Hepatitis B surface antigen in urine of hemodialysis patients

As part of an extensive epidemiological survey of chronic hemodialysis patients in Michigan, hepatitis B surface antigen (HBsAg) was identified in the sera of 79 of 701 (11%) patients. Of these patients, 59 were carriers of HBsAg for three or more months. Urine samples were collected from 36 of 39 HBsAg carriers having urinary output. Of these samples, 19 (52%) were positive for HBsAg by radioimmunoassay; this was confirmed by specific antibody neutralization. The HBsAg was not identified in the urine of seven hemodialysis patients who were lacking serum HBsAg or in urine samples from three HBsAg sero-carriers who had normal renal function. Patients undergoing maintenance hemodialysis appear to constitute a large reservoir of HBsAg chronic carriers. This study indicates that a minimum of 50% of persistent HBsAg carriers who are producing urine have detectable HBsAg in single, randomly timed, unconcentrated urine specimen. These data suggest that urine may represent a potential vehicle for transmission in nonparenterally acquired hepatitis B.     

Hepatitis B surface antigen positivity is not a contraindication for living kidney donation

Because of the organ shortage, the number of patients awaiting kidney transplantation has increased rapidly requiring physicians to implement new methods to increase the number of grafts. In this study, we compared clinical and biochemical parameters of patients who received kidneys from hepatitis B surface antigen-positive (group 1) versus other living related kidney donors (group 2). The study included 414 female (15 group 1 and 399 group 2) and 816 male (20 group 1 and 796 group 2) donors for 1195 living related kidney transplantations performed between April 21, 2008 and March 1, 2011. Group 1 kidney transplantations were undertaken only if the recipient displayed a hepatitis B antibody titer >10 mIU/mL and donor hepatitis B virus (HBV) DNA was negative. Demographic characteristics, 1- and 2-year serum creatinine levels, glomerular filtration rates (GFR), and liver function test results were similar between the 2 groups. There were no new HBV infections throughout the study period. Acute rejection rates (7/35 in group 1 vs 232/1195 in group 2; P = .988), graft loss (1/35 in group 1 vs 55/1195 in group 2; P = .624), and patient loss (0/35 in group 1 vs 34/1195; P = .311) were similar between the 2 groups. Our study showed that hepatitis B surface antigen positivity was not a contraindication to living kidney donation.     

Membranous nephropathy in 52 hepatitis B surface antigen (HBsAg) carrier children in Taiwan

To elucidate the prognosis and the causative viral antigens of hepatitis B virus (HBV)-associated childhood membranous nephropathy (MN), the clinical course and glomerular HBV antigens were studied in 52 HBsAg carrier children with MN (40 boys, 12 girls). With Fab fragments of monoclonal antibodies, hepatitis Be antigen (HBeAg) was detected in the glomerular deposits in 41 (95%) of 43 cases but HBsAg and hepatitis B core antigen (HBcAg) in none. HBeAg was detected in sera from 43 (93%) of 46 children examined. These results suggest that HBeAg plays an important role in the development of MN in HBsAg carrier children. During the follow-up period (mean, 4 years), complete remission was found in 64% and 92% of the patients followed for one and seven years, respectively; only one child had mild renal function impairment. These findings suggest a favorable outcome of HBsAg-associated childhood MN. The patient's age, disease duration, amount of glomerular deposit, focal sclerosis and disease stage appeared to affect the clinical course. HBsAg seroconversion to HBsAg-negative occurred in seven cases, and all (100%) had quick remission in two years. In patients with persistent HBsAg carriage, serum HBeAg status alone did not correlate with remission rate and remission occurred usually before the HBeAg seroconversion to anti-HBe. These findings, together with the predominant horizontal infection in these children in contrast to the frequent vertical (perinatal) transmission from HBsAg carrier mothers in HBsAg carriers in Taiwan, suggest that factors other than HBeAg per se may also play important roles.     

Hepatitis B antigen in joint irrigation fluid. A hazard for hospital personnel

We report the case of a carrier of the hepatitis B virus who required arthroscopy of the knee. The irrigation fluid was shown to contain the virus. In view of the highly infective nature of this virus, appropriate precautions are necessary when carrying out arthroscopy in such patients.     

Acid-base status in diabetic mothers and their infants following general or spinal anesthesia for cesarean section.

