OBJECTIVE: This study aimed to evaluate the impact of CMI on medication adherence and glycaemic control among patients with type 2 diabetes in Qatar.
METHODS: We developed and customised CMI for all the anti-diabetic medications used in Qatar. A randomised controlled trial in which the intervention group patients (n = 66) received the customised CMI with usual care, while the control group patients (n = 74) received usual care only, was conducted. Self-reported medication adherence and haemoglobin A1c (HbA1c ) were the primary outcome measures. Glycaemic control and medication adherence parameters were measured at baseline, 3 months, and 6 months in both groups. Medication adherence was measured using the 8-item Morisky Medication Adherence Scale (MMAS-8).
RESULTS: Although the addition of CMI resulted in better glycaemic control, this did not reach statistical significance, possibly because of the short-term follow-up. The median MMAS-8 score improved from baseline (6.6 [IQR = 1.5]) to 6-month follow-up (7.0 [IQR = 1.00]) in the intervention group. In addition, there was a statistically significant difference between the intervention and the control groups in terms of MMAS-8 score at the third visit (7.0 [IQR = 1.0]) vs 6.5 (IQR = 1.25; P-value = .010).
CONCLUSION: CMI for anti-diabetic medications when added to usual care has the potential to improve medication adherence and glycaemic control among patients with type 2 diabetes. Therefore, providing better health communication and CMI to patients with diabetes is recommended.
METHOD: A 12-month single blinded multicenter randomized control trial was designed to investigate the measured variables [Glycated Hemoglobin (HbA1c), Renal function, Albumin Creatinine Ratio (ACR) etc.]. The trial was randomized into 2 experimental parallel arms (ascorbic acid vs acetylsalicylic acid) were blinded with study supplements in combination with metformin and findings were compared to control arm with metformin alone and blinded with placebo. Withdrawal criteria was defined to maintain the equity and balance in the participants in the whole trial.
FINDING: Patients with metformin and ascorbic acid (parallel arm I) was twice more likely to reduce HbA1c than metformin alone (control arm) in a year (OR 2.31 (95% CI 1.87-4.42) p
METHODS: We used data from the KARolinska MAmmography (Karma) project, a Swedish mammography screening cohort. Insulin-treated patients with type 1 (T1D, n = 122) and type 2 (T2D, n = 237) diabetes were identified through linkage with the Prescribed Drug Register and age-matched to 1771 women without diabetes. We assessed associations with treatment duration and insulin glargine use, and we further examined MD differences using non-insulin-treated T2D patients as an active comparator. MD was measured using a fully automated volumetric method, and analyses were adjusted for multiple potential confounders. Associations with the insulin genetic score were assessed in 9437 study participants without diabetes.
RESULTS: Compared with age-matched women without diabetes, insulin-treated T1D patients had greater percent dense (8.7% vs. 11.4%) and absolute dense volumes (59.7 vs. 64.7 cm3), and a smaller absolute nondense volume (615 vs. 491 cm3). Similar associations were observed for insulin-treated T2D, and estimates were not materially different in analyses comparing insulin-treated T2D patients with T2D patients receiving noninsulin glucose-lowering medication. In both T1D and T2D, the magnitude of the association with the absolute dense volume was highest for long-term insulin therapy (≥ 5 years) and the long-acting insulin analog glargine. No consistent evidence of differential associations by insulin treatment duration or type was found for percent dense and absolute nondense volumes. Genetically predicted insulin levels were positively associated with percent dense and absolute dense volumes, but not with the absolute nondense volume (percentage difference [95% CI] per 1-SD increase in insulin genetic score = 0.8 [0.0; 1.6], 0.9 [0.1; 1.8], and 0.1 [- 0.8; 0.9], respectively).
CONCLUSIONS: The consistency in direction of association for insulin treatment and the insulin genetic score with the absolute dense volume suggest a causal influence of long-term increased insulin exposure on mammographic dense breast tissue.
METHODS: A clinically validated insulin/glucose model was used to calculate SI with the standard fasting assumption (SFA) G0 = GTARGET. Then GTARGET was treated as a variable in a second analysis (VGT). The outcomes were contrasted across twelve participants with established type 2 diabetes mellitus that were recruited to take part in a 24-week dietary intervention. Participants underwent three insulin-modified intravenous glucose tolerance tests (IM-IVGTT) at 0, 12, and 24 weeks.
RESULTS: SIVGT had a median value of 3.36×10-4 L·mU-1·min-1 (IQR: 2.30 - 4.95×10-4) and were significantly lower ( P < .05) than the median SISFA (6.38×10-4 L·mU-1·min-1, IQR: 4.87 - 9.39×10-4). The VGT approach generally yielded lower SI values in line with expected participant physiology and more effectively tracked changes in participant state over the 24-week trial. Calculated GTARGET values were significantly lower than G0 values (median GTARGET = 5.48 vs G0 = 7.16 mmol·L-1 P < .001) and were notably higher in individuals with longer term diabetes.
CONCLUSIONS: Typical modeling approaches can overestimate SI when GTARGET does not equal G0. Hence, calculating GTARGET may enable more precise SI measurements in individuals with type 2 diabetes, and could imply a dysfunction in diabetic metabolism.