Presence Of Chronic Viral Hepatitis Research Articles

Clinical efficacy of immunoglobulin on the treatment of severe fever with thrombocytopenia syndrome: a retrospective cohort study

Optimal treatment strategy for severe fever with thrombocytopenia syndrome (SFTS) remained unknown. We aimed to evaluate the efficacy of intravenous immunoglobulin (IVIG) on SFTS. A retrospective cohort study was conducted based on medical records of the laboratory-confirmed SFTS patients hospitalized during 2010-2020 in the 154th hospital, China. A 1:1 propensity score matching with age, sex, the interval from symptom onset to admission, presence of chronic viral hepatitis, diabetes and disease severity was performed between Non-IVIG group (supportive therapy) and IVIG group (IVIG plus supportive therapy). The matching variables were adjusted to compare the case fatality rates (CFRs), viral load and laboratory parameters between the two groups. Risk ratio (RR) and 95% confidence interval (CI) were reported. Totally 2219 SFTS patients were recruited. CFRs were significantly higher in 1051 patients in IVIG group than 1168 patients in Non-IVIG group (19.0% vs. 4.6%, RR=4.30, 95% CI 3.12-5.93). The difference remained significant after matching (17.2% vs. 5.1%, RR=4.02, 95% CI 2.71-5.97). The CFR of IVIG group was significantly higher in all age groups, two IVIG therapy delay groups and two therapy duration groups compared to that of Non-IVIG group (all P<0.05). IVIG therapy was related to higher viral loads and reduced counts of lymphocytes, T cells, CD4+ T cells and natural killer cells in the blood (all P<0.05). No obvious efficacy of IVIG in saving life or improving outcome of SFTS was observed. Caution is needed for clinical physicians to continue prescribing IVIG for SFTS patients. Natural Science Foundation of China.

The role of viral hepatitis B and C in the development of adverse outcomes in patients after tuberculosis

Despite the study of the epidemiology of tuberculosis and its co-infection over the past decades, a number of questions remain, including those related to the impact of co-infection on survival depending on the chosen tuberculosis treatment regimen, the likelihood of adverse outcomes in the form of gastrointestinal bleeding and cirrhosis of the liver and their relationship with the therapy of the underlying disease. The purpose of the study: to evaluate the survival of patients with tuberculosis who have co-infection (viral hepatitis B and C) and receive multicomponent chemotherapy. Materials and Methods: The study included all patients who received treatment for active tuberculosis and had viral hepatitis B and/or C from 01/01/2004 to 12/31/2020. A total of 1687 patients were included. Twenty-two patients were lost to follow-up, and attempts to ascertain their clinical status were unsuccessful. Vital status was assessed in all patients. The mean duration of follow-up was 10.5±3.0 years. Median follow-up was 11.3 years (95% confidence interval (CI) 8.2-14.3). The average age of the cohort was 53.3±7.7 years. The study assessed survival and all-cause mortality annually. Results: The frequency of chronic hepatitis B in the group of patients with active tuberculosis was 3.8%, hepatitis C - 14.8%, hepatitis B and C - 0.5% of cases. Such an incidence of viral hepatitis is associated with a high frequency of illicit drug users (62.4%). It should be noted that the frequency of hepatitis treatment was low and amounted to 8.7%. When assessing the contribution of hepatitis B and C to the mortality of patients with active tuberculosis, it was found that hepatitis is not a predictor of death in patients. At the same time, patients who did not receive hepatitis therapy had a higher risk of death (unadjusted odds ratio (OR) - 1.28, 95% CI 1.04-1.65). The adjusted OR for hepatitis B was - 1.87 95% CI 0.67-1.52, C - 1.24 95% CI 0.90-2.18, B and C - 1.72 95% CI 0.99-2.02. Conclusion: The presence of chronic viral hepatitis B and/or C in patients with active tuberculosis did not affect mortality from all causes and regardless of the type of virus during a long period of observation. Patients who did not receive treatment for viral hepatitis and who had a history of tuberculosis had a higher risk of death from all causes (OR 1.28, 95% CI 1.04-1.65).

