Hepatitis G is an infectious lesion of the liver tissue caused by hepatotropic HGV virus. The leading symptom in the clinic of the disease is prolonged (to three weeks) jaundice associated, including, with involvement of the biliary tract and the formation of intrahepatic bile stasis.
Characterized by fever, fatigue and significant loss of appetite. Diagnostic methods used to confirm infection are the isolation of RNA of the virus and the antibodies from the blood. For the treatment are the interferons with antiviral activity, symptomatic therapy (detoxification, enzyme, diuretic and other drugs).
Hepatitis G is a viral disease that primarily affects the hepatobiliary system. First HGV-the virus was isolated in 1967 from the blood of an American surgeon j. Barker, sick with hepatitis “neither A nor b”, however, to identify the causative agent was possible only in 1995, thanks to the introduction of molecular genetic diagnosis. Sick more often men, young age (under 45 years). In 91-98% of patients have concomitant disease in other parenteral hepatitis: frequency of co-infection with acute hepatitis b and C up to 37%, chronic – up to 17 %. Co-infection with Delta-hepaticopsida among 39.9% of patients. A clear seasonal affection have no infection.
Causes of hepatitis G
A pathogen is an RNA-containing virus (HGV is a virus, GBV-C, HPgV-virus), belonging to the family of flavivirus. Today, the virus includes three genotype several subtypes. The properties of the causative agent is similar to the hepatitis C virus, but is capable, unlike him, to reproduce the infection in nonhuman apes (which could potentially reduce the cost and simplify the study of the pathogenesis of hepatitis C, the body’s response to applied antiviral drugs). Infection infection occurs by parenteral contact with infected blood. Known cases of infection through unprotected sexual contact and transmission from mother to fetus.
Risk groups for the disease are considered patients of hemodialysis departments, recipients of internal organs, a person with a history of blood transfusion, hemophiliacs, HIV infection, medical personnel, people with many homosexual and bisexual contacts, practicing intravenous drug use. The prevalence of the disease widespread in West Africa HGV-infection is considered endemic. The virus is unstable in the environment, killed by boiling and exposure to standard doses of disinfectants.
Pathogenesis of hepatitis G has not been studied. It is believed that the virus does not have a primary hepatotropic properties, but has an affinity for mononuclear cells, spleen cells, bone marrow, and acts as a suppressor of the replication of human immunodeficiency virus. When the penetration into the human organism pathogen infects the lymphocytes, the blood gets into the various organs and systems, long persistira lymph.
Getting into the liver occurs passively, with lymphocytic cells, while inflammatory changes are expressed only in the intrahepatic bile ducts and biliary system. Possibly, the virus has a specific damaging effect on the biliary tract, as the appearance of the phenomenon of cholangitis with biliary sludge. There are also studies to determine the trigger of the role of the HGV virus in autoimmune liver disease and the formation of these abnormalities, such as aplastic anemia, thalassemia, porphyria cutaneous tarda, however, a clear description of the mechanism of the effect was not obtained because of the small number of observations.
Clinic HGV infection are similar to symptoms of a HCV infection, but cirrhotic changes of liver tissue, extrahepatic manifestations practically do not occur; however, this statement is true only for monoinfection. If you have both more than two viruses that affect the liver tissue, there is a mutual aggravation of pathological processes in the body.
Distinguish acute and primary chronic course of the disease, as well as two clinical forms:
- Busselton. The most common presentation of the disease. Patients complain of intoxication symptoms and sharp discomfort, laboratory tests can detect antibodies to the virus, a moderate increase in liver enzymes.
- Jaundice. Manifested jaundice staining of the mucous membranes, the skin, dark urine color (similar in color to the tea leaves), pruritus.
The symptoms of hepatitis G
The incubation period of the infection ranges from 9 days to 3 months. Often the disease is asymptomatic, and patients may be diagnosed accidentally during routine gynecological examinations, before donation of blood or organs, in the survey for planned surgical interventions. The onset is acute, with a rise in body temperature to 38-390C, chills, muscle and joint pain, weakness, sudden loss of appetite, drowsiness, nausea, rarely vomiting, bloating. There are heaviness, aching pain in the right hypochondrium, bitter taste in the mouth, itchy skin with a tendency to increase in its intensity.
Patients note a change in the colour of urine (straw-yellow to dark brown), and then the appearance of icteric coloration of the skin, sclera; but the most common for the skin remain the same color. Symptoms heralding the development of fulminant liver inflammation, can be considered as amplification and long duration of fever, increasing jaundice, the appearance of the gingival and nasal bleeding and tremor of the hands, the progressive increase of weakness, headache, inversion of sleep, episodes of memory loss, dinamichnee, reduction or lack of productive contact with the patient.
HGV-monoinfection with early detection practically does not cause complications, the most common is the formation of chronic lesions of the gallbladder and biliary tract (cholecystitis, cholangitis, cholelithiasis). When lightning is possible for the occurrence of acute liver failure, DIC-syndrome, acute hepatic encephalopathy. If necessary, invasive diagnostic and therapeutic procedures (injections, catheterization, fine-needle biopsy and others) high probability of occurrence of bacterial complications range from local to multi-systemic lesions and sepsis.
