Cellular and humoural autoimmunity markers in type 2 (non-insulin-dependent) diabetic patients with secondary drug failure.
In some cases patients with Type 2 (non-insulin-dependent) diabetes mellitus fail to respond to treatment with oral hypoglycaemic agents. These patients may respond in the same way as Type 1 (insulin-dependent) diabetic patients. Cellular immune aggression (defined as the capacity of peripheral mononuclear cells to inhibit stimulated insulin secretion by dispersed rat islet cells), insulin autoantibodies, C-peptide response and HLA antigens were determined in 31 Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents and in 22 control subjects. Nine (29.03%) of the 31 Type 2 diabetic patients showed positive cellular immune aggression (2 SD below control group) and 22 (70.97%) presented no cellular immune aggression. There was a relationship between positive cellular immune aggression and each of the following parameters: age, body mass index and microangiopathy. No correlation was found between positive cellular immune aggression and glycaemia, HbA1, blood lipids or atherosclerosis. Patients with positive cellular immune aggression showed a significantly lower glucagon-stimulated C-peptide response vs those with no cellular immune aggression. Within a sub-group of patients who had never been treated with insulin, insulin autoantibodies were present in four of six patients with positive cellular immune aggression. DR2 antigen was found with decreased frequency in patients whereas no DR3/DR4 heterozygotes were observed. Our data support the hypothesis that a group of Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents presented autoimmunity towards pancreatic Beta cells.
Zavala
A V
AV
Cátedra de Nutrición, Hospital de Clínicas General José de San Martín, Universidad de Buenos Aires, Argentina.
Fabiano de Bruno
L E
LE
Cardoso
A I
AI
Mota
A H
AH
Capucchio
M
M
Poskus
E
E
Fainboim
L
L
Basabe
J C
JC
D000704:Analysis of Variance; D000818:Animals; D000917:Antibody Formation; D001323:Autoantibodies / Q000097:blood*; D002096:C-Peptide / Q000097:blood*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000276:immunology*; D005260:Female; D005934:Glucagon; D006680:HLA Antigens / Q000097:blood*; D006683:HLA-DQ Antigens / Q000097:blood; D006684:HLA-DR Antigens / Q000097:blood*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007111:Immunity, Cellular; D007328:Insulin / Q000378:metabolism; D007330:Insulin Antibodies / Q000097:blood*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000276:immunology / Q000378:metabolism; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D051381:Rats; D012016:Reference Values; D017211:Treatment Failure
D001323:Autoantibodies; D002096:C-Peptide; D006680:HLA Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D007004:Hypoglycemic Agents; D007328:Insulin; D007330:Insulin Antibodies; D005934:Glucagon