Glucose Variability and Risk of Hepatocellular Carcinoma in Patients with Diabetes: A Nationwide Population-Based Study.

Although diabetes is a well-known risk factor for hepatocellular carcinoma, exactly which metabolic parameters of diabetes are associated with hepatocellular carcinoma remain unexplored. In this study, we investigated the relationship between glucose variability (GV) and hepatocellular carcinoma in patients with diabetes through a nationwide population-based study. A population-based cohort study including 674,178 diabetic subjects participating in more than three health examinations within 5 years from the index year (2009 and 2010) were followed until the end of 2017. The coefficient of variation, SD, variability independent of the mean, and average real variability were calculated as GV indices. During a median follow-up of 6.7 years, there were 5,494 cases of hepatocellular carcinoma. When groups were classified according to glucose level, the highest risk for hepatocellular carcinoma was observed when the basal blood glucose level was 180 mg/dL or greater [adjusted HR (aHR), 1.19; 95% confidence interval (CI), 1.08-1.31]. We observed increasing trends for the relationship between GV and hepatocellular carcinoma in multivariable Cox proportional analyses. The risk of hepatocellular carcinoma increased by 27% (aHR, 1.27; 95% CI, 1.17-1.38) for the highest quartile of GV relative to the lowest quartile. These findings were consistent regardless of the presence of chronic viral hepatitis or cirrhosis, alcohol consumption, or body mass index. GV was an independent predictor of hepatocellular carcinoma, even after adjusting for confounding factors. There was a linear relationship between increase in GV and prevalence of hepatocellular carcinoma. Visit-to-visit GV might be helpful for identifying patients with diabetes at high risk of hepatocellular carcinoma.

Impact of COVID-19 on the care of patients with liver disease: EASL-ESCMID position paper after 6 months of the pandemic.

SummaryDuring the early stages of the coronavirus disease 2019 (COVID-19) pandemic, EASL and ESCMID published a position paper to provide guidance for physicians involved in the care of patients with chronic liver disease. While some healthcare systems are returning to a more normal routine, many countries and healthcare systems have been, or still are, overwhelmed by the pandemic, which is significantly impacting on the care of these patients. In addition, many studies have been published focusing on how COVID-19 may affect the liver and how pre-existing liver diseases might influence the clinical course of COVID-19. While many aspects remain poorly understood, it has become increasingly evident that pre-existing liver diseases and liver injury during the disease course must be kept in mind when caring for patients with COVID-19. This review should serve as an update on the previous position paper, summarising the evidence for liver disease involvement during COVID-19 and providing recommendations on how to return to routine care wherever possible.

MICRORNA-122 AS A BIOLOGICAL MARKER OF CHRONIC VIRAL HEPATITIS C

New epigenetic markers are being studied in various countries around the world to diagnose, predict, and treat the patients with chronic viral hepatitis C. Epigenetics is currently studying the hereditary changes in gene expression or phenotype that are not related to the changes in DNA sequence. One field of epigenetics is the expression of RNA that does not encode a protein, namely miRNA, which is a molecule 18−22 nucleotides in length that plays a crucial role in regulating gene expression. Circulating miRNAs are a new genetic material that can be isolated from a patient's blood. The expression level of a particular miRNA has different biological and clinical effects. By means of its determination in various miRNAs it is possible to predict development of diseases. In order to study the baseline expression of miRNA−122 in patients with chronic viral hepatitis C with the first HCV genotype, 74 patients were examined. Diagnosis and monitoring of the patients was performed according to the local protocols and bioethical standards. The level of miRNA−122 expression in patients with chronic viral hepatitis C with the first HCV genotype was established by reverse transcription. Studies show that the level of miRNA−122 expression in the patients with HCV and healthy individuals showed significant variability. The obtained data indicate that the expression level of miRNA−122 in patients is 29 times higher than in healthy individuals at p = 0.0001 (U; Z). This can be an additional biomarker as an index of the presence of chronic viral hepatitis C and can be further used in practice. Therefore, the high level of miRNA−122 expression in subjects (≥ 8.771 rel. units (Log10 miR−122 ≥ 0.939 rel. units)) may be the basis for further screening of patients for HCV infection. The prospects of using this index, which will allow to personalize the diagnosis and treatment tactics for patients, that, in turn, will contribute to the implementation of the WHO global strategy for the elimination of viral hepatitis. Key words: chronic viral hepatitis C, miRNA−122, elimination of viral hepatitis, biological marker.

