Effect of α⁺ Thalassemia on the Severity of Plasmodium falciparum Malaria in Different Sickle Cell Genotypes in Indian Adults: A Hospital-Based Study

Abstract

There is a paucity of literature on the association of α⁺-thalassemia, sickle-cell hemoglobin disorders, and malaria in India. This study aimed to understand the effect of α⁺-thalassemia on the severity of Plasmodium falciparum malaria in adults with respect to sickle-cell genotypes. The study subjects were categorized into ‘severe-malaria’ and ‘uncomplicated-malaria’ and age-gender matched ‘control’ groups. Sickle-cell and α⁺-thalassemia were investigated in all the recruited subjects. The effect of α⁺-thalassemia on the severity of malaria was analyzed in HbAA and sickle-cell genotypes (HbAS and HbSS) separately. The prevalence of α⁺-thalassemia in various groups ranged from 41.5% to 81.8%. The prevalence of α⁺-thalassemia was lower (OR = 1.64; p = 0.0013) in severe malaria (41.5%) as compared to healthy controls (53.8%) with HbAA genotype. In contrast, in HbAS genotype, the prevalence of α⁺-thalassemia was higher (OR = 4.11; p = 0.0002) in severe malaria (81.8%) compared to controls (52.2%). In severe malaria with HbAA genotype, there was a significantly higher hemoglobin level and low MCV and MCH level in patients with α⁺-thalassemia compared to the normal α-globin genotype. Further, the incidence of cerebral malaria, hepatopathy, and mortality was lower in patients (HbAA) with α⁺-thalassemia as compared to normal α-globin genotype (HbAA). In severe malaria with either HbAS or HbSS genotype, only a few parameters showed statistical differences with respect to α⁺-thalassemia. Low prevalence of α⁺-thalassemia in severe malaria with HbAA genotype compared to healthy controls with HbAA genotype indicates the protective effect of α⁺-thalassemia against severe malaria. However, the high prevalence of α⁺-thalassemia in patients with HbAS genotype depicts its interference in the protective effect of sickle-cell against severe malaria.

Keywords:

• α⁺ thalassemia
• Plasmodium falciparum
• malaria
• sickle cell

Acknowledgement

The authors are indebted to the late Dr. Dilip Kumar Patel, Ex-Associate Professor, Department of Medicine, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha, India and Principal Investigator of the Department of Science and Technology (DST) (New Delhi, India) sponsored project and mentor to Dr. Prasanta Purohit (Senior Research Fellow, Indian Council of Medical Research). The authors thank all patients and families for their participation in the study.

Ethical approval

This study was approved by the Institutional Ethical Committee of Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Odisha, India.

Author contributions

PP, JP and SP designed the research; PP and KD performed the research work; PP, PKM collected the clinical data; PP, JP and SP analyzed and interpreted the data; PP, PKM, JP and SP wrote the manuscript. All authors read and approved the final manuscript.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

This work was supported by Indian Council of Medical Research (ICMR), New Delhi [ICMR IRIS ID-2012–13400] and Department of Science and Technology (DST), New Delhi [File No. SR/SO/HS- 140/2007].