Quick Reference For the Most Common Symptoms of Adrenal Hormone Replacement Excess and Deficiency
Most common symptoms of:
glucocorticoid (cortisol) deficiency |
Severe fatigue, weakness, weight loss, hyperpigmentation, nausea, loss of appetite. |
glucocorticoid (cortisol) excess |
Weight gain, fatigue, easy bruising, muscle weakness, redness in the face, pink stretch marks, mood swings, inappropriate hunger. |
mineralocorticoid (fludrocortisone acetate) deficiency |
Reduced blood pressure, nausea (sometimes to the point of vomiting), dizziness (sometimes to the point of passing out), salt craving, muscle cramps. |
mineralocorticoid (fludrocortisone acetate) excess |
Hypertension, ankle swelling, exertion headache. |
Reference: Paul Margulies, MD, FACE, FACP, Medical Director, NADF (updated 2-20-2020) Click here for a PDF of this chart.
Corticosteroid Comparison Chart
Potency relative to Hydrocortisone | Half-Life | ||||
Equivalent Glucocorticoid Dose (mg) | Anti-Inflammatory | Mineral-Corticoid | Plasma(minutes) | Duration of Action (hours) |
|
Short Acting | |||||
Hydrocortisone (Cortef, Cortisol) |
20 | 1 | 1 | 90 | 8-12 |
Cortisone Acetate | 25 | 0.8 | 0.8 | 30 | 8-12 |
Intermediate Acting | |||||
Prednisone | 5 | 4 | 0.8 | 60 | 12-36 |
Prednisolone | 5 | 4 | 0.8 | 200 | 12-36 |
Triamcinolone | 4 | 5 | 0 | 300 | 12-36 |
Methylprednisolone | 4 | 5 | 0.5 | 180 | 12-36 |
Long Acting | |||||
Dexamethasone | 0.75 | 30 | 0 | 200 | 36-54 |
Betamethasone | .6 | 30 | 0 | 300 | 36-54 |
Mineralocorticoid | |||||
Fludrocortisone | 0 | 15 | 150 | 240 | 24-36 |
Aldosterone | 0 | 0 | 400 + | 20 | – – |
Reference: Adrenal Cortical Steroids. In Drug Facts and Comparisons. 5th ed. St. Louis, Facts and Comparisons, Inc.:122-128, 1997 |
Commonly Prescribed Replacement Steroid Equivalents
Prednisone | Cortisone | Dexamethasone | Hydrocortisone (Cortef) | |||
5 mg | = | 25 mg | = | 0.75 mg | = | 20 mg |
The Hypothalamic-Pituitary-Adrenal Connection
A defect at any point along the hypothalamic-pituitary-adrenal (HPA)-axis could disrupt normal physiologic glucocorticoid levels. Administration of exogenous glucocorticoids leads to suppression of cortisol production by the adrenal cortex.
HPA-axis suppression is a well-known adverse effect of glucocorticoid therapy; however, considerable controversy exists over the dose and duration of glucocorticoid therapy required to suppress the HPA-axis.
Some of the many factors that influence HPA-axis suppression include time of day that the doses are administered, route of administration, dose and duration of therapy, and duration of action of the agent used.
Reference: Helfer EL, Rose LI. Corticosteroids and adrenal suppression: characterizing and avoiding the problem. Drugs. 1989;38(5):838-845
HPA-axis suppression is a well-known adverse effect of glucocorticoid therapy; however, considerable controversy exists over the dose and duration of glucocorticoid therapy required to suppress the HPA-axis.
Some of the many factors that influence HPA-axis suppression include time of day that the doses are administered, route of administration, dose and duration of therapy, and duration of action of the agent used.
Reference: Helfer EL, Rose LI. Corticosteroids and adrenal suppression: characterizing and avoiding the problem. Drugs. 1989;38(5):838-845
Normal Cortisol Secretion
Hormone production by the adrenal gland is influenced by many factors. Normal cortisol production follows a diurnal cycle. Levels peak in the early morning hours (6 am–8 am) and decline throughout the day with a second, lower peak in the late afternoon (4 pm–6 pm).
In an adult who is not experiencing stress, the average amount of cortisol secreted by the adrenal gland is equivalent to 5 mg of prednisone.
Reference: Katzung BG. Basic and Clinical Pharmacology. 6th ed. East Norwalk: Appleton & Lange;1995:590-607
In an adult who is not experiencing stress, the average amount of cortisol secreted by the adrenal gland is equivalent to 5 mg of prednisone.
Reference: Katzung BG. Basic and Clinical Pharmacology. 6th ed. East Norwalk: Appleton & Lange;1995:590-607