Glucocorticoids

Summary

drug class: Glucocorticoids

generic and trade names:
• Hydrocortisone
• Methylprednisolone
• Prednisone
• Dexamethasone (long acting)

Not: See also Corticosteroids.

type of drug: Anti-inflammatory.

overview of interactions:
• nutrient affected by drug: Vitamin D

• substance affecting drug performance: Aluminum-containing Antacids

• nutrient affected by drug: Calcium

• nutrient affected by drug: Potassium

• nutrient affected by drug: Selenium


Interactions

nutrient affected by drug: Vitamin D

• mechanism: Glucocorticoid drugs may decrease vitamin D availability and lower serum 25-hydrosycalciferol levels.
(Hodges R. 1980:323-331; Hahn TJ, et al. N Engl J Med. 1972 Nov 2;287(18):900-904.)

• nutritional support: Most research supports the benefit of taking daily supplemental doses of 500 IU of vitamin D. Individuals using glucorticoids for an extended period of time might consult with their prescribing physician about laboratory testing of levels of 1,25 dihydroxycholecalciferol, the activated form of vitamin D. If a deficiency is discovered, activated vitamin D can be obtained by prescription as "calcitriol."

substance affecting drug performance: Aluminum-containing Antacids

• mechanism: Aluminum-containing antacids reduce the bioavailability of glucocorticoids.
(Roe DA. 1989:84.)

• nutritional concern: Individuals taking glucocorticoids should avoid the use of antacids, especially within two hours of taking the medication.

nutrient affected by drug: Calcium

• mechanism: Glucocorticoid drugs may lower serum calcium by reducing its absorption. The long-term use of glucocorticoid drugs frequently results in the development of osteoporosis.
(Roe DA. 1985:163-164.)

• research: Reid and Ibbertson studied the metabolic effects of administering 1 g of elemental calcium/day upon 13 steroid-treated patients. After 2 months, they concluded that calcium supplementation suppresses bone resorption without detectable suppression of indices of bone formation and was, therefore, likely to result in increased bone mass.
(Reid IR, Ibbertson HK. Am J Clin Nutr. 1986 Aug;44(2):287-290.)

• nutritional support: Individuals taking glucocorticoid medications for extended periods of time would most likely be able to prevent steroid-induced osteoporosis through supplementation with 1,000 mg calcium per day.

nutrient affected by drug: Potassium

• mechanism: Hypokalemia may occur during prolonged, high-dosage corticosteroid therapy. Steroidal anti-inflammatory drugs cause increased loss of potassium through the urine. Though widely observed, it remains unclear as to whether this is clinically significant.
(Thorn GW. N Engl J Med. 1966 274:775; Thelkeld DS, ed. Apr 1991; Pronsky, Z. 1991, 60.)

• nutritional support: Supplemental potassium may be necessary in some patients. However, increasing the daily consumption of fruit can be the most effective way to obtain the potassium supplementation needed to make up for depletion due to glucocorticoid drugs. In fact, the levels of potassium available through fruit will usually exceed those found in most potassium supplements since they cannot legally exceed 99 mg each.

nutrient affected by drug: Selenium

• mechanism: Glucocorticoid drugs may lower plasma selenium levels.
(Peretz A, et al. Semin Arthritis Rheum. 1991 Apr;20(5):305-316; Peretz A, et al. J Rheumatol. 1987 Dec;14(6):1104-1107.)

• research: Peretz et al studied the plasma selenium levels, erythrocyte selenium levels and activity of the selenoenzyme glutathione peroxidase in erythrocytes of patients with rheumatoid arthritis (RA) and acute inflammatory arthritis. They determined that corticosteroid treatment, particularly at high doses (20-60 mg prednisolone/day), was significantly related to the depressed plasma selenium levels of some patients with RA.
(Peretz A, et al. J Rheumatol. 1987 Dec;14(6):1104-1107.)

• nutritional support: Individuals taking glucocorticoid medications should consult their prescribing physician and/or a healthcare provider trained in nutritional therapies about the potential benefits of supplementing with selenium. Typical therapeutic dosages of selenium are in the range of 100-200 mcg per day.

Please read the disclaimer concerning the intent and limitations of the information provided here.
Do not rely solely on the information in this article.

