Eric V Balti1, Marinette C Ngo-Nemb2, Eric Lontchi-Yimagou3, Barbara Atogho-Tiedeu4, Valery S Effoe5, Elvis A Akwo6, Mesmin Y Dehayem2, Jean-Claude Mbanya7, Jean-François Gautier8, Eugene Sobngwi9. 1. Diabetes Research Center, Brussels Free University-VUB, Brussels, Belgium; National Obesity Center, Yaounde Central Hospital and Faculty of Medicine and Biomedical Sciences, University of Yaounde 1, Yaounde, Cameroon. 2. National Obesity Center, Yaounde Central Hospital and Faculty of Medicine and Biomedical Sciences, University of Yaounde 1, Yaounde, Cameroon. 3. Molecular Medicine and Metabolism Laboratories, Biotechnology Center, University of Yaounde 1, Yaounde, Cameroon; Université Paris Diderot, Paris, France. 4. Molecular Medicine and Metabolism Laboratories, Biotechnology Center, University of Yaounde 1, Yaounde, Cameroon. 5. National Obesity Center, Yaounde Central Hospital and Faculty of Medicine and Biomedical Sciences, University of Yaounde 1, Yaounde, Cameroon; Department of Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, NC, USA. 6. National Obesity Center, Yaounde Central Hospital and Faculty of Medicine and Biomedical Sciences, University of Yaounde 1, Yaounde, Cameroon; Department of Medicine, Vanderbilt University, Nashville, TN, USA. 7. National Obesity Center, Yaounde Central Hospital and Faculty of Medicine and Biomedical Sciences, University of Yaounde 1, Yaounde, Cameroon; Molecular Medicine and Metabolism Laboratories, Biotechnology Center, University of Yaounde 1, Yaounde, Cameroon; University of Technology, Kingston, Jamaica. 8. Université Paris Diderot, Paris, France; Department of Diabetes and Endocrinology, Saint-Louis Hospital, Paris, France; INSERM, UMRS 872, Cordeliers Research Center, Paris, France; Université Pierre et Marie Curie, Paris, France. 9. National Obesity Center, Yaounde Central Hospital and Faculty of Medicine and Biomedical Sciences, University of Yaounde 1, Yaounde, Cameroon; Molecular Medicine and Metabolism Laboratories, Biotechnology Center, University of Yaounde 1, Yaounde, Cameroon. Electronic address: sobngwieugene@yahoo.fr.
Abstract
AIM: We investigated the association of HLA DRB1 and DQB1 alleles, haplotypes and genotypes with unprovoked antibody-negative ketosis-prone atypical diabetes (A(-) KPD) in comparison to type 2 diabetes (T2D). METHODS: A(-) KPD and T2D sub-Saharan African patients aged 19-63 years were consecutively recruited. Patients positive for cytoplasmic islet cell, insulin, glutamic acid decarboxylase or islet antigen-2 autoantibodies were excluded. Odds ratios were obtained via logistic regression after considering alleles with a minimum frequency of 5% in the study population. Bonferroni correction was used in the case of multiple comparisons. RESULTS: Among the 130 participants, 35 (27%) were women and 57 (44%) were A(-) KPD. DRB1 and DQB1 allele frequencies were similar for both A(-) KPD and T2D patients; they did not confer any substantial risk even after considering type 1 diabetes susceptibility and resistance alleles. We found no association between A(-) KPD and the derived DRB1*07-DQB1*02:02 (OR: 0.55 [95%CI: 0.17-1.85], P=0.336); DRB1*11-DQB1*03:01 (OR: 2.42 [95%CI: 0.79-7.42], P=0.123); DRB1*15-DQB1*06:02 (OR: 0.87 [95%CI: 0.39-1.95], P=0.731) and DRB1*03:01-DQB1*02:01 (OR: 1.48 [95%CI: 0.55-3.96], P=0.437) haplotypes. Overall, we did not find any evidence of susceptibility to ketosis associated with DRB1 and DQB1 genotypes (all P>0.05) in A(-) KPD compared to T2D. Similar results were obtained after adjusting the analysis for age and sex. CONCLUSION: Factors other than DRB1 and DQB1 genotype could explain the propensity to ketosis in A(-) KPD. These results need to be confirmed in a larger population with the perspective of improving the classification and understanding of the pathophysiology of A(-) KPD.
AIM: We investigated the association of HLA DRB1 and DQB1 alleles, haplotypes and genotypes with unprovoked antibody-negative ketosis-prone atypical diabetes (A(-) KPD) in comparison to type 2 diabetes (T2D). METHODS: A(-) KPD and T2D sub-Saharan African patients aged 19-63 years were consecutively recruited. Patients positive for cytoplasmic islet cell, insulin, glutamic acid decarboxylase or islet antigen-2 autoantibodies were excluded. Odds ratios were obtained via logistic regression after considering alleles with a minimum frequency of 5% in the study population. Bonferroni correction was used in the case of multiple comparisons. RESULTS: Among the 130 participants, 35 (27%) were women and 57 (44%) were A(-) KPD. DRB1 and DQB1 allele frequencies were similar for both A(-) KPD and T2D patients; they did not confer any substantial risk even after considering type 1 diabetes susceptibility and resistance alleles. We found no association between A(-) KPD and the derived DRB1*07-DQB1*02:02 (OR: 0.55 [95%CI: 0.17-1.85], P=0.336); DRB1*11-DQB1*03:01 (OR: 2.42 [95%CI: 0.79-7.42], P=0.123); DRB1*15-DQB1*06:02 (OR: 0.87 [95%CI: 0.39-1.95], P=0.731) and DRB1*03:01-DQB1*02:01 (OR: 1.48 [95%CI: 0.55-3.96], P=0.437) haplotypes. Overall, we did not find any evidence of susceptibility to ketosis associated with DRB1 and DQB1 genotypes (all P>0.05) in A(-) KPD compared to T2D. Similar results were obtained after adjusting the analysis for age and sex. CONCLUSION: Factors other than DRB1 and DQB1 genotype could explain the propensity to ketosis in A(-) KPD. These results need to be confirmed in a larger population with the perspective of improving the classification and understanding of the pathophysiology of A(-) KPD.
Authors: Eric Lontchi-Yimagou; Philippe Boudou; Jean Louis Nguewa; Jean Jacques Noubiap; Vicky Kamwa; Eric Noel Djahmeni; Babara Atogho-Tiedeu; Marcel Azabji-Kenfack; Martine Etoa; Gaelle Lemdjo; Mesmin Yefou Dehayem; Jean Claude Mbanya; Jean-Francois Gautier; Eugène Sobngwi Journal: J Diabetes Metab Disord Date: 2018-03-29