Hydrocortisone enhances allergen-specific IgE production by peripheral blood mononuclear cells from atopic patients with high serum allergen-specific IgE levels.

BACKGROUND: Although there is convincing evidence that human B cells can be induced to produce IgE by a combination of interleukin 4 (IL-4) and hydrocortisone (HC) in atopic subjects, it is still uncertain if this performs the same functions in allergen-specific IgE synthesis. OBJECTIVE: This study was designed to investigate the differences of IgE regulation between atopics and nonatopics, interactions of HC with IL-4, and the correlation between in vitro total IgE, allergen-specific IgE synthesis and serum IgE levels. METHODS: Peripheral blood mononuclear cells (PBMCs) from 16 atopic asthma patients sensitive to Dermatophagoides farinae and seven nonatopic controls were cultured with IL-4 and/or HC. Total IgE and D. farinae-specific IgE in culture supernatant were measured by ELISA and FAST. RESULTS: IL-4 increased total IgE synthesis in PBMCs from both atopics and nonatopics, whereas, HC had this effect only in some atopics who showed spontaneous IgE production in vitro. HC acted synergistically with IL-4 in total IgE synthesis. Their effects were more remarkable in cases with lower total serum IgE levels. PBMCs from eight of 16 atopics produced D. farinae-specific IgE in vitro either spontaneously or by IL-4 and/or HC. HC had more profound effects than IL-4 in these patients. They also showed higher total IgE synthesis by HC, and higher specific serum IgE levels than the others. IL-4 and/or HC did not induce any D. farinae-specific IgE synthesis by PBMCs from nonatopics. CONCLUSION: HC had a more profound effect than IL-4 on the induction of D. farinae-specific IgE synthesis in atopic patients with high serum allergen specific IgE levels. Further studies to determine the causes of these effects, such as the presence of long lived allergen specific B cells as the result of the priming effect of IL-4 in vivo, may be needed.     

Immunoglobulin E response during viral infections.

One hundred and three patients (90 nonatopics and 13 atopics) with respiratory infections to various viral agents were studied retrospectively with respect to IgE immunoglobulin levels during acute (1 to 7 days) and convalescent (8 to 30 days) phases of infection. It was found that 59% of patients had a decrease of 20% or more in IgE level, 27% remained the same, and only 14% showed a rise 20% or more from the acute to the convalescent phases of infection. IgE levels decreased up to 3 to 4 wk after symptoms and the degree of decrease was more apparent for the nonatopics who had higher IgE levels in their acute phase of infection. Less dramatic decrease in IgE was observed for the 13 atopics studied. The changes in IgE levels during the viral infectious period are discussed in terms of possible cellular mechanisms that may control IgE immunoglobulin.     

Liver disease--a prominent cause of serum IgE elevation.

Serum IgE concentrations were elevated in thirty-seven out of sixty-seven patients (55%) with acute or chronic liver disease of widely differing aetiology. The mean IgE concentrations in these patients showed an eight-fold increase above that observed in control subjects. Increased IgE levels in patients with liver disease occurred in the absence of eosinophilia, clinical evidence of atopy or other known causes of IgE elevation. No IgE-containing plasma cells were detected in the liver biopsies from thirty-two of the sixty-seven patients tested. Peripheral blood T cells were significantly decreased from normal in the patients with liver disease, but no correlation emerged between serum IgE levels and absolute peripheral blood T-cell numbers. These findings emphasize the importance of liver disease as a significant cause of serum IgE elevation.     

