Saudi Journal of Gastroenterology
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Year : 1997  |  Volume : 3  |  Issue : 2  |  Page : 74-77
Schistosomiasis as a possible risk factor for acquiring hepatitis C virus (HCV) infection among Saudis


1 Department of Pathology, College of Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia
2 Department of Medicine, College of Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia

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Date of Submission19-Mar-1997
Date of Acceptance29-Apr-1997
 

   Abstract 

Background -Risk factors for acquiring hepatitis C virus (HCV) infection have been elucidated in many developed countries but the picture is still not clear in many Middle Eastern Countries including Saudi Arabia. Aim -To investigate possible risk factors for acquiring HCV among Saudis. Methods -Various demographic and medical risk factors that might be associated with the spread of HCV among Saudis were investigated. The population studied included 20 anti-HCV-positive with chronic liver disease (CLD), 30 anti-HCV-positive patients without CLD and 272 anti-HCV-negative Saudi blood donors. All people investigated were of the same age group (>40 years of age). Results -None of the demographic parameters studied (type of job, type of housing, education) was found to be significantly associated with acquiring HCV infection among our Saudi patients. On the other hand up to 40% of the anti-HCV­positive patients and irrespective of the condition of liver disease had a history of surgery, and 25% of them had a history of multiple injections. Furthermore, at least 20% of our anti-HCV-positive patients had a history of schistosomiasis which is significantly higher than schistosomiasis among the blood donors (P<0.005). Conclusion -In addition to blood and blood products, schistosomiasis seems to be a possible risk factor for acquiring HCV among the Saudi population. The association between schistosomiasis and enhancement of HCV infection need to be further elucidated.

How to cite this article:
Arif MA, Al-Faleh FZ, Ramia S. Schistosomiasis as a possible risk factor for acquiring hepatitis C virus (HCV) infection among Saudis. Saudi J Gastroenterol 1997;3:74-7

How to cite this URL:
Arif MA, Al-Faleh FZ, Ramia S. Schistosomiasis as a possible risk factor for acquiring hepatitis C virus (HCV) infection among Saudis. Saudi J Gastroenterol [serial online] 1997 [cited 2020 Nov 24];3:74-7. Available from: https://www.saudijgastro.com/text.asp?1997/3/2/74/33929


Hepatitis C virus (HCV) is a major causative agent of parenterally-transmitted non-A, non-B hepatitis (PT-NANBH) worldwide [1],[2],[3] and is associated with the development of cirrhosis and hepatocellular carcinoma [4],[5],[6] . Although the route by parenteral exposure such as blood transfusion and drug abuse have been well documented [2],[7],[8] about 50% of HCV cases have no obvious risk factors including parenteral exposure [2],[9] . Risk factors for acquiring HCV infection have been elucidated in many developed countries [1],[2],[10] but the picture is still not clear in many Middle Eastern countries including Saudi Arabia [10],[11] .

Recently, we have shown that sexual and intrafamilial transmission are not the route of transmission of HCV among the Saudis [13],[14] . In this study we attempted to identify demographic and various medical risk factors that might be associated with the spread of the virus among the Saudi population.


   Subjects and Methods Top


Subjects: These included 20 anti-HCV-positive Saudi patients with chronic liver disease (CLD) (18 males, 2 females; mean ± SD 49.4 ± 9.5 years), 30 anti-HCV-positive Saudi patients without CLD (22 males, 8 females; mean ± SD 47.2 ± 5.2 years) and 272 Saudi blood donors (240 males, 32 females) chosen at random during a six-month period from the blood donor population at King Khalid University Hospital (KKUH), Riyadh and were matched with age to the patient group (mean ± SD 48.5 ± 2.9 years). All the patients were seen at KKUH and the diagnosis of CLD was confirmed by liver biopsies. All patients investigated were HBs­Ag-negative and none had a history of alcoholism or exposure to hepatotoxic chemicals.


   Epidemiological and clinical investigations Top


An interviewer-administered questionaire about demography, clinical condition and risk factors for parenteral exposure (blood transfusion, surgery, hemodialysis, intravenous drug use, multiple injections, folk medicine, and a history of schistosomiasis) were filled on each subject investigated. During the interview, serum samples were obtained for testing liver biochemistry and anti-HCV status.Serum samples were stored at -20°C Until use.


   Laboratory investigations Top


All samples were tested for HBsAg (Organon Teknika, N.V. Veedijk, Turnhout) and for anti-HCV (UBI HCV EIA 4.0, Beijing United Biochemical Co., Ltd.) using ELISA system. The assay for anti­HCV employs an immunosorbent that consists of synthetic peptides corresponding to highly antigenic segments of core, NS3, NS4, and NS5 regions of HCV, bound to wells of the microplate. Anti-HCV­positive samples were additionally tested by a supplemental assay (LiaTek HCVIII, Organon Teknika, N.V. Veedijk, Turnhout). In all assays manufacturer's instructions were followed.


