Prevalence of antibodies against hepatitis A virus, hepatitis B virus, and treponema pallidum in mauritius

1991 ◽  
Vol 23 (5) ◽  
pp. 535-541 ◽  
Author(s):  
Tino F. Schwarz ◽  
Clement Chan Kam ◽  
George Law Min ◽  
Wolfgang Jilg ◽  
Bettina Wilske ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Treponema Pallidum ◽  
Virus Hepatitis ◽  
B Virus

Hepatitis b virus, hepatitis a virus and persistently elevated aminotransferases in hemophiliacs

1980 ◽  
Vol 6 (2) ◽  
pp. 111-118 ◽  
Author(s):  
R. J. Gerety ◽  
M. E. Eyster ◽  
E. Tabor ◽  
J. A. Drucker ◽  
C. J. Lusch ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Virus Hepatitis ◽  
B Virus

scholarly journals Viral and parasitic pathogen burden and the association with stroke in a population-based cohort

2017 ◽  
Vol 13 (5) ◽  
pp. 481-495 ◽  
Author(s):  
Brad D Pearce ◽  
Anna Bracher ◽  
Jeffrey L Jones ◽  
Deanna Kruszon-Moran
Keyword(s):  
Hepatitis B Virus ◽  
Toxoplasma Gondii ◽  
Hepatitis B ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Virus Hepatitis ◽  
Serological Evidence ◽  
B Virus ◽  
Cytomegalovirus Hepatitis ◽  
Prior Infection

Background Higher cumulative burden of viral and bacterial pathogens may increase the risk of stroke, but the contribution of parasitic infections in relation to cumulative pathogen burden and risk of stroke has rarely been examined. Aim To estimate the association of multiple persistent viral and parasitic infections with stroke in a representative sample of adults in the United States. Methods Serological evidence of prior infection was categorized as positive for 0–1, 2, 3, or 4–5 infections based on immunoglobulin G seropositivity to cytomegalovirus, hepatitis A virus, hepatitis B virus, Toxoplasma gondii, and Toxocara spp. in 13,904 respondents from the National Health and Nutrition Examination Survey III. Regression analysis was used to estimate the cross-sectional association between serological evidence of prior infection and history of stroke adjusting for demographic risk factors, and potential mediators of stroke. Results Age-adjusted models that included serological evidence of prior infection to cytomegalovirus, hepatitis A virus, hepatitis B virus, Toxoplasma gondii, and Toxocara spp. showed that adults in the highest serological evidence of prior infection category (4–5 infections) had a higher prevalence of stroke (5.50%, 95% confidence interval 2.44–10.46%) than those in the lowest serological evidence of prior infection categories (1.49%, 95% confidence interval 1.01–2.11%), and a trend test suggested a graded association between serological evidence of prior infection and stroke ( p = 0.02). In multivariable logistic regression models, the positive association of serological evidence of prior infection with stroke prevalence remained significant after adjustment for other significant risk factors (odds ratio = 1.4, p = 0.01) but was only significant among those aged 20–59 (odds ratio = 2.0, p = 0.005) and not among those aged 60–69 ( p = 0.78) or 70 and older ( p = 0.43). Conclusion We found support for a connection between serological evidence of prior infection to cytomegalovirus, hepatitis A virus, hepatitis B virus, Toxoplasma gondii, and Toxocara spp. and stroke among those aged 20–59. There may be a need to consider common parasitic infections in addition to viral and bacterial pathogens when calculating serological evidence of prior infection in relation to cerebrovascular disease.

Role of environmental factors in the etiology of hepatocellular carcinoma

2010 ◽  
Vol 151 (28) ◽  
pp. 1132-1136 ◽  
Author(s):  
István Tornai
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Environmental Factors ◽  
Hepatitis B ◽  
Hepatitis A ◽  
Virus Hepatitis ◽  
B Virus

A krónikus vírushepatitisek jelentik ma a legismertebb okokat a hepatocellularis carcinoma (HCC) kialakulásában. A krónikus B- és C-vírus-hepatitis a májrákok körülbelül 40-50%-át okozza. A nyugati típusú társadalmakban a HCC előfordulása folyamatosan növekvő tendenciát mutat. Az alkohol számít a környezeti tényezők közül a legfontosabbnak, bár az alkoholfogyasztás a legtöbb országban csökken. Ez aláhúzza az egyéb környezeti tényezők fontosságát is. Az elfogyasztott alkoholmennyiséggel egyenes arányban növekszik a cirrhosis és a következményes HCC gyakorisága nőkben és férfiakban egyaránt. A kémiai anyagok közül a legismertebb a Kínában és Afrikában elterjedt aflatoxin, amely a gabonaféléket szennyező mycotoxin. Hasonló területeken endémiás, mint a hepatitis B-vírus, együtt szinergista hatást fejtenek ki. A dohányzás is egyértelműen bizonyított hepatocarcinogen hatással rendelkezik. Ez is jelentősen fokozódik, ha alkoholfogyasztással vagy vírushepatitisszel társul. Társadalmilag talán a legfontosabb az elhízás, a következményes nem alkoholos zsírmáj, illetve steatohepatitis és a 2-es típusú cukorbetegség, amelyek prevalenciája egyre fokozódik. Feltehetően ezek állnak a növekvő HCC-gyakoriság hátterében. Az inzulinrezisztencia és az oxidatív stressz képezik a legfontosabb patogenetikai lépéseket a májsejtkárosodásban. További fontos rizikótényező az orális fogamzásgátlók elterjedt használata. Egyes foglalkozások esetén a tartós szervesoldószer-expozíció is növeli a HCC rizikóját. Védelmet jelenthetnek az antioxidánsok, a szelén, a gyógyszerek közül a statinok és a feketekávé-fogyasztás.

