Hepatitis Hepatitis E
All About Hepatitis E
HEV is an RNA virus, 32-34 nm in diameter, came from families calici virus, first identified in 1983. Like HAV, HEV infection is also transmitted through the faecal-oral, and has been associated with the epidemic through water in developing countries. (Adler, 2005). The incident was first reported in India in 1955 that about 29,000 people. The existence of cases in Western countries is associated with the case of a visit to an endemic area. Most often attack in young adults to middle-aged and pregnant women mrtalitas a very high rate (20%) (Sylvia and Lorrainne, 2003).
Hepatitis E from a virus called hepatitis non-A non-B transmitted enteric (ET-NANB), hepatitis non-A non-B Epidemika, Hepatitis non-A non-B faecal-oral route. (Chin J, 2006)
Clinical symptoms of this disease similar to hepatitis A, chronic form is not found. Case fatality rate of this disease is similar to hepatitis A except in pregnant women, where the figure can reach 20% of pregnant mothers infected during the third trimester of pregnancy. Cases occur sporadically and in epidemic form. (Chin J, 2006)
Diagnosis based on clinical symptoms and epidemiological picture and in a way to get rid of another etiology of hepatitis, especially hepatitis A with serological examination. Serologic tests currently being developed to detect antibodies to HEV, but not yet commercially available in the United States. However, some types of diagnostic tests are available in various research laboratories including: enzyme immunoassay and Western blot assay to detect anti-HEV IgM and IgG in serum; PCR tests to detect HEV RNA in the blood serum and feces, and immunofluorescent antibody blocking assays to detect terhdap HEV antigen antibodies in blood serum and liver. (Chin J, 2006)
The cause of the disease is hepatitis E virus (HEV), spherical, not bound, single stranded RNA virus with a diameter of 32 to 34 nm. HEV are grouped into the family Caliciviridae. Nevertheless, the organization / structure of the HEV genome differs fundamentally with the other calicivirus and HEV should be grouped into separate families. (Chin J, 2006)
Distribution of Disease
HEV is a major cause of hepatitis non-A non-B enteric worldwide. Hepatitis E outbreaks and sporadic cases have occurred covering a vast territory, especially arising in countries with poor environmental sanitation. Outbreaks often occur as outbreaks of waterborne, but it has been reported sporadic cases and outbreaks is not clearly related to water. Figures Distribution of disease is highest in young to middle age; lower rates found in younger age groups as a result of anicteric infection and / or subclinical HEV infection. In the United States and most other developed countries, cases of hepatitis E reported among travelers returning from HEV endemic areas. Outbreaks have been found in India, Myanmar (Burma), Iran, Bangladesh, Ethiopia, Nepal, Pakistan, Central Asian Republics of the former Soviet Union, Algeria, Libya, Somalia, Mexico, Indonesia and China. Outbreaks due to transmission through an extensive water with 3.682 casualties occurred in 1993 patients in Uttar Pradesh. (Chin J, 2006)
From numerous studies conducted at this time indicates that the reservoir is likely to be domestic animals, including pigs, however, has not been proven. HEV can be transmitted to chimpanzees, cynomolgus macaque, tamarin and pigs. (Chin J, 2006)
Modes of Transmission
HEV is transmitted primarily through fecal-oral route, drinking water contaminated with feces is the most common transmission media occurs. Transmission may also occur from person to person by faecal-oral route, but the environment of the household secondary cases rarely occur during outbreaks. From various studies conducted at this time indicates that hepatitis E may be a zoonotic infection, which incidentally quickly spread to humans. (Chin J, 2006)
Ranging from 15 to 64 days.; Average incubation period varies from 26 to 42 days in different outbreaks. (Chin J, 2006)
Period of communicability
It is not known. However, HEV is found in the feces 14 days after onset of symptoms of icterus (jaundice) and an average of 4 weeks after consuming contaminated food or water and lasts for about 2 weeks. (Chin J, 2006)
Susceptibility and resistance
The vulnerability of a person unknown. Over 50% of possible anicteric HEV infection, symptoms of icterus increased with increasing age. Women in the third trimester of pregnancy are particularly vulnerable to the occurrence of fulminant disease. The occurrence of several large outbreaks have occurred in young adult age groups in some areas where other enteric viruses endemic in the region was high and most people get infections in infancy, can not be explained complete. (Chin J, 2006)
When the hepatitis virus entry into hepatocytes and to replicate the cellular immune activation occurs primarily cells that are cytotoxic T lymphocytes. Nature of T lymphocyte cells are hepatocyte cells that will destroy more and more damaged cells simultaneously. Hepatitis A virus will come out of the patient’s body through the feces after 14 to 30 days of virus-infected patients. Once out of the body then transmission can occur when poor quality patient hygiene and sanitation. (Anthony F. E, 2005)
Morphological changes in the liver are often similar to a variety of different viruses. In the case of a classic, size and color of the liver appear normal, but sometimes a little edema, enlarged and colored like bile. The histological, occurs composition hepatocellular become chaotic, injury and necrosis of liver cells and peripheral inflammation. These changes are perfectly reversible, when the acute phase of illness subsided. In some cases, submasif or massive necrosis can lead to severe liver failure and death. (Sylvia and Lorrainne, 2003).
