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      Prevalence of Hepatitis B, Hepatitis C, and HIV in Multiply Transfused Sickle Cell Disease Patients from Oman

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          Abstract

          Background

          In Oman, the prevalence of hepatitis B (HBV) infection is 5.8%, with 2.8–7.1% HBV carriers. Hepatitis C (HCV) prevalence among Omanis is 0.41%. A total of 2917 human immunodeficiency virus (HIV) infections were notified among Omanis by 2017. This study was performed as there was no data on the prevalence of HIV, HBV and HCV in sickle cell disease (SCD) patients from Oman.

          Study Design and Methods

          In this retrospective, cross-sectional study, medical records of all SCD patients who attended our hospital between 2011 to 2017 were retrieved from the hospital information system. Following approval by the local medical research and ethics committee, data on HIV, HBV, and HCV exposure were recorded to estimate the prevalence.

          Results

          Among a total of 1000 SCD patients (491 males and 509 females), twenty-three (2.3%) patients showed positive serology for hepatitis B surface antigen (HbsAg), of whom sixteen (1.6%) were HBV DNA positive. 126 (12.6%) had anti-HCV antibodies (anti-HCV), of whom fifty-two (5.2%) were HCV RNA positive. None of the patients had positive serology for HIV. A normal liver was observed on abdominal ultrasound in 788 (78.8%) patients, whereas 208 (20.8%) had hepatomegaly, and 4 (0.4%) had liver cirrhosis. Thirty-six (3.6%) patients died, but in only two patients, the mortality was due to cirrhosis of liver.

          Conclusions

          This study provides the first comprehensive data on the prevalence of HBV and HCV infections among Omani SCD patients exposed to blood transfusions. Reassuringly, no case with HIV was observed.

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          Most cited references35

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          Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group.

          The acute chest syndrome is the leading cause of death among patients with sickle cell disease. Since its cause is largely unknown, therapy is supportive. Pilot studies with improved diagnostic techniques suggest that infection and fat embolism are underdiagnosed in patients with the syndrome. In a 30-center study, we analyzed 671 episodes of the acute chest syndrome in 538 patients with sickle cell disease to determine the cause, outcome, and response to therapy. We evaluated a treatment protocol that included matched transfusions, bronchodilators, and bronchoscopy. Samples of blood and respiratory tract secretions were sent to central laboratories for antibody testing, culture, DNA testing, and histopathological analyses. Nearly half the patients were initially admitted for another reason, mainly pain. When the acute chest syndrome was diagnosed, patients had hypoxia, decreasing hemoglobin values, and progressive multilobar pneumonia. The mean length of hospitalization was 10.5 days. Thirteen percent of patients required mechanical ventilation, and 3 percent died. Patients who were 20 or more years of age had a more severe course than those who were younger. Neurologic events occurred in 11 percent of patients, among whom 46 percent had respiratory failure. Treatment with phenotypically matched transfusions improved oxygenation, with a 1 percent rate of alloimmunization. One fifth of the patients who were treated with bronchodilators had clinical improvement. Eighty-one percent of patients who required mechanical ventilation recovered. A specific cause of the acute chest syndrome was identified in 38 percent of all episodes and 70 percent of episodes with complete data. Among the specific causes were pulmonary fat embolism and 27 different infectious pathogens. Eighteen patients died, and the most common causes of death were pulmonary emboli and infectious bronchopneumonia. Infection was a contributing factor in 56 percent of the deaths. Among patients with sickle cell disease, the acute chest syndrome is commonly precipitated by fat embolism and infection, especially community-acquired pneumonia. Among older patients and those with neurologic symptoms, the syndrome often progresses to respiratory failure. Treatment with transfusions and bronchodilators improves oxygenation, and with aggressive treatment, most patients who have respiratory failure recover.
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            Recovery, persistence, and sequelae in hepatitis C virus infection: a perspective on long-term outcome.

