affected sex hormones within one month . Including 37 patients with posthepatitis B decompensated cirrhosis, 2 patients with decompensated alcoholic cirrhosis, 4 patients with decompensated mixted cirrhosis(posthepatitis B and alcoholic cirrhosis), 2 patients with decompensated posthepatitis C cirrhosis , 1 patients with decompensated cirrhosis which was induced by medicine to the damage of the liver, 26 patients merging with ascites, 31 patients with feminization ,8 patients with uper gastrointestinal hemorrhage, 9 patients with primary carcinoma of the liver. Some patients have two or more than two kinds of complications at the same time. Another choosing 20 health males for matched control, age 22-70 years old, average 49 years old, without disease history in lung, liver, kidney and endocrine disease., various liver function index signs are all normal, age , weight index , blood pressure, food habit etc. all were comparable between patients and controls. The blood(4 milliliter) of all patients without meal was obtained in the next morning in the hospital. Serum was preserved in refrigerators(- 83 centigrade) to measure after being separated Centrifugal machine. Serum components of sex hormone, testosterone(T), Estrone(Ei), Estradiol(E2), and estriol(E3) were measured by radioimmunoassay in 45 cases decompensated cirrhosis, then compared with 20 cases normal subjects. Other biochemical indexes were measured by the lab of the hospital in the next morning . patients with hepatic cirrhosis(45 cases) were divided into Child-pugh grade A(5-6 score)group (14 cases), Child-pugh grade B(7-9 score)group (19 cases),and Child-pugh grade C(>10 score)group(12 cases) according to Child-pugh grade to compare. The data were analyzed by soft ware SPSS 10.0 .P value of less than 0.05 was considered statistically. Results1. Serum E, values were 41.73±25.05 and 23.95± 10.20 in patients with cirrhosis and control group, Ei values were significantly higher in cirrhosis than in control group (P<0.01) .There was no significant difference in E2 between patients with cirrhosis( 20.15±l 1.67)and control group (19.78±7.07) (P>0.05). Serum E3 values were 1.66±1.04 and 1.17±0.42 in patients with cirrhosis and control group, E3 values were significantly higher in patients with cirrhosis than in control group (P<0.05). Serum T were 223.10±100.16 and 400.09±108.36 in patients with cirrhosis and control group, T value was significantly lower in patients with cirrhosis than in control group (P<0.01).2. Patients with cirrhosis(45 cases) were divided into Child-pugh grade A(5-6 score)group (14 cases), Child-pugh grade B(7-9 score)group (19 cases),and Child-pugh grade C(>10 score)group(12 cases) according to Child-pugh grade Serum Ei values were 25.65±7.71, 41.55±12.47, 60.75±38.25 in Child-pugh grade A group, B group , C group, respectively. Ei progressively and significantly increased from cirrhosis Child A to C(A and B PO.05, A and C PO.01, B and C P<0.05); Serum E2 values were 18.6±27.36 ,20.52±12.96 ,22.19±13.43, in Child-pugh grade A group, B group , Cgroup, respectively. No difference was found in serum E2 from cirrhosis Child A to C(P>0.05); Serum E3 values were 1.32±0.56,1.60±1.01,2.16±1.37 in Child-pugh grade A group, B group, C group, respectively. There was no significant difference in serum E3 from cirrhosis Child A to B(P>0.05) and from Child B to C (P>0.05), but significant difference between Child B and C(P<0.05); Serum T values were 293.81±84.43,226.40±76.84,135.41±85.31 in Child-pugh grade A group, B group , C group, respectively. T progressively and significantly decreased from cirrhosis Child A to C (A andBP<0.05, A and CPO.01, B andCPO.Ol) .3. There was no significant difference in Ei between patients with ascites (45.56±29.13) and without ascites (42.82±27.95)(P>0.05); There was no significant difference in E2 between patients with ascites (20.62±11.85) and without ascites (19.52±11.72)(P>0.05); There was no significant difference in E3 between patients with ascites (1.79±1.25) and without ascites (1.42±0.71)(P>0.05); There was no significant difference in T between patients with ascites (206.59±105.97)without