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Inherited haemoglobin disorders: an increasing global health problem.

TLDR
It takes considerable time to establish expertise in developing programmes for the control and management of these conditions, and the lessons learned in developed countries will need to be transmitted to those countries in which they occur at a high frequency.
Abstract
Despite major advances in our understanding of the molecular pathology, pathophysiology, and control and management of the inherited disorders of haemoglobin, thousands of infants and children with these diseases are dying through lack of appropriate medical care. This problem will undoubtedly increase over the next 20 years because, as the result of a reduction in childhood mortality due to infection and malnutrition, more babies with haemoglobin disorders will survive to present for treatment. Although WHO and various voluntary agencies have tried to disseminate information about these diseases, they are rarely mentioned as being sufficiently important to be included in setting health care priorities for the future. It takes considerable time to establish expertise in developing programmes for the control and management of these conditions, and the lessons learned in developed countries will need to be transmitted to those countries in which they occur at a high frequency.

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Medical genetics in developing countries in the Asia-Pacific region: challenges and opportunities

TL;DR: Challenges provide opportunities for both developing and developed nations to work together to reduce the inequalities and to ensure a caring, inclusive, ethical, and cost-effective genetic service in the Asia-Pacific region.
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Acceptability of prenatal diagnosis by a sample of parents of sickle cell anemia patients in Cameroon (sub-Saharan Africa).

TL;DR: The results of this study suggest Cameroonian parents with children affected with Sickle Cell Anemia generally accept the principles of prenatal diagnosis and in some cases termination of a pregnancy affected with sickle cell Anemia.
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Quantitative proteomics of plasma vesicles identify novel biomarkers for hemoglobin E/β-thalassemic patients.

TL;DR: This work highlights haptoglobin, hemopexin, and cathepsin S as potential clinically relevant biomarkers for levels of hemolysis and inflammation and monitoring of these plasma proteins could help in the clinical management of thalassemia.
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Analysis of survival data in thalassemia patients in Shiraz, Iran

TL;DR: Sociodemographic and hematological factors were found to be significantly associated with the survival rate of thalassemia and addressing these factors may help healthcare providers and physicians to provide the best possible care and to improve the survival rates.
Journal ArticleDOI

Sonographic Markers of Fetal α-Thalassemia Major

TL;DR: The cardiothoracic ratio, placental thickness, and middle cerebral artery peak systolic velocity are the sensitive markers most used in clinical practice and can predict fetal α‐thalassemia major and assess the efficacy of treatment noninvasively.
References
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Sickle cell disease

TL;DR: New strategies for specific therapy, including expanded use of chronic transfusions, bone marrow transplantation, and hydroxyurea, now offer hope for prevention of many or all of the hemolytic and vaso-occlusive manifestations of sickle cell disease.

World development report 1993 : investing in health

TL;DR: This report examines the controversial questions surrounding health care and health policy and advocates a threefold approach to health policy for governments in developing countries and in the formerly socialist countries, based in large part on innovative research.
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Effect of Hydroxyurea on the Frequency of Painful Crises in Sickle Cell Anemia

TL;DR: Hydroxyurea therapy can ameliorate the clinical course of sickle cell anemia in some adults with three or more painful crises per year and Maximal tolerated doses of hydroxyurea may not be necessary to achieve a therapeutic effect.
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Pathogenesis and Treatment of Sickle Cell Disease

TL;DR: A wealth of information is produced on the mechanisms by which a single base substitution in the gene encoding the human β-globin subunit, with the resulting replacement of β6 glutamic acid by valine, leads to the protean and devastating clinical manifestations of sickle cell disease.