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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 1995  |  Volume : 6  |  Issue : 2  |  Page : 140-143
Hepatitis C Virus Infection in Hemodialysis Patients in Jordan

1 Department of Medicine, Medical School, Jordan University, Amman, Jordan
2 Al-Basheir Hospital, Amman, Jordan
3 Princes Basma Hospital, Irbid, Jordan

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To evaluate the prevalence of hepatitis C virus infection in our hemodialysis population, we carried out a survey of 273 adult hemodialysis patients in three hemodialysis units in Jordan using a second generation rapid enzyme immunoassay. Sixty seven patients were seropositive with a prevalence of 24.5%. All patients were transfusion dependent except two. More than 85% of the patients have been on hemodialysis for more than two years. Co-infection with hepatitis B virus was observed in six patients. Abnormal liver functions were seen in five patients, but liver biopsies were not done. The prevalence of hepatitis C antibody in healthy blood donors in Jordan is 1.7%. We conclude that HCV infection prevalence in hemodialysis patients in Jordan is 24.5%, a percentage similar to what has been reported around the world and in the neighboring countries.

Keywords: Hepatitis C, Hemodialysis, Jordan.

How to cite this article:
Said RA, Hamzeh YY, Mehyar NS, Rababah MS. Hepatitis C Virus Infection in Hemodialysis Patients in Jordan. Saudi J Kidney Dis Transpl 1995;6:140-3

How to cite this URL:
Said RA, Hamzeh YY, Mehyar NS, Rababah MS. Hepatitis C Virus Infection in Hemodialysis Patients in Jordan. Saudi J Kidney Dis Transpl [serial online] 1995 [cited 2020 Jun 6];6:140-3. Available from: http://www.sjkdt.org/text.asp?1995/6/2/140/40855

   Introduction Top

Anemia is an inevitable feature of chronic renal failure and is particularly severe in anephric hemodialysis patients [1] . Prior to the advent of the genetically engineered recombinant human erythropoietin (rHuEPO), nearly 25% of the hemodialysis patients required regular blood transfusions and consequently were at risk for infections [2] . Non-A, non-B (NANB) hepatitis was first described in 1975 when a substantial number of post-transfusion hepatitis B virus (HBV). At that time nearly one third of all transfusions were followed by this of infection [3] . The diagnosis was rarely made, because the acute disease often had or no symptoms. Inspite of all efforts to exclude paid blood- donors, blood units carrying markers for HBV (HBsAg and anti-HBc), and blood units with increased levels of serum transminases, the incidence of NANB hepatitis is still high and ranges between 5-7% [4] .

Recently, hepatitis C virus (HCV) was identified as the leading cause of NANB hepatitis [5] . Since then HCV infection has been recognized as a major health hazard in dialysis patients with high prevalence of elevated transaminases [6],[7] . In fact, in the last EDTA annual meeting in Vienna, the prevalence of anti-hepatitis C positive hemodialysis patients was reported as 17.7% in all EDTA Registry [8] . Yet there was a big difference between countries, with high percentages in countries bordering the Mediterranean Sea and East Europe [Table - 1]. In Saudi Arabia, an alarming prevalence of 68% among 1147 dialysis patients was reported in a multicenter study [9] .

   Subjects and Methods Top

We are reporting a survey in the hemodialysis units in Jordan in an attempt to define the prevalence of hepatitis C viral infection. In Jordan, currently we have nearly 700 patients with ESRD, and 630 patients are on maintenance hemodialysis. Screening for hepatitis C infection among our hemodialysis patients was carried out in 273 patients in three major dialysis units in the country during the second half of 1994. Two of the dialysis centers are in Amman, the capital. Serum samples from all the 273 patients were routinely screened for hepatitis B surface antigen using Enzyme Linked Immunosorbent Assay (ELISA) technique (Sorin Biomedia­ Italy), antibody to hepatitis C virus using Murex anti-HCV rapid enzyme immunoassay second generation, (Murex Diagnostic Limited, Dartford, England), and antibodies to human immunodeficiency virus types 1 and 2 by rapid enzyme immunoassay wellcozyme HIV 1+2, Murex, (Murex diagnostic Limited, Dartford, England).

Significant liver dysfunction was defined as alanine aminotransferase (ALT) more than twice the upper limit of normal persistently for longer than six months during the last year. The number of blood transfusions and the duration of dialysis were also analysed.