丙型肝炎病毒准种多样性与病毒血症水平、疾病活动度及干扰素疗效的关系

目的　了解丙型肝炎病毒 (HCV)准种变异与病毒血症水平、疾病活动度及干扰素疗效的关系。方法　采用针对HCVE2高变区 1 (HVR1 )的单链构象多态性分析法 (SSCP)对 68例慢性丙型肝炎患者进行HCV准种检测 ,分析准种数目与HCVRNA、ALT、AST水平及肝组织活动指数 (HAI)的相关性。对其中 48例给予干扰素治疗 ,分析准种数目对干扰素应答效果的影响。结果　 61例HVR1SSCP阳性 ,HCV准种数目为 (6 2± 2 4)条。准种数量与HCVRNA水平显著相关 (P <0 0 1 ) ,与ALT、AST及HAI无明显相关 (P >0 0 5)。干扰素治疗患者中 ,43例HVR1阳性 ,持续应答者治疗前HCV准种数量 (3 3± 1 2 ,n =1 1 )显著少于获得治疗终点应答 (ETR)伴复发者 (6 3± 2 2 ,n =1 2 ,P <0 0 5)或无应答者 (8 0± 3 3 ,n=2 0 ,P <0 0 1 )。治疗结束时 ,干扰素组仍有 1 6例检测出HCV准种 ,但准种条数降为 (3 4± 1 2 )条 ,与未接受干扰素治疗病例的准种数目 (6 8± 2 5)相比差异有显著性 ,P <0 0 1 ) ,且其中 1 0例准种模式发生了改变。结论　HCV准种多样性可引起较高的病毒血症水平 ,但与疾病活动度无关 ;准种数目可作为预测慢性丙型肝炎干扰素疗效的指标。     

Increased serum IgE in alcohol abusers

Background: It has been reported that total serum IgE is increased in patients with alcoholic cirrhosis, but it is not clear if this fact is related to alcoholic liver disease or to alcohol intake. Objective: To measure serum IgE in a group of chronic alcoholics with different stages of liver injury in order to elucidate if IgE increase is related to alcoholic liver damage. Patients and methods: Total serum IgE was determined by enzyme immunoassay in 186 chronic alcoholic patients (137 male/49 female) and 101 healthy controls. Patients and controls with known reasons for IgE elevation were excluded. Among alcoholic patients, 24 had fatty liver, 28 hepatic fibrosis, 29 alcoholic hepatitis, and 67 liver cirrhosis (38 patients were not evaluable concerning liver injury). Results: Total serum IgE was found to be increased in alcoholics (median 154.5IU/mL, range 1–7329IU/mL) with respect to healthy controls (median 20IU/mL, range < 1–1417 IU/mL) (P < 0.001). IgE increase was moderate (180–1000 IU/mL) in 60 alcoholics (32.3%) and marked (> 1000 IU/mL) in 27 (14.5%). Male alcoholics had higher IgE levels than females (median 191 IU/mL and range 1–7329 IU/mL vs 105IU/mL and range 2–2189IU/mL) (P= 0.009). On logistic regression analysis, alcoholism, male sex and younger age (but not smoking) were independently associated with higher IgE levels. No clear relationship was noted between serum IgE and severity of alcoholic liver disease. Thus, no correlation was observed between IgE and parameters of liver function (serum bilirubin, albumin or prothrombin index). Likewise, IgE concentrations were not significantly different in patients with liver cirrhosis with respect to patients with less severe liver disease. Serum IgE was increased (> 180 IU/mL) in 47.8 % of cirrhotics and in 44% of patients without liver cirrhosis. In contrast, other immunoglobulins (IgG, IgA and IgM) were significantly correlated with liver dysfunction. Conclusion: Chronic alcoholism should be considered as a cause of increased total serum IgE, regardless of the severity of the underlying liver disease.     

Serum Carnitine Levels in Chronic Hepatitis C Patients Before and After Lymphoblastoid Interferon-α Treatment

