Adding rosiglitazone to metformin in patients with type 2 diabetes: effect on diabetes control and metabolic parameters

To evaluate the efficacy and tolerability, any changes in lipid parameters including free fatty acids and effect on weight and blood pressure, of adding Rosiglitazone to patients with type 2 DM who are not adequately controlled on maintenance dose of Metformin. Prospective study of 14 patients with type 2 DM who were maintained on Metformin alofte [1.5-2.5 g/day]. Twelve patients met the inclusion criteria, and received 4 mg of Rosiglitazone daily in addition to Metformin. Patients were followed for 24 weeks and seen for 6-7 visits. The dose of Rosiglitazone was increased after 8 weeks if FBG was still >/= 160 mg/dl. Full biochemical evaluation was done and safety parameters were observed at base line, at intervals during the study and at the end of the study. All patients completed the study. T test was used for comparison. Eight males and four females were studied. They had the following characteristics: Mean age was [52 +/- 6.9] years, weight was [78.2 +/- 10.1] kg BMI was [28 +/- 4] kg/m[2], waist circumference was [97.5 +/- 6.5] cm, and duration of DM was [7.3 +/- 6] years. Four patients required an increase of Rosiglitazone dose to 8 mg after 8 weeks. All patients showed improvement of HbAlc levels by the end of the study. When mean base line parameters were compared to those at the end of study: HbAlc level dropped from [8.9% +/- 1.5] to [7.1% +/- 1.1] [P: 0.00003] and FBG from [205 + 50.6] to [150 +/- 28] mg/dl [P: 0.002]. Free Fatty Acids [FFA] dropped from [703 +/- 213] to [510 +/- 303.6] by 8 weeks and to [574 +/- 184.6] microeq/L by the end of the study, [P: 0.01 and 0.06, respectively]. Improvement in HbAlc did not however correlate with the level of FFA drop. There was also significant increase in HDL level [1.15 +/- 0.14]-[1.27 +/- 0.2] mmol/L, [P: 0.02], and weight [78.2 +/- 10.1]-[80.1 +/- 10.9] kg [P: 0.01]. The changes in LDL [3.02 +/- 0.57] - [3.23 +/- 0.5] mmol/L, TG [2.16 +/- l.l]-[2.2 +/- 1.33] mmol/L, waist circumference [97.5 +/- 6.5]-[99 +/- 8.1] cm, and BP [132.5 +/- 17]-[130.2 +/- 18.8] mm Hg [systolic], were not significant. When [Good Responders], [HbAlc drop of >1.5%], [nine subjects] were compared to those with less than 1.5% drop [three subjects], there were no specific characteristics to define responders. Rosiglitazone, added to Metformin in type 2 DM patients, was effective and well tolerated. There was a significant decrease in FFA levels with treatment. The response to treatment, however could not be predicted from biochemical or clinical parameters. A larger study may be needed to define respon-der characteristics

case of vitamin D deficiency masquerading as occult malignancy

At present, the diagnosis of a [brown tumor] is a clinical curiosity. It is considered to be a complication of severe and rapidly progressive hyperparathyroidism [HPT]. Indeed, such a presentation is typical of a patient harboring a parathyroid carcinoma. The incidence of brown tumors is 3% in the benign form of primary hyperparathyroidism [1]. In secondary HPT, the incidence of brown tumors is under 2% and is caused by chronic renal failure.[1] Brown tumors are locally destructive lesions consisting of fluid-filled cysts that are rich in highly vascularized fibrous tissue containing hemorrhagic spots. Blood pigment [hemosiderin] will accumulate, which imparts a reddish-brown hue and hence the name [brown tumor].[1] Brown tumors are demonstrated radiologically as lesions of osteitis fibrosa cystica [1]. We describe a young lady who was erroneously diagnosed elsewhere as a case of metastatic bone disease. Our evaluation documented this as a case of vitamin D deficiency [VDD] causing secondary hyperparathyroidism [SHPT] with diffuse distribution of brown tumors in her skeleton. Following vitamin D and calcium treatment, the patient improved