Clinical Manifestations Of Hepatitis Research Articles

A Comparison of Clinical Manifestations and Outcomes between Acute Sporadic Hepatitis A and Hepatitis E Infections in Thailand.

Hepatitis A virus (HAV) and hepatitis E virus (HEV) infections often present as acute hepatitis with prodromal symptoms. These infections, transmitted via the oral-enteral route, constitute significant public health challenges, particularly in developing countries with subpar sanitary systems. The aim of the study was to describe the clinical manifestations, laboratory findings, and outcomes of hepatitis A and hepatitis E infections in Thailand. We conducted a retrospective chart review and analysis of 152 patients diagnosed with acute hepatitis A or hepatitis E from January 2007 to August 2018 at Siriraj Hospital. The hepatitis E cohort was older with a greater prevalence of comorbidities (hypertension, diabetes mellitus, chronic kidney disease, chronic hepatitis B, and post-kidney transplantation status) than the hepatitis A cohort. While the majority of hepatitis A patients presented with fever (98%) and jaundice (96%), these symptoms were less pronounced in hepatitis E patients. Furthermore, hepatitis A patients exhibited significantly higher aminotransferase and total bilirubin levels. However, clinical outcomes, such as hospitalization rates, progression to acute liver failure, and mortality, were comparable across both groups. In conclusion, although the clinical manifestations of hepatitis A and hepatitis E were similar, fever and jaundice were more prevalent and aminotransferase and bilirubin levels were higher in the HAV-infected group.

Association of TNF-α, IFN-γ, IL-6, and IL-10 with different clinical manifestations of hepatitis B infection

Cytokines have a crucial part in the pathogenesis, persistence of infection, and prognosis of hepatitis B virus (HBV) infection as HBV does not cause direct liver destruction; rather, disease-related complications and prognosis are more associated with immune system action, specifically cytokines such as TNF-α, IFN-γ, IL-6, IL-10, and other cytokines. This study sought to link TNF-, IFN-, IL-6, and IL-10 to various clinical manifestations of HBV infection. Ninety sera were taken from HBV-infected patients, 30 (33.3%) of whom had liver cirrhosis, 30 (33.3%) were HBV carriers, 19 (21.2%) were acute HBV patients, and 11 (12.2%) were recently HBV infected. ELISA was used to determine the serum levels of TNF-α, IFN-γ, IL-6, and IL-10. HBV-infected patients with liver cirrhosis had considerably higher mean serum levels of IFN-γ (P=0.005) and IL-10 (P=0.003), but TNF-α and IL-6 were significantly higher in recent HBV-infected patients (P values 0.034 and 0.004, respectively). There were substantial changes in mean serum levels of TNF-α, IFN-γ, IL-6, and IL-10 at different phases of HBV infection, implying a role for cytokines in HBV etiology, chronicity, and consequences.

A clinical manifestation of Hepatitis C among the population of Hyderabad, Pakistan

A clinical manifestation of Hepatitis C among the population of Hyderabad, Pakistan

Clinical Manifestations of Hepatitis E.

The clinical manifestations of hepatitis E are similar to those of other types of viral hepatitis. While acute hepatitis E is usually self-limited, pregnant women and chronic liver disease patients suffering from acute hepatitis E usually present with severe clinical manifestations that may develop into fulminant hepatic failure. Chronic HEV infection is typically seen in organ transplant patients; most HEV cases are asymptomatic and rarely display jaundice, fatigue, abdominal pain, fever, fatigue, or ascites. The clinical manifestations of HEV infection in neonates are diverse and have varied clinical signs, biochemistry, and virus-biomarkers. Lastly, the extrahepatic manifestations and complications of hepatitis E are in need of further study.

Prognosis of hepatitis E infection in patients with chronic liver disease: A meta-analysis.

