title: HLA class II alleles susceptibility markers of type 1 diabetes fail to specify phenotypes of ketosis-prone diabetes in adult Tunisian patients.
abstract: We aimed to characterize the different subgroups of ketosis-prone diabetes (KPD) in a sample of Tunisian patients using the Aβ scheme based on the presence or absence of β-cell autoantibodies (A+ or A-) and β-cell functional reserve (β+ or β-) and we investigated whether HLA class II alleles could contribute to distinct KPD phenotypes. We enrolled 43 adult patients with a first episode of ketosis. For all patients we evaluated clinical parameters, β-cell autoimmunity, β-cell function and HLA class II alleles. Frequency distribution of the 4 subgroups was 23.3% A+β-, 23.3% A-β-, 11.6% A+β+ and 41.9% A-β+. Patients from the group A+β- were significantly younger than those from the group A-β- (P = .002). HLA susceptibility markers were significantly more frequent in patients with autoantibodies (P = .003). These patients also had resistance alleles but they were more frequent in A+β+ than A+β- patients (P = .04). Insulin requirement was not associated to the presence or the absence of HLA susceptibility markers. HLA class II alleles associated with susceptibility to autoimmune diabetes have not allowed us to further define Tunisian KPD groups. However, high prevalence of HLA resistance alleles in our patients may reflect a particular genetic background of Tunisian KPD population.
authors: Immunology Department, La Rabta Hospital, Al Manar University Tunis, Tunisia. lilia_laadhar@yahoo.com
authors: Lilia
authors: L
authors: Laadhar
authors: Fatma
authors: F
authors: Harzallah
authors: Mondher
authors: M
authors: Zitouni
authors: Maryam
authors: M
authors: Kallel-Sellami
authors: Moncef
authors: M
authors: Fekih
authors: Naziha
authors: N
authors: Kaabachi
authors: Hádia
authors: H
authors: Slimane
authors: Sondès
authors: S
authors: Makni
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D016883:Diabetic Ketoacidosis / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D005260:Female; D005787:Gene Frequency; D005819:Genetic Markers; D005838:Genotype; D006683:HLA-DQ Antigens / Q000235:genetics* / Q000276:immunology; D059866:HLA-DQ beta-Chains; D006684:HLA-DR Antigens / Q000235:genetics* / Q000276:immunology; D059811:HLA-DRB1 Chains; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011446:Prospective Studies; D014416:Tunisia / Q000453:epidemiology
chemical_list: D001323:Autoantibodies; D005819:Genetic Markers; D006683:HLA-DQ Antigens; D059866:HLA-DQ beta-Chains; C069051:HLA-DQB1 antigen; D006684:HLA-DR Antigens; D059811:HLA-DRB1 Chains; D007004:Hypoglycemic Agents; D007328:Insulin