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.
METHODS: Genetic analysis was performed in 42 patients with MODY aged 1 month to 18 years among a cohort of 759 patients with diabetes, identified with the following four clinical criteria: age of diagnosis ≤18 years; negative pancreatic autoantibodies; family history of diabetes; or persistently detectable C-peptide; or diabetes associated with extrapancreatic features. GCK gene mutations were first screened by Sanger sequencing. GCK mutation-negative patients were further analyzed by WES.
RESULTS: Mutations were identified in 24 patients: 20 mutations in GCK, 1 in HNF4A, 1 in INS, 1 in ABCC8, and a 17q12 microdeletion. Four previously unpublished novel GCK mutations: c.1108G>C in exon 9, and c.1339C>T, c.1288_1290delCTG, and c.1340_1343delGGGGinsCTGGTCT in exon 10 were detected. WES identified a novel missense mutation c.311A>G in exon 3 in the INS gene, and copy number variation analysis detected a 1.4 Mb microdeletion in the long arm of the chromosome 17q12 region. Compared with mutation-negative subjects, the mutation-positive subjects had lower hemoglobin A1c and initial blood glucose levels.
CONCLUSIONS: Most MODY cases in this study were due to GCK mutations, which is in contrast to previous reports in Chinese patients. Diabetes associated with extrapancreatic features should be a clinical criterion for MODY genetic analysis. Mutational analysis by WES provided a precise diagnosis of MODY subtypes. Moreover, WES can be useful for detecting large deletions in coding regions in addition to point mutations.
METHODS: We randomized 108 overweight and obese patients with T2D (46 M/62F; age 60 ± 10 years; HbA1c 8.07 ± 1.05%; weight 101.4 ± 21.1 kg and BMI 35.2 ± 7.7 kg/m2) into three groups. Group A met with RDN to develop an individualized eating plan. Group B met with RDN and followed a structured meal plan. Group C did similar to group B and received weekly phone support by RDN.
RESULTS: After 16 weeks, all three groups had a significant reduction of their energy intake compared to baseline. HbA1c did not change from baseline in group A, but decreased significantly in groups B (- 0.66%, 95% CI -1.03 to - 0.30) and C (- 0.61%, 95% CI -1.0 to - 0.23) (p value for difference among groups over time
OBJECTIVE: To investigate prevalence and predictors of PREM defined by IDAA1c.
METHODS: Six hundred fourteen of 678 children (aged <15 years) with new-onset T1D (2000-2013) from a regional pediatric diabetes service (Auckland, New Zealand).
RESULTS: Overall rate of PREM at 3 months was 42.4%, and lower in Māori/Pacific children (28.6%; P = .006) and those of other ethnicities (28.8%; P = .030) compared with New Zealand Europeans (50.4%). Comparing the most and least deprived socioeconomic quintiles, the odds of PREM were lower among the most deprived (adjusted odds ratio [aOR] 0.44; P = .019). Lower rates of PREM were seen in children aged 0 to 4.9 years (23.8%) and 10 to 14 years (40.9%) than in children aged 5 to 9.9 years (57.4%; P
MATERIALS AND METHODS: This was an investigator-initiated, single-center, randomized, controlled, clinical trial in patients with T2DM and DKD, comparing 12-weeks of low carbohydrate diet (<20g daily intake) versus standard low protein (0.8g/kg/day) and low salt diet. Patients in the VLCBD group underwent 2-weekly monitoring including their 3-day food diaries. In addition, Dual-energy x-ray absorptiometry (DEXA) was performed to estimate body fat percentages.