In individuals with underlying chronic liver disease (CLD), hepatitis E virus (HEV) infection is a potential trigger of acute-on-chronic liver failure. In this systematic review, seven electronic databases were searched. Pooled incidence rates with 95% confidence intervals (95% CIs) were calculated by the Freeman-Tukey double arcsine transformation method. The association between death or liver failure and HEV superinfection in CLD patients was estimated by the odds ratios (OR) with a 95% CI. A total of 18 studies from 5 countries were eligible for systematic review. The prevalence of acute HEV infection in hospitalized CLD patients with clinical manifestations of hepatitis was 13.6%, which was significantly higher than that in CLD patients from the community (pooled prevalence 1.1%). The overall rates of liver failure and mortality in CLD patients with HEV superinfection were 35.8% (95% CI: 26.7%-45.6%) and 14.3% (95% CI: 10.6%-18.5%), respectively, with the rates in cirrhotic patients being approximately 2-fold and 4-fold higher than those in noncirrhotic patients, respectively. The risks of liver failure (OR=5.5, 95% CI: 1.5-20.1) and mortality (OR=5.0, 95% CI: 1.9-13.3) were significantly higher in CLD patients with HEV superinfection than in those without HEV superinfection. HEV testing in hospitalized CLD patients is necessary due to the high prevalence of HEV infection observed in hospitalized CLD patients. HEV superinfection could accelerate disease progression in patients with underlying CLD and increase mortality in these patients. HEV vaccination is appropriate for patients with pre-existing CLD.

Epidemiological Characteristics and Clinical Manifestations of Hepatitis E in a Tertiary Hospital in China: A Retrospective Study.

BackgroundHepatitis E virus (HEV) infection is the most common cause of acute viral hepatitis worldwide and one of the main causes of death in the last decade, causing chronic hepatitis and liver failure in some populations. The aging population and obesity are two major factors threatening human health. Therefore, we want to understand the relationship between these two groups and HEV infection.ObjectivesThe study aimed to analyze the epidemiological, clinical, and laboratory features of HEV infection and evaluate probable high-risk factors for disease progression and the current diagnostic strategies of hepatitis E infection.Study DesignPatients diagnosed with acute hepatitis E with symptoms and liver dysfunction were enrolled. For statistical analysis, clinical features and laboratory findings were collected between the elderly and non-elderly and HEV+ fatty liver disease (FLD) groups. Statistical analysis was performed using Excel and the platform VassarStats, and statistical significance was taken as P < 0.05.ResultsJaundice and the bilirubin peak were significantly deeper, the duration of hospitalization was significantly longer, and the proportion of ascites and liver failure was significantly higher in the elderly group. The aging population is one of the risk factors of severe hepatitis E. Hepatitis E becomes more serious in the HEV + FLD group, although the results did not reach statistical significance.ConclusionThe aging and FLD were suggested to aggravate HEV infection. However, the diagnosis of HEV infection remains a challenge. A prospective study with sufficient sample size is needed to confirm this conclusion.

Phase 1 Study of Axatilimab (SNDX-6352), a CSF-1R Humanized Antibody, for Chronic Graft-Versus-Host Disease after 2 or More Lines of Systemic Treatment

Phase 1 Study of Axatilimab (SNDX-6352), a CSF-1R Humanized Antibody, for Chronic Graft-Versus-Host Disease after 2 or More Lines of Systemic Treatment

