Cell-mediated immunity in acute and chronic hepatitis.

Peripheral lymphocytes from patients with hepatitis-B surface antigen (HBsAg)-positive and -negative acute hepatitis (AH), chronic active hepatitis (CAH), chronic persistent hepatitis (CPH), and normal controls were tested for in vitro cytotoxicity and blast transformation. Cytotoxicity was measured by chrominum (21Cr) release into the medium from 51Cr-labeled Chang liver cells after incubation for 6 h with peripheral lymphocytes at a lymphocyte target cell ratio of 200:1. Concomitant 72-h incubation studies were performed to assess thymus cell-dependent (T) lymphocyte function as measured by conccanavalin A (Con A)- stimulated incorporation of tritiated thymidine (blast transformation) and by cytotoxicity. It was found that (a) lymphocytes from patients with AH are cytotoxic to Chang liver cells compared to controls (P less than 0.001); (b) lymphocytes from patients with acute and chronic hepatitis are less cytotoxic when incubated with autologous and homologous HB2Ag-positive and -negative AH, CAH, and CPH are as cytotoxic as normal controls when stimulated with a nonspecific mitogen such as Con A; and (d) lymphocytes from patients with CAH while on prednisone therapy showed marked depression of cytotoxicity when stimulated with Con A. Thus these studies show that patients with AH have circulating T lymphocytes which are capable of causing the destruction of Chang liver cells. There is no defect in T-cell function as measured by Con A-stimulated cytotoxicity. There is a serum factor (s) in patients with acute and chronic hepatitis which inhibits spontaneous and induced lymphocyte cytotoxicity and blast transformation. Finally, prednisone treatment appears to inhibit lymphocyte cytotoxicity in patients with CAH.     

Serum HBV-DNA (hepatitis B virus DNA) in acute and chronic hepatitis B infection

HBV DNA was measured in the sera of 69 patients with hepatitis B virus infections. Sixteen patients had acute hepatitis B, 24 had chronic active hepatitis (CAH), 6 had chronic persistent hepatitis (CPH), 5 had cirrhosis without CAH and 18 were asymptomatic HBsAg carriers. In patients with acute hepatitis B who recovered, HBV DNA was present in the serum transiently early in the illness. HBV DNA persisted in the serum in the two patients who developed chronic hepatitis. Sera of 23 of 24 patients with CAH were persistently positive for HBV DNA. There was no relationship between the quantity of HBV DNA in the serum and the histological intensity of activity. Thirteen of the 24 patients with CAH had histological evidence of cirrhosis in addition to CAH and HBV DNA was detected in the sera of all 13. The sera of 2 of 6 patients with CPH were positive for HBV DNA. In one it was positive only where there was clinical evidence of reactivation of HBV infection. The other patient subsequently developed CAH. Sera of 5 patients with established HBsAg positive cirrhosis but without evidence of CAH were negative for HBV DNA. Two of these patients had hepatocellular carcinoma. Sera of 18 asymptomatic anti-HBe positive carriers with normal ALT were negative for HBV DNA. HBeAg and HBV DNA were not always found in the serum together. In acute hepatitis 5 patients with HBV DNA in the serum were HBeAg positive, but in 6 patients the sera were HBeAg positive inthe absenceof HBV DNA.     

Alfuzosin-induced acute hepatitis in a patient with chronic liver disease

OBJECTIVE: To report a new case of probable alfuzosin-induced hepatitis. CASE SUMMARY: An 80-year-old man was evaluated because of jaundice and pruritus. He was diagnosed as having Child-Pugh A chronic liver disease due to hepatitis B virus. Other etiologies of hepatitis were appropriately ruled out, and the hepatitis B was non-replicative. Therefore, elevated liver enzyme levels were ascribed to alfuzosin treatment. DISCUSSION: Although alfuzosin-related mixed-type hepatotoxicity has been previously reported, this is the first published case describing probable hepatocellular-type hepatotoxicity resulting from use of alfuzosin in a patient with underlying chronic liver disease. According to the Naranjo probability scale, alfuzosin was a probable cause of the hepatotoxicity. The mechanism of alfuzosin-induced liver damage is unknown. Several features, such as absence of predictable dose-dependent toxicity of alfuzosin in previous studies and absence of hypersensitivity manifestations in our case, are suggestive of a metabolic type of idiosyncratic toxicity. CONCLUSIONS: Alfuzosin rarely causes hepatotoxicity; however, clinicians must be alert for this adverse effect while using alfuzosin.     