One important prediction of clinical hepatitis A is age, where children rarely show obvious symptoms, but in adults of about 75-95% of infections with hepatitis A symptoms are real. (PAPDI, 1996). More than 80% of young children that transmit hepatitis to family members are asymptomatic, while more than three-quarters of adults who are exposed to hepatitis A in the outbreak is symptomatic. (Sherker A. H, 2005)
Clinical features of acute viral hepatitis consists of 3 phases. The first phase is the phase of pre jaundice (prodromal) phase of viral hepatitis from exposure to 2 weeks. The symptoms that often arise are gastrointestinal symptoms such as nausea, vomiting, diarrhea and decreased appetite, besides that it also appeared symptoms of "flu-like syndrome" such as fever, headache, body feels weak. In this phase usually more yellow urine from feces began to brown and paler color. After a phase of pre jaundice (prodromal) phase it will continue to be jaundice. Phase jaundice usually lasts for 1-2 weeks. In this phase, gastrointestinal symptoms and "flu-like syndrome" will be reduced or even disappear. Symptoms
that arise are usually weak body, accompanied by the emergence of yellow color on the eyes, sebah abdomen and tenderness in the right hypocondrium. Urine will be light golden brown (like tea). The third phase is the healing period that lasted 3-4 months (12-15 weeks). Healing period marked by the emergence of appetite, yellow color began to diminish to disappear and the color of urine started younger. Jaundice is generally missing in the 2 6 weeks.
Earliest biochemical abnormality is an increase in ALT (SGPT) and AST (SGOT), which began to increase at approximately 18 days after infection with the virus, 1 week later there was an increase of serum bilirubin levels. This bilirubin levels showed significant symptoms of jaundice in patients. Examination of urine at the time awitan will reveal the existence of excess bilirubin and urobilinogen. Jaundice in viral hepatitis found in most patients have symptoms that can menunjukka high hyperbilirubinemia jaundice clinically. In general, jaundice pada new conjungtiva in serum as high as 2 to 4 mg / dl. (Braunwald et al, 1998)
IgM Antibodies first appeared after 25 days of virus infection, while IgG appeared after 28 days of virus infection. The presence of IgM indicates that ongoing viral infection, while IgG showed that the patient was infected with a virus and have immunity against the virus. (Anthony F. E, 2005)
Pada urine examination and bilirubin urobilin found positive at the time of prodromal phase and will grow in phases and jaundice disappeared in phase blood konvalensens.Pemeriksaan will get increased AST and ALT levels began to rise in the late prodromal phase and phase change high on jaundice and began declining in the phase konvalensens. High levels of transaminase was no correlation with the degree of liver damage. Blood bilirubin levels will rise and if> 2 mg%, it will cause the yellow color in the sclera. Serum bilirubin continued to rise despite transaminases began to fall birirubin The total value can be used as one indicator of disease prognosis. When the total bilirubin value> 20 mg% and prolonged it can be concluded more severe disease. Memanjangnya prothrombin time indicates the extensive necrosis of hepato cellular and showed a poor prognosis. On serological examination will be obtained IgM anti-HAV positive. (Harijono et al, 1994)
Hepatitis A and E is a disease that can heal on its own (Self-Limited Disease). For that, there is no specific therapy to treat acute viral hepatitis caused by HAV and HEV. Bed rest during the acute phase, accompanied by adequate nutritious diet is the usual recommendation. Intravenous feeding may be needed during the acute phase when patients constantly vomiting. Physical activity usually need to be restricted until symptoms subside and liver function tests return to normal physiology. (Sherker A. H, 2005)
Because of the limited treatment of hepatiis the emphasis is more focused on prevention through immunization. Imunsasi can be either passive immunization for hepatitis, active and passive immunization for hepatitis B, while for HEV still missing immunizations. (PAPDI, 1996)
Treatment in patients with hepatitis are:
Rest lying on the many grievances, mobilization gradually begins when a complaint or symptom is reduced, decreasing serum bilirubin and transaminase. Normal daily activities initiated after complaints disappeared and normal laboratory data.
There are no special diet, what is important is the amount of calories and adequate protein, adjusted to slera patient, sometimes less nutrition and fluid intake due to nausea and vomiting, so to be supported by parenteral nutrition: 10-20% dextrose infusion, 1500 calories / day.
Until now there has been no specific treatment for acute viral hepatitis. There is no indication of corticosteroid therapy for acute viral hepatitis, the addition of vitamins to foods high in calories of protein given to patients who experience weight loss or malnutrition.
General Prevention (Includes advice to patients):
Improved hygiene of food and drinks, Improvement of environmental sanitation and personal hygiene. Also Isolation of patients (children are prohibited to school or day care until 2 weeks after onset of symptoms)
Prevention Special with Passive with human normal immunoglobulin (NHIG: Normal Human Immune Globulin), so do Active with the inactive HAV vaccine.
Characteristics of Hepatitis
Characteristic is something that has a distinctive character in accordance with a certain disposition. Characteristics of a disease comprised disease frequency, distribution and risk factors that influence the development of the disease. (Kjellstrom T, et al, 1995)
Cases of hepatitis that often occurs is epidemic hepatitis A. Approximately 1.4 million per year in the world’s population are infected and the majority of cases unreported. In the United States reported an epidemic in the 1980s, where an increase in cases from 1983 to 1989 by 58%. And then the number of cases gradually declined because of the quality of food sanitation and hygiene improved. Generally disease epidemic is related to food contaminated by viral hepatitis A. Sanitation and hygiene of food becomes a major role in the spread of this disease. (Willner, 2005)
Hepatitis E was found in 1983 while on the epidemic of waterborne hepatitis was first reported in India in 1955. Furthermore, many reports of similar epidemics in the USSR (1955-1956), India (1975-1976), Burma (1976-1977), Nepal (1973), Algeria (1980-1981), Borneo (1987), Ivory Coast (1983 – 1984), Los Angeles, USA (1987), Mexico (1987) dank amp refugees in Somalia and Sudan (1985-1986). Populations are often infected by the age between 15 to 40 years. (Mirrian, 2000)