[SIMINA]

Buna!Indaraznesc si eu.Am de vre-o trei ani hepatita B.Eu am luat-o printr-o transfuzie de singe.Am avut acum trei ani o operatie prin care a fost nevoie de transfuzie de singe.Nu am avut nici un fel de simtome din care se spun.Raceala,oboseala,temperatura.Am facut analiza de HIV printre care si aceasta analiza si am constatat ca am hepatita B si mi sa spus ca sunt purtator sanatos.Va rog sa imi explicati si mie ce inseamna.Va multumesc!

Aceasta postare a fost editata de SIMINA: 02 December 2005 - 08:14 PM

[Sky]

Daca nu e cu suparare iti pot oferi un articol in engleza. Dc nu stii prea bine te pot ajuta si cu traducerea peste ceva timp.
"Inactive carriers forms the largest group in chronic HBV infected patients. Around 300 million people are inactive carriers The inactive HBsAg carrier state is diagnosed by absence of HBeAg and presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based assays, repeatedly normal ALT levels, and minimal or no necroinflammation, slight fibrosis, or even normal histology on biopsy [3,4]. Inactive cirrhosis may be present in patients who had active liver disease during the replicative phase of infection. The prognosis of the inactive HBsAg carrier state is usually benign. Long-term follow- up (up to 18 years) of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma (HCC) [40-42]. Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state [40-43]. In addition, approximately 20 to 30% of persons in the inactive HBsAg carrier state may undergo spontaneous reactivation of hepatitis B during follow-up [29,33,34,40]. Multiple episodes of reactivation or sustained reactivation can cause progressive hepatic damage and even hepatic decompensation. HBV reactivation is usually asymptomatic but on occasion can mimic acute viral hepatitis [44]. Acute flares of hepatitis should be differentiated from superinfection with other hepatotropic viruses. As many as 20 to 30% of these acute exacerbations may be caused by superinfection with HDV, HCV, or hepatitis A virus and can be associated with an increased risk of fulminant hepatic failure [44]. Some carriers eventually become HBsAg negative and develop anti-HBs. The incidence of delayed HBsAg clearance has been estimated to be 1 to 2% per year in Western countries, where HBV infection is usually acquired in adulthood, but a lower rate from 0.05 to 0.8% per year in endemic areas, where HBV infection is mostly acquired perinatally or in early childhood. Clearance of HBsAg has been reported to be higher in women than in men and in older than younger carriers. Prognosis is improved by loss of HBsAg as liver disease is usually inactive and nonprogressive, but HBsAg clearance does not completely prevent occurrence of decompensation or HCC in patients who have already developed cirrhosis [45,46]."

sau poti citi aici http://www.presspro-pediatru.ro/articole/h...cronica-119.php

Multa sanatate.