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EDITORIAL
Year : 1997  |  Volume : 4  |  Issue : 1  |  Page : 9-11  

Viral hepatitis, the battle continues


Professor of Medicine and Gastroenterology, King Saud University & Secretary General, Saudi Council for Health Specialties, P.O. Box 94656, Riyadh 11614, Saudi Arabia

Date of Web Publication31-Jul-2012

Correspondence Address:
Hussein M AI-Freihi
Professor of Medicine and Gastroenterology,King Saud IJniversity& Secretary General, Saudi Councitfor Health Specialities,P.O.Box 94656,Riyadh 11614
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


PMID: 23008560

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How to cite this article:
AI-Freihi HM. Viral hepatitis, the battle continues. J Fam Community Med 1997;4:9-11

How to cite this URL:
AI-Freihi HM. Viral hepatitis, the battle continues. J Fam Community Med [serial online] 1997 [cited 2019 Dec 13];4:9-11. Available from: http://www.jfcmonline.com/text.asp?1997/4/1/9/98444

Hepatitis is a disease of varied etiologies. Ethnic, economic, social, environmental, behav­ioral and iatrogenic factors can significantly influence its epidemiology. Undoubtedly viral causes are by far the most common and dominant ones. Since the discovery of the Hepatitis B surface antigen (HBsAg) in 1964 by Blumberg, [1] a number of viruses referred to alphabeti­cally with letters such as A, B, C, D, E and G have been identified.

Extensive data pertinent to viral hepatitis are now established: its prevalence, incidence, mode of transmission to a certain extent, clinical features, complications, serological markers and effective prevention for A and B. In this issue of the journal, two papers addressing the epidemiology of the two most important causes of chronic viral hepatitis (B and C) in a well-defined homogeneous group [2] and among general population are published. [3] The overall prevalence of HBsAg among the selected group at Yanbu and general population in Hail of 7.7% and 3.5% respectively is similar to previously published data. [4] The Kingdom of Saudi Arabia (KSA) is considered to be endemic for Hepatitis B virus (HBV) infection. By adult age, 7-8% of the public in the KSA test positive for HBsAg while 6.7% of Saudi children are already positive by the age of 7-10 years. [4] Prevalence of HBV infection in the KSA is steady in all age groups indicating a horizontal transmission route in early life. Epidemiological studies have failed to reveal any sexual differences or relationship to socioeconomic status and the family size of affected individuals either for Hepatitis B or C. Patients with schisto­somiasis, however, appear to be at higher risk to acquire both HBV and Hepatitis C vines (HCV) infection. [5],[6] The fact that infection with HBV in the KSA takes place in early life and via horizontal transmission, provides an excellent basis and effective strategy for control through mass vaccine. [7] Therefore, a nationwide campaign was launched in the KSA on October 1, 1989 aiming at vaccinating all newborn and children entering primary schools. The program has been integrated with the expanded program on immunization (EPI). [8] The impact of this massive campaign is expected to become apparent in the follow-up study which has just been started throughout the KSA. This study, among others, aims at determining the prevalence of HBsAg among Saudi children less than 12 years of age. Owing to the high efficacy (95-99% seroconversion rate) of the vaccine and the nearly nationwide coverage (>90%), marked reduction in HBsAg prevalence, and thus HBV infection reservoir, should occur within the targeted age group. [8] This expectation would have been noted in the present two studies, had they included a larger number of children 12 years of age or less. However, the present prevalence rate of 7-8% among adult Saudis will persist for the next few decades. This fact entails that HBV will continue to play an important role in the pathogenesis of acute and chronic liver disease, including cirrhosis and hepatocellular carcinoma in the KSA, as previously demonstrated. [1],[9],[10],[11],[12]

Sustained response rate to antiviral therapy does not exceed 45% for HBV and 15-40% for HCV infection at its best. Furthermore, development of vaccine for HCV will be difficult because of the heterogeneous nature of the genom. [13]

Reported HCV prevalence in KSA ranges from 0.3 to 3% among general population and up to 68% among hemodialysis patients. [14],[15],[16] The 0.6% prevalence for HCV infection re­ported in this issue of the journal compares well with previously reported data. [2],[15],[16] The prevalence of anti-HCV in Saudi patients with chronic liver disease ranges from 25% to 63.6%, [14] indicating a major role for the virus in this disease entity. [14]

Due to an improved living standard, prevalence of Hepatitis A infection (HAV) in the KSA is declining among children less than 15 years old and steadily increasing with advancing age. [17] HAV infection is usually asymptomatic in children but can be severe if it first occurs in adulthood. Therefore vaccine policies for HAV infection needs to be seriously addressed.

