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HLA- B*5701 Allele in HIV-infected Indian Children and its Association with Abacavir Hypersensitivity
Mamta V Manglani1, Yashwant R Gabhale2, Mamatha M Lala1
1Pediatric Centre of Excellence for HIV Care (PCoE), Department of Pediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai, India.
Insights
In HIV-infected children, 11% carried the HLA-B*5701 allele. This allele is linked to Abacavir hypersensitivity, with two cases identified in this study.
Area of Science:
- Immunogenetics
- Pediatric Infectious Diseases
- Pharmacogenomics
Background:
- Abacavir is a crucial antiretroviral medication for treating HIV infection in children.
- Hypersensitivity reactions to Abacavir are a significant clinical concern, potentially linked to specific genetic markers.
- The HLA-B*5701 allele is a known predictor of Abacavir hypersensitivity.
Purpose of the Study:
- To investigate the prevalence of the HLA-B*5701 allele in a cohort of HIV-infected children.
- To determine the association between the presence of the HLA-B*5701 allele and the occurrence of Abacavir hypersensitivity.
- To inform clinical practice regarding Abacavir use in pediatric HIV management.
Main Methods:
- A cohort of 100 HIV-infected children (aged 2-18 years) was enrolled.
- Polymerase Chain Reaction (PCR) sequencing was employed to detect the HLA-B*5701 allele.
- Clinical monitoring for Abacavir hypersensitivity reactions was conducted.
Main Results:
- The HLA-B*5701 allele was identified in 11% (11 out of 100) of the HIV-infected children.
- Two children who tested positive for the HLA-B*5701 allele developed Abacavir hypersensitivity.
- No hypersensitivity reactions were observed in children who did not carry the HLA-B*5701 allele.
Conclusions:
- The HLA-B*5701 allele is present in 11% of HIV-infected children, confirming its relevance in this population.
- A strong association exists between the HLA-B*5701 allele and Abacavir hypersensitivity in pediatric patients.
- Pre-treatment screening for the HLA-B*5701 allele is recommended to prevent Abacavir hypersensitivity in HIV-infected children.
Objective:
To determine the prevalence of HLA-B*5701 allele in HIV-infected children, and to find its association with Abacavir hypersensitivity.
Methods:
Children (2 to 18 y) already on, or to be initiated on Abacavir were included for PCR sequencing to detect HLA-B*5701.
Outcome Measures Were:
proportion with HLA B*5701 allele and hypersensitivity with Abacavir. Abacavir was stopped if patient tested positive for HLA-B*5701 allele.
Results:
100 children (median age 11 y) were enrolled; 10 were already on Abacavir. HLA-B*5701 positivity was observed in 11 (11%) children. Two of these 11 children developed hypersensitivity after initiation of Abacavir. Abacavir was thereafter stopped in all who tested HLA-B*5701 positive, irrespective of the development of hypersensitivity reaction.
Conclusion:
HLA-B*5701 allele was present in 11 (11%) of HIV-infected children, of which two developed Abacavir hypersensitivity. None of the patients without the allele developed hypersensitivity.
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