Objective: Chronic liver disease is often a hypocarnitinaemic condition. Since carnitine affects lipid metabolism, modifications of lipid pattern and energy metabolism can be expected in patients affected by chronic viral hepatitis. The aim of this study was to assess the relationship between serum carnitine levels and the grading of chronic hepatitis C, and to evaluate the effects of lymphoblastoid interferon (IFN)-αnl on carnitine levels in patients with hepatitis C. Design: We evaluated carnitine serum levels in a group of 32 patients with chronic hepatitis C before and after treatment with intramuscular IFNα 3MU 3 times/week for 6 months, comparing them with levels in 20 healthy controls. Statistical correlations between serum carnitine, histological activity index score, duration of disease and lipid pattern were also evaluated. Results: Serum carnitine levels, which were statistically lower in hepatitis C patients than in controls before therapy, increased after IFNα (p = 0.0003 vs pretreatment). There were no significant changes in total cholesterol in any patient after treatment, although serum triglyceride levels increased (p = 0.0003). Serum carnitine levels were correlated with age (r = 0.35; p = 0.02), type of response (r = ?03; p = 0.04), duration of disease (r = ?0.8; p = 0.0001) and high-density lipoprotein cholesterol levels (r = 0.43; p = 0.005) after completion of IFNα treatment. Conclusion: It is suggested that the post-treatment increase in serum carnitine observed in this study could be considered a new index of improved liver function. Also, exogenous administration of carnitine may be useful in patients with chronic hepatitis C who have reduced endogenous synthesis of this substance.     

Serum procalcitonin levels in chronic hepatitis C patients under pegylated interferon-alpha plus ribavirin treatment.

OBJECTIVES: To evaluate the alterations of serum procalcitonin (PCT) levels in patients with chronic hepatitis C during pegylated interferon-alpha (PEG-IFNa) plus ribavirin (RIB) treatment and to correlate them with clinical and virological outcomes. STUDY DESIGN: Fifty-two consecutive patients (29 males, age=41.2+/-14.7 years) with chronic HCV-related liver disease (six cirrhotics) were evaluated for PCT levels at baseline and during the treatment course (at week 12, 24, 48 and 72) with PEG-IFNa plus RIB. Sustained virological response (SVR) was confirmed by undetectable serum HCV-RNA at the end of treatment and again 6 months after completion of treatment. RESULTS: Two patients exhibited culture-proved bacterial infections during the treatment course. Thirty-six patients (69.2%) exhibit SVR and 16 (30.8%) were non-responders. Serum PCT levels remained within normal limits (0.1-0.5 ng/mL) in all treated patients throughout the follow-up period except those two who exhibited bacterial infections during the treatment course. Virological responders exhibited significant decline of serum PCT levels over time compared to non-responders (p<0.001), even when adjusted for multiple baseline parameters (p=0.037). CONCLUSION: Serum PCT levels decline in chronic hepatitis C patients during PEG-IFNa plus RIB treatment, especially in the sustained virological responder group, while they elevate only when bacterial infections complicate the treatment course.     

Recombinant interferon alfa therapy for chronic hepatitis C. A randomized, double-blind, placebo-controlled trial

Infection with the hepatitis C virus may result in chronic liver disease for which no effective therapy is now available. We studied the effects of recombinant human interferon alfa in a prospective, randomized, double-blind, placebo-controlled trial in patients with well-documented chronic hepatitis C. Forty-one patients were enrolled in the trial, 37 of whom were later found to have antibody to hepatitis C virus. Twenty-one patients received interferon alfa (2 million units) subcutaneously three times weekly for six months, and 20 received placebo. The mean serum aminotransferase levels and the histologic features of the liver improved significantly in the patients treated with interferon but not in the patients given placebo. Ten patients treated with interferon (48 percent) had a complete response, defined as a decline in mean serum aminotransferase levels to the normal range during therapy; three others had a decrease in mean aminotransferase levels of more than 50 percent. After treatment ended, however, serum aminotransferases usually returned to pretreatment levels; 6 to 12 months after the discontinuation of interferon therapy, only two patients (10 percent) still had normal values. We conclude that interferon alfa therapy is beneficial in reducing disease activity in chronic hepatitis C; however, the beneficial responses are often transient.     