急性戊型肝炎重叠慢性乙型肝炎感染的实验室特性分析

目的：研究HEV重叠慢性乙型肝炎感染患者的临床、实验室特征及分析戊型肝炎病毒感染对慢性乙型肝炎患者肝纤维化的影响。方法：随机选取单纯HBV感染患者和HBV重叠HEV感染患者各40例,对他们的临床及实验室检查资料进行分析,研究HEV感染对慢性乙型肝炎患者临床及实验室指标的影响。结果：（1）两组患者HBeAg 、HbeAb和HBV-DNA阳性率比较,差异无统计学意义（P〉0.05）（2）重叠组重型肝炎率及自发性腹膜炎率均高于乙型肝炎组,差异有统计学意义（重型肝炎率：χ^2=10.476,P〈0.001;自发性腹膜炎率χ^2=5.878,P=0.015）。而死亡率两组比较未见统计学意义（χ^2=0.263,P=0.608）（3）两组患者血清总胆红质、丙氨酸氨基转移酶、天冬氨酸氨基转移酶比较,差异有统计学意义（4）两组患者肝纤维化指标（层粘连蛋白、Ⅲ型前胶原氨基端肽、Ⅳ型胶原及血清透明质酸）差异均有统计学意义。结论：慢性乙型肝炎重叠戊型肝炎感染可以加重患者的症状和并发症,造成严重的肝功能损伤及加重患者的肝纤维化。     

Fibronectin is an acute phase reactant in mice

Tissue injury and inflammation are potent stimuli for the immediate increased synthesis of several plasma proteins collectively known as acute phase phase reactants. This dramatic phenomenon is thought to play an important role in inflammation and tissue repair. Plasma fibronectin is a normal plasma glycoprotein and a major non-specific opsonin apparently involved in maintaining the integrity of the mononuclear phagocytic system. Because of its ability to mediate clearance of intravascular particulate matter, increased production following tissue injury could be of benefit to the organism. We now report that plasma fibronectin is a significant acute phase reactant in mice with levels increasing from a baseline mean value of 257 ug/ml to 595 ug/ml by 24 hours (p less than 0.01) after a subcutaneous injection of silver nitrate. Similar findings were observed when subcutaneous casein was used as the acute phase stimulus. This data provides further circumstantial evidence that plasma fibronectin is involved in host defence and tissue repair.     

慢性乙型肝炎重叠急性戊型肝炎63例HBV基因型的检测和分析

目的:探讨HBV基因型与慢性乙型肝炎重叠急性戊型肝炎发病机制的相关性.方法:采用Caliper微流芯片法测定63例慢性乙型肝炎重叠急性戊型肝炎患者的HBV基因型.同时对HBV-DNA定量采用荧光定量PCR技术测定,生化指标采用全自动生化分析仅检测.结果:63例慢性乙型肝炎重叠急性戊型肝炎患者B型和C型分别为22例和39例,C型HBV重叠HEV感染率明显高于B型(P<0.05),HbeAg(-)和HbeAg(+)分别为31例和32例,HbeAg(-)和HbeAg(+)的慢性乙型肝炎患者重叠HEV感染率相仿(P>0.05);C型患者血清ALT、AST、TBIL水平明显高于B型(JD<0.05),血清CHE、ALB、PTA水平明显低于B型(P<0.05);B型和C型患者HbeAg阳性率分别为31.8%和61.5%,C型患者HBeAg阳性率明显高于B型(P<0.05);在HbeAg(-)组中,B、C型HBV-DNA的阳性率分别为55.3%和26.7%,B型患者的HBV-DNA阳性率明显高于C型(P<0.05).结论:C型HBV感染的慢性乙型肝炎患者比B型更易重叠HEV感染,同时,C型患者肝功能损害要明显重于B型.B型HBV易发生前C区变异,可能是B型HBV感染的慢性乙型肝炎患者重叠HEV感染率低于C型的原因之一.     

