Multicentre evaluation of the DCA 2000 system for measuring glycated haemoglobin. DCA 2000 Study Group.

The recommended method for assessing long-term blood glucose control in diabetic patients is the measurement of glycated haemoglobin (Hb). The Ames DCA 2000 system for assaying glycated Hb uses an immunoassay with a monoclonal antibody specific for an aminoacid sequence within the HblAc molecule. This study compared the performance of the DCA 2000 system for HblAc measurement with that of high-performance liquid chromatography (HPLC). A total of 1.016 insulin-dependent and non-insulin-dependent diabetic patients from 5 outpatient clinics took part. The correlation coefficients between DCA 2000 and HPLC data ranged between 0.94 and 0.98, depending on site. The mean variations and 95% confidence intervals for the differences between the results for each sample were: site A 0.172 (-1.186 to 1.53), site B -0.275 (-1.317 to 0.767), site C -0.146 (-0.868 to 0.576), site D -0.088 (-0.864 to 0.688), and site E -0.251 (-1.099 to 0.597). The sensitivity of the DCA 2000 assay ranged between 80 and 94%, and the specificity between 88 and 100%, depending on site. For pooled results, the correlation coefficient assayed by the two methods was 0.95. The mean variation was -0.116 and the 95% confidence interval -1.23 to 0.998. The sensitivity of DCA 2000 was 91%, and the specificity 94%. DCA tended to underestimate HbAlc slightly as compared to HPLC. This study confirms the reliability of DCA 2000 for measuring glycated Hb. The system is easy to use and provides valuable information for the care of the diabetic patients.

[Current data on the physiopathology of massive obesity]. / Données actuelles sur la physiopathologie de l'obésité massive.

It is now believed that the factors leading to massive obesity are a caricature of those which are responsible for common obesity. The lipid component of daily diet is as important as the amount of calories ingested. Putting on weight occurs only in subjects with metabolic abnormalities or with genetically determined neuro-hormonal anomalies. The weight increase tends to correct the initial metabolic disturbances, and in fact obesity is nothing but a phenomenon of adaptation. The development of molecular biology techniques should help us, in the near future, to understand these major physiopathological disorders.

[Oral and dietary treatments of type 2 diabetes]. / Traitements oraux et diététiques du diabète de type 2.

Non insulin-dependent diabetes mellitus requires a metabolic and vascular treatment in order to prevent macroangiopathy. Personal diet management, which is similar in diabetic and non diabetic comparable patients, is the basis of therapy. Any significant result cannot be expected without its observance. Sulfonylurea and biguanide drugs can enhance diet action and must be prescribed secondarily according to the level of hyperglycaemia. Blood pressure and lipid control is as important as glycaemic normalization. Early diet management of obese people should be the best approach to prevent type II diabetes.

Effects of a combination of bedtime intermediate-acting insulin and glibenclamide in type 2 (non-insulin-dependent) diabetic patients with secondary failure to respond to oral hypoglycaemic agents.

The effect of a subcutaneous injection of an intermediate-acting insulin at bedtime combined with glibenclamide has been evaluated in 16 non-insulin-diabetic patients with secondary failure to respond to oral agents. The patients showed poor metabolic control (HbA1 greater than 11%) after two months on diet and glibenclamide treatment (15 mg.day-1). For 3 months the glibenclamide was continued together with an injection of an intermediate-acting insulin at bedtime in order to maintain fasting blood glucose under 120 mg.dl-1. A significant reduction in fasting blood glucose and HbA1 (15.50 vs 10.35%) and fructosamine (2.03 vs 1.69 mmol.l-1) was observed (230 to 141 mg.dl-1) at a mean insulin dose of 0.28 U.kg-1. The peak blood glucose after a standard test meal was also significantly improved (290 vs 203 mg.dl-1). Two months after the bedtime insulin injection had been withdrawn, only one patient was still being treated with oral agents alone. Except for another patient who dropped out, all the others had to be treated again with insulin because their fasting blood glucose exceeded 180 mg.dl-1. It is concluded that a single subcutaneous injection of an intermediate-acting insulin at bedtime combined with glibenclamide improved fasting and post-meal blood glucose concentrations in non-insulin-dependent patients resistant to diet and oral hypoglycaemic treatment. Almost all of the patients relapsed after insulin was withdrawn.

Class II MHC antigen induction on rat insulinoma (RINm5F) and colon carcinoma (TS) cells by co-culture with diabetic and normal xenogenic lymphocytes.

Two MHC Class II-negative rat epithelial cell lines (RINm5F beta-cells and TS colic cells) were co-cultured with xenogenic lymphocytes from Type I diabetic patients or from low-dose streptozotocin (SZ) diabetic mice. MHC Class II antigens (Ag) were easily induced on both cell lines in such co-culture conditions, representing an experimental approach to insulitis. Our data indicate that: (1) lymphocytes from diabetic patients or from SZ mice were more efficient than lymphocytes from healthy controls in inducing Class II Ag on RIN cells. Lymphocytes from patients with autoimmune thyroid diseases were also more efficient than control lymphocytes, indicating that the ability to induce Class II may be related to the activation of lymphocytes rather than being diabetes-specific. (2) Rat colon carcinoma cells (TS) were also induced to express high levels of Class II Ag upon co-culture with SZ or control mouse lymphocytes. (3) Class II+ RIN cells were observed after 24 h of co-culture; their number increased after 48 and 72 h. The number of class II+ RIN increased proportionally to the number of lymphocytes in the culture. (4) Induction of Class II Ag was obtained by cell-free supernatants of mouse lymphocytes/RIN co-cultures and was inhibited by cyclosporine A, suggesting that Class II induction in this model is mediated by lymphokines. (5) Depletion experiments indicate that both monocytes and lymphocytes play a role in this Class II induction.