Serum levels of IL-10, IL-15 and soluble tumour necrosis factor-alpha (TNF-α) receptors in type C chronic liver disease

We previously reported that the number of TNF-α-producing cells was increased in the liver of patients with type C chronic liver disease. To understand further the pathophysiology of this change, we examined serum levels of two soluble TNF receptors, TNF-αRI (p55) and -αRII (p75), and IL-10, all of which act as TNF-α buffer, and IL-15, a novel cytokine sharing many immunological activities with IL-2, using ELISA methods. We studied control individuals and patients with type C chronic liver disease, including asymptomatic hepatitis C virus (HCV) carriers with persistently normal serum ALT values, and those with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Both types of sTNF-αR closely correlated with disease progression. Patients with LC and HCC had significantly elevated levels for sTNF-αRII compared with the other patient groups and controls. Serum IL-10 levels were significantly greater in all chronic liver disease groups than in controls. With respect to IL-15, the values were high in CH, LC and HCC compared with those of controls. Notably, HCC patients showed highest values for both IL-10 and IL-15, with significant differences from the other patient groups. Serial determinations revealed that interferon (IFN) treatment for CH patients resulted in the suppression of circulating IL-10 and IL-15 levels along with decrease in serum aminotransferase values. Both cytokines remained at decreased levels after cessation of therapy in patients who went into clinical and virological remission. On the other hand, treatment did not affect serum levels of sTNF-αRs. These findings indicate that serum levels of these molecules correlated with disease progress in chronic HCV infection, and that IL-10 and IL-15 may reflect the degree of inflammation in the liver. It is also suggested that both cytokines may be related to the development of HCC.     

Interferon-alpha treatment for severe atopic dermatitis

Patients with both severe atopic dermatitis (AD) and chronic myeloid leukemia, chronic hepatitis B, or chronic hepatitis C were treated with interferon-alpha (IFN-α). IFN-α treatment improved AD. Moreover, there were also significant decreases in serum IgE and IgG4 levels and in in vitro spontaneous IgE and IgG4 production by patients' mononuclear cells.     

Significance of serum IgM anti-HBc in chronic hepatitis B virus infection.

Because of widely differing reports on the significance of IgM anti-HBc in chronic hepatitis B virus (HBV) infection, paired sera and liver biopsies from 49 patients with chronic HBV infection were analysed for serum IgM anti-HBc, HBsAg titre, HBeAg/anti-HBe, HBV DNA, serum aspartate transaminase, intrahepatic HBcAg expression, and liver histology. High levels of IgM anti-HBc, in the diagnostic range of acute hepatitis B (greater than 1.2), were detected in seven patients (14.3%) and a total of 34 patients (69.6%) had an index of more than 0.2. No correlation was found between IgM anti-HBc and the serum markers of active viral replication or HBsAg titre but it correlated significantly with intrahepatic expression of cytoplasmic HBcAg (r2 = 0.165, P = 0.002). IgM anti-HBc also correlated with active liver histology (P = 0.015) but there was a considerable overlap of the IgM anti-HBc index values between the various disease groups, indicating a poor specificity. Serial assessment of IgM anti-HBc in eight patients treated with interferon-alpha (four responders) showed an increase in IgM anti-HBc in three out of four patients corresponding to the e-seroconversion period followed by a drop in IgM anti-HBc levels. However, an increase in IgM anti-HBc was also seen in one non-responder, indicating that this feature is not unique to interferon-alpha responders. These data indicate that serum IgM anti-HBc cannot be used alone as a certain diagnostic measure of HBV replication nor in the prediction of liver histology.     

Raised IgE levels in beta-thalassaemia: correlation with splenectomy and hepatitis B virus infection.

IgE values obtained in 117 beta-thalassaemia patients were significantly higher than in age matched normal subjects. In 31 patients (26.5%) IgE levels were above 2 s.d. of normal values for age, but the frequency of IgE with reaginic activity was lower in patients (5.1%) than in controls (11.9%). The highest values were observed in splenectomized patients who were also positive for one or more serological markers of hepatitis B virus infection. The increase of IgE levels was directly correlated with the number of years after splenectomy, and patients with biopsy proven chronic liver disease had higher IgE levels than those without evidence of liver damage. On the other hand, IgE levels were not correlated with the number of transfusions, age, IgG, IgA, IgM levels or T cell subsets and mitogen responsiveness. These results show that beta-thalassaemia patients develop elevated IgE levels to which splenectomy and hepatitis B virus infection contribute in a synergistic manner.     

