STEROIDS & DIABETES by sSO47VQ4

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									STEROIDS & DIABETES




     Michael M. Barsotti, M.D.
       What is the prevalence of SDM ?

   What is the best way to screen for SDM ?

 What is the typical pattern of hyperglycemia in
these patients-how should they be monitored ?

   What is the best strategy to treat SDM ?
                  GLUCOCORTICOIDS:
                  Insulin antagonistic hormones


• Liver: promote gluconeogenesis
• Muscle & adipose tissue: antagonize uptake and utilization of
  insulin
• Pancreas: inhibitory effect on insulin release and stimulation of
  glucagon secretion
      Normal Beta-cell Reserve




Basal and stimulated hyperinsulinemia
(insulin resistance) resulting in none or
minimal glucose intolerance
         Impaired Beta-cell Reserve



•   Impaired glucose tolerance
•   Overt diabetes
•   Marked hyperglycemia
•   DKA and NHH
        TYPICAL PATTERN OF SDM



• Elevated glucose after meals

• Decrease to normal glucose overnight
Clinical consequences of hyperglycemia:
    increased morbidity and mortality


•   Post Cardiac Surgery (Furnary)
•   Surgical & Medical ICU (Van den Berghe)
•   Solid Organ Transplant (Duclos)
•   Myocardial Infarction (Malmberg)
•   Acute Lymphocytic Leukemia (Weisers)
•   General Medical Ward (Umpierrez)
    Prevalence of Steroid Diabetes in
          Hospitalized Patients



• 50% or more of patients

• Less than half of these patients will have
  had a history of diabetes


                        • Endocr Pract. 2006:12:358-362
         Diagnosing Steroid Diabetes

25 patients with neurological disease treated with 30-60mg
  of prednisolone orally after breakfast for 2 weeks

No prior history of DM, family history of DM, or medications
  that might affect blood sugar (thiazides, B-blockers, etc.)




                            Pharmacotherapy 2004;24(4):508-514
                NORMAL       IMPAIRED          SDM*        SENSITIVITY


AC BREAKFAST          24           1             0               0%

PC BREAKFAST          17            4            4           30.8%

PC LUNCH              2             10           13         100.0%

PC DINNER             7                7         10          76.9%




            *Fasting > or = 126 mg/dl; Random > or = 200 mg/dl
    COMORBIDITIES ASSOCIATED WITH
          HYPERGLYCEMIA


•   Pre-existing diabetes
•   Family Hx of diabetes
•   Age
•   Obesity
•   Long-term corticosteroid use
             Oral Diabetes Medications

• In general minimal benefits

• Long acting agents like glyburide and glimiperide will have minimal
  effect on post prandial hyperglycemia and increase risk of fasting
  hypoglycemia.

• The use of repaglinide, nateglimide, acarbose, precose, TZDs, and
  metformin all make physiological sense but in clinical practice often
  are ineffective.

• Incretins (?)
                             INSULIN

• Most effective
• Peak action of the insulin needs to correspond to the post absorptive
  state - the primary affect of steroids is on glucose disposal following
  the meal.
    – Rapid acting analog insulin before the meals
    – AM: R/NPH Supper: R
    – Insulin resistance: ICR often < 1:5
• Cautious use of long acting insulin
    – Ratio prandial:basal 70:30
                 CHALLENGES

• Steroid dosing
  –   AM
  –   Multiple daily doses
  –   Potency (prednisone, dexamethasone)
  –   Alternate day dosing
  –   Tapering
• Meal schedule
  – Variable time
  – Variable amounts
  – Omitting meals

								
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