ascites (248.3 l±90.21)(P>0.05).4. Serum E, values were 74.08±42.43^ 37.83±19.32 in patients with Hepatic encephalopathy and without hepatic encephalopathy, E, were significantly higher inpatients with hepatic encephalopathy than without hepatic encephalopathy (P<0.01); There was no significant difference in E2 between patients with hepatic encephalopathy (21.74±16.07) and without hepatic encephalopathy (19.91±ll.ll)(P>0.05); There was no significant difference in E3 between patients with hepatic encephalopathy (2.27±1.66) and without hepatic encephalopathy (1.57±0.91)(P>0.05); Serum T values were 141.93±69.36, 239.36±111.65 in patients with Hepatic encephalopathy and without Hepatic encephalopathy, T in patients with hepatic encephalopathy were significantly lower than without Hepatic encephalopathy (P<0.01);5. E] positively correlated with total bilirubin ( r=0.442vP<0.01 ) and prothrombin time(r=0.553,P<0.05),but didn't correlate with albumin(P>0.05). E2 was positively correlated with total bilirubin(r=0.335,/><0.05), but didn't correlate with albumin and prothrombin time (P>0.05). E3 didn't correlate with total bilirubin , prothrombin time and albumin(P>0.05). T positively correlated with albumin (r=0.323,P<0.05)and negatively correlate with total bilirubin(r=-0.455, PO.01) and prothrombin time(r= -0.472, PO.01).6. Child-pugh score was correlated positively with Ei (r=0.511,P<0.01)and was correlated negatively with T(r=-0.53,P<0.01)in cirrhosis group. Not correlated in E2, E3 (P>0.05).7.Serum Ei values were 47.48±27.76 and 29.01±9.70 in group with feminization and group without feminization , E] values were significantly higher in group with feminization than without feminization (P<0.05) .There was no significant difference in E2 between group with feminization (21.13±12.11 )and without feminization (18.00±10.76) (P>0.05). .There was no significant difference in E3 between group with feminization (1.78±1.14)and without feminization (1.40±0.74) (P>0.05). Serum T values were 217.16±108.27^ 260.35±112.18 in group with feminization and without feminization , T values were lower in group with feminization than without feminization, but there wasn't significant difference (P>0.05) . Conclusions1. Ei,E3 were significantly higher in patients with cirrhosis in control. T were significantly lower in patients with cirrhosis than in control. Our data suggests that disturbance of sex hormones existed in decompensated liver cirrhosis, and hinted that the damage of the liver may be a important reason of resulting in sex hormonesabnormality.2. Ej progressively and significantly increased from cirrhosis Child A to C ; No difference was found in serum E2 from cirrhosis Child A to C(P>0.05); There was significant difference between Child B and C; T progressively and significantly decreased from cirrhosis Child A to C. it indicated that the degree of sex hormones dysfunction and serious degree of decompensated cirrhosis were closely correlated.3. Ei values were significantly higher in hepatic encephalopathy. Ei positively correlated with total bilirubin , prothrombin time and Child-pugh score. E2 positively correlated with total bilirubin. T were significantly lower in patients with hepatic encephalopathy. T positively correlated with albumin and negatively with total bilirubin , prothrombin time and Child-pugh.; Sex hormones, especially increased Ei and decreased T were consistent with the damage of the liver. Measuring sex hormones .especially Ei, T can reflect degree of the liver damage, and also can be indexes to estimate the prognosis and therapy affection of patients with decompensated hepatic cirrhosis.4. Ei values were significantly higher in group with feminization than that in group without feminization. T values were lower in group with feminization than that in group without feminization, but there was no significant difference. There was no significant difference in E2, E3 between group with feminization and without feminization. Speculating that the feminization has certain connection with Ei , no direct connection with E2.
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