Benign Hepatitis Research Articles

Incidence of hepatitis A in children with acute icteric hepatitis of district Shopian of Kashmir

Background: Viral hepatitis is a major health problem worldwide. It is caused by at least five hepatotropic viruses, hepatitis A virus being the commonest one. The virus is responsible for most forms of acute benign hepatitis, although fulminant hepatic failure can occur. HAV spreads mainly through the fecal-oral route and hence is preventable by precautionary methods. Hepatitis A vaccine is available and highly effective in preventing disease. Objective of current study was to find the incidence of hepatitis A in children with features of acute icteric hepatitis of district Shopian of Kashmir.Methods: We sampled 83 children aged above 1 year to 17 years who attended the hospital for different features suggestive of hepatitis and evaluated them after proper and detailed history followed by relevant investigations and serology. Cases were labelled positive or negative on the basis of HAV IgM antibody.Results: We had 83 cases, 36 were boys (43.37%) and 47 were girls (56.62%). The girls made just more than a half of the cases and the boys just below half the cases. 13.25% (11 cases) were aged 1 to 4 years (none was below 2 years), 32.53% (27) were 4 to 7years, 32.53% (27) were 7 to 10 years, 16.87% (14) were 10 to 13 years, only 4.82% (4 cases) reported were 13 to 17 years. All 83 proved to be hepatitis A (100%).Conclusions: This study found that the incidence of hepatitis A in children with features of acute icteric hepatitis is very high in the children of district Shopian & a survey with a very large sample size will be ideal.

Differences in radiotherapy application according to regional disease characteristics of hepatocellular carcinoma.

There are differences in opinion regarding the application of external beam radiotherapy in the treatment of hepatocellular carcinoma. Some major guidelines state that external beam radiotherapy is yet to attain a sufficient level of evidence. However, caution should be exercised when attempting to understand the clinical need for external beam radiotherapy solely based on the level of evidence. Previously, external beam radiotherapy had low applicability in the treatment of hepatocellular carcinoma before computed tomography-based planning was popularized. Modern external beam radiotherapy can selectively target tumor cells while sparing normal liver tissues. Recent technologies such as stereotactic body radiotherapy have enabled more precise treatment. The characteristics of hepatocellular carcinoma differ significantly according to the regional etiology. The main cause of hepatocellular carcinoma is the hepatitis B virus. It is commonly diagnosed as a locally advanced tumor but with relatively preserved hepatic function. The majority of these hepatocellular carcinoma cases are found in the East Asian population. Hepatocellular carcinoma caused by hepatitis C virus or other benign hepatitis tends to be diagnosed as a less locally aggressive tumor but with deteriorated liver function. The western world and Japan tend to have patients with such causes. External beam radiotherapy has been more commonly performed for the former, although the use of external beam radiotherapy in the latter might have more concerns with regard to hepatic toxicity. This review discusses the above subjects along with perspectives regarding external beam radiotherapy in recent guidelines.

Prevalece of Hepatitis A Virus in Libian Children

Hepatitis A virus (HAV) is the most hepatotropic. This virus is responsible for the most forms of acute and benign hepatitis although fulminant hepatic failure can occur in 1% more often in adults. It is a member of Picornaviridae famil, it is a heat stable and has limited host range. The incidence of infection by Hepatitis A virus shows regional variation being highest in developing countries. Determination of age specific Hepatitis A virus (HAV) seroprevalence and the associated risk factors would help better plan for national preventive strategies including vaccination. We carried out a cross-sectional study on 315 children from Tripoli and Gharian cities in Libya during the years 2018-2020. The age range of the patients was 1-18 years and were from different socioeconomic status (SES) families.....attending teaching hospitals casualty seeking medical help and checkup. The indicators of SES included employment status, residence, number of family members, source of drinking water and social status. Serum samples were collected and investigated for HAV antibodies. The data were statistically analyzed. HAV antibodies were positive in 113 patients (36%) Males were 161(53%) while Females were 154 (49%). HAV antibodies was significantly higher among children of low SES,60 % by the age of 18 years compared to children of high SES, 35% by the same age. Crowded household and parental education were significantly associated with high seropositivity and seronegativity respectively. There is significant rate of seronegativity amongst the studied population especially those from richer backgrounds making them more susceptible to severe infection in future with concomitant complications. We propose that revision of national vaccination program should be considered to include Hepatitis A vaccination

