Sexually Transmitted Diseases - I. I. Mavrov 2005

Viral Hepatitis

Viral hepatitis is a systemic infectious disease characterized primarily by damage to the reticuloendothelial system of The Liver and the digestive tract. It typically has an insidious onset. Today, modern approaches allow for a fresh perspective in assessing the Epidemiology, Differential Diagnosis, and outcomes of both acute and chronic viral hepatitis.

Etiology. The causative agents are hepatitis B and C Viruses. Recently, new hepatitis-causing viruses, G and TTV, have been discovered, along with the SEN virus, which has eight variants and is closely related to the TTV virus.

Hepatitis viruses are resilient against chemical and physical agents. They withstand heating up to 100 °С for 1–2 minutes, with their thermal resistance increasing when suspended in Blood serum. Their antigenic properties remain intact even after boiling for 10 minutes, as well as at pH 2.4 for 6 hours, although infectivity is lost. The viral antigen is destroyed by a 0.5% sodium hypochlorite solution within 3 minutes at a low disinfectant concentration. The infectious activity of the virus also persists following ultraviolet irradiation (UV) of plasma or other blood products.

To date, no cellular systems capable of supporting viral Replication have been identified. The hepatitis B virus causes subclinical infection in certain species of monkeys, particularly chimpanzees.

The TTV virus has been isolated from animals, including pigs, chickens, and cows, making it a zoonotic virus shared between humans and animals.

Transmission routes. The infection is transmitted parenterally. The highest risk of infection is associated with intravenous drug use, blood transfusions (typically sourced from asymptomatic carriers), or blood products (such as plasma and packed red Blood Cells) in which the virus retains its infectivity. The hepatitis B virus has been detected in semen, uterine secretions, menstrual blood, saliva, and nasopharyngeal washings. Consequently, sexual contact plays a significant role in the spread of the infection. Domestic transmission is also possible, as is the vertical transmission of the hepatitis B virus from an infected or carrier pregnant woman to the fetus, either transplacentally, through contact with infected Amniotic Fluid, or during childbirth.

A significant number of individuals become infected due to inadequate sterilization of syringes, needles, scalpels, or during tattooing. Hepatitis B is commonly encountered among patients and staff in hemodialysis units. It frequently affects surgeons, pathologists, dentists, nurses, laboratory technicians, blood transfusion station personnel, and others.

Sexual transmission of viral hepatitis B is more widespread than previously believed. In such cases, microtraumas to the Skin or mucous membranes of the genitals, rectum, or Oral Cavity serve as the entry gate for viruses present in the semen or uterine secretions of an infected sexual partner.

Epidemiology. In the final decade of the 20th century, the incidence of viral hepatitis B and C rose sharply. According to WHO data, approximately 10 million people die from the consequences of hepatitis C annually, and at least 900 million worldwide are infected, with signs of chronic hepatitis and liver cirrhosis observed in 300–350 million patients. Drug Addiction and prostitution are cited as the primary drivers of this rapid surge in incidence.

Eight genotypes of the hepatitis C virus are known. Genotype 3a is frequently associated with intravenous drug use and serves to some extent as a "marker" for drug users, even in cases of a single episode. Hence, hepatitis C is also known as "addicts' hepatitis." The disease is highly prevalent due to a high susceptibility to both hepatitis B and C viruses. It is characterized by a long incubation period (ranging from 9 to 26 weeks). There are no seasonal peaks in incidence, nor is there any hypersensitivity among specific age groups. However, certain high-risk groups are distinguished: individuals practicing promiscuity or homosexuality; patients who abuse parenteral medications and those receiving frequent blood transfusions; individuals undergoing hemodialysis; children born to mothers with viral hepatitis B; and medical personnel and dentists in contact with hepatitis B patients or carriers.

According to expert estimates, there are over 200 million carriers of the hepatitis B virus worldwide. Hepatitis B can progress into chronic liver disease, such as chronic persistent hepatitis, chronic active hepatitis, liver cirrhosis, and hepatocellular carcinoma. Persistent infection is observed in 5–15% of adults who have recovered from the acute form, and in certain geographic regions, in more than 90% of adults infected during childhood.

Positive test results for the hepatitis B virus correlate with a history of other Sexually Transmitted Infections, repeated homosexual contacts, promiscuity, and the practice of anorectal and orogenital intercourse (R. Catterall, 1978; A. Jassus et al., 1980).

In recent years, A number of publications have emphasized The Link Between sexual activity and the contraction of viral hepatitis B and C. Evidence indicates that in the blood serum of patients visiting venereologists, hepatitis B Antigens or Antibodies are found 10 times more frequently compared to a control group of voluntary blood Donors. Among homosexual men, antibodies to the hepatitis B virus are detected in 30% of those examined, compared to 5% in men with exclusively heterosexual contacts; thus, sexual transmission among heterosexual partners is relatively rare. An exception is made for men who are chronic carriers of the hepatitis B virus, who pose a risk to their female sexual partners but do not serve as a source of infection through household contact. The number of cases of heterosexual transmission of hepatitis B increases with each year.

