Voglibose in PPHG Dr Mohammed Riyaz MBBS MDMedicinePG Dip Diabetology USA Diploma EndocrinologyUK Master Endocrinology USA Consultant Endocrinologist amp Diabetologist The triad of glucose control in DM ID: 767859
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Voglibose in PPHG Dr. Mohammed RiyazMBBS, MD(Medicine),PG Dip Diabetology (USA), Diploma Endocrinology(UK),Master Endocrinology (USA)Consultant Endocrinologist & Diabetologist
The triad of glucose control in DM Contributors to effective glycaemic control ? Fasting plasma glucose ? Postprandial glucose ?HbA1c?Acute glucose fluctuations ?Sustained chronic hyperglycemia
Dysglycaemia and oxidative stress Activation of oxidative stress with glucose fluctuations increases the risk of associated complicationsIncrease of risk with impaired glucose control and decrease of risk with improved glucose control is as represented by the diagonal arrow in the geometric cube
CV risk in the DM patient Diabetic patients are also seen to have increased subclinical atherosclerosis, increase in carotid intima media thickness with worsening grades of glucose tolerance, and an overall increase in the components of the metabolic syndrome.
The diabetic picture First step in deterioration of glucose homeostasis in DM is the loss of postprandial glucose control.
Fasting , postprandial, and postabsorptive states Real fasting state is only limited to a 3 to 4 hour period of time at the end of night.
Post meal glucose excursions Post meal glucose responses are influenced by the quality and quantity of carbohydrates contained in the meal.
Glycaemic variability and PPHG Looking beyond HbA1c
PPHG: Relation to HbA1c FPG (HbA1c > 7.5%) PPG (HbA1c 6.5% to 7.5%)
PPHG and FPG: The interrelation Gerich JE. Clinical significance, pathogenesis, and management of postprandial hyperglycemia. Arch Intern Med 2003 June 9;163(11):1306-16.
PPHG related complications Oxidative stress and endothelial dysfunction Increased carotid intima media thickness Atherosclerosis, myocardial infarctionStroke, neurologic complicationsRenal failure RetinopathyDerosa G, Maffioli P. Alpha glucosidase inhibitors and their use in clinical practice. Arch Med Sci. 2012; 8(5): 899-906Gerich J. Pathogenesis and management of postprandial hyperglycemia: role of incretin-based therapies. Int J Gen Med. 2013;6:877-95.Ismail TSES, Deshmukh SA. Comparative study of effect of alpha glucosidase inhibitors- miglitol, acarbose, and voglibose on postprandial hyperglycemia and glycosylated hemoglobin in type-2 diabetes mellitus. Int J of Pharma and Bio Sciences. 2012; 3(3):337-343
The Diabetes Intervention Study demonstrated postprandial hyperglycaemia to be a better predictor of subsequent myocardial infarction and mortality than fasting hyperglycaemia. This observation was later confirmed by landmark studies that suggested PPHG to be an independent risk factor for macrovascular diseases. Production of free radicals due to stimulation of oxidative stress is increased during the postprandial period and is proportional to the magnitude of postprandial glucose excursions. Derosa G, Maffioli P. Alpha glucosidase inhibitors and their use in clinical practice. Arch Med Sci. 2012; 8(5): 899-906Hurel SJ, Mohan V. Clinical decision making: managing postprandial hyperglycemia. J Assoc Physicians India. 2006; 54:871-6Monnier L, Collette C. Glycemic variability. Should we and can we prevent it? Diab Care. 2008; 31(2):S150-S154
Importance of PPHG control Emphasis remains on fasting glucose and A1c to guide management of diabetes
In the clinical context PPHG can prove to be a rate-limiting factor in achieving optimal glycemic control.
The diabetic picture in the Indian population India is termed as the diabetic capital of the world
DM in Indians Reasons for an increased propensity
Indian diet and glycaemic variability
Carbohydrates account for 90% of the total variability in blood glucose response
Can we restrict carbohydrates in diet? Low carbohydrate diets are not recommended in the management of diabetes. Avoiding carbohydrates will not return the blood glucose levels to normal. Yes/ No
Management of PPHG IDF recommends PPG goals to not exceed 140 mg/dL. ADA 2015 mentions 2-hour PPG ≥ 200 mg/dL during OGTT to be diagnostic of DM.
Alpha glucosidase inhibitors (AGIs) in PPHG management
AGIs for the Indian patient Why are they better?
AGI - Voglibose in therapy An alpha glucosidase inhibitor. Delays absorption of carbohydrates from the small intestine. About 20 to 30 times more potent than acarbose. Reduces postprandial glucose levels. Suppresses daily glycaemic excursions in NIDDM. Reduces total cholesterol and TGs, and increases HDL-C. Useful first-line treatment in patients with a combination of slightly raised basal glucose concentrations and marked postprandial hyperglycaemia.
Voglibose - Mechanism of action
Voglibose - Place in therapy
Voglibose in IGT Prevented the development of type II DM in patients with IGT.
Voglibose in NIDDM Changes in plasma glucose levels before and after treatment.
Voglibose in DM patients with CV disease
Voglibose effect on lipid profile in patients with DM Reduction in total cholesterol levels. Sustained increase in HDL levelsReduces triglyceride levels Outweighs acarbose in its beneficial effect on lipids.
Voglibose added to insulins
Voglibose in combination with OHAs such as metformin and glimepiride significantly reduces FPG, PPG, and HbA1c. The combination favourably influences lipid levels.
The triple combination of voglibose, glimepiride, metformin Well tolerated and effective in controlling FPG and PPG
Comparative adverse effect profile
New insights in AGIs
Future in DM management Continuous glucose monitoring systems Inhaled insulin