Background: Till date, there is no Cochrane meta-analysis available which has analyzed efficacy and safety of tirzepatide in type-2 diabetes. This meta-analysis was undertaken to address this knowledge gap. Methods: Electronic databases were searched for randomized controlled trials (RCTs) involving people with diabetes receiving tirzepatide compared to a placebo/active comparator. Primary outcome was to evaluate changes in HbA1c. Secondary outcomes were to evaluate alterations in blood–glucose, glycemic targets, weight, lipids, and adverse events. Results: From 34 articles initially screened, data from six RCTs involving 3484 patients were analyzed. Over 12–52 weeks, individuals receiving tirzepatide had significantly greater lowering of HbA1c [mean difference (MD) = -0.75% (95% confidence interval (CI): -1.05 to -0.45); P < 0.01; I 2 = 100%], fasting glucose [MD = -0.75 mmol/L (95% CI: -1.05 to– -0.45); P < 0.01; I 2 = 100%], 2-h post-prandial-glucose [MD = -0.87 mmol/L (95% CI: -1.12 to -0.61); P < 0.01; I 2 = 99%], weight [MD = -8.63 kg (95% CI: -12.89 to -4.36); P < 0.01; I 2 = 100%], body mass index [MD = -1.80 kg/m 2 (95% CI: -2.39 to -1.21); P < 0.01; I 2 = 99%], and waist circumference [MD = -4.43 cm (95% CI: -5.31 to -3.55); P < 0.01; I 2 = 95%] as compared to dulaglutide, semaglutide, degludec, or glargine. Patients receiving tirzepatide had higher odds of achieving HbA1c <6.5% compared to active controls [odds ratio (OR) = 4.39 (95% CI: 2.44–7.92); P < 0.01; I 2 = 90%]. Tirzepatide use had significantly higher odds of weight loss >5% [OR = 19.18 (95% CI: 2.34–157.17); P < 0.01; I 2 = 99%], >10% [OR = 21.40 (95% CI: 2.36–193.94); P < 0.01; I 2 = 98%], and >15% [OR = 32.84 (95% CI: 2.27–474.33); P = 0.01; I 2 = 96%] compared to active-control group. Treatment-emergent adverse events [risk ratio (RR) = 1.43 (95% CI: 1.14–1.80); P < 0.01; I 2 = 40%] and severe adverse events [RR = 1.00 (95% CI: 0.64–1.57); P = 1.00; I 2 = 49%] were not different. High data heterogeneity and the presence of publication bias limits the grading of current data from “moderate to low.” Conclusion: ...

Background No meta-analysis has holistically analysed and summarised the efficacy and safety of gemigliptin in type 2 diabetes. The meta-analysis addresses this knowledge gap. Methods Electronic databases were searched for randomised controlled trials (RCTs) involving diabetes patients receiving gemigliptin in the intervention arm and placebo/active comparator in the control arm. The primary outcome was change in haemoglobin A1c (HbA1c). The secondary outcomes were alterations in glucose, glycaemic targets, lipids, insulin resistance, and adverse events. Results Data from 10 RCTs involving 1,792 patients were analysed. Four had an active control group (ACG), with metformin/dapagliflozin/sitagliptin/glimepiride as the active comparator; six had a passive control group (PCG), with placebo/rosuvastatin as controls. HbA1c reduction by gemigliptin at 24 weeks was comparable to ACG (mean difference [MD], 0.09%; 95% confidence interval [CI], −0.06 to 0.23; P =0.24; I 2 =0%; moderate certainty of evidence [MCE]), but superior to PCG (MD, −0.91%; 95% CI, −1.18 to −0.63); P <0.01; I 2 =89%; high certainty of evidence [HCE]). Gemigliptin was superior to PCG regarding achieving HbA1c <7% (12 weeks: odds ratio [OR], 5.91; 95% CI, 1.34 to 26.08; P =0.02; I 2 =74%; 24 weeks: OR, 4.48; 95% CI, 2.09 to 9.60; P <0.01; I 2 =69%; HCE). Gemigliptin was comparable to ACG regarding achieving HbA1c <7% after 24 weeks (OR, 0.92; 95% CI, 0.52 to 1.63; P =0.77; I 2 =66%; MCE). Adverse events were similar between the gemigliptin and control groups (risk ratio [RR], 1.06; 95% CI, 0.82 to 1.36; P =0.66; I 2 =35%; HCE). The gemigliptin group did not have increased hypoglycaemia (RR, 1.19; 95% CI, 0.62 to 2.28; P =0.61; I 2 =19%; HCE). Conclusion Gemigliptin has good glycaemic efficacy and is well-tolerated over 6 months of use.

Men with decreased skeletal mass, age, severe immune dysfunction at diagnosis, having rapid increase in CD4 count following ART and IRIS have higher risk of osteoporosis in the long run.

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Screening of two sites (knee and 1st MTP) has similar sensitivity, specificity, PPV, NPV and positive LR as compared to six sites in diagnosing gout.

The current classification of both diabetes and antidiabetes medication is complex, preventing a treating physician from choosing the most appropriate treatment for an individual patient, sometimes resulting in patient-drug mismatch. We propose a novel, simple systematic classification of drugs, based on their effect on adenosine monophosphate-activated protein kinase (AMPK). AMPK is the master regular of energy metabolism, an energy sensor, activated when cellular energy levels are low, resulting in activation of catabolic process, and inactivation of anabolic process, having a beneficial effect on glycemia in diabetes. This listing of drugs makes it easier for students and practitioners to analyze drug profiles and match them with patient requirements. It also facilitates choice of rational combinations, with complementary modes of action. Drugs are classified as stimulators, inhibitors, mixed action, possible action, and no action on AMPK activity. Metformin and glitazones are pure stimulators of AMPK. Incretin-based therapies have a mixed action on AMPK. Sulfonylureas either inhibit AMPK or have no effect on AMPK. Glycemic efficacy of alpha-glucosidase inhibitors, sodium glucose co-transporter-2 inhibitor, colesevelam, and bromocriptine may also involve AMPK activation, which warrants further evaluation. Berberine, salicylates, and resveratrol are newer promising agents in the management of diabetes, having well-documented evidence of AMPK stimulation medicated glycemic efficacy. Hence, AMPK-based classification of antidiabetes medications provides a holistic unifying understanding of pharmacotherapy in diabetes. This classification is flexible with a scope for inclusion of promising agents of future.

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