PubMed Health⌕ Search

PubMed · 7513276

Chronic hepatitis C.

Abstract

Formerly the diagnosis of acute and chronic non-A, non-B hepatitis was made by the exclusion of other causes. However, in 1989 cloning of an antigenic component of the hepatitis C virus (HCV) was reported. This led to first- and second-generation tests for antibody to HCV (anti-HCV) in serum. HCV has been associated with acute and chronic posttransfusion and sporadic non-A, non-B hepatitis, and with hepatocellular carcinoma. Viral HCV RNA can be estimated with the polymerase chain reaction test, but this technically difficult test is not generally available. The entire viral genome has been sequenced. The envelope region shows considerable variation, and mutant HCV infections are being described already. There are geographic variations in the prevalence of anti-HCV, but usually about 0.5% to 1% of healthy blood donors test positive. Parenteral exposure to blood, especially by transfusion or drug abuse, remains a certain means of acquiring HCV infection. The method by which millions without parenteral risk factors acquire HCV remains uncertain. Vertical transmission and sexual and family spread occur only rarely. Body secretions are free of the virus. The mode of transmission may become clarified when tests for viral HCV as opposed to anti-HCV become generally available. Acute HCV infection usually is mild, and the chronic disease is also indolent. Carriers of hepatitis B virus or alcoholics who also test positive for HCV have more serious disease. Chronic HCV infection must be distinguished from autoimmune chronic active hepatitis. The most important difference is the response to corticosteroid therapy, which is good in autoimmune hepatitis and poor in HCV-related disease. Hepatocellular carcinoma can complicate HCV-related cirrhosis, usually about 20 years after infection with HCV. Recombinant interferon-alpha is used to treat chronic HCV disease, but selection of patients, dose, and duration of therapy are uncertain. In general, 50% of patients respond to the treatment, but 50% of these will have a relapse, with an overall response rate of 25%. Liver transplantation in patients with end-stage HCV disease usually is followed by infection of the graft.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D S Sherlock. 1994. Chronic hepatitis C.. https://pubmed.ncbi.nlm.nih.gov/7513276/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

FGF21 suppresses alcohol consumption through an amygdalo-striatal circuit.

Excessive alcohol consumption is a major health and social issue in our society. Pharmacologic administration of the endocrine hormone fibroblast growth factor 21 (FGF21) suppresses alcohol consumption through actions in the brain in rodents, and genome-wide association studies have identified single nucleotide polymorphisms in genes involved with FGF21 signaling as being associated with increased alcohol consumption in humans. However, the neural circuit(s) through which FGF21 signals to suppress alcohol consumption are unknown, as are its effects on alcohol consumption in higher organisms. Here, we demonstrate that administration of an FGF21 analog to alcohol-preferring non-human primates reduces alcohol intake by 50%. Further, we reveal that FGF21 suppresses alcohol consumption through a projection-specific subpopulation of KLB-expressing neurons in the basolateral amygdala. Our results illustrate how FGF21 suppresses alcohol consumption through a specific population of neurons in the brain and demonstrate its therapeutic potential in non-human primate models of excessive alcohol consumption.

Alcohol Drinking↗