Viral Hepatitis: 1985 Update

1985 ◽  
Vol 7 (1) ◽  
pp. 3-11
Author(s):  
Saul Krugman
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Viral Hepatitis ◽  
Hepatitis A ◽  
Viral Infections ◽  
Hepatitis A Virus ◽  
Fatal Outcome ◽  
Specific Marker ◽  
Hepatitis D ◽  
B Virus

During the past two decades extraordinary advances in hepatitis research have clarified the etiology and natural history of the disease. At least four types of hepatitis have been identified: A, B, D (delta), and non-A, non-B. Hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis D virus (HDV) have been characterized. Serologic tests have been developed to detect the antigens and antibodies associated with these three hepatitis infections. As of the present time, the non-A, non-B viral agents have not been identified. Therefore, non-A, non-B hepatitis is diagnosed by excluding other viral causes of hepatitis, such as hepatitis A virus, hepatitis B virus, Epstein-Barr virus (EBV), cytomegalovirus (CMV), and others. A recent report indicating that non-A, non-B hepatitis may be caused by a retrovirus, if confirmed, may provide a specific marker of this infection. The course of viral hepatitis is variable; it may be an asymptomatic, anteric infection, or it may be an acute illness characterized by fever, malaise, anorexia, nausea, abdominal pain, and jaundice. Most patients recover completely, but occasionally the infection may be complicated by chronic hepatitis, cirrhosis, and, occasionally, by a fulminant fatal outcome. This review will be devoted predominantly to a discussion of the diagnostic and prophylactic aspects of hepatitis A and hepatitis B viral infections.

scholarly journals Prolonged and biphasic acute hepatitis A in hepatitis B virus carrier

2016 ◽  
Vol 10 ◽  
Author(s):  
Elena Garlatti Costa ◽  
Michela Ghersetti ◽  
Silvia Grazioli ◽  
Pietro Casarin
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Acute Hepatitis ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Inactive Carrier ◽  
B Virus ◽  
Acute Hepatitis A ◽  
Hepatitis B Virus Carrier ◽  
Life Threatening

Acute hepatitis A is generally a self-limited disease in healthy subjects within few weeks, but an uncommon type of prolonged and biphasic acute course of hepatitis A infection has been also described. This type of presentation is observed in about 6-10% of patients, but a small number of reports, concerning this topic, are available in literature. In addition hepatitis A virus (HAV) infection in hepatitis B virus (HBV) carriers has rarely been discussed. A 41-year-old Italian man, already known to our Department for HBV infection as an inactive carrier HBsAg(+)ve, experienced a prolonged and biphasic course of acute hepatitis A, lasting about 7 months. In this patient possible factors, causing the second flare of transaminases, were excluded (in particular autoimmunity). Liver biopsy as well HAV RNA search in blood/stools were not performed. In conclusion, the hepatologist should take into account this type of atypical course in patients with HAV-related hepatitis and should promote HAV vaccination in subjects with HBV-chronic hepatitis, to prevent possible life-threatening acute exacerbation of hepatic damage, mainly in HBV-carriers with more severe forms of liver diseases.

Non-A, non-b hepatitis in chimpanzees: Interference with acute hepatitis A virus and chronic hepatitis B virus infections

1983 ◽  
Vol 11 (3) ◽  
pp. 207-213 ◽  
Author(s):  
Daniel W. Bradley ◽  
James E. Maynard ◽  
Karen A. McCaustland ◽  
Bert L. Murphy ◽  
E. H. Cook ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Virus Infections ◽  
Chronic Hepatitis B Virus ◽  
B Virus ◽  
Acute Hepatitis A ◽  
Hepatitis B Virus Infections

scholarly journals Viral Superinfection in Previously Unrecognized Chronic Carriers of Hepatitis B Virus with Superimposed Acute Fulminant versus Nonfulminant Hepatitis

1999 ◽  
Vol 37 (1) ◽  
pp. 235-237 ◽  
Author(s):  
Chia-Ming Chu ◽  
Chau-Ting Yeh ◽  
Yun-Fan Liaw
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Acute Hepatitis ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Hepatitis B Surface Antigen ◽  
Significant Difference ◽  
B Virus ◽  
Hdv Infection

The role of viral superinfection in hepatitis B surface antigen carriers with superimposed fulminant (n = 60) versus nonfulminant (n = 90) acute hepatitis was studied. The frequency of hepatitis A virus (HAV) (0 versus 2.2%), HCV (18.3 versus 21.1%), HDV (15.0 versus 7.8%), and HEV (1.7 versus 4.4%) infection showed no significant difference, while simultaneous HCV and HDV infection was significantly more prevalent in the former (8.3 versus 0%). Only 3.6% of fulminant cases and 3.3% of nonfulminant controls were HGV RNA positive.

Sign in / Sign up

Export Citation Format

Share Document