Factors affecting hepatitis B immunization in celiac disease

Aim: While 90-95% of the adult population responds to hepatitis-B vaccination, it is known that, this rate is lower in patients with CD. In our study, determination of response rates of vaccinated celiac patients, and the affecting factors associated with vaccine responses were the aims of our investigation. Material and Methods: The study included 280 celiac patients who applied to the polyclinic between 2015-2019 years. Demographic, anthropometric characteristics (age, gender, onset age, disease duration, smoking, body mass index(BMI), waist-hip ratios) and symptoms in patients were documented. Hepatitis B, C, delta serology were examined. The prevalence of chronic hepatitis and associated risk factors were evaluated. Hepatitis-B vaccination rates and vaccine responses were determined. The risk factors associated with the immune response were reviewed. Results: 212 (75.7%) of the patients were female, the mean-age of the patients was 33.4±10.8 and the disease duration was 4.9±3.7 years. In 14 (5%) of the patients there were chronic viral infections, 18 (6.4%) had natural immunity, 92 (32.9%) were immunized, 58 (56.4%) were not encountered with viral infection. No significant correlation was found between the presence of chronic viral hepatitis and risk factors. 28 (30.4%) patients who had not vaccine response. It was observed that; the dietary incompatibility and absence of immunological remission were significantly higher, the BMI and the waist size were significantly lower in non-response group (P0.05). Conclusions: Considering the mild-high prevalence of chronic viral infection in celiac patients, it is important to vaccinate these patients against infections. It is of great importance to implement re-vaccination protocol in the patients without vaccine response.Keywords: Celiac disease; hepatitis B; vaccination.

Approach and management of patients with chronic hepatitis B and C during the course of inflammatory bowel disease.

Inflammatory bowel disease and chronic viral hepatitis are 2 distinct but common conditions throughout the world. Mostly, both need life-long follow-up. Since immunosuppressive drugs remain corner stones of inflammatory bowel disease management, one should be aware of the concomitant presence of chronic viral hepatitis in such patients to prevent serious (even fatal) outcomes. Recently, new treatment options have become available in the treatment of both inflammatory bowel disease and chronic viral hepatitis. In this review, we have discussed and summarized current treatment and follow-up strategies for those 2 important public health issues in light of available literature.

Incidence of Hyperbilirubinemia and Jaundice Due to Atazanavir in a Cohort of Hispanic Patients

Incidence of Hyperbilirubinemia and Jaundice Due to Atazanavir in a Cohort of Hispanic Patients

Ritonavir Greatly Impairs CYP3A Activity in HIV Infection With Chronic Viral Hepatitis

Ritonavir is a powerful inhibitor of cytochrome P450 3A (CYP3A) that metabolizes many antiretrovirals. We examined the effect of ritonavir and of chronic viral hepatitis (CVH) status on CYP3A activity. Twenty-six HIV-positive men (13 with CVH, 16 on chronic ritonavir-based highly active antiretroviral therapy) received oral and intravenous midazolam, a probe for CYP3A phenotypic activity. CYP3A activity was expressed as oral clearance of the midazolam probe. In HIV-positive subjects not on ritonavir, CYP3A activity (mean +/- SD) did not differ between subjects by CVH (no CVH, controls: 28.5 +/- 9.0 vs. CVH+: 23.2 +/- 6.2 mL/min/kg, not significant). In those on ritonavir (R), CYP3A activity was 7% of controls (R: 2.1 +/- 0.8 vs. no R 28.5 +/- 9.0 mL/min/kg, P < 0.0004). CYP3A activity in subjects on ritonavir and with CVH was further reduced to 4% of controls (no CVH, R+ 2.1 +/- 0.8 vs. R+, CVH+ 1.0 +/- 0.4 mL/min/kg, P < 0.006). Ritonavir markedly decreases CYP3A activity. In the presence of CVH, ritonavir-based therapy further reduces CYP3A activity by half. Coinfection with CVH impairs CYP3A activity in the presence of the CYP3A inhibitor ritonavir.