慢性丙型肝炎患者血清leptin含量与HA、PⅢP水平的相关分析

目的：探讨了慢性丙型肝炎患者血清leptin含量与HA、PⅢP水平的关系。方法：应用放射免疫分析对32例慢性丙型肝炎患者进行了血清leptin和HA、PⅢP水平检测,并与35名正常健康人作比较。结果：慢性丙型肝炎患者血清leptin和HA、PⅢP水平均非常显著地高于正常人组（P〈0．01）,相关分析显示,血清leptin与HA、PⅢP水平呈明显的正相关（r=0．6178．0．5706,P〈0．01）。结论：慢性丙型肝炎患者血清leptin水平的升高与肝脏炎症病变严重程度有关,leptin测定可作为—个判断肝脏炎症严重程度的指标,具有重要的临床价值。     

慢性肝病患者TPO水平与肝纤维化指标关系的探讨

目的：探讨慢性肝病患者血清中血小板生成素（TPO）水平与肝纤维化指标的关系。方法：ELISA测定正常人群及肝病患者的TPO水平,肝纤维化指标用放射免疫分析。结果：血小板生成素水平在慢性肝炎[（120.41±99.73）pg/ml]轻、中、重组,肝硬化[（125.84±100.40）pg/ml]与正常人群[（144.18±48.01）pg/ml]中比较均无显著性差异（P〉0.05）;肝硬化组（18例）的ⅣC与TPO水平有显著相关性（r=0.517,P〈0.05）,其余各组HA、LN、PCⅢ、ⅣC与TPO均无相关性（P〉0.05）。结论：慢性肝病患者血清TPO水平与疾病的严重程度无关,而肝硬化患者TPO水平与肝纤维化程度有一定的关系。     

Lymphocyte subsets and beta 2-microglobulin expression in chronic hepatitis C/non-A, non-B. Effects of interferon-alpha treatment.

Thirty-three patients with chronic hepatitis C/non-A, non-B were included in a randomized controlled study of interferon-alpha 2b (IFN-alpha 2b) treatment, 3 x 10(6) U three times weekly for 36 weeks. Using an immunoperoxidase technique, frozen liver biopsy specimens were examined with MoAbs for the presence of T helper cells (CD4), T suppressor/cytotoxic cells (CD8), total T cells (CD2) and B cells (CD22) before and after treatment. beta 2-microglobulin (beta 2-MG) expression on hepatocytes was semiquantified using a scoring system on sections from paraffin-embedded biopsy specimens. Serum levels of beta 2-MG were analysed with a radioimmunoassay technique. Intralobular T helper and T suppressor/cytotoxic cells declined significantly in the treated patients but not in the controls. The portal CD4/CD8 ratio did not change. Before treatment, serum beta 2-MG levels and hepatocyte beta 2-MG expression were significantly higher in patients with chronic active hepatitis compared to patients with chronic persistent hepatitis. Serum beta 2-MG levels increased significantly in responders during IFN treatment, with a maximum after 12 weeks. However, in the liver, the hepatocyte beta 2-MG expression was significantly decreased after treatment. Thus, IFN-alpha treatment does not seem to induce an increased HLA class I antigen hepatocyte expression in chronic non-A, non-B hepatitis, which favours the hypothesis that its anti-viral effects are more important in modulating the disease activity.     

