Prevalence of Secondary Arterial Hypertension (PAH) in Patients With Sickle Cell Disease in Nigeria and the Role of HIV/AIDS and Endemic Parasitic Infections in the Natural History of Pulmonary Hypertension in Sickle Cell Disease
Sponsor study identifier
Secondary identifiers
observational
308
1 country
1
Study Start
June 15, 2006
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
Not reported
Date not reportedStudy Completion
September 28, 2017
Date type not reportedThis date has not been verified as actual or estimated.
This study will explore how people with sickle cell disease (SCD) develop a complication called pulmonary hypertension (PHTN), a serious disease in which blood pressure in the lungs is higher than normal. PHTN is also caused by HIV, hepatitis C and schistosomiasis. Patients who have both SCD and one of these other infections may develop more severe PHTN. The number of Nigerians with SCD who also have PHTN is not known, nor is the cause of PHTN in this population. This study will examine genetic material in people with and without SCD to determine whether certain genes will allow doctors to predict which patients with SCD are likely to develop PHTN. Nigerian males and females 10 years of age and older with or without SCD may be eligible for this study. Patients must have SS, SC, or SB thalassemia or other genotype; control subjects must have hemoglobin A or AS genotype. Participants undergo a complete medical history and physical examination, blood tests, electrocardiogram (EKG), ultrasound tests of the heart and abdomen, and a 6-minute walk (distance test) to determine exercise capacity. Blood tests include screening for HIV, hepatitis B and C, schistosomiasis, hookworm and malaria. Patients who test positive for HIV, hepatitis B or C, schistosomiasis, hookworm or malaria are referred for treatment at Ahmadu Bello University Teaching Hospital in Zaria, Nigeria, and those who test negative for hepatitis B are referred for vaccination. Genetic tests focus on genes involved in SCD, PHTN, inflammation, blood vessel function and red blood cell function.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
September 28, 2017
Date type not reportedThis date has not been verified as actual or estimated.
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Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
June 15, 2006
Date type not reportedThis date has not been verified as actual or estimated.
August 22, 2006
Actual (reported)August 23, 2006
Actual (reported)September 28, 2017
Date type not reportedThis date has not been verified as actual or estimated.
Ahmadu Bello University Teaching Hospital
Kaduna, Nigeria
Aliyu ZY, Tumblin AR, Kato GJ. Current therapy of sickle cell disease. Haematologica. 2006 Jan;91(1):7-10. No abstract available.
Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. JAMA. 2005 Apr 6;293(13):1653-62. doi: 10.1001/jama.293.13.1653.
Morris CR, Kato GJ, Poljakovic M, Wang X, Blackwelder WC, Sachdev V, Hazen SL, Vichinsky EP, Morris SM Jr, Gladwin MT. Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease. JAMA. 2005 Jul 6;294(1):81-90. doi: 10.1001/jama.294.1.81.
Swee Lay Thein, M.D.
National Heart, Lung, and Blood Institute (NHLBI)
308 participants (actual enrollment reported by the registry).
First Submitted
August 22, 2006
First Posted
August 23, 2006
Study Start
June 15, 2006
Date type not reportedThis date has not been verified as actual or estimated.
Contact the study team to confirm eligibility.
Study Completion
September 28, 2017
Date type not reportedThis date has not been verified as actual or estimated.
Last Updated
November 29, 2019
Record last verified: 2017-09-28
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