Hépatite fulminante à virus Epstein-Barr : évolution favorable après transplantation hépatique

Viral hepatitis are the leading cause of fulminant hepatitis. Epstein Barr virus is the viral agent involved in infectious mononucleosis, associated with a frequent and usually benign hepatitis, except in case of immunodeficiency, congenital or acquired. We report the case of an immunocompetent young woman who presented an EBV induced fulminant hepatic failure, requiring liver transplantation that was successful. This observation emphasizes that EBV must be known as a possible cause of fulminant hepatitis and that liver transplantation is probably the unique therapeutic option to avoid a usually fatal course.

Delta infection and hepatitis B virus replication in Danish patients with fulminant hepatitis B.

The presence of hepatitis B virus and delta agent markers was investigated in 41 patients referred during the years 1970-1985 with fulminant hepatitis classified as type B or non-A non-B and compared to findings in patients with uncomplicated hepatitis B and chronic hepatitis B infection. 13 patients had no markers of hepatitis B and delta infection and were classified as non-A non-B hepatitis. The remaining 28 patients were all HBsAg and IgM anti-HBc positive and 14 (50%) had evidence of delta infection. In contrast, only 13/71 patients (18%) with acute benign hepatitis B had evidence of delta coinfection (p less than 0.005). This corresponds to an odds ratio of 4.5 for development of fulminant hepatitis among patients with hepatitis B and delta coinfection. In 100 chronic HBsAg carriers 29% were positive for delta markers. 12 of the delta infected patients with fulminant hepatitis were positive for total antibody to the delta antigen, and 2 were delta antigen positive. Three were HBeAg positive/anti-HBe negative. None had hepatitis B virus DNA. Among the 14 patients without delta infection, hepatitis B virus DNA was found in 2/4 HBeAg positive/anti-HBe negative patients and in 1/8 patients negative for both markers. The present data indicate that a high proportion of Danish patients with fulminant hepatitis B have hepatitis B and delta agent coinfection. Further, the findings suggest that hepatitis B and delta coinfection may be associated with an increased risk of development of fulminant hepatitis as compared to that of hepatitis B alone.

Sequences of Hepatitis B Virus DNA in the Serum and Liver of Patients with Acute Benign and Fulminant Hepatitis

We investigated hepatitis B virus (HBV) DNA in liver samples from 22 patients with acute benign hepatitis (AH) and 26 with acute fulminant hepatitis (FH) and compared the results with those obtained by detection of serum HBV DNA and HBV serological markers. Free HBV DNA forms were detected in 11 patients with AH and one with FH, a reflection of active HBV DNA replication in three patients and the end of viral multiplication in nine. Free monomeric HBV DNA was present in three patients with AH and six with FH, and free oligomers were identified in three patients with AH. Results from two patients with AH and seven with FH suggested the presence of dimeric or multimeric HBV DNA. Thus, the various forms of HBV DNA previously described in chronic HBV carriers may be observed at the acute stage of the viral infection. After comparing serological and hybridization data, we found that nine of 19 patients (one with AH and eight with FH) lacking serum HBV surface antigen might have had acute hepatitis related to infection with HBV or HBV variants.

Search for hepatitis B virus DNA in sera from patients with acute type B or non-A, non-B hepatitis

One hundred and three single sera from adults hospitalized with acute type B (78) or non-A, non-B (25) hepatitis were tested for the presence of hepatitis B virus DNA (HBV DNA). All sera from patients with type B hepatitis were IgM anti-HBc-positive. These patients were classified as benign (47) or fulminant (31) hepatitis. The 25 acute non-A, non-B patients were also classified as benign (21) or fulminant (4) hepatitis and were negative for serologic markers of past HBV infection. Serum HBV DNA was detected with similar frequency in benign (38.5%) and fulminant (FH, 34.6%) HBsAg-positive cases. HBV DNA was not detected in either the 26 acute HBsAg-negative hepatitis B cases who were positive for anti-HBc and anti-HBs or the 25 acute non-A, non-B hepatitis cases. The absence of HBV DNA in 43.8% of benign hepatitis B patients who were positive for HBsAg and HBeAg could possibly be attributed to either low level replication of HBV that was not detectable by the [32P]HBV DNA probe or to a period of delayed clearance of free HBeAg following cessation of HBV replication. Emergence of anti-HBs in the presence of HBsAg did not always correspond to clearance of HBV in fulminant type B cases. However, in acute type B hepatitis, irrespectively of severity, disappearance of HBsAg and appearance of anti-HBs was accompanied by reduction of HBV replication to undetectable levels.