Transmission of hepatitis B and C viruses from infected carrier mothers to their children is possible. In a fraction of these children, viral persistence develops, leading to primary chronic hepatitis. The high carrier rate and widespread prevalence of viral hepatitis B observed even in early childhood are attributed by researchers to perinatal infection.

Clinical Features. Viral hepatitis B and C begin gradually. The pre-icteric period is prolonged and accompanied by dyspepsia, arthralgia, and skin rashes. When the virus is transmitted sexually, the acute stage of the disease is mild and subclinical—clinical manifestations are subtle, and jaundice (if it develops) resolves quickly and completely. However, observations show that the majority of homosexual men with acute viral hepatitis B exhibit pronounced clinical symptoms. These patients remain contagious to their sexual partners for several weeks. The prognosis is favorable in most cases (R. Catterall, 1978). Indicators of a past acute infection include anti-HBc and anti-HBc antibodies.

Chronic viral hepatitis B is a sequela of acute hepatitis, occurring in 10–12% of adult patients and accompanied by sporadic fluctuations in transaminase levels and hepatomegaly. Such changes are also frequently observed in virus carriers but generally do not progress to liver cirrhosis. The prognosis is favorable. Liver function tests in patients with chronic viral hepatitis B are typically normal, but their blood serum tests positive for HBsAg, which is considered characteristic of the chronic course of viral infection. In some patients, particularly carriers of the delta agent, a chronic active form is observed, characterized by a wide spectrum of histological Changes in the liver; HBsAg is detected in 10–15% of these patients. The marker for the delta agent is anti-delta antibodies. The prognosis in such cases is guarded, as the progressive process may lead to macronodular liver cirrhosis.

A key feature of chronic viral hepatitis B is its paucisymptomatic nature, regardless of morphological changes in the liver or the profile of serum viral markers. The disease may remain in a stable phase, and patients can remain contagious to their sexual partners for 10 years or more (P. Ya. Grigoriev et al., 1984; R. Tudson et al., 1980).

The onset of the disease is characterized by nausea, vomiting, and fever, which frequently mimic Influenza. Jaundice may appear during the prodromal phase, though it is typically absent in the Initial Stages of hepatitis B.

The main clinical signs of the disease include lethargy, weakness, headache, varying degrees of pain in the right upper quadrant, dyspeptic disorders (a bitter taste in the Mouth, flatulence, bowel irregularities), and, in some patients, tenderness along the path of the intestines. These symptoms generally persist in patients for a prolonged period.

In addition to hepatic alterations, viral hepatitis B may manifest with:

1) urticaria and other rashes, along with non-migratory polyarthralgia developing in 15–20% of patients 1–6 weeks prior to the onset of hepatitis symptoms; 2) polyarteritis nodosa; 3) Glomerulonephritis. It is hypothesized that circulating immune complexes in the blood are the underlying cause of these syndromes.

It was previously believed that "healthy" carriage of hepatitis viruses could persist for many years without causing damage to the liver or other Organs. It has now been conclusively proven that signs of hepatitis are detectable in 85–90% of "healthy" hepatitis B virus carriers, and in 82–100% of hepatitis C antibody carriers.

Hepatitis C predominates among chronic liver diseases. Its characteristic feature is that only 20% of patients recover following the acute phase, while 80% develop a chronic form. The most favorable variant is slow progression, where the hepatitis spans 25–30 years and culminates in liver cirrhosis. In 25–30% of patients, rapid progression is observed, advancing to fatal cirrhosis twice as fast—within just 10–15 years.

Young adults under the age of 30 predominate among those affected, and many do not live to reach mature adulthood. Despite progressive hepatitis, the majority of patients feel well for a long time, and 15% exhibit no changes in biochemical liver function tests.

Diagnosis. Important diagnostic indicators of viral hepatitis B and C include a history of surgeries, blood and blood product transfusions, frequent injections, sexual excesses, homosexual contacts, drug addiction, and other factors promoting the breach of skin or mucous membrane integrity within 9–30 weeks prior to the appearance of the initial symptoms.

Clinical and epidemiological data are supplemented by laboratory findings, among which the most sensitive are enzymological tests measuring serum aminotransferase activity. In acute hepatitis, their serum levels range from 500-2000 IU and almost never drop below 100 IU. The level of Alanine aminotransferase (ALT) is typically higher than that of serum aspartate aminotransferase (AST). A sharp increase in ALT levels within 3-19 days of disease onset points to viral hepatitis A, whereas a gradual rise (over 35-200 days) is more characteristic of viral hepatitis B.

Liver dysfunction in viral hepatitis is also manifested by a decrease in serum albumin and an elevation in serum globulins. Gamma-globulin and serum transaminase levels are frequently used to assess the severity of the disease course and the degree of liver damage. In many patients with viral hepatitis A, high levels of IgM are detected 3-4 days after the increase in ALT. In contrast, the concentration of this immunoglobulin Class in patients with viral hepatitis B usually remains within the normal range or is only slightly elevated.

