Evidence map›Paper›PMID 41575919›Full record

ArticlePloS one2026

HbA1c underperforms in identifying abnormal glucose tolerance in the presence of G6PD deficiency: Insight from the Africans in America study.

Amy R Bentley, Kauthrah Ntabadde, Claudine B Kabeza, Kenneth Ekoru, Christopher W DuBose, David B Sacks, Adebowale A Adeyemo, Charles N Rotimi, Anne E Sumner

Abstract read
In one paragraph

Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Amy R BentleyCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID https://orcid.org/0000-0002-0827-9101
Kauthrah NtabaddeSection on Diabetes, Nutrition and Health, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID https://orcid.org/0000-0002-6130-6535
Claudine B KabezaSection on Diabetes, Nutrition and Health, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Kenneth EkoruOmnigen Biodata Limited, Cambridge, United Kingdom.
Christopher W DuBoseSection on Diabetes, Nutrition and Health, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
David B SacksClinical Center, National Institutes of Health, Bethesda, Maryland, United States of America.
Adebowale A AdeyemoCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Charles N RotimiCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Anne E SumnerSection on Diabetes, Nutrition and Health, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G6PD deficiency (G6PD-D) variants are associated with lower hemoglobin A1c (HbA1c) concentrations, raising concerns about the diagnostic efficacy of HbA1c for abnormal glucose tolerance (Abnl-GT) in Africans, in whom risk of G6PD-D and Abnl-GT is high. G6PD-D is assessed using genotyping or an enzymatic assay, but because G6PD-D is X-linked, the enzymatic assay is necessary for determining status for women heterozygous for deficiency variants. We assessed: 1) ability of HbA1c to detect Abnl-GT by G6PD-D; 2) concordance of genotyping and enzymatic assay for G6PD-D in sub-Saharan Africans living in the US. 534 participants of the Africans in America study were included, with HbA1c ranging from 3.1-11.3%. Abnl-GT determined by HbA1c (≥5.7%) was compared to the diagnostic standard, the oral glucose tolerance test (fasting glucose≥100 mg/dL and/or 2h glucose≥140 mg/dL). G6PD-D status was determined by genotype (n = 263), enzymatic assay (n = 83), or both (n = 188). G6PD-D could not be determined for 13 women heterozygotes with only genotype data. In the remaining participants, HbA1c was 0.9% lower among those with G6PD-D (4.6 ± 0.5; range 3.1-5.6) compared to those with normal G6PD activity (5.5 ± 0.6; range 4.2-11.3; P < 0.001). Glucose concentrations did not differ between groups. HbA1c sensitivity and specificity for Abnl-GT were 0% (0/17) and 100% (37/37) among those with G6PD-D, and 50% (98/195) and 80% (217/272) among those with normal activity. After excluding women heterozygotes, concordance for G6PD-D detection by genotype and the enzymatic assay was 100%. G6PD-D was associated with ~0.9% lower HbA1c in this study, leading to a failure of HbA1c to identify Abnl-GT in these participants. Such a dramatic difference in a screening tool could have consequences in practice, including late diagnosis, undertreatment, and increased complications among those with G6PD-D. Additionally, the results for the enzymatic assay were perfectly concordant with the genotype results for G6PD-D. However, as genotype alone cannot predict G6PD-D in heterozygous women, the enzymatic assay was more informative.

Indexed as

Glucose IntoleranceGlucosephosphate Dehydrogenase DeficiencyGlycated HemoglobinAdultBlack PeopleBlood GlucoseFemaleGenotypeGlucosephosphate DehydrogenaseGlucose Tolerance TestHumansMaleMiddle AgedSub-Saharan African PeopleUnited StatesBlood GlucoseGlucosephosphate DehydrogenaseGlycated Hemoglobinhemoglobin A1c protein, human

Identifiers

PMID41575919
PMCPMC12829870

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.