Chronic viral hepatitis is a group of infectious liver lesions occurring with inflammatory dystrophic-proliferative changes in the parenchyma of the organ. Clinical manifestations are dyspeptic, asthenovegetative and hemorrhagic syndromes, persistent hepatosplenomegaly, liver dysfunction. Diagnostics includes determination of markers of hepatitis B, C, D, F and G in serum; assessment of biochemical liver samples, liver ultrasound, rheohepatography, puncture liver biopsy, hepatoscintigraphy. Treatment is conservative, including diet, taking eubiotics, enzymes, hepatoprotectors, antiviral drugs.
B18 Chronic viral hepatitis
Chronic viral hepatitis in clinical gastroenterology is understood as etiologically heterogeneous anthroponotic diseases caused by hepatotropic viruses (A, B, C, D, E, G), having a manifest course lasting more than 6 months. Disease is more common at a young age and, in the absence of adequate therapy, leads to the early development of cirrhosis, liver cancer and death of patients. The progression of the disease is accelerated by drug abuse, alcohol, simultaneous infection with several hepatitis or HIV viruses.
Chronic hepatitis is etiologically closely related to acute forms of viral hepatitis B, C, D, E, G, especially occurring in a mild jaundice, non-jaundice or subclinical variant and taking a protracted character. Chronic viral hepatitis usually develops against the background of unfavorable factors – improper treatment of acute hepatitis, incomplete convalescence at the time of discharge, burdened premorbid background, alcohol or drug intoxication, infection with other viruses (including hepatotropic), etc.
The leading pathogenetic mechanism in chronic viral hepatitis is a violation of the interaction of immune cells with virus-containing hepatocytes. At the same time, there is a deficiency of the T-system, depression of macrophages, weakening of the interferogenesis system, the absence of specific antibody genesis against virus antigens, which ultimately disrupts the adequate recognition and elimination by the immune system of virus antigens on the surface of hepatocytes.
Taking into account the etiology, there are chronic viral hepatitis B, C, D, G; combinations of B and D, B and C, etc., as well as unverified chronic viral hepatitis (of unclear etiology).
Depending on the degree of activity of the infectious process, chronic viral hepatitis with minimal, mild, moderate, pronounced activity, fulminant hepatitis with hepatic encephalopathy are isolated. The minimum degree of activity (chronic persistence of viral hepatitis) develops with a genetically determined weak immune response, when there is a proportional suppression of all indicators of cellular immunity (T-lymphocytes, T-suppressors, T-helpers, T-killers, etc.). Low, moderate and pronounced activity occurs with a sharp imbalance of immune regulation.
During chronic viral hepatitis, there are stages:
- with the absence of fibrosis;
- with the presence of mild periportal fibrosis;
- with the presence of moderate fibrosis with portoportal septa;
- with the presence of pronounced fibrosis with portocentral septa;
- with the development of cirrhosis of the liver;
- with the development of primary hepatocellular carcinoma.
Disease can occur with a leading cytolytic, cholestatic, autoimmune syndrome. Cytolytic syndrome is characterized by intoxication, increased transaminase activity, decreased PTI, dysproteinemia. With cholestatic syndrome, the predominant manifestations are skin itching, an increase in the activity of alkaline phosphatase, GGTP, bilirubin. Autoimmune syndrome occurs with asthenovegetative phenomena, arthralgia, dysproteinemia, hypergammaglobulinemia, increased activity of AlAT, the presence of various autoantibodies.
Depending on the developing complications, chronic viral hepatitis is distinguished, burdened with hepatic encephalopathy, edematous ascitic syndrome, hemorrhagic syndrome, bacterial complications (pneumonia, intestinal phlegmon, peritonitis, sepsis).
The clinic of chronic viral hepatitis is determined by the degree of activity, etiology of the disease, and the severity of symptoms – the concomitant background and duration of the lesion. The most characteristic manifestations are asthenovegetative, dyspeptic and hemorrhagic syndromes, hepatomegaly and spenomegaly.
Asthenovegetative manifestations in chronic viral hepatitis are characterized by increased fatigue, weakness, emotional lability, irritability, aggressiveness. Sometimes there are complaints of sleep disorders, headache, sweating, subfebrility.
The phenomena of dyspepsia are associated with both a violation of the normal functioning of the liver, and with frequent concomitant lesions of the biliary tract, duodenum and pancreas, therefore accompany most cases of chronic viral hepatitis. Dyspeptic syndrome includes feelings of heaviness in the epigastrium and hypochondrium, flatulence, nausea, belching, intolerance to fatty foods, loss of appetite, instability of the stool (tendency to diarrhea). Jaundice is not a pathognomonic symptom of chronic viral hepatitis; in some cases, subictericity of the sclera may be noted. Obvious jaundice appears more often and increases with the development of cirrhosis and liver failure.