Acid-base status was studied in 30 diabetic mothers and their infants and in 30 healthy mothers and their babies after general or spinal anesthesia for cesarean section. A normal acid-base state was found for the diabetic subjects following general or spinal anesthesia. However, the infants of diabetic mothers given spinal anesthesia had an average pH of 7.20 and a base excess value of -5.67 mEq/l in umbilical-artery blood at delivery. These values were significantly lower than those observed in the infants of the other groups, where the average pH was between 7.28 and 7.30 and the base excess between -1.87 mEq/l and 1.00 mEq/l. These findings were significantly related to maternal diabetes and maternal hypotension.     

Hepatitis B x antigen and p53 in the development of hepatocellular carcinoma

Hepatitis B virus (HBV) is one of the major etiological agents responsible for the appearance of chronic liver diseases, including hepatocellular carcinoma (HCC). There is increasing evidence that the HBV excoded x antigen (HBxAg) is involved in one or more steps that contribute to multistep hepatocarcinogenesis. Recent work has now defined one of these steps as the physical binding and functional inactivation of the tumor suppressor protein, p53, by HBxAg. The centrality of p53 to genomic stability, cell cycle arrest, induction of apoptosis, and in senescence related pathways, suggests that its disruption by HBxAg will result in genomic instability, loss of cell cycle control, a lower apoptotic rate, and an extension in the life span of HBV-infected cells. It is proposed that HBxAg/p53 complex formation represents one of several steps whereby HBV contributes to the development of HCC. Received for publication on Jan. 6, 1998; accepted on June 10, 1998     

The role of hepatitis B surface antigen in the pathogenesis of glomerulopathies.

The frequency of hepatitis B surface antigen (HBsAg) has been studied in the sera and renal biopsies of 276 patients with various forms of glomerulonephritis (GN), the nephrotic syndrome and other nephropathies. Using a modified Hepanosticon method, HBs antigenemia was detected in 32 of 196 patients (16.3%) with immune complex (IC) GN and the nephrotic syndrome. Indirect immunofluorescence revealed HBsAg in 33 renal biopsy tissue specimens (16.8%). HBsAg was found in the sera of four of the 80 remaining patients with other renal diseases (5%), and in the renal biopsy tissues of another four (5%). Antibody against HBsAg could only be demonstrated in the serum of one glomerulonephritic patient. The sera of 18,799 normal blood donors were used as controls; of these 186 (0.99%) had positive tests for HBsAg. It is concluded that, in some patients with GN and the nephrotic syndrome, HBsAg-containing IC may be implicated in the development and/or progression of the disease.     

Hepatitis B virus large surface protein: function and fame

Chronic infection with hepatitis B virus (HBV) is the leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. HBV life cycle begins with viral attachment to hepatocytes, mediated by the large HBV surface protein (LHBs). Identification of the sodium-taurocholate cotransporting polypeptide (NTCP) as a HBV receptor has revealed a suitable target for viral entry inhibition. Analysis of serum hepatitis B surface antigen (HBsAg) level is a non-invasive diagnostic parameter that improves HBV treatment opportunities. Furthermore, HBsAg plays an important role in manipulation of host immune response by HBV. However, observations in patients with chronic hepatitis B under conditions of immune suppression and in transgenic mouse models of HBV infection suggest, that in absence of adaptive immune responses cellular mechanisms induced by HBV may also lead to the development of liver diseases. Thus, the multifaceted pathological aspects of HBsAg predetermine the design of new therapeutical options modulating associated biological implications.     

乙型肝炎病毒表面大蛋白在抗病毒治疗中的临床意义

目的探讨乙型肝炎病毒表面大蛋白（LHBs）在监测抗病毒疗效上的临床意义。方法跟踪监测46例阿德谲韦酯治疗患者60周,分别采用ELISA法、时间分辨免疫荧光分析法和实时定量PCR法检测患者小同时间的LHBs、HBV血清学标志物和HBV DNA载量,并进行相关性分析。结果LHBs和HBV DNA下降趋势一致,其相关系数r=0．97,但LHBs消退晚于HBV DNA。治疗60周时共有20例患者的HBV DNA〈5×10^2／mL,其中8例LHBs转阴;疗效反复组14例患者HBV DNA转阴后又转阳,3例患者LHBs转阴;治疗无效组12例患者,2例LHBs转阴。结论动态监测LHBs可作为抗病毒治疗效果评价指标的有益补充.     

Antibody to hepatitis B surface antigen is not cytotoxic to antigen-secreting hepatocytes.

A continuously growing cell line which produces hepatitis B surface antigen was grown in the presence of antibody to the surface antigen. Antibody from animal and human sources was used. Neither growth rate nor cell morphology was affected and the cells did not inactivate the antibody over a 4-day incubation period. The surface antigen produced was specifically neutralized. These results suggest that hepatic injury occurring in response to hepatitis B virus infection is not mediated by humoral immunity to the surface antigen.     

