Viral Hepatitis
Thomas T. Yoshikawa, Shobita Rajagopalan in Antibiotic Therapy for Geriatric Patients, 2005
Common clinical varieties of viral hepatitis include hepatitis A, B, C, D, and E (Table 1). Both hepatitis A and hepatitis E are often self-limiting diseases, acquired by fecal-oral transmission, and hence require no specific therapy. Hepatitis B and hepatitis D are transmitted parenterally and have a tendency for chronicity. Hepatitis C spreads by parenteral routes and is associated with the highest chronicity rate among the viral hepatitides. Various forms of viral hepatitides cannot be distinguished from each other clinically or by biochemical tests, and hepatitis serology is necessary for accurate diagnosis. Currently available antiviral therapies for hepatitis B and hepatitis C show promising results; however, novel treatments for these infections continue to evolve. Vaccination against hepatitis A and hepatitis B are available. Although the overall incidence of hepatitis A and hepatitis B may be less in the elderly in comparison to younger individuals, older individuals suffer from higher morbidity and mortality from these illnesses.
Diseases of the Hepatobiliary Tree and Pancreas Associated with Fever
Benedict Isaac, Serge Kernbaum, Michael Burke in Unexplained Fever, 2019
At least five distinct types of viral hepatitis have been recognized: A, B, two types of non-A, non-B (NANB), or the recently described D or delta virus.15 These agents may produce a wide range of clinical features, from asymptomatic infection, through anicteric hepatitis, cholestatic jaundice, to acute fulminant hepatitis or chronic liver disease (in hepatitis B, delta, and NANB). Fever and flu-like symptoms may predominate during the preicteric phase of hepatitis, whose duration may range from 1 or 2 days to 3 weeks.16,17 Fever and chills occur in about 30% of adults and 40% of children with hepatitis A, and diarrhea is common in children.18 The patient with anicteric hepatitis may complain of unexplained fever, anorexia, nausea, and weakness; important clues to the correct diagnosis are abdominal discomfort and brown urine. In hepatitis B, a febrile polyarthritis may develop and precede other systemic features.19 Fever may accompany several complications of hepatitis: fulminant hepatitis, chronic active hepatitis, cirrhosis, hepatocellular carcinoma, aplastic anemia, necrotizing vasculitis,20,21 and mixed cryoglobulinemia.22
Clinical Pharmacology of the Anti-Tuberculosis Drugs
Peter D O Davies, Stephen B Gordon, Geraint Davies in Clinical Tuberculosis, 2014
Subclinical hepatitis occurs in up to 10% of patients on INH [16,18,23,28]. A clinical picture similar to viral hepatitis may develop, with anorexia, nausea, vomiting, abdominal pain and weight loss. Laboratory changes include elevations in plasma aspartate transaminase (AST), alanine aminotransferase (ALT) and occasionally bilirubin. The hepatitis is independent of INH plasma concentrations. Risk factors include age more than 35 years, chronic alcohol intake, preexisting hepatic disease and concurrent hepatotoxic agents [23,28]. Hepatitis in combination with rifampicin is additive, but not synergistic [28,29]. INH should be stopped immediately, allowing time for the liver enzymes to return to baseline and for any clinical symptoms to resolve before carefully reintroducing the drug.
Clinical experience with the inactivated hepatitis A vaccine, Avaxim 80U Pediatric
Published in Expert Review of Vaccines, 2019
Catherine Bravo, Larissa Mege, Claire Vigne, Yael Thollot
The incubation period of acute hepatitis A is usually 14–28 (up to 50) days. The clinical outcome is strongly correlated with age; young children usually experience asymptomatic infection or mild nonspecific viral-like illness, while adults who have not been infected when young commonly experience symptomatic icteric infection [2,5]. Hepatitis A cases are not clinically distinguishable from other types of acute viral hepatitis [12]. Symptoms in young children include malaise, nausea, fever, and diarrhea in approximately 50% of cases; joint pain, abdominal pain, or vomiting in 20–30% of cases, and jaundice in up to 10% [2]. Liver enzyme levels may be raised; dark urine and clay-colored stools along with jaundice are all possible characteristic manifestations [5]. Specific diagnosis is primarily through detection of anti-HAV immunoglobulin M (IgM) antibodies, which gradually disappear over 6 months post-infection [20]. Additional tests include reverse transcriptase polymerase chain reaction (RT-PCR) to detect for HAV RNA [12], but these are mainly used for research purposes. There is no specific anti-viral treatment for hepatitis A [12] and supportive care remains the mainstay of treatment [21].
Management of chronic viral hepatitis in the hematological patient
Published in Expert Review of Anti-infective Therapy, 2018
Laura Ambra Nicolini, Emanuela Zappulo, Claudio Viscoli, Malgorzata Mikulska
Viral hepatitis is of concern in the hematological patient for several reasons. First, HCV and, to a lesser extent, HBV have been associated with an increased risk of certain hematological disorders. Particularly, there is strong evidence of a causal relationship between HCV and type II mixed cryoglobulinemia and B-cell non-Hodgkin lymphoma (B-NHL) [7,8]. Second, HBV, HCV, and possibly even HEV may reactivate during immunosuppression, with clinical presentation varying from asymptomatic or mild transaminitis to significant liver impairment, with consequent delays or changes of chemotherapy regimens, and acute failure [9]. Third, also in case of resolved HBV infection, that is previous HBV infection, defined by the absence of HBsAg in the presence of antibodies against HBV core antigen (HBcAb), with or without antibodies against HBsAg (HBsAb), reactivation occurs in certain settings [10]. Therefore, screening for viral hepatitis and correct management is mandatory to prevent unfavorable outcomes.
Severe dengue and liver involvement: an overview and review of the literature
Published in Expert Review of Anti-infective Therapy, 2020
Po Ying Chia, Tun-Linn Thein, Sean Wei Xiang Ong, David Chien Lye, Yee Sin Leo
Moderate liver disease is defined when a patient has all 3 of (i) an acute illness with discrete onset of signs and symptoms consistent with acute viral hepatitis (e.g. fatigue, abdominal pain, loss of appetite, intermittent nausea, vomiting, dark urine, clay-colored or light stools), (ii) alanine aminotransferase (ALT) greater than 10 times upper limit of normal consistent with grade 4 toxicity in the FDA 2007 toxicity tables or ≥400 U/L and (iii) does not meet criteria for acute liver failure (i.e. no mental status changes and international normalized ratio [INR] <1.5) [21]. Severe liver disease is defined when a patient has all 3 of (i) an acute clinical syndrome consistent with acute hepatitis, (ii) change in mental status or any grade of hepatic encephalopathy and (iii) coagulopathy with INR ≥1.5 [21].
Related Knowledge Centers
- Cirrhosis
- Cytomegalovirus
- Hepatitis
- Hepatitis B Virus
- Hepatocellular Carcinoma
- Viral Disease
- Acute
- Chronic Condition
- Asymptomatic
- Epstein–Barr Virus