The information presented in Interactions is for informational and educational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, case reports, and/or traditional usage with sources as cited in each topic. The results reported may not necessarily occur in all individuals and different individuals with the same medical conditions with the same symptoms will often require differing treatments. For many of the conditions discussed, treatment with conventional medical therapies, including prescription drugs or over-the-counter medications, is also available. Consult your physician, an appropriately trained healthcare practitioner, and/or pharmacist for any health concern or medical problem before using any herbal products or nutritional supplements or before making any changes in prescribed medications and/or before attempting to independently treat a medical condition using supplements, herbs, remedies, or other forms of self-care.


References

Hahn TJ, Hendin BA, Scharp CR, Haddad JG Jr. Effect of chronic anticonvulsant therapy on serum 25-hydroxycalciferol levels in adults. N Engl J Med. 1972 Nov 2;287(18):900-904.

Hodges R. Drug-nutrient interaction, In: Nutrition in Medical Practice. Philadelphia: W.B. Saunders, 1980:323-331.

Peretz A, Neve J, Famaey J. Selenium in rheumatic diseases. Semin Arthritis Rheum. 1991 Apr;20(5):305-316. (Review)
Abstract: Selenium is involved in several important biochemical pathways relevant to rheumatic diseases. Experimental and clinical studies suggest that selenium modulates the inflammatory and immune responses. Patients suffering from inflammatory rheumatic diseases often have low selenium levels, but this finding does not correlate with disease severity. Selenium supplementation needs stricter selection criteria and better ascertainment of dose to obtain a stimulatory or inhibitory effect relevant to the disease state. Prevention of marginal selenium deficiency by moderate supplementation might enhance host defense mechanisms.

Peretz A, Neve J, Vertongen F, Famaey JP, Molle L. Selenium status in relation to clinical variables and corticosteroid treatment in rheumatoid arthritis. J Rheumatol. 1987 Dec;14(6):1104-1107.
Abstract: Plasma selenium levels, erythrocyte selenium levels and activity of the selenoenzyme glutathione peroxidase in erythrocytes were determined in patients with rheumatoid arthritis (RA) and acute inflammatory arthritis. Results were compared with those from age and sex matched controls. These variables were not statistically different from controls in patients with inflammatory arthritis and in patients with RA not treated with corticosteroids. No correlation was found in RA between plasma selenium biological variables of inflammation and most clinical indices of disease severity. Therefore, acute or chronic inflammation was not the main factor that accounted for low plasma selenium levels in RA. Corticosteroid treatment, particularly at high doses (20-60 mg prednisolone/day), was significantly related to the depressed plasma selenium levels of some patients with RA. The mechanisms underlying this modification remain poorly understood.

Pronsky Z. Powers and Moore's Food-Medications Interactions. Ninth Edition. Food-Medication Interactions. Pottstown, PA, 1991, 60.

Reid IR, Ibbertson HK. Calcium supplements in the prevention of steroid-induced osteoporosis. Am J Clin Nutr. 1986 Aug;44(2):287-290.
Abstract: The long-term use of glucocorticoid drugs frequently results in the development of osteoporosis. To assess the value of calcium supplementation in preventing this loss of bone, the metabolic effects of administering 1 g of elemental calcium/day have been studied in 13 steroid-treated patients. After 2 mo, the fasting urine hydroxyproline-creatinine ratio decreased from 27.1 +/- 2.5 (SEM) to 21.8 +/- 2.4 (p less than 0.001) and there was an increase in fasting urine-calcium excretion (p less than 0.05). Serum alkaline phosphatase and osteocalcin showed no change. We concluded that calcium supplementation suppresses bone resorption without detectable suppression of indices of bone formation and is, therefore, likely to result in increased bone mass. The safety and low cost of calcium make it a very suitable prophylactic agent in glucocorticoid-treated patients.

Reid IR, Ibbertson HK. Corticosteroids and osteoporosis. Aust N Z J Med. 1987 Dec;17(6):611-612. (Letter)

Roe DA. Diet and Drug Interactions. New York: Van Nostrand Reinhold, 1989:84.

Roe DA. Drug-induced Nutritional Deficiencies. 2nd ed. Westport, CT: Avi Publishing, 1985:163-164.

Thorn GW. Clinical considerations in the use of corticosteroids. N Engl J Med. 1966 274:775.

Thelkeld DS, ed. Hormones, Adrenal Cortical Steroids, Glucocorticoids. In: Facts and Comparisons Drug Information. St. Louis, MO: Facts and Comparisons, Apr 1991.