Glimepiride in type 2 diabetes mellitus Thai patients.

This study aimed to confirm the efficacy of glimepiride given once daily in the treatment of Thai type 2 diabetic patients and to find out the optimum dosage for Thai patients. The patients were enrolled at the diabetic clinics of 5 hospitals (Rajavithi, Chulalongkorn, Pramongkutklao, Siriraj and Theptarin Hospitals). All patients started glimepiride 1 mg once daily and escalated to 2, 3, 4 and until 6 mg every 4 weeks if fasting plasma glucose (FPG) exceeded 140 mg/dL. Subjects were 60 females and 29 males with an average age of 52.2 +/- 10.0 years. Mean BMI was 25.5 +/- 3.8 kg/m2. Fifty seven patients (64.0%) were drug naïve and thirty two patients (36.0%) had been previously treated with oral hypoglycemic agents. Seventy three per cent of the drug naïve and 37 per cent of the previously treated patients could be controlled with 1-2 mg of glimepiride once daily. At the twelfth week of treatment, mean fasting plasma glucose decreased from 224.6 to 156.6 mg/dL (30% reduction) and mean HbA1c decreased from 10.0 to 7.5 per cent (25% reduction). At the end of the study 49.4 per cent of the patients had HbA1c < 7.0 per cent, 21.3 per cent had HbA1c 7.0-8.0 per cent and 29.3 per cent had HbA1c > 8.0 per cent. Adverse events that were probably or possibly related to the drug were reported in 5 patients (5.6%). Three of them were hypoglycemia and two patients had skin rash. All hypoglycemic episodes were mild. Glimepiride was indicated to be safe. There were no clinically significant changes in clinical laboratory values, physical examinations and vital signs. In conclusion, glimepiride was efficacious and safe in type 2 diabetes Thai patients and 1-2 mg of glimepiride appeared to be a sufficient dose for most newly diagnosed type 2 diabetic patients.

Lack of association between a polymorphism of human thyrotropin receptor gene and autoimmune thyroid disease.

A polymorphism in codon 52 of the human thyrotropin receptor results in a proline to threonine substitution in the extracellular domain of the receptor, but the association with autoimmune thyroid disease has been uncertain and there is no report the prevalence of this polymorphism in Orientals. To investigate this polymorphism and the association with autoimmune thyroid disease, we studied 113 normal unrelated individuals, 142 autoimmune thyroid disease patients including 112 Graves' disease and 30 Hashimoto's thyroiditis in the Thai population. We screened genomic DNAs of these subjects for the presence of A253 by PCR amplification using a degenerate oligonucleotide primer which produces a Tth111 I restriction site only in the presence of A253. The variant allele was present in 5.3 per cent of normal and 3.5 per cent of autoimmune thyroid disease, 2.7 per cent of Graves' disease and 6.7 per cent of Hashimoto's thyroiditis. The allele distribution in autoimmune thyroid disease patients did not differ significantly from that observed in controls. No association was found between this TSH-R polymorphism and the occurrence of autoimmune thyroid disease.

Simple and sensitive test for thyroid hormone autoantibodies.

We presented a simple and sensitive test for thyroid hormone autoantibodies. The normal range for T4 and T3 autoantibodies in Thai people considering mean +/- 3 S.D. were 1.8-9.4 per cent and 3.1-8.6 per cent, respectively. Although positive low titer of thyroid hormone autoantibodies had almost no interference of thyroid hormone levels, high titer might cause great interference. This method can be used for screening patients who have unexpectably high levels of serum T4, T3 or discrepancy between thyroid hormone levels and clinical findings.