scholarly journals Analysis of hepatitis C virus infection among sickle cell anemia patients by an antigen-antibody combination assay

2011 ◽  
Vol 2 (1) ◽  
pp. 26
Author(s):  
Obeid E. Obeid ◽  
Alhusain J. Alzahrani

Hepatitis C virus (HCV) has a major impact on public health. In spite of the progress made in the prevention of transfusion-transmitted infections over the last years, these still occur, especially in multi-transfused patients such as sickle cell anemia patients. Sickle cell disease (SCD) is highly prevalent in Eastern Saudi Arabia. Little is known about the prevalence of HCV in Saudi sickle cell disease patients. The present study aimed to assess HCV and HBV antigens, antibodies and viral genome among sickle cell anemia patients in a tertiary hospital in Eastern Saudi Arabia. Methods used included measurement of HCV antigen and antibodies using the novel HCV antigen/antibody combination assay, assessment of HCV core antigen and measurement of viral genome using standard commercial kits. Of the 138 sickle cell disease samples tested, 5 (3.6%) samples gave positive results. Their hemoglobin ranged between 7.8 and 10.1 g/dL, their erythrocyte count ranged between 3.1¥106 and 3.9¥106. Out of these 5 samples, 4 were also positive by the HCV Core Ag assay and by the HCV RNA PCR test (80%). None of the control group was positive. Seven patients were positive for HBs antibodies. One sample was positive for HBsAg, and this indicates chronic carrier state. Improving the testing for blood-borne infections such as HCV and HBV will result in better control of these infections in sickle cell disease patients which will inevitably lead to lower mortality and morbidity in this group of patients.

Blood ◽  
1986 ◽  
Vol 67 (5) ◽  
pp. 1404-1410 ◽  
Author(s):  
BA Miller ◽  
M Salameh ◽  
M Ahmed ◽  
J Wainscoat ◽  
G Antognetti ◽  
...  

Abstract Homozygous sickle cell disease in the eastern province of Saudi Arabia is clinically mild. Circulating fetal hemoglobin levels of 16.0 +/- 7.4% were found in these anemic patients, but only 1.09 +/- 0.97% in their sickle trait parents. To determine whether these sickle cell anemia patients inherit an increased capacity to synthesize fetal hemoglobin, a radioimmunoassay of fetal and adult hemoglobin was performed on erythroid progenitor (BFU-E)-derived erythroblasts from Saudi Arabian sickle cell patients and their parents. Mean fetal hemoglobin content per BFU-E-derived erythroblast from Saudi Arabian sickle cell patients was 6.2 +/- 2.4 pg/cell or 30.4 +/- 8.6% fetal hemoglobin (normal 1.1 +/- 0.7 pg/cell and 5.1 +/- 1.8%). Linear regression analysis of % HbF in peripheral blood versus % HbF per BFU-E- derived cell showed a positive correlation with an r of 0.65. The variance of the intrinsic capacity to produce HbF may account for almost 40% (r2) of the variance of circulating fetal hemoglobin but other factors, particularly selective survival of F cells, must also contribute significantly. Despite virtually normal HbF levels in sickle trait parents of these Saudi patients, mean fetal hemoglobin production per BFU-E-derived erythroblast in these individuals was elevated to 3.42 +/- 1.79 pg/cell or 16.1 +/- 6.4% fetal hemoglobin, and the magnitude of fetal hemoglobin production found in parents correlated with that of the patients. These data indicate that the high fetal hemoglobin in Saudi sickle cell disease is genetically determined but expressed only during accelerated erythropoiesis. Further evidence of such genetic determination was provided by analysis of DNA polymorphisms within the beta-globin gene cluster on chromosome 11. This revealed a distinctive 5′ globin haplotype (+ + - + +) on at least one chromosome 11 in all high F SS and AS tested. The precise relationship of this haplotype to HbF production in this population remains to be defined.