S2614 Cholestatic Hepatitis From Acute Epstein-Barr Virus Infection

INTRODUCTION: Primary Epstein-Barr Virus infection (EBV) presents as a triad of fever, posterior lymphadenopathy and pharyngitis. Hepatocellular involvement is limited to transient, mild, asymptomatic elevations of aminotransferases. Clinical manifestations of hepatitis are rarely the presenting feature of the disease and severe cholestasis is exceedingly rare. We present a patient with atypical presenting features found to have cholestatic hepatitis due to acute EBV infection. CASE DESCRIPTION/METHODS: A 38-year-old male with no medical history presented with right upper quadrant (RUQ) abdominal pain for 1 week associated with malaise, dyspnea, nausea, emesis, and fever to 38.8 degrees Celsius. His social history consisted of safe sex practices, no sick contacts, and no drug or alcohol use. On examination, he was afebrile and hemodynamically stable. There was no jaundice, scleral icterus or lymphadenopathy. There was mild tonsillar erythema without edema or exudate. He had RUQ and epigastric tenderness to palpation without notable hepatosplenomegaly. His labs showed no leukocytosis with elevated aspartate aminotransferase (AST) 234 IU/L, alanine aminotransferase (ALT) 383 IU/L, alkaline phosphatase 432 IU/L, and total and direct bilirubin of 3.4 and 1.6 mg/dL, respectively. ALT and AST peaked at 743 and 582 IU/L, respectively. HIV and hepatitis panel were negative. RUQ ultrasound showed normal gallbladder (GB) wall thickness of 2.7 mm with mild distention, trace pericholecystic fluid, and no biliary dilation. Magnetic resonance cholangiopancreatography showed mild hepatosplenomegaly, a normal GB and no biliary obstruction. Further workup revealed a positive Monospot with >160 units/ml of EBV antibodies to viral capsid antigen IgM and indeterminate EBV antibody to viral capsid antigen IgG, indicating acute EBV infection. DISCUSSION: EBV cholestasis is thought to be secondary to inflammation of the bile duct and direct damage to hepatic cells by autoantibody-mediated activation of free radicals. A literature review revealed that EBV has been reported to cause a hepatocellular pattern of elevated aminotransferases however cholestatic patterns are infrequently reported and thus may cause a diagnostic dilemma. The existing literature reports this phenomenon in pediatrics, adolescents, or patients in the second decade of life. Our case highlights the importance of including EBV infection in the differential diagnosis of cholestatic hepatitis at any age, particularly when no demonstrable cholecystitis is present.Table 1.: Liver and biliary marker trend throughout hospitalizationFigure 1.: Abdominal MRI demonstrating hepatomegaly and splenomegaly, measuring 15.1 cm anterior-posteriorly, and 13.9 cm craniocaudally.Figure 2.: Abdominal MRI demonstrating hepatosplenomegaly.

Hepatitis E virus infection in liver transplant recipients: a descriptive literature review.

Hepatitis E virus infection has been recognized as a rising hepatotropic viral infection in the developing countries but overlooked in the developed countries, due to its lower prevalence. However, hepatitis E virus prevalence is on rise in the liver transplant recipients due to immunosuppression, which needs prompt recognition by healthcare practitioners. Hepatitis E virus infection is commonly believed to be transmitted via an animal host; but in the post-liver transplant patients, it can also be acquired via blood and blood products transfusion and autochthonous route. Previous studies have shown the significance of hepatitis E virus infection in post-liver transplant, as the patients at a high risk of progressing to chronic hepatitis and cirrhosis. Pediatric patients are at higher risk of hepatitis E virus infection post-liver transplant. Specific hepatitis E virus genotypes have the potential for greater severity. The clinical manifestation of hepatitis E virus can also present as extrahepatic features which need high level of suspicion for early recognition and treatment. Treatment options of hepatitis E virus range from immunosuppressive drug minimization, ribavirin therapy to novel direct-acting antiviral regimens. Herein, we aim to explore epidemiology, prevalence, risk factor, diagnosis, and management of hepatitis E virus infection giving special attention to liver transplant recipients.

Viral load and clinical manifestations of hepatitis E virus genotype 3 infections.

A fraction of plasma donations undergoes hepatitis E virus (HEV) RNA screening since late 2014 in France. The aim of this study was to determine the frequency of HEV RNA as well as the viral load and the evolution of genotype distribution over a 3-year period (2015-2017) in asymptomatic blood donors in comparison with symptomatic patients routinely diagnosed. The overall detection rate of HEV RNA in plasma donations was 0.10% during the 3-year period, with a median viral load of 717 IU/mL (range: <60-168000 IU/mL) in the 189 samples found HEV RNA positive. One hundred and twenty samples (64.4%) were successfully HEV genotyped. Most strains were HEV3f (n=54; 44.3%) and HEV3c (n=46; 37.7%). The genotype distribution was not different throughout the 3-year period and we found no association between the genotype and where the blood donors lived (P=0.96). The HEV genotype distributions in infected blood donors and symptomatic patients were similar. However, the symptomatic patients had a higher viral load (median 282000 IU/mL; range: <60-136000000 IU/mL; P<0.01) than the blood donors. Overall, asymptomatic blood donors and patients with symptomatic hepatitis E had similar genotype distributions but the blood donors had lower viral loads.