Chronic viral hepatitis C, oxidative stress and the coagulation/fibrinolysis system in haemodialysis patients

Introduction The aim of the present study was to establish whether the presence of chronic viral hepatitis (PVH) could be implicated in the elevation of oxidative stress (SOX) and haemostasis system in haemodialysis (HD) patients. Matherials and methods In HD patients with and without PVH and in controls we compared the markers of: coagulation pathway- tissue factor (TF) and its inhibitor (TFPI), prothrombin fragment F 1 + 2 (F 1 + 2 ); fibrinolysis: tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA) and its soluble receptor (suPAR), plasminogen activator inhibitor 1 (PAI-1), plasmin/antiplasmin complexes (PAP); and a marker of SOX - Cu/Zn superoxide dismutase (Cu/Zn SOD) levels. Results Patients, particularly those with PVH, showed a significant increase in the markers of the coagulation, fibrinolysis and oxidative status as compared to controls. All parameters of coagulation/fibrinolysis system were directly associated with the PVH and Cu/Zn SOD levels, and there was a relationship between the PVH and Cu/Zn SOD levels. Multivariable analysis showed that PVH and increased SOX were identified as independent variables significantly associated with the disturbances of coagulation/fibrinolysis system in these patients. Conclusions We concluded that PVH is a novel determinant of the increased oxidative stress as well as the disturbances of coagulation/fibrinolysis system in haemodialysis patients.

Idiosyncratic drug-induced liver injury: an overview

Drug-induced liver injury (DILI) encompasses a spectrum of clinical disease ranging from mild biochemical abnormalities to acute liver failure. The majority of adverse liver reactions are idiosyncratic, occurring in most instances 5 – 90 days after the causative medication was last taken. The diagnosis of DILI is clinical, based on history, probability of the suspect medication as a cause of liver injury and exclusion of other hepatic disease. DILI can be hepatocellular (predominant rise in alanine transaminase), cholestatic (predominant rise in alkaline phosphatase) or mixed liver injury. An elevated bilirubin level more than twice the upper limit of normal in patients with hepatocellular liver injury implies severe DILI, with a mortality of ∼ 10% and with an incidence rate of 0.7 – 1.3 per 100,000. Although acute liver failure is rare, 13 – 17% of all acute liver failure cases are attributed to idiosyncratic drug reactions. Response to drug withdrawal may be delayed up to 1 year with cholestatic liver injury with occasional subsequent progressive cholestasis known as the vanishing bile duct syndrome. Overall, chronic disease may occur in up to 6% even if the offending drug is withdrawn. Antibiotics and NSAIDs are the most common cause of DILI. Statins rarely cause significant liver injury whereas antiretroviral therapy is associated with hepatotoxicity in 10% of treated patients. Multiple mechanisms of DILI have been implicated, including TNF-α-activated apoptosis, inhibition of mitochondrial function and neoantigen formation. Risk factors for DILI include age, sex and genetic polymorphisms of drug-metabolising enzymes such as cytochrome P450. In patients with human immunodeficiency virus, the presence of chronic viral hepatitis increases the risk of antiretroviral therapy hepatotoxicity. Over the next decade, the combination of accurate case ascertainment of DILI via clinical networks and the application of genomics and proteomics will hopefully lead to accurate prediction of risk of DILI, so that pharmacotherapy can be optimised with avoidance of adverse hepatic events.