   Results Top

Samples from 67 patients out of 273 screened (24.5%) were reactive for antibody to HCV. There were 26 males and 41 females, and their ages ranged between 16-73 years. Eight patients were previously transplanted; seven from living related, and one living non related, transplant donors. Sixty-five patients were transfusion dependant, and more than 50% of them received more than 30 transfusions. Duration on dialysis was an important factor among the positive patients. Thirty two patients (44.5%) were on dialysis for a minimum of five years or more, 27 patients for 2-5 years, while eight patients were on dialysis for less than one year. Abnormal liver functions were seen in five patients (7.5%), but tissue diagnosis was not available.

Six patients (8.9%) were positive for HBsAg, five of them were in one unit, and serum aminotransferases were normal in all. All the HCV seropositive patients were negative for HIV antibodies.

   Discussion Top

The reported prevalence of HCV infection in long-term dialysis patients varies between 1-48% around the world, with higher rates being reported from areas where the incidence in general population is high [10],[11] . In Jordan, this is the first study to be conducted among our dialysis population and shows a prevalence of 24.5%, a value similar to what has been reported in the neighboring countries in the Mediterranean basin [12] . This is definitely higher than what has been reported among healthy blood donors; 0.9-1% in USA, 1% in Japan, 0.7% in Itlay, 1.5% in Saudi Arabia and 1.7% in Jordan [13] . Two important aspects were present in our patients that possibly contributed to this high prevalence of HCV infection. Firstly, the long duration of dialysis among the majority of the seropositve patients; nearly 48% of our patients were on dialysis for more than five years, 40% for 2-5 years, and nearly 15% for less than one year. Secondly, the large number of transfusions among this group of patients; 50% of the patients received more than 30 transfusions, and only two patients received less than five transfusions. Both the duration of dialysis and the number of transfusions correlated well with the high prevalence of HCV infection, among hemodialysis patients [14],[15],[16] .

Only eight patients (11.9%) were transplanted, seven were from living-related donors, one patient from living-non related donor. All of them were on dialysis prior to transplantation for at least 3-4 years, and all received multiple blood transfusions. So it is difficult to assume that transplantation has contributed to HCV infection, as found by others [17],[18] . Co-infection with hepatitis B virus was observed in six patients (8.9%) and five of them were in one hemodialysis unit. One of the dialysis units had the highest prevalence rate in the participating dialysis units (51.5%). Accordingly, the staff members of this unit were screened for evidence of HCV infection, and three members were seropositive. In addition strict adherence to the universal infection control policy was lacking. All these factors demonstrate the possible role of cross-infection and nosocomial transmission of HCV in addition to blood transfusion [10],[19],[20],[21] .

None of our three units practiced the dialyzer reuse policy and our current practice is to perform chemical disinfection of the machines by using bleach between dialysis sessions if HCV positive patients used those machines. We did not isolate patients in a separate room or assigned them to isolated machines, as reported by others [20],[22] . The clinical manifestations of HCV infection in our patients were minimal and evident only by a transient and slightly elevated transaminases in 7.5% of patients. None of the patients were acutely sick but liver biopsies were not done, so we were unable to assess the pathological correlation of HCV infection as was dis'cussed by others [23] . Finally none of our patients so far received interferon alpha, and hopefully we will start a few patients on such a treatment regimen soon [24],[25] .

In conclusion, nearly 24.5% of 273 hemodialysis patients in Jordan were found to have evidence of HCV infection, Blood transfusion seems to be the major route of infection. We hope that with the introduction of screening for HCV antibodies in blood donors, started in May 1994, and the use of rHuEPO in treating anemic hemodialysis patients together with strict adherence to the universal infection control precautions, a decline in the prevalence and incidence of HCV infection in our hemodialysis population will occur.