Management of Hepatitis B Virus (HBV) in transplantation

Clinical manifestations of hepatitisB virus (HBV) infection are ranged from fulminant hepatitis to decompensated cirrhosis or hepatocellular carcinoma. Liver transplantation (LT) is one therapeutic option of these HBV infection complications. Intrahepatic viral persistence and low levels of circulating viral particles despite treatment optimization may lead to HBV recurrence after LT, which jeopardizes graft and patients survival after LT. HBV recurrence prophylactic strategies are based on nucleos(t)ides analogues (NUCs) treatment to block viral replication and anti-HBs immunoglobulin administration to neutralize circulating viral particles. The risk of HBV recurrence is also important in case of transplantation with a graft from a donor with a history of HBV infection (HBc+) to a "HBV naive" recipient or in case of immunosuppressive therapy after solid organ or hematopoietic stem cell transplantation for a HBc+ recipient. Prophylactic strategies are mainly focused on biological monitoring and NUCs therapy for high-risk situations.

P2‐104: Analysis of the sero‐epidemiology and clinical manifestations of hepatitis E virus in South America

P2‐104: Analysis of the sero‐epidemiology and clinical manifestations of hepatitis E virus in South America

Natural History, Clinical Manifestations, and Pathogenesis of Hepatitis A.

Hepatitis A virus (HAV) is transmitted by the fecal-oral route and is a major cause of acute viral hepatitis. The clinical manifestations of HAV infection range from asymptomatic infection to acute liver failure (ALF), but do not include progression to chronic hepatitis. Risk factors for severe acute hepatitis A are older age (>40 years) and preexisting liver disease. Some patients may show atypical clinical features such as relapsing hepatitis, prolonged cholestasis, or extrahepatic manifestations. Almost all hepatitis A patients spontaneously recover with supportive care. However, in the case of ALF (<1%), intensive care and urgent decision on liver transplantation are required. Liver injury during hepatitis A is not directly caused by HAV but is known to be caused by immune-mediated mechanisms. In this review, the natural history and clinical manifestations of hepatitis A are described. In addition, mechanisms of immunopathogenesis in hepatitis A are discussed.

SOCS3 genetic variants and promoter hypermethylation in patients with chronic hepatitis B.

The clinical manifestations of hepatitis B viral infection (HBV) include chronic hepatitis B (CHB), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). The contribution of negative regulator suppressor of cytokine signaling-3 (SOCS3) promoter variants in HBV disease and SOCS3 hypermethylation in tumor tissues were investigated The SOCS3 promoter region was screened for polymorphisms in 878 HBV patients and in 272 healthy individuals. SOCS3 promoter methylation was examined by bisulfite sequencing. SOCS3 mRNA expression was quantified in 37 tumor and adjacent non-tumor liver tissue specimens. The minor allele rs12953258A was associated with increased susceptibility to HBV infection (OR=1.3, 95%CI=1.1-1.6, adjusted P=0.03). The minor allele rs111033850C and rs12953258A were observed in increased frequencies in HCC and LC patients compared to CHB patients (HCC: OR=1.7, 95%CI=1.1-2.9, adjusted P=0.046; LC: OR=1.4, 95%CI=1.1-1.9, adjusted P=0.017, respectively). HBV patients with rs111033850CC major genotype had decreased viral load (P=0.034), whereas the rs12953258AA major genotype contributed towards increased viral load (P=0.029). Tumor tissues revealed increased hypermethylation compared to adjacent non-tumor tissues (OR=5.4; 95%CI= 1.9-17.1; P=0.001). Increased SOCS3 expression was observed in HBV infested tumor tissues than non-HBV related tumor tissues (P=0.0048). SOCS3 promoter hypermethylation was associated with relatively low mRNA expression in tumor tissues (P=0.0023). In conclusion, SOCS3 promoter variants are associated with HBV susceptibility and SOCS3 hypermethylation stimulates HCC development.

An unusual presentation of Epstein-Barr Virus induced hepatitis in a 15-month-old child

