Chronic hepatitis C: diagnosis

Laboratory diagnosis of chronic hepatitis C

At the time of treatment, the activity of serum transaminases rarely exceeds the upper limit of the norm by 6 times, on average, it is about 3 times higher than normal. The activity of serum transaminases does not reflect the degree of changes in the liver; it can be normal for multiple determinations, despite significant morphological changes. However, if it is more than 10 times higher than the upper limit of the norm, then it presupposes the presence of chronic hepatitis with necrotic and inflammatory changes.

Levels of albumin and bilirubin in serum at the time of treatment are usually normal and increase with time slightly. The level of prothrombin is not changed.

Concentration of HCV-RNA in serum is essential for assessing the contagiousness and for monitoring the results of treatment. Quantitative methods, such as the investigation of branched DNA strands (rDNA), although they are used in diagnostics, but have low sensitivity. Their results require confirmation by PCR. If there is a liver biopsy in the blood of HCV-PHK, it usually reveals a change. The concentration of HCV-RNA in the serum, exceeding 10 ⁵ molecular equivalents (copies) in 1 ml, is observed in the active phase of the disease and coincides with the peak activity of transaminases.

Serum anti-core-HCV IgM can serve as a measure of the effectiveness of treatment.

If possible, the genotype of the virus should be established. Type 1b is associated with a more severe course, a poor response to antiviral drugs, relapses after liver transplantation and the possibility of developing cancer. Type 4 is characterized by resistance to antiviral treatment.

In the differential diagnosis of chronic hepatitis C with autoimmune chronic hepatitis, especially when the possibility of IFN therapy is being considered, blood should be examined for autoantibodies.

For early detection of hepatocellular carcinoma in patients with cirrhosis of the liver, especially in men older than 40 years, the level of serum a-fetoprotein is determined every 6 months and ultrasound of the liver is performed.

Histological examination of the liver

The histological picture is not pathognomonic, but characteristic changes are often revealed. A distinctive feature is lymphoid aggregates or follicles in portal tracts, which can be both isolated and part of inflammatory changes in portal tracts. The core of the aggregates consists of B cells in combination with a number of T-helper / inducers and is surrounded by a ring formed predominantly from T-suppressors of cytotoxic lymphocytes. By cellular composition, these aggregates resemble primary lymphoid follicles in the lymph nodes. Their formation is not accompanied by manifestations of an autoimmune process. The degree of involvement of bile ducts in different series of studies was different. Interstitial hepatitis occurs in mild form, although usually accompanied by intra-lobular cellular infiltration. Fat dystrophy is found in 75% of cases, its mechanism is unclear. A pattern of mild chronic hepatitis is characteristic. Chronic hepatitis can be combined with cirrhosis of the liver, or a histological examination reveals a picture of inactive liver cirrhosis. Changes are not related to the duration of the disease or the activity of serum transaminases during treatment. A liver biopsy plays a significant role in clarifying the diagnosis and assessing the activity and stage of the disease. Repeated biopsies, apparently, are justified only in the case of scientific research, otherwise the need for them does not arise.

HCV-RNA can be detected in liver tissue by PCR.

Immunological diagnosis of chronic hepatitis C

Approximately 5% of patients with autoimmune hepatitis have an anti-HCV test that is false-positive and approximately 10% of patients with hepatitis C have circulating autoantibodies. However, these states are fundamentally different. The clinical picture of hepatitis C does not change in the presence of autoantibodies.

A relationship was found between HCV infection and a positive LKM I test. It may be due to the presence of cross-sectional antigenic determinants in chronic HCV infection and autoimmune chronic active hepatitis with LKM 1, although detailed analysis has shown that these determinants differ from each other. Between these two types of hepatitis there are clinical differences. HCV infection usually affects older men and with a low LKM I titer.

Anti-GOR is an autoantibody against host proteins found in LKM 1-positive patients with chronic hepatitis C. They have no clinical significance.

Autoimmune hepatitis can be initiated by interferon in patients with chronic HCV infection. Predicting this by the level of autoantibodies before treatment is impossible. Autoimmune hepatitis is manifested with sudden increases in serum transaminase activity and autoantibody titers. Immunodepressive therapy is effective.

The detection of autoantibodies in patients with anti-HCV and HCV-RNA may lead to difficulties in the choice of treatment: immunosuppressive therapy, which responds to patients with true chronic autoimmune hepatitis, or antiviral - for infected HCV.

Comparative characteristics of autoimmune hepatitis and chronic hepatitis C

Index	Autoimmune Hepatitis	Hepatitis C
Age	Young and middle	Any
Floor	Mainly female	Uniform distribution
ACAT activity:
10 times the norm	Usually	Rarely
"Fluctuates"	Rarely	Usually
HCV-RNA	Absent	Present
Contact with blood	Absent	Often
Response to corticosteroids	Rapid decrease in serum transaminase activity	Missing or weak

Differential diagnosis of chronic hepatitis C

It is necessary to exclude the role in the development of the disease of all possible hepatotoxic drugs.

There should be no hepatitis B markers. However, in some patients with chronic hepatitis B at too low, undetectable titers of HBsAg and HBV-DNA, erroneous diagnosis of hepatitis C is possible.

Chronic autoimmune hepatitis is indicated by the very high activity of serum transaminases and the level of y-globulin in combination with high titer of autoantibodies in serum.

It should be deleted Wilson's disease.

[1], [2], [3], [4], [5],