Hepatitis G is an infectious lesion of liver tissue caused by the hepatotropic HGV virus. The leading symptom in the clinic of the disease is prolonged (up to three weeks) jaundice, associated, among other things, with the defeat of the biliary tract and the formation of intrahepatic stagnation of bile. Fever, increased fatigue and a significant decrease in appetite are characteristic. Diagnostic methods used to confirm infection consist in the isolation of the virus RNA, as well as antibodies to the pathogen from the blood. Interferons with antiviral activity, symptomatic therapy (detoxification, enzymes, choleretic and other drugs) are used for treatment.
ICD 10
B17.8 Other specified acute viral hepatitis
General information
Hepatitis G is a viral disease affecting mainly the human hepatobiliary system. For the first time, the HGV virus was isolated in 1967 from the blood of American surgeon J. Barker, who had hepatitis “neither A nor B”, but it was possible to identify the pathogen only in 1995 thanks to the introduction of molecular genetic diagnostics. Men and young people (up to 45 years old) are most often ill. In 91-98% of cases, patients have concomitant disease with other parenteral hepatitis: the frequency of co–infection with acute hepatitis B and C is up to 37%, with chronic hepatitis – up to 17%. Coinfection with delta hepatitis occurs among 39.9% of patients. The infection has no clear seasonal attachment.
Causes
The causative agent of infection is an RNA-containing virus (HGV virus, GBV-C, HPgV virus) belonging to the flavivirus family. Today, the virus includes three genotypes and several subtypes. By its properties, the pathogen is similar to the hepatitis C virus, but, unlike it, it is able to reproduce the infection on non-human monkeys (which can potentially reduce the cost and simplify the study of the pathogenesis of hepatitis C, the body’s response to the antiviral drugs used). Infection occurs parenterally through contact with infected blood. There are known cases of infection during unprotected sexual intercourse and transmission of the virus from the mother to the fetus.
The risk groups for the disease are patients of hemodialysis departments, recipients of internal organs, persons who have undergone hemotransfusion, patients with hemophilia, HIV infection, medical personnel, people with numerous homosexual and bisexual contacts, practicing intravenous drug use. The prevalence of the disease is ubiquitous, for West Africa, HGV infection is considered an endemic disease. The virus is unstable in the environment, dies when boiled and exposed to standard doses of disinfectant solutions.
Pathogenesis
The pathogenesis of hepatitis G has not been studied enough. It is believed that the virus does not have primary hepatotropic properties, but has an affinity for mononuclears, spleen cells, bone marrow, and also acts as a suppressor of human immunodeficiency virus replication. Upon penetration into the human body, the pathogen affects lymphocytes, enters various organs and systems with the blood flow, persisting in the lymph for a long time. Ingestion into the liver occurs passively, together with lymphocytic cells, while inflammatory changes are expressed only in the intrahepatic bile ducts and the biliary system. Probably, the virus has a specific damaging effect on the biliary tract, since the occurrence of cholangitis with the phenomenon of biliary sludge has been described. There are also studies to determine the trigger role of HGV virus in autoimmune liver lesions and the formation of pathologies such as aplastic anemia, thalassemia, cutaneous porphyria of the Tardis, but a clear description of the mechanism of influence has not been obtained due to the small number of observations.
Classification
The clinic of HGV infection is similar to the symptoms of HCV infection, but cirrhotic changes in liver tissue, extrahepatic manifestations are practically not found; however, this statement is true only for monoinfection. In the presence of more than two viruses affecting the liver tissue at the same time, there is a mutual aggravation of pathological processes in the body. There are acute and primary chronic course of the disease, as well as two clinical forms:
- Heartless. The most common picture of the disease. Patients complain of intoxication symptoms and severe malaise, during laboratory examination, antibodies to the virus, a moderate increase in liver enzymes can be detected.
- Jaundice. It is manifested by jaundice staining of mucous membranes, skin, dark urine color (similar in color to tea leaves), skin itching.
Hepatitis g symptoms
The incubation period for infection ranges from 9 days to 3 months. Often, the disease is asymptomatic, and patients can be identified by chance: at a professional examination, before donating blood or organs, during an examination for planned surgical interventions. The onset of the disease is acute, with a rise in body temperature to 38-390C, chills, muscle and joint pain, weakness, a sharp decrease in appetite, drowsiness, nausea, less often vomiting, bloating. There are heaviness, aching pains in the right hypochondrium, bitterness in the mouth, skin itching with a tendency to increase its intensity.
Patients note a change in the color of urine (from straw yellow to dark brown), and then the appearance of a jaundiced skin color, sclera; but with the most common course, the skin remains the same shade. Symptoms foreshadowing the development of fulminant inflammation of the liver can be considered an increase and prolonged course of fever, an increase in jaundice, the appearance of gingival and nasal bleeding, tremor of the hands, a progressive increase in weakness, headache, sleep inversion, episodes of memory lapses, adynamicity, a decrease or lack of productive contact with the patient.
Complications
HGV-monoinfection with timely detection practically does not cause complications; most often there is the formation of chronic lesions of the gallbladder and biliary tract (cholecystitis, cholangitis, cholelithiasis). With a lightning-fast course, acute liver failure, DIC syndrome, acute hepatic encephalopathy may occur. If invasive diagnostic and therapeutic procedures are necessary (injections, catheterization, fine needle biopsy, etc.), there is a high probability of bacterial complications in the range from local to multisystem lesions and sepsis.