IL-33和ST2在慢加急性乙型肝炎肝衰竭和慢性乙型肝炎患者中水平差异及应用研究

目的探讨白细胞介素-33(IL-33)和ST-2蛋白(ST2)在慢加急性乙型肝炎肝衰竭(ACHBLF)和慢性乙型肝炎患者中水平差异及应用价值。方法选取该院42例ACHBLF患者作为研究组A组,45例慢性乙型肝炎患者作为研究B组,另选取45例同期于该院行健康体检的健康志愿者作为健康对照组。采用酶联免疫吸附试验对血清IL-33和ST2水平进行检测,并对比检测结果。分别采用赖氏法、酶联免疫吸附试验、溴甲酚绿法对3组研究对象丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、清蛋白(ALB)水平进行检测,并分析在研究A组和研究B组中血清IL-33和ST2分别与ALT、AST和ALB的临床关系。结果研究A组血清IL-33和ST2、ALT和AST水平较研究B组和健康对照组显著升高,差异均有统计学意义(P0.05),且研究B组IL-33和ST2、ALT和AST水平也较健康对照组显著升高,差异有统计学意义(P0.05);研究A组血清ALB水平较研究B组和健康对照组显著降低,差异有统计学意义(P0.05),且研究B组ALB水平显著低于健康对照组,差异有统计学意义(P0.05);研究A组血清IL-33和ST2与ALT、AST水平呈显著正相关,与血清ALB呈显著负相关;研究B组血清IL-33和ST2与ALT、AST水平呈显著正相关,与血清ALB无明显相关性。结论 ACHBLF患者血清IL-33和ST2水平较慢性乙型肝炎患者显著升高,推测可能与加重炎性反应和肝损伤有关。     

Interferon preparations in the treatment of acute and chronic forms of hepatitis B

The therapeutic efficacy of human leucocytic alpha-interferon and combiferon produced in the N.F. Gamaleya Institute of Epidemiology and Microbiology, was assessed in 27 patients with different types of hepatitis B and in 30 controls. A marked clinical effect was noted in therapy of acute types of hepatitis B: the improvement of clinical and immunological indices, the reduction of the duration of HBs-antigenemia. The treatment of chronic types was effective in 5 out of 8 patients. A therapeutic scheme for acute and chronic types of hepatitis B was given.     

Central hemodynamics and portal-hepatic blood flow in patients with acute and chronic virus hepatitis

AIM: To characterize central hemodynamics and portal-hepatic blood flow in patients with acute and chronic viral hepatitis. MATERIAL AND METHODS: Ultrasound investigation, tetrapolar rheography, hepatic scintigraphy were made in 149 patients with acute and chronic viral hepatitis B, C and B + C. RESULTS: The above patients had disturbances in central hemodynamics manifesting with developing myocardiodystrophy and hyperkinetic hemodynamics syndrome; decreased intensity and increased amplitude of respiratory fluctuations of volumic hepatic blood flow; impairment of peripheral blood flow. CONCLUSION: The above changes were most prominent in patients with chronic hepatitis B + C.     

Fibronectin and factor VIII-related antigen in liver cirrhosis and acute liver failure

The liver is involved in the turnover of fibronectin in two different ways: hepatic synthesis contributes substantially to the plasma fibronectin pool, while Kupffer-cells, performing an important role of the reticuloendothelial system, remove fibronectin opsonized material from the circulation. In 45 patients with histologically confirmed liver cirrhosis and six patients with acute liver failure due to intoxication we determined fibronectin concentration in plasma by electroimmunoassay and additionally measured factor VIII-related antigen, which is a large glycoprotein not synthesized in the liver. Fibronectin levels in plasma were decreased in liver cirrhosis. This decrease was correlated with the extent of porto-caval collateral circulation. Very low levels were found in patients with acute liver failure. Factor VIII-related antigen levels were greatly increased as a function of the hepatic insufficiency. Between both parameters there was a significant inverse correlation. It is concluded that the simultaneous determination of both proteins provides reliable information about the remaining liver function.