Chronic viral hepatitis and iron affect the plasma levels of LIGHT—a new member of the TNF superfamily in uraemic haemodialyzed patients

LIGHT (lymphotoxin-like inducible protein that competes with glycoprotein D for binding herpesvirus entry mediator on T cells) is a recently identified of the tumor necrosis factor α (TNF-α) ligand superfamily. We wanted to establish whether the presence of chronic viral hepatitis could be implicated in enhanced inflammation as well as the elevation of plasma LIGHT levels in haemodialyzed (HD) patients. The plasma levels of LIGHT, high sensitivity C-reactive protein (hs CRP) and TNF-α were measured in HD patients with hepatitis in comparison to subjects without hepatitis and to healthy volunteers. The values of hs CRP and TNF-α were significantly elevated in HD patients when compared to the controls. TNF-α levels were significantly higher in the hepatitis-positive relative to the hepatitis-negative group ( p < 0.01). LIGHT levels were significantly decreased in hepatitis-negative patients as compared to controls ( p < 0.001) and hepatitis-positive group ( p < 0.01). Both LIGHT and TNF-α were directly associated with the presence of hepatitis. Multiple stepwise regression analysis identified increased iron levels as the only independent variable significantly associated with increased LIGHT ( β = 0.475, p = 0.003). These results suggest the presence of chronic viral hepatitis and iron levels are novel determinants of the increased LIGHT in the plasma of HD patients.

The Effects of Hepatic Artery Chemotherapy on Viral Hepatitis in Patients With Hepatocellular Carcinoma

Transcatheter arterial chemoembolization (TACE) or arterial Yttrium-90 (90Y) microspheres are used to treat unresectable hepatocellular carcinoma (HCC), but little is known about their effects on viral hepatitis. The aim of this study was to determine their effect on viral hepatitis in patients with HCC. We carried out a retrospective review of patients treated for HCC. Worsening of viral hepatitis was determined by serum chemistry and viral loads where available. Fifty-two patients treated with TACE were followed for a mean of 22.0 months. Thirty-nine patients (75%) had decreased/stable tumor. Two of the 39 (5%) patients with decreased/stable tumor burden had a sustained increase in bilirubin. None had a sustained ALT elevation or significant increase in viral load after TACE. Twenty-four patients treated with 90Y microspheres were followed for a mean of 12.0 months. Twenty-two of these had a decreased/stable tumor burden and no patient had a significant elevation of ALT. However, 7 of the 22 had a sustained bilirubin elevation. We conclude that neither TACE nor 90Y treatment was associated with worsening viral hepatitis in this group of HCC patients. The presence of chronic viral hepatitis with normal bilirubin should not exclude the use of these therapies in patients with unresectable HCC.

Is Carbohydrate‐Deficient Transferrin a Specific Marker for Alcohol Abuse? A Study in Patients with Chronic Viral Hepatitis

Carbohydrate-deficient transferrin, a transferrin isoform, is hailed as a new marker of chronic alcohol abuse, but its specificity is, however, not unequivocally accepted. The aim of the present study was therefore to determine carbohydrate-deficient transferrin levels in patients with chronic hepatitis B and C with or without documented chronic alcohol intake. Carbohydrate-deficient transferrin was measured using a double-antibody radioimmunoassay (CDTect, Pharmacia) in serum samples from 66 patients (45 males and 21 females; mean age: 39 years) with chronic viral hepatitis B (n = 20) or C (n = 46). Diagnosis of the underlying liver disease was established by liver biopsy. Carbohydrate-deficient transferrin levels were raised in 15 patients [23%; hepatitis B (n = 2) and hepatitis C (n = 13)]. In patients with chronic hepatitis B, the carbohydrate-deficient transferrin level was raised in two abstainers. In the 46 patients with chronic hepatitis C, 10 (22%) patients with an alcohol consumption of < 60 g/day for the men and 30 g/day for the women had raised carbohydrate-deficient transferrin levels. The overall specificity of carbohydrate-deficient transferrin for chronic alcohol abuse was thus 78%, suggesting an association between elevated carbohydrate-deficient transferrin levels and the presence of chronic viral hepatitis. Carbohydrate-deficient transferrin levels were not correlated with the histological grading or staging of chronic hepatitis B and C, or with biological markers of hepatic synthesis and cellular damage. Thus, an increased carbohydrate-deficient transferrin level may occur in patients with chronic viral hepatitis in the absence of chronic alcohol abuse. This fact should be kept in mind by physicians when using this marker to detect alcohol abuse.