METHODS: A cross-sectional investigation was conducted at General Penang Hospital, Malaysia. Demographic criteria and laboratory tests of patients were investigated. Controlled glycemia (CG) was recognized as glycated hemoglobin (HbA1c) ≤7% depending on American Diabetes Association guidelines 2018. Charlson Comorbidity Index (CCI) was used to estimate the confounding influence of co-morbidities and predict ES-10Y. Data was managed by IBM-SPSS 23.0.
RESULTS: A total of 400 cases categorized to (44.25%) patients with CG, and (55.75%) cases had uncontrolled glycemia (UCG). HbA1c mean in CG and UCG group was (6.8 ± 0.9 vs 9.5 ± 1.6, P-value: 0.001). Fasting blood glucose was (7 ± 2.3 vs. 9.9 ± 4.3, P-value: 0.001) in CG and UCG group. CCI was (3.38 ± 2.38 vs. 4.42 ± 2.70, P-value: 0.001) and, ES-10Y was (62% vs 46.2%, p-value: 0.001) in CG vs. UCG respectively. Spearman test indicates a negative correlation between CG and CCI (r: 0.19, p-value: 0.001). Logistic regression confirmed HbA1c as a significant predictor of CCI (r2: 0.036, P-value: 0.001). CG has a positive correlation with survival (r: 0.16, P-value: 0.001) and logistic regression of survival (r2: 0.26, P-value: 0.001).
CONCLUSIONS: More than one-half of the investigated persons had UCG. Controlled HbA1c was associated with lower co-morbidities and higher ES-10Y.
Methodology: A 12-week prospective, non-controlled, interventional study in suboptimal-controlled T2DM patients with DFU was conducted. Antidiabetic medications were adjusted with the aim of at least 1% in relation to patient's individualised HbA1c target. The wound area was determined by using specific wound tracing. The daily wound area healing rate in cm2 per day was calculated as the difference between wound area at first visit and the subsequent visit divided by the number of days between the two visits.
Results: 19 patients were included in the study. There was a significant HbA1c reduction from 10.33 %+1.83% to 6.89%+1.4% (p<0.001) with no severe hypoglycaemia. The median daily wound area healing rate was 0.234 (0.025,0.453) cm2/day. There was a strong positive correlation between these two variables (r=0.752, p=0.01). After dividing the patients into four quartiles based on final HbA1c and comparing the first quartile vs fourth quartile, there was a significant difference in daily wound area healing rates (0.597 vs 0.044 cm2/day, p=0.012).
Conclusion: There was a positive correlation between HbA1c reduction and wound healing rate in patients with DFU. Although this is an association study, the study postulated the benefits of achieving lower HbA1c on wound healing rate in DFU which require evidence from future randomised controlled studies.
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.
Methodology: This sub-analysis included Filipino patients with T1DM or T2DM, aged 18 years and older, treated with insulin for more than 12 months, who completed the two-part self-assessment questionnaires (SAQ1 and SAQ2) and patient diaries that recorded hypoglycemia during retrospective (6 months/4 weeks before baseline) and prospective period (4 weeks after baseline) (ClinicalTrials.gov number: NCT02306681).
Results: A total of 671 patients were enrolled and completed the SAQ1 (62 patients with T1DM and 609 patients with T2DM). Almost all patients (100% in T1DM and 99.3% in T2DM) experienced at least 1 hypoglycemic event prospectively. The incidence of any hypoglycemia was also high in the prospective period compared to retrospective period (72.6 [95% CI: 64.8, 80.9] events PPY and 43.6 [95% CI: 37.8, 49.9] events PPY; p=0.001, respectively) in T1DM patients.
Conclusion: Among insulin-treated patients, higher rates of hypoglycemia were reported prospectively than retrospectively. This indicates that the patients in real-life setting often under-report hypoglycemia. Patient education can help in accurate reporting and appropriate management of hypoglycemia and diabetes.
MATERIALS AND METHODS: We pooled data from 17 observational studies involving 1,699 patients treated with either CSII or non-CSII (including premixed and MDI) regimen. The study outcomes were the frequencies of hypoglycemia, hyperglycemia and/or ketosis. Given the lack of patient-level data, separate analyses for premixed and MDI regimen were not carried out.
RESULTS: The CSII-treated group (n = 203) was older (22.9 ± 6.9 vs 17.8 ± 4.0 years), and had longer diabetes duration (116.7 ± 66.5 vs 74.8 ± 59.2 months) and lower glycated hemoglobin (7.8 ± 1.1% vs 9.1 ± 2.0%) at baseline than the non-CSII-treated group (n = 1,496). The non-CSII-treated group had less non-severe hypoglycemia than the CSII-treated group (22%, 95% CI 13-34 vs 35%, 95% CI 17-55). Of the non-CSII-treated group, 7.1% (95% CI 5.8-8.5) developed severe hypoglycemia, but none from the CSII-treated group did. The non-CSII-treated group was more likely to develop hyperglycemia (12%, 95% CI 3-25 vs 8.8%, 95% CI 0-31) and ketosis (2.5%, 95% CI 1.0-4.6 vs 1.6%, 95% CI 0.1-4.7), and discontinue fasting (55%, 95% CI 34-76 vs 31%, 95% CI 9-60) than the CSII-treated group.
CONCLUSIONS: The CSII regimen had lower rates of severe hypoglycemia and hyperglycemia/ketosis, but a higher rate of non-severe hyperglycemia than premixed/MDI regimens. These suggest that appropriate patient selection with regular, supervised fine-tuning of the basal insulin rate with intensive glucose monitoring might mitigate the residual hypoglycemia risk during Ramadan.
AIMS OF STUDY: The aim of the present study is to evaluate the repeated dose toxicity of the standardized aqueous extract administered daily for 30 days through oral administration at its effective hypoglycemia doses.
MATERIALS AND METHODS: The seeds were dried, ground and extracted in deionized water. A HPLC-photodiode array method was developed and validated for the standardization of both the hypoglycemia agents, namely bruceine D and E in aqueous extract. Both normoglycemia and streptozotocin (STZ)-induced diabetic rats were fed orally with 15, 30 and 60mg/kg body weight of standardized aqueous extract. The blood glucose was measured at 0-8h. In repeated dose toxicity, similar doses were administered orally to rats for 30 days. At the end of 30 days, the blood was withdrawn and subjected to biochemical and haematology analysis while organs were harvested for histology analysis.
RESULTS: Oral administration of standardized aqueous extract exhibited a dose-response relationship in both the normoglycemia and STZ-induced diabetic rats. Daily oral administration of 15, 30 and 60mg/kg standardized aqueous extract for 30 days to rats did not show signs to toxicity in its biochemical, haematology and histology analysis.
CONCLUSION: In conclusion, although the seeds were reported to contain compounds with various pharmacological activity, the daily oral administration to rats for 30 days do not showed signs of toxicity at its effective hypoglycemia doses.