Objective: We report an atypical case of hepatitis in an infant that could be helpful to physicians of various specialties, as it demonstrates an atypical clinical and laboratorial manifestation of a disease not so common at that age and that could have gone undiagnosed. Case Description: A 15-month-old female, immunocompetent patient was referred to the hospital with a 3-day history of fever, vomiting, and diarrhea. The patient presented with alternation between sleepiness and irritation associated with rapid increase in serum liver enzymes levels, but no jaundice. Neurologic evaluation showed no meningeal signs and no encephalic morphological abnormalities were observed in a cranial CT scan. Treatment consisted of symptomatic medication and daily evaluation for signs of hepatic encephalopa- thy or bleeding. A serological panel showed negative IgM but positive IgG reactivity against Cytomega- lovirus (CMV) and IgM and IgG negative immunoreactivity against HAV. She was not tested for Hepatits B (HBV) or Hepatits C (HCV). Positive immunoreactivity against the Epstein-Barr virus capsid antigen (EBV VCA) IgM and negative reactivity against IgG, indicated a diagnosis of EBV-induced acute hepatitis. The patient was discharged asymptomatic after 11 days, with decreasing serum liver enzymes levels. A 15-day follow up evidenced complete remission of symptoms and normalized laboratory tests. Comments: Hepatic involvement in infections by Epstein-Barr Virus is common, presenting with moderate and transient increase in liver enzymes. It can go undetected and resolve spontaneously, while clinical manifestations of hepatitis are infrequent. In this report, we present an unusual case of a pediatric patient with hepatitis induced by EBV infection, along with a review of the literature. According to our search, no other EBV-induced hepatitis case reports have been published involving an immunocompetent patient under 2 years of age

Thrombocytopenia as a Clinical Manifestation of Hepatitis C Among Patients With a Positive Anti-HCV Test

Background: The hepatitis C virus (HCV) has been recognized as the cause of thrombocytopenia (defined as a platelet count of < 150,000 platelets/uL) occurring in patients with chronic hepatitisC. Thrombocytopenia occurs in 64% - 76% of patients with cirrhosis and/or fibrosis, compared with 6% of non-cirrhotic patients with chronic liver disease. Objectives: The aim was to study the prevalence of thrombocytopenia in HCV patients without cirrhosis and splenomegaly. Patients and Methods: A cross-sectional study was carried out in the gastrointestinal out patient department (G.I. OPD) of the Sindh institute of urology and transplantation (SIUT) from September-November 2013. 30 patients aged between 18 - 60 years with a positive anti-HCV result were included. Patients with enlarged spleen, liver cirrhosis on an ultrasound of the abdomen, and throm- bocytopenia related to other causes were excluded from the study. Results: A total of 30 patients satisfying the inclusion criteria were selected for study. The mean age of the patients was 42.2 11.4 (16 - 60), and they included 21 females and 7 males. The majority of patients had normal liver function tests with normal spleen size. On the CBC, 13 had platelets of less than 150,000/ L and 17 patients had a platelet count in the normal range, i.e., 150,000 - 400,000/ L. The prevalence of thrombocytopenia was found to be 43.3% among those with hepatitis C. Conclusions: The conducted study showed moderate frequency of hepatitis C-induced thrombocytopenia in patients without hep- atic fibrosis and splenomegaly among the Pakistani population.

Clinical Manifestations of Hepatitis E.

The clinical manifestations of hepatitis E are similar to those of other types of viral hepatitis. While acute hepatitis E is usually self-limited, pregnant women and chronic liver disease patients suffering from acute hepatitis E usually present with severe clinical manifestations that may develop into fulminant hepatic failure. Chronic HEV infection is typically only seen in organ transplant patients; most HEV cases are asymptomatic and rarely display jaundice, fatigue, abdominal pain, fever, fatigue, or ascites. The clinical manifestations of HEV infection in neonates are diverse and have varied clinical signs, biochemistry, and virus biomarkers. Lastly, the extrahepatic manifestations and complications of hepatitis E are in need of further study.

Epidemiological characteristics and clinical manifestations of hepatitis E virus infection in Bulgaria: A report on 20 patients.