Incidence of Hepatitis C Virus (HCV), Hepatitis B Virus (HBV) and Dual Infection in Egyptian Patients on Haemodialysis

Hepatitis viral infections are important causes of morbidity and mortality in haemodialysis patients. The aim of the present work is to study the prevalence and possible risk factors of hepatitis C virus (HCV), hepatitis B virus (HBV) and dual infection in haemodialysis patients. Three hundred forty patients with end-stage renal disease, 266 males (78.2%) with mean age of 50.9?±?11.6 years and 74 females (21.8%) with mean age of 53.5?±?10.5 years on haemodialysis, were recruited from four haemodialysis units. They were screened for the presence of HCV, HBV and dual HCV and HBV infections and possible risk factors for acquiring these infections in those patients during the period between June 2007 and August 2009. One hundred ninety-six (57.7%) patients were HCV positive while 12 (3.5%) patients had HBV infection. A dual infection with both viruses was observed in 26 patients (7.6%).There was a significant difference in the number of blood transfusions among HCV-positive, HBV-positive and dual infection patients and negative patients (12.4?±?7.6, 13.8?±?6.8, 13.5?±?8.3 vs. 5.2?±?3.4 transfusions, p?<?0.01). HCV, HBV and dual HCV and HBV patients have been on dialysis for a longer period than the negative patients (7.5?±?5, 6.2?±?3.6, 7.5?±?5.4 vs. 4.4?±?4 years, p?<?0.01). Higher HCV was associated with longer haemodialysis duration and history of previous blood transfusion and not associated with dialysis in multicentres. HBV and dual infection is less prevalent than HCV in haemodialysis units.     

Cardiac changes in infants of diabetic mothers

Diabetes mellitus (DM) is a systemic chronic metabolic disorder characterized by increased insulin resistance and/or β- cell defects. It affects all ages from the foetal life, neonates, childhood to late adulthood. Gestational diabetes is a critical risk factor for congenital heart diseases (CHDs). Moreover, the risk increases with low maternal education, high body mass index at conception, undiagnosed pre-gestational diabetes, inadequate antenatal care, improper diabetes control, and maternal smoking during pregnancy. Maternal DM significantly affects the foetal heart and foetal–placental circulation in both structure and function. Cardiac defects, myocardial hypertrophy are three times more prevalent in infants of diabetic mothers (IDMs). Antenatal evaluation of the cardiac function and structures can be performed with foetal electrocardiography and echocardiography. Postnatal cardiac evaluation can be performed with natal and postnatal electrocardiography and echocardiography, detection of early atherosclerotic changes by measuring aortic intima-media thickness, and retinal vascular changes by retinal photography. Ameliorating the effects of diabetes during pregnancy on the offspring depends mainly on pregestational and gestational diabetes prevention. However, other measures to reduce the risk, such as using medications, nutritional supplements, or probiotics, still need more research. This review discusses the mechanism of foetal sequels and the risk factors that increase the prevalence of CHDs in gestational DM, the various cardiac outcomes of gestational DM on the foetus and offspring, cardiac evaluation of foetuses and IDMs, and how to alleviate the consequences of gestational DM on the offspring.     

Quantitative morphology of B, A, D, and PP cells in infants of diabetic mothers

Pancreatic specimens from 34 infants of diabetic mothers (IDM) and 32 control infants of gestational ages 26-44 wk were examined histologically using immunocytochemical stains for insulin, glucagon, somatostatin, and pancreatic polypeptide (PP). Each section was divided into PP-rich and PP-poor regions that are thought to be derived from the ventral and dorsal lobes of the gland, respectively. In some of these, the fractional area (%) occupied by positively stained B, A, and PP cells was determined by automatic image analysis, and the area occupied by D cells was determined by conventional point counting. The B cell fractional area was significantly higher in the IDM in both PP-poor and PP-rich areas (P less than 0.02). the fractional area of A cells in PP-poor areas and of PP cells in PP-rich areas was also significantly greater in IDM (P less than 0.02). The total endocrine cell fractional area was significantly greater in IDM in PP-poor but not in PP-rich regions of the pancreas. These results are not compatible with the hypothesis that maternal hyperglycemia results in specific fetal B cell hyperplasia and raise the possibility that hyperplasia of B, A, and PP cells in IDM may result from a variety of stimuli or that one stimulus acts on a pluripotential stem cell.