Hepatitis G virus is an RNA virus belonging to the Flavivridae family. It is parenterally transmitted and usually causes self-limited acute hepatitis without chronic sequelae. [18] To my knowledge, there is no data available with regard to the epidemiology of HGV in the KSA.

Despite the progress made in elucidating various causes of viral hepatitis, the availability of efficacious vaccine for HBV and HAV, the introduction of modern antiviral therapy and the improvement in health education and standard of living, viral hepatitis will continue to dominate the scene of medical practice in the KSA and probably will continue to do so in the years to come.

 
   References Top

1.Blumberg GS, Alter HJ, Visnich S. A "new" antigen in leukemia sera. JAMA 1965;191:541-6.  Back to cited text no. 1
    
2.Kashgari RH, Mohamad AA. Seroepidemiology of hepatitis B virus (HBV) and hepatitis C virus (HCV) and rela­tionship to alanine transferase (ALT) in Saudi workers at Yanbu industrial city. J of Family and Community Medicine 1997;4(l):24-9.  Back to cited text no. 2
    
3.Mahaba HM, El-Tayeb AA, EI-Sekibi DK, El Gofaei AF, El-Baz HS, Ismail NA. Pattern of HBsAg positivity in selected groups at King Khalid General Hospital, Hail Region, KSA J of Family and Community Medicine 1997; 4(1):30-6.  Back to cited text no. 3
    
4.Al-Faleh FZ, Ayola EA, Arif A1. Seroepidemiology of hepatitis B virus infection in Saudi Arabian children: a base­ line survey for mass vaccination against hepatitis B. J Infect 1992;24:197-206.  Back to cited text no. 4
    
5.AI-Freihi HM. Prevalence of hepatitis B surface antigenernia among patients with Schistosoma mansoni. Ann SaudiMed 1993;13:121-5.  Back to cited text no. 5
    
6.Arif NIA, Al-Faleh FZ, Ramia S. Schistosomiasis as a possible risk factor for acquiring hepatitis C virus (HCV) infection among Saudis. J Saudi Gastro 1997;3:74-7.  Back to cited text no. 6
    
7.Barin F, Perrin J, Chotard J, et al. Cross sectional and longitudinal epidemiology of hepatitis B in Senegal. Prog Med Virol 1981;27:148-62.  Back to cited text no. 7
    
8.Al-Faleh FZ, Ayola EA, Al-Jeffrey MA, Arif M, Al-Rashed RS, Ramia S. Integration of hepatitis B vaccine into the expanded program on immunization: The Saudi Arabian experience. Ann Saudi Med;13:231-6.  Back to cited text no. 8
    
9.El-Hazmi MAF, AI-Faleh FZ, Warsy AS. Epidemiology of viral hepatitis among the Saudi population: a study of viral markers in Kahiber. Saudi hoed J 19R6;7:122-9.  Back to cited text no. 9
    
10.Al-Faleh FZ. Hepatitis B infection in Saudi Arabia. Ann Saudi Med 19R8;8:474-80.  Back to cited text no. 10
    
11.Shobokshy OA, Serebeer FE. The etiology of acute viral hepatitis in the western region of Saudi Arabia. Trans R Soc Trop Tied Hyg 1987;81:219-21.  Back to cited text no. 11
    
12.Ashraf SJ, Arya C, Sayed M, et al. A profile of primary hepatocellular carcinoma patients in Gizan area of Saudi Arabia. Cancer 1986;2163-R.  Back to cited text no. 12
    
13.Shikata T. Strategies for the development of hepatitis C and E vaccine. In: Nishioka K et al, editors. Viral hepatitis and liver disease. Springer Verlag 1993, p. 501-2.  Back to cited text no. 13
    
14.Al-Faleh FZ. Hepatitis C virus infection: An update. Saudi Journal Kidney 1995;6:118-21.  Back to cited text no. 14
    
15.AI-Mofarreh M, Fakunle YM, El-Karamany WM, Ezzat HO, Ballesteros MN, Khawaji MZ, et al. Prevalence of antibodies to hepatitis C virus in blood donors in Riyadh. Ann Saudi Med 1991;11:501-3.  Back to cited text no. 15
    
16.Bemvil SS, Andrews VJ, Kariem AA. Hepatitis C antibody prevalence in Saudi Arabian blood donor population. Ann Saudi Med 1991;11:563-7.  Back to cited text no. 16
    
17.Al-Mazrou Y, Khalil M, Al-Jeffri M, AI-Howasi D4. A serosurvey of hepatitis A (HAV IgM positive) amongst children in Riyadh, Saudi Arabia. Riyadh: Ministry of Health; 1997.  Back to cited text no. 17
    
18.Alter MJ, Gallagher At, Morris TT, et al. Acute Non-A-E hepatitis in the United States and the role of hepatitis G virus infection. NEJM 1997;336:741-6.  Back to cited text no. 18
    




 

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