Hepatitis E is one of the leading clinical manifestations of acute viral hepatitis in developing countries. In industrialized countries, during the past several years, sporadic "autochthonous" cases of HEV infection have been increased. The aim of this study was to analyze the epidemiological, clinical and laboratory features of HEV infection among patients hospitalized at the Department of Infectious Diseases in Military Medical Academy, Sofia, Bulgaria. A retrospective study of 806 cases of acute viral hepatitis was performed at the Department of Infectious Diseases in Military Medical Academy, Sofia, Bulgaria, between December 2004 and September 2012.The etiological diagnosis was established by ELISA. The statistical analysis was performed using Excel 2007 (Microsoft, Redmond, Washington, USA) and SPSS Statistics 19.0 (IBM Corp., Armonk, NewYork, USA). Specific reaction to anti-HEV-IgM and anti-HEV-IgG antibodies were detected in 20 (2.48%) of 806 patients. The most observed clinical presentations were jaundice (85%), fatigue (85%), anorexia (65%), abdominal discomfort (55%) and fever (40%). The mean values of aspartate transaminase and alanine transaminase were 521 IU/l and 881 IU/l, respectively. The cholestasis was slight, marked with mean values of gamma-glutamyl transferase and alkaline phosphatase, respectively 418 IU/I and 486 IU/I. We report twenty autochthonous sporadic cases of acute infection with HEV. The zoonotic etiology of the virus as well as the foodborne transmission of the infection is discussed. We found that aging and pre-existing underlying diseases are risk factors for a severe course of the HEV infection.

Clinical Factors and Viral Load Influencing Severity of Acute Hepatitis A.

Background and AimsClinical manifestations of hepatitis A virus (HAV) infection vary from mild to fulminant hepatic failure (FHF) in adults. We investigated the relationship between laboratory findings, including viral load, and clinical outcomes in patients with acute hepatitis A (AHA) and evaluated predictive factors for severe acute hepatitis (s-AH).MethodsWe analyzed the clinical manifestations of AHA in 770 patients. Patients with a prothrombin time (PT) of less than 40% of normal were classified as s-AH and included 4 patients with FHF, 11 patients with acute renal failure, and 3 patients with prolonged jaundice (n = 128). Other patients were defined as mild acute hepatitis (m-AH) (n = 642). Serum samples were obtained from 48 patients with acute hepatitis A. Among them, 20 with s-AH, and 28 with m-AH, were tested for HAV RNA titer.ResultsIn a multivariate analysis, age (HR = 1.042, P = 0.041), peak creatinine (HR = 4.014, P = 0.001), bilirubin (HR = 1.153, P = 0.003), alanine aminotransferase (ALT) (HR = 1.001, P<0.001), initial lactate dehydrogenase (LDH) (HR = 1.000, P = 0.045) and total cholesterol (HR = 0.978, P<0.001) were independent factors for s-AH. Serum HAV RNA was detected in 20/20 (100%) patients with s-AH and 22/28 (78.6%) patients with m-AH. In a multivariate analysis of the 48 patients who were tested for HAV RNA, peak ALT (HR = 1.001, P = 0.004) and HAV RNA titer (HR = 2.076, P = 0.012) were independent factors for s-AH.ConclusionsClinical factors including age, peak creatinine, bilirubin, ALT, initial LDH and total cholesterol were independent factors for s-AH in a multivariate analysis. In particular, HAV load strongly correlated with the severity of hepatitis A.

Clinical manifestations of Hepatitis B: its association with serum profile of cytokine genetic polymorphism

&lt;p class="MsoNormal" style="text-align: justify;"&gt;&lt;strong&gt;&lt;em&gt;&lt;span style="font-size: 10.0pt; mso-ansi-language: EN-US;" lang="EN-US"&gt;Objective&lt;/span&gt;&lt;/em&gt;&lt;/strong&gt;&lt;em&gt;&lt;span style="font-size: 10.0pt; mso-ansi-language: EN-US;" lang="EN-US"&gt;: This systematic review aims to review the correlation among the genetic polymorphism of cytokine, production and clinical presentation of these serum hepatitis B chronic. &lt;strong&gt;Methodology&lt;/strong&gt;: For this we conducted a systematic review of articles obtained by searching the databases Journals Portal CAPES and Pub Med The papers selected were published between the years 200 and 2013. We used the following descriptors: 1. Chronic hepatitis B, 2. Cytokine gene polymorphism 3. Anti-hepatitis B / genetics, 4. Hepatitis B virus / genetics. &lt;strong&gt;Results: &lt;/strong&gt;the articles found in the search, twenty-five (25), which were used in this review. &lt;strong&gt;Conclusion&lt;/strong&gt;: The research on the correlation between the genetic polymorphism of cytokine production of these serum and clinical presentation of chronic hepatitis B is still incipient, although this may elucidate the immunological mechanisms responsible for viral clearance and the chronicity of the infection.&lt;/span&gt;&lt;/em&gt;&lt;/p&gt;