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Post prandial blood glucose has been linked to diabetic complications like cardiovascular problems. Achieving diet control in diabetic patients remain a significant challenge in our country. The value of good glycemic control by intensified insulin therapy in type 1 diabetes patients has been established by DCCT trial. Subsequent studies confirm that the extent of benefit of tight control also be seen in type 2 patients. In one shady almost half the patients has post prandial values more than 70 mg over fasting values. 1/3 of patients had glucose excursion over 100 mg/dl. Elevated post prandial blood glucose with normal fasting blood glucose can cause complications like retinopathy. Some of the micro and macro vascular complications are seen even before the diagnosis of DM clinically.
Contributing factors for elevated post prandial blood glucose.
1. Unusually high intake of carbohydrate diet.
2. OHA or insulin when given at pre-lunch or pre-breakfast time is not able to bring post
lunch blood sugar but is controlling fasting blood glucose. Any attempt to increase the
dose of medication in such situation results in 5.00 pm hypoglycaemia (Evening
Hypoglycaemia) hence is not the preferred mode of treatment.
3. In these DM especially Type 2 DM meal stimulated insulin secretion seems to be lost.
This occurs even before overt DM develops. Normally after IV Glucose, insulin peaks
within 10 minutes and second phase peaks after 20 minutes. In DM insulin in 1st phase
is absent and second stage secretion is blunted and delayed. Fasting hyperglycaemia
occurs when a loss of approximately 75% in beta cells occur.
Effect of PPBG elevations in DM
Glucose is a potent inducer of oxidative stress and induces free radical oxidation of low
density lilpoprotein. This leads to increased vessel wall atherogenesis. Increased PPBG produces dyslipidemia, activates prothrombotic activity and reduces insulin sensitivity. All these factors lead to chronic complications of DM.
Management
1. Reduce carbohydrate intake at lunch.
2. Nosulin / Glycomanon can be tried before lunch.
3. Metformin 0.5 gm twice before meals can be tried to increase insulin sensitivity.
4. In a person is taking 30/70 mixture of injection Human Mixtard insulin it can be changed
to 50/50 i.e. containing equal parts of short acting and intermediate acting insulin.
5. Use of Lispro : Lispro insulin is a insulin analogue, has proline from position B28 to B29,
thus Lispro hexamers dissociate more readily than regular human insulin hexamers into
monomers. It is indicated for reduction of preprandial and post prandial blood sugar. As
it is a short acting insulin and it has to be used in conjunction with a longer acting
human insulin. It can be taken with meals. It has rapid onset action and shorter duration
of action than regular human insulin.
6. Role of Acarbose : It is a complex oligosaccharide which reversibly inhibited alpha
glucosidase present in brush border of small intestinal rmicosa and hence delays the
production of monosaccharides. Side effects are flatulence, abdominal distension,
borborgymi and diarrhoea. The drug lowers insulin raise in post prandial
hyperglycaemia, no weight gain occurs with the therapy and there is no hypoglycemic
episodes when given as monotherapy. Available as 50 mgm tablets, maximum is 100
mgm/day. If hypoglycaemia occurs when used in combination therapy, glucose to be
used and not sucrose or table sugar.
Conclusion
Persistent post prandial hyperglycaemia in a diabetic is not desirable. It will need to long
term macrovascular and micro vascular complications. Every effort should be made to bring it down tonormal acceptable level. Current modalities of therapy to bring down prandial hyperglycaemia are briefly reviewed.
REFERENCES
1. Sephen P. Clissol, Clive Edward. Acarbose—A pulmonary review of its
pharmacodynamics' and pharmacokinetic properties and therapeutic potentials.
2. Anderson, JH, Brunelle RL, Keohane P., Koivisto VA et. Mealtime treatment with
insulin analogue improves Post Prandial Hyperglycaemia and Hypoglycaemia in
NIDDM patients—Arch Internal Medicine 1997 : 157; 1249 : 1255.
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