2018 ◽  
Vol 12 (3) ◽  
pp. 629-632 ◽  
Author(s):  
Hassan Al Moussawi ◽  
Abhishek D. Polavarapu ◽  
Divya Asti ◽  
Zainab Awada ◽  
Stephen  Mulrooney

Around 8% of patients diagnosed with sickle cell disease (SCD) are hepatitis C virus (HCV) carriers. Previously, HCV treatment was seldom considered in SCD patients, as the ribavirin-induced hemolysis and interferon-induced cytopenias could lead to more profound anemia. Nowadays, several oral direct-acting antiviral drugs have been developed and approved by the FDA for hepatitis C treatment. While direct-acting antivirals mitigate many of these risks, their safety and efficacy in SCD patients remains insufficiently explored. Here, we report on successfully treating HCV with ledipasvir/sofosbuvir in a compensated cirrhotic patient with SCD and thalassemia minor.


Blood ◽  
1986 ◽  
Vol 67 (5) ◽  
pp. 1404-1410
Author(s):  
BA Miller ◽  
M Salameh ◽  
M Ahmed ◽  
J Wainscoat ◽  
G Antognetti ◽  
...  

Homozygous sickle cell disease in the eastern province of Saudi Arabia is clinically mild. Circulating fetal hemoglobin levels of 16.0 +/- 7.4% were found in these anemic patients, but only 1.09 +/- 0.97% in their sickle trait parents. To determine whether these sickle cell anemia patients inherit an increased capacity to synthesize fetal hemoglobin, a radioimmunoassay of fetal and adult hemoglobin was performed on erythroid progenitor (BFU-E)-derived erythroblasts from Saudi Arabian sickle cell patients and their parents. Mean fetal hemoglobin content per BFU-E-derived erythroblast from Saudi Arabian sickle cell patients was 6.2 +/- 2.4 pg/cell or 30.4 +/- 8.6% fetal hemoglobin (normal 1.1 +/- 0.7 pg/cell and 5.1 +/- 1.8%). Linear regression analysis of % HbF in peripheral blood versus % HbF per BFU-E- derived cell showed a positive correlation with an r of 0.65. The variance of the intrinsic capacity to produce HbF may account for almost 40% (r2) of the variance of circulating fetal hemoglobin but other factors, particularly selective survival of F cells, must also contribute significantly. Despite virtually normal HbF levels in sickle trait parents of these Saudi patients, mean fetal hemoglobin production per BFU-E-derived erythroblast in these individuals was elevated to 3.42 +/- 1.79 pg/cell or 16.1 +/- 6.4% fetal hemoglobin, and the magnitude of fetal hemoglobin production found in parents correlated with that of the patients. These data indicate that the high fetal hemoglobin in Saudi sickle cell disease is genetically determined but expressed only during accelerated erythropoiesis. Further evidence of such genetic determination was provided by analysis of DNA polymorphisms within the beta-globin gene cluster on chromosome 11. This revealed a distinctive 5′ globin haplotype (+ + - + +) on at least one chromosome 11 in all high F SS and AS tested. The precise relationship of this haplotype to HbF production in this population remains to be defined.


2018 ◽  
Vol 7 (1) ◽  
pp. 158
Author(s):  
AzarDanesh Shahraki ◽  
Azam Zafarbakhsh ◽  
AmirrezaFarhadian Dehkordi

2013 ◽  
Vol 33 (6) ◽  
pp. 610-613
Author(s):  
Adnan Agha ◽  
Rafaat Chakik ◽  
Mamdouh M. Abdulhadi Ali ◽  
Dib Alsaudi ◽  
Giorgio Sammito ◽  
...  

Hemoglobin ◽  
2020 ◽  
Vol 44 (2) ◽  
pp. 78-81 ◽  
Author(s):  
Amein K. Al-Ali ◽  
Ahmed Alsulaiman ◽  
Alhusain J. Alzahrani ◽  
Obeid T. Obeid ◽  
Chitti Babu Vatte ◽  
...  

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