            Hepatitis C has emerged in recent years as the most common basis for liver disease in the United States, having infected an estimated 3.9 million people in this country and an estimated 170 million worldwide. Currently, it is the predominant reason for undergoing liver transplantation. The disease it causes is characterized by silent onset in most infected individuals, a high rate of viral persistence, and the potential for development of ever-worsening chronic liver disease, ranging from chronic hepatitis to cirrhosis and occasionally to hepatocellular carcinoma. Such progression, when it occurs, is also most commonly a silent process that may take 20-40, and occasionally even more, years to reach its end point. Because of these characteristics, it has been exceedingly difficult to accurately assess the natural history. Efforts to accomplish this have consisted of retrospective, prospective, and cohort studies. The most concerning data have derived from the retrospective study approach, generally performed at tertiary referral centers. Because these centers commonly attract persons with existing chronic liver disease, they have tended to describe a high rate of progression to cirrhosis and cancer. This "referral bias" is avoided in the prospective and cohort study approach, and data derived from these studies indicate a lower rate of progression and a correspondingly higher rate of either recovery or minimal liver disease. In this review, we briefly describe potential mechanisms of viral persistence; present detailed information on outcomes that have derived from retrospective, prospective, and cohort studies, involving both adults and children; examine the data regarding progression of fibrosis and of progression to hepatocellular carcinoma; consider cofactors that might enhance liver disease progression; and report the emerging data that suggest that spontaneous viral clearance may be higher than is currently believed. We conclude with the view that severe, life-threatening, progressive liver disease clearly occurs in a sizable minority (perhaps 30%) of chronically infected persons but speculate that fibrosis progression is neither linear or inevitable and hence that most hepatitis C virus carriers will have either a stable nonprogressive course or such indolent progression that they will die from an unrelated disease before the severe sequelae of hepatitis C become manifest or will have a sustained "curative" response to therapy. Although this view provides reasonable hope to the hepatitis C virus-infected individual, it does not deny the enormous burden this infection presents as the result of its high prevalence and global distribution. The sheer magnitude of the infected population will result in a large number with severe life-threatening liver disease even if the proportion of infected individuals that develop progressive disease is relatively small.
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              The declining risk of post-transfusion hepatitis C virus infection.

              The most common serious complication of blood transfusion is post-transfusion hepatitis from the hepatitis C virus (HCV). Blood banks now screen blood donors for surrogate markers of non-A, non-B hepatitis and antibodies to HCV, but the current risk of post-transfusion hepatitis C is unknown. From 1985 through 1991, blood samples and medical information were obtained prospectively from patients before and at least six months after cardiac surgery. The stored serum samples were tested for antibodies to HCV by enzyme immunoassay, and by recombinant immunoblotting if positive. Of the 912 patients who received transfusions before donors were screened for surrogate markers, 35 seroconverted to HCV, for a risk of 3.84 percent per patient (0.45 percent per unit transfused). For the 976 patients who received transfusions after October 1986 with blood screened for surrogate markers, the risk of seroconversion was 1.54 percent per patient (0.19 percent per unit). For the 522 patients receiving transfusions since the addition in May 1990 of screening for antibodies to HCV, the risk was 0.57 percent per patient (0.03 percent per unit). The trend toward decreasing risk with increasingly stringent screening of donors was statistically significant (P less than 0.001). After we controlled for the method of donor screening, the risk of seroconversion was strongly associated (P less than 0.001) with the volume of blood transfused, but not with the use of particular blood components. The incidence of post-transfusion hepatitis C has decreased markedly since the implementation of donor screening for surrogate markers and antibodies to HCV. The current risk of post-transfusion hepatitis is about 3 per 10,000 units transfused.
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                Author and article information

                Journal
                Mediterr J Hematol Infect Dis
                Mediterr J Hematol Infect Dis
                Mediterranean Journal of Hematology and Infectious Diseases
                Mediterranean Journal of Hematology and Infectious Diseases
                Università Cattolica del Sacro Cuore
                2035-3006
                2019
                01 November 2019
                : 11
                : 1
                : e2019058
                Affiliations
                [1 ]Department of Haematology, Sultan Qaboos University Hospital, Muscat, Oman
                [2 ]College of Medicine & Health Sciences, Muscat, Oman
                Author notes
                Correspondence to: Dr. Salam Alkindi, BA, MB, BCh, BAO, MSc, FRCP. Professor in Haematology and Consultant Haematologist, Department of Haematology, College of Medicine & Health Sciences, Sultan Qaboos University, P. O. Box 35, Muscat 123, Sultanate of Oman. Tel.: +96824141182, Fax: +96824144887. E-mail: sskindi@ 123456yahoo.com
                Article
                mjhid-11-1-e2019058
                10.4084/MJHID.2019.058
                6827606
                31700583
                bb61482b-5585-4c86-b155-b3a5de8617ce
                Copyright @ 2019

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by-nc/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 July 2019
                : 24 September 2019
                Categories
                Original Article

                Infectious disease & Microbiology
                prevalence,hepatitis,hbv,hcv,hiv,infection
                Infectious disease & Microbiology
                prevalence, hepatitis, hbv, hcv, hiv, infection

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