Interferon-α-2a

Interferon-alpha-2a, a single interferon-alpha subtype manufactured by use of recombinant DNA technology, has immmunomodulatory, antiviral and antiproliferative properties. It is a beneficial treatment for about 30% of patients with well-compensated chronic hepatitis C. Biochemical responses [defined as normalisation of serum alanine aminotransferase (ALT) levels] are achieved in 37 to 76% of patients at the end of treatment with interferon-alpha-2a at dosages of 3 to 6MU 3 times weekly (given intramuscularly or subcutaneously) for 6 to 12 months. In contrast, evidence of disease remission is seldom observed in untreated patients. Improvements in liver histology in patients receiving interferon-alpha-2a are associated with complete biochemical responses to the drug. Virological responses (defined as an absence of hepatitis C-RNA in the serum) occur in up to 86% of patients after treatment with interferon-alpha-2a 3 to 6MU 3 times weekly for 12 months. After cessation of interferon-alpha-2a therapy, a considerable proportion of treatment responders experience disease reactivation. Rates of sustained biochemical response are generally higher after 12 months' therapy (27 to 57%) than after 6-month courses of treatment (27 to 30%). The long term efficacy of interferon-alpha-2a in patients with chronic hepatitis C is improved by the concomitant administration of ribavirin. Interferon-alpha-2a shows efficacy similar to that of interferon-alpha-2b or interferon-alpha-n1 in patients with chronic hepatitis C. During the first few days of therapy with interferon-alpha-2a (or other forms of interferon-alpha), most patients experience a transient 'influenza-like' reaction, characterised by fatigue, fever, chills and headache. These symptoms are usually alleviated by paracetamol (acetaminophen). Lethargy, mild myelosuppression, alopecia and neuropsychiatric symptoms are dose-limiting adverse effects that may occur during longer term therapy. Severe adverse effects, experienced by <2% of interferon-alpha-2a recipients, include severe depression, seizures and generalised bacterial infections. Autoimmune thyroid dysfunction develops in 3 to 12% of patients during treatment with interferon-alpha-2a. Conclusion. Interferon-alpha-2a produces sustained responses in about 30% of adults with chronic hepatitis C. Its efficacy appears to be similar to that of other interferon-alpha products. Thus, the drug remains a useful first-line treatment option for adults with well-compensated chronic hepatitis C. Further research into the optimal dosage of interferon-alpha-2a and its role in combination with other agents is likely to contribute towards future advances in the management of chronic hepatitis C.     

GBV-C/HGV infection in chronic hepatitis C patients: Its effect on clinical features and interferon therapy

A novel virus (GBV-C/HGV) may be associated with some liver diseases including fulminant hepatitis and acute and chronic hepatitis. On the other hand, many investigations showed that this infection does not contribute to liver disease. GBV-C/HGV has been found to occur in association with infection with other hepatitis viruses. We investigated the effect of GBV-C/HGV infection on the clinical features and interferon treatment in patients with chronic hepatitis C. A total of 262 hepatitis C virus (HCV) RNA positive patients with chronic hepatitis were examined in this study. The detection of serum GBV-C/HGV RNA was done by RT-PCR using specific primers from the NS5 regions. Interferon-alpha was given at a dose of 6 MU/day for 16 or 24 weeks. A responder was defined as a patient with ALT normalization and HCV RNA disappearance after treatment. GBV-C/HGV RNA was detected in 28 (11%) patients. No significant difference was detected in clinical features (age, sex, liver-related biochemical tests, and histological examination) between the 28 GBV-C/HGV-positive patients and the GBV-C/HGV-negative patients. Using interferon therapy for hepatitis C, the responder rates of GBV-C/HGV-positive and -negative patients were 14% and 20%, respectively. Of the 28 patients with GBV-C/HGV RNA, GBV-C/HGV RNA was tested after interferon therapy in 16 and of these GBV-C/HGV RNA was not detected in nine patients after therapy. These findings suggest that GBV-C/HGV infection dose not affect the clinical features in patients with HCV and the efficacy of interferon therapy for chronic hepatitis C. J. Med. Virol. 55:98–102, 1998. © 1998 Wiley-Liss, Inc.     

