Nasri F, Dib S A, Sá J R, Russo E M, Vieira J P, Chacra A R
Departamento de Medicina, Escola Paulista de Medicina, São Paulo.
Rev Assoc Med Bras (1992). 1995 Jan-Feb;41(1):37-42.
Although rare, ketoacidosis may be induced by the occurrence of antibody mediated insulin resistance. Cases of 3 patients with ketoacidosis precipitated by immunologic insulin resistance (IIR) are reported. CASE REPORT--Three patients were admitted to the primary care unit of Hospital São Paulo in Diabetic Ketoacidosis. Demographic data of the patients (HML, DRJ and DIS) included: age (46.39 and 54 y.o.); sex (2F, 1M); diabetes mellitus (2 DM II and 1 pancreatic); duration of diabetes (6, 11 and 9 years) and BMI (17.5; 25.5 and 24.3 kg/m2. Admission laboratory data were: glucose (40, 38 and 22 mmol/L); pH (7.2; 6.9 and 7.2) and all had ketonuria. Insulin requirements for metabolic control were: HML: 1494U; DRJ: 1496U; DIS: 450U in a period of: 212, 206 and 72h. The plasmatic leves of Anti insulin antibodies (IA) measured by RIA (nU/mL) and ELISA (EI), where: HML: 7186, 3.26; DRJ: 7879, 3.42 and DIS: 8377, 2.88. HI was associated with marked decrease of both, insulin requirements and IA (HML: 3393, 1.39 after 10 months and DRJ: 4673, 2.34; DIS: 1510, after 18 months) at follow-up. DISCUSSION--The High Insulin requirements and time necessary to achieve the metabolic control guided us to the diagnosis of IIR. It was confirmed by high levels of AI and by the improvement in the metabolic control after the introduction of HI. CONCLUSION--The physician must be alert to severe IIR if there is no response after standard therapy to ketoacidosis. HI can be considered a valid alternative of treatment for IIR.