In half of the observations, patients with chronic viral hepatitis have hemorrhagic syndrome, characterized by a tendency to skin hemorrhages, nosebleeds, petechial rashes. Hemorrhages are caused by thrombocytopenia, a violation of the synthesis of clotting factors. In 70% of patients, the appearance of extrahepatic signs is noted: telangiectasia (vascular asterisks), erythema palmar, capillaritis (capillary dilation), increased vascular pattern on the chest.
Extrahepatic manifestations include myalgia and arthralgia, peripheral polyneuropathy, amenorrhea, gynecomastia, decreased libido, damage to the eyes and salivary glands. With the predominant autoimmune syndrome, nodular periarteritis, cardiomyopathy, antiphospholipid syndrome, dermatomyositis, granulomatosis, Takayasu’s disease, autoimmune hepatitis, chronic glomerulonephritis, diabetes mellitus, etc. can join.
In this disease, hepatomegaly is noted: the liver can protrude from under the costal arch by 0.5-8 cm; the upper border is determined percutorially at the level of VI-IV intercostals. The consistency of the liver becomes densely elastic or dense, there may be increased sensitivity or soreness during palpation. Splenomegaly is also detected in most patients. The expansion of the veins of the esophagus, hemorrhoidal veins, the development of ascites indicate the neglect and the formation of cirrhosis of the liver.
The diagnosis of chronic viral hepatitis is established with a long-term (over 6 months) infectious process caused by hepatitis B, C, D, F, G viruses; the presence of hepatosplenomegaly, asthenic, dyspeptic and hemorrhagic syndromes. To confirm the diagnostic hypothesis, the following is carried out:
- Determination of infectious markers. In order to verify the form of the disease, the markers of viral hepatitis are determined by the ELISA method, the detection of RNA viruses using PCR diagnostics.
- Blood test. Of the biochemical parameters of liver function, the most interesting is the study of AlAt and AsAT, alkaline phosphatase (ALP), gamma-glutamyltranspeptidase (GGT), lecithin aminopeptidase (LAP), serum cholinesterase (SC), lactate dehydrogenase (LDG), bilirubin, cholesterol, etc., which allow us to judge the degree of damage to the liver parenchyma in chronic viral hepatitis. In order to assess the state of hemostasis, a coagulogram is examined, the number of platelets is determined.
- Visualization methods. Ultrasound of the liver allows you to see changes in the hepatic parenchyma (inflammation, compaction, sclerosis, etc.). Rheohepatography is used to study information about the state of intrahepatic hemodynamics. Hepatoscintigraphy is indicated for signs of cirrhosis of the liver.
- Invasive diagnostics. Liver biopsy and morphological examination of the biopsy is performed at the final stage of the examination to assess the activity of chronic viral hepatitis.
At the stage of remission of chronic viral hepatitis, it is necessary to adhere to a diet and a gentle regime, carry out preventive courses of multivitamins, hepatoprotectors, choleretics. Exacerbation requires inpatient treatment.
The basis of the basic therapy is diet table No. 5; the appointment of drugs that normalize the intestinal microflora (lactobacterin, bifidumbacterin, bifikol); enzymes (festal, enzystal pancreatin); hepatoprotectors (riboxin, karsil, heptral, essentiale, etc.). It is advisable to take infusions and decoctions with antiviral (calendula, St. John’s wort), antispasmodic and weak choleretic and action (knotweed, mint).
With cytolytic syndrome, intravenous infusions of protein preparations and freshly frozen plasma, plasmapheresis are necessary. The relief of cholestatic syndrome is carried out with the help of adsorbents (activated charcoal, polyphepam, bilignin), preparations of unsaturated fatty acids (henofalk, ursofalk). With autoimmune syndrome, immunosuppressants, glucocorticoids, delagil are prescribed, hemosorption is carried out.
Etiotropic therapy requires the appointment of antiviral drugs: synthetic nucleosides (retrovir, famvir), interferons (viferon, roferon A), etc.
Prognosis and prevention
Patients with chronic viral hepatitis are on lifelong dispensary registration with an infectious diseases specialist-hepatologist. The unfavorable course is acquired with a burdened background: simultaneous infection with several viruses, alcohol abuse, drug addiction, HIV infection. The outcome of chronic viral hepatitis is cirrhosis and liver cancer.
Prevention of the chronization of the infectious process consists in the identification of low-symptomatic forms of viral hepatitis, adequate treatment and control of convalescents. Patients who have had viral hepatitis should adhere to the diet and lifestyle recommended by the doctor.