   References Top

1.Eschbach JW. Hemotological problems of dialysis patients. In Drukker W, Parsons FM, Maher JF (eds). Replacement of renal function by dialysis. Boston, Martinus Nijhoff. 1983;630-45.  Back to cited text no. 1    
2.Paganini EP, Latham D, Abdulhadi M. Practical considerations of recombinant human erythropoietin therapy. Am J Kidney Dis 1989;14:19-25.  Back to cited text no. 2    
3.Druwe PM, Michielsen PP, Ramon AM, De Broe ME. Hepatitis C and Nephrology. Nephrol Dial Transplant 1994;9:230-7.  Back to cited text no. 3    
4.Weisiger RA. Non-A, non-B hepatitis. Promise and implications of the hepatitis C assay. Modern Medicine 1990;7(7):35-46.  Back to cited text no. 4    
5.Choo QL, Kuo G, Weiner AJ, Overby LR, Bradley DW, Houghton M. Isolation of cDNA clone derived from a blood­borne rion-A, non-B viral hepatitis genome. Science 1989;244:359-62.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Galbraith RM, Dienstag JL, Purcell RH, Gower PH, Zuckerman AJ, Williams R. Non-A, non-B hepatitis associated with chronic liver disease in a haemodialysis unit. Lancet 1979;l:951-3.  Back to cited text no. 6    
7.Conway M, atterall AP, Brown EA, et al. Prevalence of antibodies to hepatitis C in dialysis patients and transplant recipients with possible routes of transmission. Nephrol Dial Transplant 1992;7:1226-9.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Annual report of management of renal failure in Europe XXIV, 1993. Vienna, 1994.  Back to cited text no. 8    
9.Huraib S, Al-Rasheed R, Aldress A, Arif M, Saleh FA. High prevalence and risk factors for hepatitis C in Saudi Arabia: a need for new strategies in dialysis practice (Abstract). Saudi Kidney Dis Transplant Bull 1993;4:73.  Back to cited text no. 9    
10.Knudsen F, Wantzin P, Rasmussen K, et al.Hepatitis C in dialysis patients: Relationship to blood transfusions, dialysis and liver disease. Kidney Int 1993;43:1353-6.  Back to cited text no. 10  [PUBMED]  
11.Ponz E, Campistol JM, Bruguera M, et al. Hepatitis C virus infection among kidney transplant recipients. Kidney Int 1991;40:748-51.  Back to cited text no. 11  [PUBMED]  
12.Da Porto A, Adami A, Susanna F, et al. Hepatitis C virus in dialysis units: a multicenter study. Nephron 1992;61:309-10.  Back to cited text no. 12  [PUBMED]  
13.Padmanabhan R. Hepatitis C Virus infection in nemo dialysis patients in Saudi Arabia. Saudi J Kidney Dis Transplant 1994;5(2):157-8.  Back to cited text no. 13    
14.Giammaria U, De Meo F, Acitelli S, et al. HCV infection in hemodialyzed patients: incidence and correlation with dialytic age. Nephron 1992;61:335-6.  Back to cited text no. 14  [PUBMED]  
15.Esteban JI, Esteban R, Viladomiu L, et al. Hepatitis C virus antibodies among risk group in Spain. Lancet 1989;2:294-7.  Back to cited text no. 15  [PUBMED]  
16.Moroni GA, Cori P, Marelli F, et al. Indirect evidence transfusion role in conditioning hepatitis C virus prevalence among dialysis patients. Nephron 1991;57:371-2.  Back to cited text no. 16  [PUBMED]  
17.Huang CC, Lia MK, Lin MW, Pao CC, Fang JT, Yao DS. Transmission of hepatitis C virus by renal transplantation. Transplant Proc 1993;25:1474-5.  Back to cited text no. 17    
18.Vincenti F, Weber P, Kuo G, et al. Hepatitis C virus in cadaver organ donors: prevalence and risk of transmission to transplant recipients. Transplant Proc 1991;23:2651-2.  Back to cited text no. 18  [PUBMED]  
19.Calabrese G, Vagelli G, Guaschino R, Gonella M. Transmission of anti-HCV within the household ofhaemodialysis patients (letter). Lancet1991;338:1466.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Teruel JL, Pascual J, Liano F, Ortuno J. Importance of nosocomial transmission of hepatitis C virus infection in dialysis units (letter). Clin Nephrol 1992;38:117-8.  Back to cited text no. 20    
21.oshida C, Vanderborght B, Stuyvor L, Rouzere C, et al. Tracing non­transfusional transmission of HCV infection through genomic typing of HCV in hemodialysis unit (Abstract). In Xllth International Congress of Nephrology, 1993, Jerusalem 314.  Back to cited text no. 21    
22.Ng Y, Lee S, Wus, et al. Re-use of dialysis as a risk factor of transmission of hepatitis C virus in hemodialysis patients (Abstract). In XII th International Congress of Nephrology, 1993, Jerusalem 394.  Back to cited text no. 22    
23.Rosello L, Fernandez E, Lopez TJ, et al. Hepatitis C in hemodialysis patients: prognosis and diagnosis value of transjugular liver biopsy (Abstract). In Xllth International Congress of Nephrology 1993, Jerusalem 394.  Back to cited text no. 23    
24.Nordio M, Guarda L, Belussi F, et al. Treatment of hepatitis C in dialysis patients with alpha-2B-interferon. A first experience. J Am Soc Nephrol 1991;2:341.  Back to cited text no. 24    
25.Alfurayh O, Ellis M, Qunibi W, et al. Chronic hepatitis C treated by recombinant interferon alpha in patients on hemodialysis. J Am Soc Nephrology 1992;3:352.  Back to cited text no. 25    

Correspondence Address:
Riyad A Said
Jordan University, P.O. Box 13132, Amman 11942
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