In the diagnostic phase of compulsory examinations of a patient with infectious disease specialist, internist, gastroenterologist, surgeon. The detection of violations and the change of consciousness necessary to consult a neurologist, psychiatrist. Patients in critical condition require immediate intensive care treatment.
The diagnostic procedure necessary for verification of CHF include:
- Assessment of objective status. Physical examination helps to determine the degree of impairment of consciousness, the shade of the skin, mucous membranes, the presence of scratching (the criterion of intensity of pruritus), enlarged liver, spleen, positive symptoms Grekova-Ortner (pain when tapping the right costal arch), Kera (pain when pressure is applied to the projection point of the gall bladder). May be determined by tremor of the limbs.
- Laboratory studies of blood and urine. In clinical analysis of blood – leukocytosis, shift formula to the left, increased ESR. For biochemical studies the characteristic increase in the level of activity of gamma-glutamyltranspeptidase and alkaline phosphatase, slight increase in ALT, AST. Total bilirubin is 2-or more fold increase, mainly due to the direct. Urinalysis demonstrates the color change, the presence of bile pigments.
- Identification of infectious agents. Determination of the presence of virus in the blood is by PCR. HGV-RNA can be detected up to six months from the moment of infection in acute in periods of replication in chronic process. Antibodies to the pathogen detected again after 4-6 months of infection (ELISA).
- Instrumental diagnostics. Ultrasound of the abdomen and retroperitoneal space allow defianately, to determine the presence of enlarged liver and spleen, low echogenicity of the liver tissue, bile sludge in the gallbladder thickening hyperechogenicity of the body wall. Rarely is Mr-cholangiography, CT and cpgre.
- Biopsy. Fine-needle liver biopsy are shown in the period of remission to verify the diagnosis and determine the degree of fibrosis. The resulting material allows for PCR, histopathological and immunohistochemical examination. An alternative to the invasive method is the study of the device “Fibroscan”.
Differential diagnosis is carried out with such diseases as viral hepatitis (A, b, C, D, E, F, TTV, etc.), leptospirosis, SARS, alveococcosis, sepsis, HFRS, opisthorchiasis, tuberculosis, hydatid disease, influenza. Similar clinical picture can give of obstructive jaundice, primary sclerosing cholangitis, malignant neoplasms of the hepatobiliary system, metastatic lesions of the liver, rarely purulent processes (carbuncles internal organs). Symptoms similar to hepatitis G, may meet patients with fatty liver, drug-induced liver injury, pancreatitis, abnormalities of the intestine, long-term abuse of alcohol and drugs, poisoning by mushrooms, methyl alcohol, salts of heavy metals.
Treatment of hepatitis G
Patients with suspected pathology hospitalized in the infectious Department. For sex partners and intravenous drug use needs to be identified, informed and invited to exclude or confirm the diagnosis. Newborns, breastfeeding, away from the breast and examined. The older children also once donate blood for determination of antibodies to causative agents of parenteral infections.
Therapy of hepatitis G imply sparing diet (strictly prohibited alcohol, sodas, fresh baked goods, fried and fatty meals, confectionery, seasonings, marinades, coffee), increase fluid intake (bottled water), bed rest until stable reduction of the temperature of the case within 2-3 days. Not recommended for lifting more than 10 kg, exercising, running, sudden changes of temperature, pressure (sauna, pool). As causal treatment the best results showed preparations of alpha-interferon. Drug treatment also consists of detoxification (chlosol, Trisol, glucose, Reamberin), reception of sorbents (the activated coal, diosmectite, a polymethylsiloxane polyhydrate), enzymes (Pancreatin), choleretic agents (ursodeoxycholic acid) and symptomatic therapy.
Prognosis and prevention
The prognosis for this infection is considered more favorable than hepatitis C. It is associated with minimal liver damage and low variability of the virus. However, given the small percentage of monoinfection (2-8%), and its coexistence with other viral lesions of the liver, the prognosis will depend on early detection and regular follow-up. Proven impact on the frequency of fulminant flow HGV virus does not have, although mutant forms of the virus were detected in 12-50% of cases. Jaundice often lasts three weeks, hepatic failure in the case of lightning the course of monoinfection increases for 6-45 days.
Methods of specific prophylaxis of the disease are currently under development. A promising direction in vaccine development may be the use of protein E2 of the HCV genome of the virus, because persons with antibodies to proteins of the data, not observed cases of infection with hepatitis G. Additional protection may be available for vaccination of adults against hepatitis b virus (particularly those at risk). Existing methods of treatment of chronic viral inflammation of the liver (etiotropic antiviral drugs) may also be considered as preventive methods.
The non-specific protection measures should include strict control of indications and techniques for blood transfusions and transplantations, a thorough inspection of blood products, donor organs, the introduction into medical practice of modern methods of sterilizing instruments, disposable supplies, pregnancy planning, accounting and examination in the antenatal clinic during pregnancy, condom use, avoidance of traumatic sexual practices and intravenous drug use.