RESULTS: The study population (n = 30) had a median age of 57 years old and a BMI of 30.68kg/m2. Both groups showed similar total calorie intake, i.e. 739.33 (IQR288.48) vs 789.92 (IQR522.4) kcal, by the end of the study. The VLCBD group showed significantly lower daily carbohydrate intake 27 (IQR25) g vs 89.33 (IQR77.4) g, p<0.001, significantly higher protein intake per day 44.08 (IQR21.98) g vs 29.63 (IQR16.35) g, p<0.05 and no difference in in daily fat intake. Both groups showed no worsening of serum creatinine at study end, with consistent declines in HbA1c (1.3(1.1) vs 0.7(1.25) %) and fasting blood glucose (1.5(3.37) vs 1.3(5.7) mmol/L). The VLCBD group showed significant reductions in total daily insulin dose (39(22) vs 0 IU, p<0.001), increased LDL-C and HDL-C, decline in IL-6 levels; with contrasting results in the control group. This was associated with significant weight reduction (-4.0(3.9) vs 0.2(4.2) kg, p = <0.001) and improvements in body fat percentages. WC was significantly reduced in the VLCBD group, even after adjustments to age, HbA1c, weight and creatinine changes. Both dietary interventions were well received with no reported adverse events.
CONCLUSION: This study demonstrated that dietary intervention of very low carbohydrate diet in patients with underlying diabetic kidney disease was safe and associated with significant improvements in glycemic control, anthropometric measurements including weight, abdominal adiposity and IL-6. Renal outcomes remained unchanged. These findings would strengthen the importance of this dietary intervention as part of the management of patients with diabetic kidney disease.
MATERIALS AND METHODS: A total of 100 type 2 diabetes participants with stage 3-4 CKD were recruited. Blood for glycated hemoglobin (HbA1c ), serum 25(OH)D, renal and lipid profiles were drawn at enrollment. Correlation and regression analyses were carried out to assess the relationship of serum 25(OH)D, HbA1c and other metabolic traits.
RESULTS: A total of 30, 42, and 28% of participants were in CKD stage 3a, 3b and 4, respectively. The proportions of participants based on ethnicity were 51% Malay, 24% Chinese and 25% Indian. The mean (±SD) age and body mass index were 60.5 ± 9.0 years and 28.3 ± 5.9 kg/m2 , whereas mean HbA1c and serum 25(OH)D were 7.9 ± 1.6% and 37.1 ± 22.2 nmol/L. HbA1c was negatively correlated with serum 25(OH)D (rs = -0.314, P = 0.002), but positively correlated with body mass index (rs = 0.272, P = 0.006) and serum low-density lipoprotein cholesterol (P = 0.006). There was a significant negative correlation between serum 25(OH)D and total daily dose of insulin prescribed (rs = -0.257, P = 0.042). Regression analyses showed that every 10-nmol/L decline in serum 25(OH)D was associated with a 0.2% increase in HbA1c .
CONCLUSIONS: Lower serum 25(OH)D was associated with poorer glycemic control and higher insulin use among multi-ethnic Asians with type 2 diabetes and stage 3-4 CKD.
METHODS: Two reviewers searched MEDLINE for studies of ≥12 weeks duration in adults with type 2 diabetes. The key search word was "gliclazide", filtered with "randomized controlled trial", "human" and "19+ years". Differences were explored in mean change in glycated hemoglobin (HbA(1c)) from baseline (primary outcome) and risk of hypoglycemia (secondary outcome) between gliclazide and other oral insulinotropic agents; and other sulfonylureas.
RESULTS: Nine out of 181 references reported primary outcomes, of which 7 reported secondary outcomes. Gliclazide lowered HbA1c more than other oral insulinotropic agents, with a weighted mean difference of -0.11% (95%, CI -0.19 to -0.03%, P=0.008, I(2)=60%), though not more than other sulfonylureas (-0.12%; 95%, CI -0.25 to 0.01%, P=0.07, I(2)=77%). Risk of hypoglycemia with gliclazide was not different to other insulinotropic agents (RR 0.85; 95%, CI 0.66 to 1.09, P=0.20, I(2)=61%) but significantly lower than other sulfonylureas (RR 0.47; 95%, CI 0.27 to 0.79, P=0.004, I(2)=0%).
CONCLUSION: Compared with other oral insulinotropic agents, gliclazide significantly reduced HbA1c with no difference regarding hypoglycemia risk. Compared with other sulfonylureas, HbA1c reduction with gliclazide was not significantly different, but hypoglycemia risk was significantly lower.