Hepatitis g diagnosis
At the diagnostic stage, examinations of the patient by an infectious disease specialist, therapist, gastroenterologist, surgeon are mandatory. If violations and changes in consciousness are detected, a consultation of a neurologist, a psychiatrist is necessary. Patients in critical condition require immediate resuscitation. Diagnostic procedures necessary for the verification of nosology include:
- Assessment of the objective status. Physical examination makes it possible to determine the degree of impaired consciousness, the shade of the skin, mucous membranes, the presence of scratching (the criterion for the intensity of itching), an increase in the size of the liver, spleen, positive symptoms of Grekov-Ortner (soreness when tapping on the right rib arch), Kera (pain when pressing on the projection point of the gallbladder). Tremor of the extremities can be determined.
- Laboratory tests of blood and urine. In a general clinical blood test – leukocytosis, a shift of the formula to the left, an increase in ESR. The biochemical study is characterized by an increase in the activity level of gamma-glutamyltranspeptidase and alkaline phosphatase, a slight increase in ALT, AST. Total bilirubin is determined in a 2 or more fold increase, mainly due to direct. Urine analysis shows a change in color, the presence of bile pigments.
- Identification of infectious agents. The presence of the virus in the blood is determined by PCR. HGV-RNA can be detected up to six months from the moment of infection in acute course, during periods of replication in the chronic process. Antibodies to the pathogen begin to be determined only after 4-6 months from infection (ELISA).
- Instrumental diagnostics. Ultrasound of the abdominal cavity and retroperitoneal space allow for diffdiagnosis, to determine the presence of an increase in the liver and spleen, reduced echogenicity of hepatic tissue, bile sediment in the gallbladder, thickening, hyperechogenicity of the organ wall. MR cholangiography and CT are performed less frequently.
- Biopsy. A fine needle liver biopsy is indicated during remission in order to verify the diagnosis and determine the degree of fibrosis. The obtained material allows for PCR, pathohistological, immunohistochemical studies. An alternative to the invasive method is a study using the “Fibroscan” device.
Differential diagnosis is carried out with diseases such as viral hepatitis (A, B, C, D, E, F, TTV and others), leptospirosis, ARVI, alveococcosis, sepsis, HFRS, opisthorchiasis, tuberculosis, echinococcosis, influenza. A similar clinical picture can be given by mechanical jaundice, primary sclerosing cholangitis, malignant neoplasms of the hepatobiliary system, metastatic liver lesions, rarely purulent processes (carbuncles of internal organs). Symptoms similar to hepatitis G can occur with hepatic steatosis, medicinal liver damage, pancreatitis, intestinal pathologies, prolonged abuse of alcohol and narcotic substances, poisoning with mushrooms, methyl alcohol, heavy metal salts.
Treatment
Patients with suspected pathology are hospitalized in the infectious diseases department. Partners in sex and intravenous drug use should be identified, informed, invited to exclude or confirm the diagnosis. Newborns who are breastfed are weaned and examined. Older children also donate blood once to determine antibodies to pathogens of parenteral infections.
Hepatitis G therapy implies a mandatory sparing diet (alcohol, carbonated drinks, fresh pastries, fried and fatty dishes, confectionery, seasonings, marinades, coffee are strictly prohibited), an increase in drinking regime (boiled water), bed rest until a steady decrease in body temperature for 2-3 days. Lifting weights of more than 10 kg, sports exercises, running, sudden changes in temperature, pressure (sauna, swimming pool) are not recommended. Alpha-interferon preparations showed the best results as etiotropic therapy. Drug treatment also consists of detoxification (chlosol, trisol, glucose, reamberin), intake of sorbents (activated charcoal, diosmectite, polymethylsiloxane polyhydrate), enzymes (pancreatin), choleretic drugs (ursodeoxycholic acid) and symptomatic therapy.
Prognosis and prevention
The prognosis for this infection is considered more favorable than for hepatitis C. This is due to minimal liver damage and low variability of the virus. However, given the small percentage of monoinfection (2-8%), and its predominant coexistence with other viral liver lesions, the prognosis of the disease will depend on early detection and regular follow-up. The HGV virus has no proven effect on the frequency of fulminant course, although mutant forms of the virus were detected in 12-50% of cases. Jaundice most often lasts three weeks, liver failure in the case of lightning-fast monoinfection increases within 6-45 days.
Methods of specific prevention of nosology are currently under development. The use of E2 proteins of the HCV virus genome may be a promising direction in creating a vaccine, since there are no cases of hepatitis G infection among people who have antibodies to these proteins. An additional measure of protection may be the affordable vaccination of the adult population against viral hepatitis B (especially risk groups). Existing methods of treatment of chronic viral liver inflammation (etiotropic antiviral drugs) can also be considered as preventive methods.
Measures of non-specific protection should include strict control of indications and techniques of blood transfusions and transplantations, thorough testing of blood products, organ donors, introduction into medical practice of modern methods of sterilization of instruments, disposable consumables, pregnancy planning, registration and examination in the antenatal clinic during gestation, the use of condoms, avoidance of traumatic types of sexual practices and intravenous drug administration.