七项肝纤维化血清标志物的诊断意义

目的 检测肝病患者血清基质金属蛋白酶1(MMP-1)、基质金属蛋白酶抑制剂1(TIMP-1)、转化生长因子B1(TGF-β1)、透明质酸(HA)、Ⅲ型前胶原(PⅢP)、Ⅳ型胶原(CⅣ)和层粘连蛋白(LN)含量,评价其对肝纤维化的诊断价值.方法 酶标法检测血清MMP-1、TIMP-1、TGF-β1含量.放射免疫法检测血清HA、PⅢP、CⅣ、LN含量.结果 肝病患者血清TGF-β1、HA、PⅢP、CⅣ、LN水平与健康对照组比较均有升高,差异均有统计学意义(P＜0.05).慢性肝病患者血清TIMP-1水平明显高于健康对照组(P＜0.01),而肝病患者血清MMP-1水平与健康对照组比较,差异无统计学意义(P＞0.05).结论 慢性肝病患者存在MMP-1和TIMP-1的严重失衡,是慢性肝病患者肝脏细胞外基质沉积的重要原因.血清TIMP-1、TGF-β1、HA、PⅢP、CⅣ和LN对肝纤维化具有较好的临床诊断价值,而MMP-1的临床诊断价值欠佳.     

Decreased nitric oxide production in chronic viral hepatitis B and C

Nitric oxide is a free radical gas molecule which may be implicated in antiviral defense. However, there is no information about its possible role in chronic viral hepatitis B and C. In this study we have analyzed the serum levels of NO₂⁻ (as an index of nitric oxide generation) from patients with chronic viral hepatitis B and C and relationship of same with the response to interferon therapy. Serum samples were analysed from 61 patients with chronic hepatitis B, 60 patients with chronic hepatitis C, 11 with chronic liver disease of nonviral origin, and 23 healthy controls. Levels of NO₂⁻ were statistically higher in healthy controls (P < 0.001) than in patients with chronic liver disease. No relation was found between NO₂⁻ and viremia or response to interferon therapy in patients with chronic hepatitis B. In contrast in chronic hepatitis C, responder patients had significantly higher NO₂⁻ than nonresponders (P < 0.01). With respect to the relation between NO₂⁻ levels and liver damage, patients with cirrhosis had lower NO₂⁻ levels than the rest of the patients (P < 0.001)². In conclusion, patients with chronic viral hepatitis have low serum NO₂⁻ levels. J. Med. Virol. 51:326–331, 1997. © 1997 Wiley-Liss, Inc.     

TT virus infection in patients with chronic hepatitis B or C: influence on clinical, histological and virological features

Concomitant infection with TT virus and hepatitis B virus (HBV) or hepatitis C virus (HCV) is common. However, the effect of TTV infection on chronic hepatitis B or C is unknown. The prevalence of TTV infection, the effect of TTV infection on the clinical, histological and virological features of patients with chronic hepatitis B or C, and the influence of TTV infection on the HCV response to interferon alfa therapy were studied. A total of 100 asymptomatic hepatitis B surface antigen carriers, 220 patients with HBV-related chronic liver diseases, and 110 patients with chronic hepatitis C treated with interferon alfa (3 million units subcutaneously three times a week for 24 weeks) were enrolled. Serum HCV RNA and serum TTV DNA were detected by the polymerase chain reaction (PCR). Serum HBV DNA and serum HCV RNA level were quantified by branched DNA assays. Infection with TTV was detected in 21.5% of HBV carriers and 37% of HCV carriers. TTV infection had little effect on the clinicopathological course of chronic HBV infection. In chronic hepatitis C, clinical features, histological severity, serum HCV RNA levels, and the response to interferon alfa therapy did not differ between those with and without TTV infection. The loss of serum TTV DNA did not correlate with the biochemical response as did in the loss of serum HCV RNA. In conclusion, TTV infection is found frequently in patients with chronic hepatitis B or C in Taiwan; however, coinfection with TTV does not affect the clinicopathological course of chronic hepatitis B or C and the response to interferon alfa therapy.