Risk of hyperglycemia from glucocorticoids

A 65 year old patient with COPD sees his primary care provider for worsening shortness of breath over the past week.  His current medications include tiotropium and albuterol.  He has no other significant past medical history but has a family history of diabetes.  His current labs include a fasting plasma glucose of 96 mg/dL, HbA1c of 6.1%, Scr = 0.8 mg/dL.  His primary care provider determines that the patient is having a COPD exacerbation and is opting to initiate a 5 day course of prednisone 40 mg orally daily (click here for more on a 5 days course versus longer steroid courses for COPD exacerbations).  What are some of the risk factors, the time-course, and the mechanism for developing hyperglycemia in a situation like this?

Converting systemic corticosteroids

Let’s start with a patient case.  A patient is being treated with methylprednisolone 20 mg IV q6 hours for some inflammatory process and is clinically improving.  She can now tolerate oral medication and we would like to simplify her dosing regimen to transition to outpatient care. How can we manage her methylprednisolone dosing?

One issue that comes up frequently on the internal medicine service is the potency of different corticosteroids relative to each other and the correct way to convert the doses. Below is the chart that shows the equivalent dose of the various agents we commonly use.

Update on steroid recommendations for COPD exacerbations

Let’s start with a patient case.  An elderly patient is admitted through the emergency department with markedly worsening dyspnea and purulent sputum production over the last three days.  When reviewing his history, you find that he has GOLD grade 4 (very severe) COPD and experiences roughly one exacerbation per year that requires hospitalization.  His home medications for COPD include tiotropium (Spiriva) 18 mcg/inhalation once daily, albuterol MDI (Proventil HFA, ProAir HFA, or Ventolin HFA) 90 mcg/inhalation 2 inhalations every 4-6 hours as needed for dyspnea, and fluticasone/salmeterol (Advair Diskus) 250/50 mcg inhaled twice daily.  You are now deciding what steroid regimen should be initiated to manage this exacerbation.

Use of dexamethasone for vasogenic edema

Vasogenic edema is a result of a disruption of the blood brain barrier that is frequently related to tumors.  The edema can lead to increased intracranial pressure in addition to tissue shifts and brain displacement.  Injury can occur not only from this mechanical shift but also from decreased perfusion that is associated with elevated intracranial pressure.

Dexamethasone is a potent, long-acting glucocorticoid which has no inherent mineralocorticoid activity.  Glucocorticoids have a number of mechanisms for how they reduce inflammation in the body including reduction in lymphocytes, monocytes, basophils, and eosinophils (neutrophils decrease at the site of inflammation but increase in the blood); suppression of the arachadonic acid cascade by inhibiting phospholipase A2 which reduces prostaglandins and leukotrienes; inhibition of other antigen presenting cells; vasoconstriction and decreased capillary permeability; and at large doses, reduced production of antibodies.