   Statistical analysis Top


One way analysis of variance, Chi-square test and Fisher's exact test were used in our analysis.


   Results Top


Demographic characteristics of the Saudi subjects investigated are shown in [Table - 1]. None of the parameters studied (type of job, type of housing and education) was shown to be significantly associated with acquiring HCV infection. In contrast to this, 10% of patients with CLD had a history of blood transfusion [Table - 2] while up to 40% of the anti­HCV-positive patients had a history of surgery [Table - 2]. Among the anti-HCV-positive patients with or without CLD, at least 20% had a history of multiple injections which is significantly higher than the 3% who had a history of multiple injections among the anti-HCV-negative blood donor group (P<0.005) [Table - 2]. Similarly, 25% of the anti­HCV-positive patients with CLD had a history of schistosomiasis compared to 20% among antiHCV-­positive patients without CLD which is significantly higher than schistosomiasis among the blood donors (P<0.005) [Table - 2].

Intravenous drug use and folk medicine did not seem to be an important risk factor for acquiring HCV infection among these Saudi population [Table - 2].


   Discussion Top


The three groups investigated in this study were of similar age groups. The results obtained demonstrate that at least 50% of our anti-HCV-positive patients with or without CLD had a history of parenteral exposure which included blood transfusion, surgery or multiple injection. The results confirm our earlier observations [13] and those of others [1],[2] that about 50% of HCV infection cases had no obvious parenteral risk factor and other possible modes of transmission need to be elucidated. Behavioral risk factor for acquiring HCV infection such as intravenous drug abuse [7],[8] was not found in this study population and hence its role in spreading HCV is negligible. It was always speculated that folk medicine such as venesection might play a role in transmitting HCV infection in the Saudi population [12] . This factor as well as sharing razors and toothbrushes did not seem to have an effect on spreading HCV infection in our population studied.

Other than parenteral exposure, our results show that at least 20% of our anti-HCV-positive subjects had a documented medical history of schistosomiasis compared to only 1.5% in those who were anti-HCV-negative (P<0.005). It seems therefore that a history of schistosomiasis is a possible risk factor significantly associated with HCV infection. It must be mentioned that eight out of the 30 anti-HCV-positive patients with CLD had no obvious risk factors for acquiring HCV infection. This is in agreement with others where the mode of infection in community-acquired HCV remains uncertain [15] although parenteral route is suggested to be the most likely route [16] . The mechanism(s) by which schistosomiasis enhances HCV seropositivity is still unknown but several possibilities can be cited. First, it is well established that Schistosoma mansoni enhances several viral infections such as hepatitis B and D viruses (HBV and HDV) in the liver [17],[18] and hence it may similarly enhance HCV infection. In our questionaire, we did not distinguish between infection by S. mansoni or S. hematobium and future studies are needed to confirm which of these enhances HCV infection. Secondly, it has been shown that during S. mansoni infection there is a down regulation of Th 1 cytokine production accompanied by induction of Th 2 cytokine [19],[20] . This modulation of the cytokine system in the liver could inhibit a protective intrahepatic cytotoxic T lymphocyte to HCV [21] and enhance viral replication and consequently liver damage. Thirdly, it was postulated that tarter emetic therapy given in a series of 15 injections in the past for schistosomiasis in Egyptians may have contributed to the high endemicity of HCV among Egyptians [22],[23] perhaps via contaminated needles and syringes. This type of treatment was widely used in many Arab countries including Saudi Arabia before introducing the oral treatment.

It can be concluded from our study that schistosomiasis could be a possible risk factor in acquiring HCV infection among the Saudi population. The association between schistosomiasis and enhancement of HCV infection need to be further elucidated and confirmed in future studies.