Detecting serological markers of viral hepatitis B (HBsAg, anti-HBs, HBeAg, and anti-HBe) is crucial for diagnosis. The following Methods are used for this purpose: Agar gel precipitation test (AGPT), counter-Immunoelectrophoresis (CIEP), Complement fixation test (CFT), indirect hemagglutination assay (IHA), enzyme-linked immunosorbent assay (ELISA), and radioimmunoassay (RIA). The most sensitive and specific among these are the radioimmunoassay and enzyme-linked immunosorbent assay. The latter can replace RIA, which requires expensive gamma counters and radionuclide-labeled Proteins. The widespread adoption of enzyme-linked immunosorbent and molecular biological methods will undoubtedly help improve clinical diagnosis, epidemiological surveillance, and the detection of virus carriers in this disease.

Treatment and Prevention. Therapeutic measures for viral hepatitis are primarily based on antiviral, pathogenetic, and symptomatic agents. Treatment is aimed at creating favorable conditions for the resorption of damaged liver cells and the promotion of reparative processes. The Use of corticosteroid preparations, with or without azathioprine, generally promotes disease remission. Patients who have recovered from viral hepatitis should avoid heavy physical labor for 6-12 months (depending on the form of the disease and the recovery period) as well as hepatotoxins such as alcohol. All convalescents are subject to follow-up medical observation (dispensarization).

Currently, therapy using alpha-interferon preparations, as well as combination therapy with interferon and ribavirin—which doubles treatment efficacy—is widely accepted for chronic hepatitis B and C. This combined treatment suppresses the virus, reduces The activity of necrosis and inflammatory processes in the liver, and slows down or inhibits its fibrotic (cirrhotic) transformation.

Immunization against the hepatitis B virus should be carried out in high-risk groups, taking into account the epidemiological situation, socioeconomic factors, Sexual Behavior patterns, and environmental conditions. Furthermore, due to high rates of perinatal hepatitis B transmission, immunization is particularly urgent in certain areas for women of childbearing age at risk, as well as for infants in their first year of life born to carrier mothers, since this is the only realistic way to prevent infection. Immunization should also be conducted among populations in certain predominantly tropical and subtropical regions where hepatitis B is highly endemic, with 10-20% (or more) of the population being virus carriers, as well as in regions with a high incidence of hepatocellular carcinoma. The latter ranks among the top ten most common malignancies worldwide. Over 250,000 new cases are registered annually, and there is strong evidence that approximately 80% of these neoplasms are caused by the hepatitis B virus.

Prevention of viral hepatitis must focus on interrupting the routes of transmission of the causative agent. An analysis of clinical and epidemiological studies allows us to recommend the following preventive measures:

1. All confirmed cases of viral hepatitis must be reported to local public health authorities or infectious disease clinics. This will allow for more targeted Structure/175.html">Implementation of anti-epidemic measures.

2. Transient and permanent virus carriers must be informed about the risks they pose to others and the ways to minimize viral transmission.

3. The risk of infection is higher during sexual contact with patients suffering from acute viral hepatitis than with virus carriers. Individuals should be warned about situations that may pose a risk of contracting or transmitting the viral infection.

4. Women who contract viral hepatitis during Pregnancy can transmit the infection to the fetus. The risk of transmission increases in the third trimester and the postpartum period. Infants become HBsAg-positive primarily within the first 2 months postpartum, but it is recommended to screen children for HBsAg at 1-month intervals for at least half a year. Persistent antigenemia develops in the majority of such children.

5. Patients with acute viral hepatitis must be isolated, strict precautions must be observed while caring for them, and gloves or other protective clothing must be worn when handling blood and instruments. Both medical personnel and patients must observe personal hygiene.

6. Isolating HBsAg carriers is impractical, as there is no evidence that they (particularly food handlers) can be a source of infection. However, they should be informed about the possibility of transmitting the infection to their sexual partners.

7. HBsAg screening is advisable for patients attending sexually transmitted disease clinics and outpatient departments. Specially trained staff should be assigned to examine and counsel these patients.

8. Careful monitoring of blood donors (especially regular ones). Timely suspension from blood donation of individuals with current or past viral hepatitis, regardless of how long ago the illness occurred or the treatment outcome, as well as individuals suspected of harboring this infection.

9. Mandatory in-depth re-examination of individuals deferred from donation due to clinical or serological suspicions of viral hepatitis.

10. Prompt tracing, examination, and serological monitoring of recipients who received blood or blood components from patients with viral hepatitis.

11. Restriction of blood transfusions (especially small volumes of 150-200 ml) and performing them only under strict clinical indications.

12. Thorough sterilization of needles and other instruments used for parenteral Procedures.

Combating sexually transmitted viral hepatitis requires comprehensive anti-epidemic work, accurate record-keeping, medical follow-up (dispensarization) of all patients and virus carriers, and broad Public Health Prevention measures with active participation not only from medical and sanitary-epidemiological institutions and various government agencies, but also from public organizations. The fight against this infection must be carried out in accordance with the country's existing system for monitoring and treating patients with Sexually Transmitted Diseases.