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Development of Steroid induced dysglycemia during the 48 hours of steroid therapy in hospitalized patients; its correlation with the type of steroid.

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Presentation on theme: "Development of Steroid induced dysglycemia during the 48 hours of steroid therapy in hospitalized patients; its correlation with the type of steroid."— Presentation transcript:

1 Development of Steroid induced dysglycemia during the 48 hours of steroid therapy in hospitalized patients; its correlation with the type of steroid used and the presence of risk factors for diabetes. DR. SHIKHA SHARMA, DR APARNA AGRAWAL Department Of General Medicine LHMC & SSK Hospital New Delhi

2 INTRODUCTION Glucocorticoid use leads to hyperglycemia. 1 Mechanism
>Decreases insulin synthesis >Increases insulin resistance2 >Glucose uptake and glucose storage in muscles, stored as glycogen3,4 >Increased lipolysis and proteolysis5 >Permissive effects upon hormones like catecholamines and glucagon

3 DEFINITION AND INCIDENCE
FBG level of ≥ 126 mg/dL, glycaemia at any time ≥ 200 mg/dL, glycated hemoglobin ≥ 6.5% or blood glucose ≥ 200 mg/dL two hours after an oral glucose load with classic signs and symptoms of hyperglycemia.6 Incidence of steroid induced hyperglycemia= 34-68%7,8 Incidence of steroid induced diabetes mellitus=1.6-64%8,9

4 AIMS AND OBJECTIVES To study the changes in blood glucose levels between 6-48 hours of starting corticosteroid therapy. To study the various factors associated with steroid induced hyperglycemia with special reference to the :- -Nature of the corticosteroid used. -Presence of risk factors for diabetes.

5 INCLUSION CRITERION Age≥ 18years to be started on oral or parenteral steroid therapy irrespective of their underlying disease and comorbid illness.

6 EXCLUSION CRITERION Pregnant or lactating woman. Known diabetic
RBG≥200 mg/dl prior to steroid therapy. Presteroid RBG mg/dl with Hba1c ≥6.5% Patients on oral/parenteral steroid in the last 4 weeks. Patients on dextrose containing iv drips Non consenting patients. Note-Patient already on inhaled and/or topical corticosteroids will not be excluded from the study

7 METHODOLOGY Hundred in-patients to be started on oral/parenteral steroids. Evaluation of risk factor for diabetes > Age > BMI {overweight = kg/m2, obese ≥30kg/m2} > Waist circumference{Men=90cm, Women=80cm} > Hypertension{BP ≥140/90 mmHg} > Dyslipidemia.{Total cholesterol ≥200mg/dl or Triglycerides ≥150mg/dl}

8 METHODOLOGY EXCLUDED STUDY POPULATION
Patients to be started on steroid therapy Not a known diabetic Known diabetics Meeting other exclusion criterias RBG <140mg/dl EXCLUDED ≥200mg/dl Hba1c STUDY POPULATION ≥6.5% <6.5%

9 STUDY POPULATION Start steroids RBS at 6,12,24 and 48 hours
Consent Start steroids RBS at 6,12,24 and 48 hours Lipid profile

10 OBSERVATIONS AND RESULTS
DEMOGRAPHY

11 DYSGLYCEMIA

12 p=0.001

13 ≥60 mg/dl rise in blood glucose value after 48 hours of steroid therapy with regard to steroid used
hydrocortisone (N=54) dexamethasone (N=32) prednisolone (N=14) Number of patients 19(35.18%) 3(9%)

14 RISK FACTORS TOTAL(N) N=100 DYSGLYCEMIA N=70 IGT N=48 SDM N=22 P value Age≥50years 43 41(95.3%) 24(55.8%) 17(39.5%) 0.001 BMI≥23kg/m2 20 20(100%) 14(70%) 6(30%) 0.005 HTN 14 14(100%) 8(57.1%) 6(42.9%) 0.015 WC≥90cm (in males) ≥80cm (in females) 25 25(100%) 15(60%) 10(40%) Dyslipidemia 33 28(84.8%) 14(42.4%)

15 Number of risk factors and dysglycemia
No of risk factors Normoglycemia(%) Dysglycemia(%) SDM(%) 75 25 1 18.5 81.5 11.1 2 4 96 44 3 100 83.3 33.3 5 p=0.001

16 CONCLUSION Steroid induced dysglycemia was observed in 70% of the patients within 48 hours of therapy. Patients receiving parenteral hydrocortisone are more likely to develop dysglycemia which is also more severe compared to parenteral dexamethasone and oral prednisolone. Older age, presence of hypertension, dyslipidemia and presence of central or generalised obesity increases the risk of development of steroid induced hyperglycemia. The risk further increases with increasing number of risk factors. Thus, it becomes imperative to monitor blood sugar for patients starting on steroid therapy.

17 REFERNCES 1)Clore JN, Thurby-Hay L: Glucocorticoid-induced hyperglycemia.Endocr Pract 15: 469–474, 2009;15: ) Strohmayer EA, Krakoff L.R.Glucocorticoids and cardiovascular risk factors.Endocrinol Metab Clin North Am. 2011;40: , ix. 3)Perez A, Jansen-Chaparro S, Saigi L, Bernal-Lopez MR, Minambres L, Gomez-Huelgas R_Glucocorticoid induced hyperglycemiaJ Diabetes.2014;6: )Ruzzin J, Wagman AS, Jensen J. Glucocorticoid induced insulin resistance in skeletal muscles: defects in insulin signaling and the effects of a selective glycogen synthase-kinase-3 inhibitor. Diabetologia. 2005;48: ) Van Raalte DH, Ouwens DM, Diamant M. Novel insights into glucocorticoid mediated diabetogenic effects:towards expansion of therapeutic options? Eur J Clin Invest.2009;39:81-93.

18 6)Diagnosis and classification of diabetes mellitus. Diabetes Care
6)Diagnosis and classification of diabetes mellitus. Diabetes Care. 2012;35(Suppl 1): S64–71. 7)Ito S, Ogishima H, Kondo Y, Sugihara M, Hayashi T, Chino Y et al. Early diagnosis and treatment of steroid-induced diabetes mellitus in patients with rheumatoid arthritis and other connective tissue diseases. Mod Rheumatol Jan;24(1):52-59 8)Donihi AC, Raval D, Saul M, Korytkowski MT, DeVita MA. Prevalence a nd  predictors  of corticosteroid related  hyperglycemia  in  hospitalized  patients.  Endocr Pract.  2006;1 2:358–362. 9)Papang R, John AS, Abhraham S, Rao PSSS. A study of steroid-induced diabetes mellitus in leprosy. Indian J Lepr. 2009; 81:

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