Costs and benefits of the passive prophylaxis of hepatitis B in an Italian hospital.

The authors report the clinical results and the cost/benefit analysis of a protocol of passive prophylaxis of hepatitis B based on the administration of two doses of three ml each of HBIG and on the control of anti-HBs levels by RIA for six months after accidental exposure in health-care personnel. Only two out of 351 susceptible subjects developed viral hepatitis instead of the expected 70 if passive prophylaxis had not been performed. The cost/benefit analysis showed a saving of 356 509 US$ in the past 36 months. Furthermore, the cost of each case of hepatitis prevented was 2194 US$, whereas the cost of one case of acute, benign hepatitis was 6180 US$. Since a saving of 3.39 US$ for each dollar spent is achieved, this protocol of passive prophylaxis appears more than adequate both clinically and economically. It is believed that the adoption of some general prophylactic measures will further stress the advantages of this procedure.

INFLUENCE OF DELTA INFECTION ON SEVERITY OF HEPATITIS B

The prevalence of serum markers of primary delta infection was determined in 532 patients with acute benign hepatitis B seen in Italy, and in 111 patients with fulminant hepatitis B seen in Italy, France, and England. Patients with fulminant hepatitis had a significantly higher prevalence of delta markers (43/111, 39%) than did those with benign hepatitis (101/532, 19%). In 25 of the 43 patients with delta-positive fulminant hepatitis, serum markers indicated a primary hepatitis B infection while in the remaining 18, IgM antibody to hepatitis B core antigen was absent, indicating that hepatitis B preceded superinfection with the delta agent. The increased morbidity of HBsAg hepatitis with delta infection may result from the cumulative simultaneous exposure to hepatitis B virus and delta, or from superinfection of HBsAg carriers with delta.

Clinical aspects of neonatal hepatitis.

Over a period of nine years, 316 newborn infants with prolonged nonhemolytic jaundice have been observed (Table 1). Fifty-four percent of them were classified as having hepatitis; 29% were diagnosed as having anatomical malformations of the extrahepatic biliary ducts; in the remaining 17% the jaundice was ascribed to a variety of causes (Table 2). Most (90%) of the 169 infants with viral hepatitis could be classified (Table 3) as having either benign hepatitis (94 patients) or cholestatic hepatitis (59 patients). Among the 92 infants with malformations of the bile-duct system (Table 4), the most frequent lesion was an atresia of the extrahepatic biliary ducts (66 patients). There were 151 infants who exhibited a prolonged obstructive type of jaundice (Table 5). In this group the etiology was almost evenly divided between cholestatic hepatitis (18%) and extrahepatic duct atresia (21%). Thus, the efforts of recent years have been oriented toward

The Liver in Secondary (Early) Syphilis

When syphilis was in its heyday sophisticated investigation of patients with liver disease was in its infancy. In particular needle hepatic biopsy was introduced only in the 1940's just before syphilis received a setback with the advent of penicillin. There have therefore been few detailed accounts of hepatic histology during the various stages of syphilis. Older writers relied on autopsy findings, and so the pericellular hepatic fibrosis of congenital syphilis (the liver teeming with spirochetes) was recognized and the hobnailed, scarred appearance of the gummatous liver had always to be distinguished from a macronodular (post-necrotic) cirrhosis.1 An acute benign hepatitis . . .

Subacute hepatitis.

ACUTE viral hepatitis of both the epidemic and *■ serum varieties continues to be a common medical illness and is regarded correctly as a typical benign, self-limited disease. Despite considerable variation in the degree and duration of clinical illness associated with the virus-induced liver-cell damage most patients recover completely, with no lasting evidence of hepatic dysfunction. Rarely, for unknown reasons, massive liver necrosis is produced by the hepatitis viruses and results clinically in usually fatal fulminant acute hepatitis. Most physicians recognize these two extremes of the hepatitis clinicopathological "spectrum," — acute benign hepatitis and fatal fulminant hepatitis, — but . . .