 
   References Top

1.Esteban JI, Esteban R, Viladomiu L, et al. Hepatic C virus antibodies among risk groups in Spain. Lancet 1989; 2:294­-6.  Back to cited text no. 1  [PUBMED]  
2.Alter MJ, Hadler SC, Judson FN, et al. Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection. JAMA 1990; 264:2231-5.  Back to cited text no. 2  [PUBMED]  
3.Choo QL, Weiner AJ, Overby LR, et al. Hepatitis C virus: The major causative agent of viral non-A, non-B hepatitis. Br Med Bull 1990; 46:423-41.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Choo QL, Kuo G, Weiner AJ, et al, Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome. Science 1989; 244:359-62.  Back to cited text no. 4    
5.Ohkoshi S, Kojima H, Tawaraya H, et al. Prevalence of antibody against non-A, non-B hepatitis virus in Japanese patients with hepatocellular carcinoma. Jpn J Cancer Res 1990; 81:550-3.  Back to cited text no. 5  [PUBMED]  
6.Ayoola EA, Al-Mofleh IA, Al-Faleh FZ, et al. Prevalence of antibodies to hepatitis C virus among Saudi patients with chronic liver diseases. Hepato-Gastroenterology 1992; 39:337-9.  Back to cited text no. 6  [PUBMED]  
7.Bell J, Batey RG, Farrell GC, et al. Hepatitis C virus in intravenous drug users. Med J Aust 1990; 153:274-6.  Back to cited text no. 7  [PUBMED]  
8.Guida B, Torresin A, Piersantelli N. Hepatitis C virus in Italian drug addicts. Ann Int Med 1990; 113:559-60.  Back to cited text no. 8  [PUBMED]  
9.Al Faleh FZ, Ayoola EA, Al Jeffry M, et al. Prevalence of antibody to hepatitis C virus among Saudi Arabian children: A community-based study. Hepatology 1991; 14:215-8.  Back to cited text no. 9    
10.Stevens CE, Taylor PE, Pindyck J. Epidemiology of hepatitis C virus: A preliminary study in volunteer blood donors. JAMA 1990; 263:49-53.  Back to cited text no. 10    
11.Scott DA, constantine NT, Callahan J, et al. The epidemiology of hepatitis C virus antibody in Yemen. Am J Trop Med Hyg 1992; 46:63-8.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Al Faleh FZ, Ramia S. Hepatitis C virus in Saudi Arabia: a review. Ann Saudi Med 1996; (accepted for publication).  Back to cited text no. 12    
13.Al Faleh FZ, Ramia S, Arif M, et al. Profile of hepatitis C virus (HCV) and the possible modes of transmission of the virus in Gizan area, Kingdom of Saudi Arabia: A community-based study. Ann Trop Med Parasite] 1995; 89:431-7.  Back to cited text no. 13    
14.Arif M, Al Swayeh M, Al Faleh FZ, Ramia S. Risk of hepatitis C virus (HCV) infection among household contacts of Saudi patients with chronic liver disease. J Viral Hepatitis 1995;  Back to cited text no. 14    
15.Hollinger FB, Lin HJ. Community-acquired hepatitis C virus infection. Gastroenterol 1992; 102:1426-9.  Back to cited text no. 15    
16.Conry-Cantilena C, Van Raden M, Gibble J, et al. Routes of infection, viremia, and liver disease in blood donors found to have hepatitis C virus infection. N Engl J Med 1996; 334:1691-6.  Back to cited text no. 16    
17.Ghaffar YA, Fattah SA, Kamel M, et al. The impact of endemic schistosomiasis on acute viral hepatitis. Am J Trop Med Hyg 1991;45:743-50.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]
18.Darwish MA, Shaker M, Raslan O, Raouf T. Hepatitis B and D viral infections among schistosomiasis patients in Egypt. J Egyptian Publ Hlth Assoc 1992; 67:547-63.  Back to cited text no. 18    
19.Pearce EJ, Caspar P, Grzych JM, Lewis FA, Sher A. Down regulation of the Th I cytokine production accompanies induction of the Th 2 responses by a parasitic helminth, Schistosoma mansoni. J Exptl Med 1991; 173:159-66.  Back to cited text no. 19    
20.Kullberg MC, Pearce EJ, Hieny SE, Sher A, Berzofsy JA. Infection with Schistosoma mansoni alters Th 1/Th 2 cytokine responses to a non-parasite antigen. J Immunol 1992; 148:3264-70.  Back to cited text no. 20    
21.Koziel MJ, Dudley D, Wong JT, Dienstag J, Houghton M, Ralston R, Walker BD. Intrahepatic cytotoxic T lymphocyte specific for hepatitis C virus in persons with chronic hepatitis. J Immunol 1992: 149:3339-44.  Back to cited text no. 21    
22.Darwish ME, Raouf TA, Rusdhy P, Constantine NT, Rao MR, Edelman R. Risk factors associated with a high seroprevalence of hepatitis C virus infection in Egyptian blood donors. Am J Trop Med Hyg 1993; 49:440-7.  Back to cited text no. 22    
23.Kishy A, Al Nakib B, Al Mufti S, Madda JP, Hira PR. Anti­HCV-positive cirrhosis associated with schistosomiasis, Am J Gastroenterol 1993;88:1428-31.  Back to cited text no. 23    

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Correspondence Address:
Mohammed A Arif
Department of Pathology (32), College of Medicine, P.O. Box 2925, Riyadh 11461
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


PMID: 19864797

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