Corticosteroid-induced hypothalamo-pituitary-adrenal axis suppression. Prospective study using two regimens of corticosteroid therapy.

Abstract

Long-term oral corticosteroid therapy leads to suppression of the hypothalamo-pituitary-adrenal (HPA) axis (Paris, 1961;Treadwell, Savage, Sever, and Copeman, 1963; Jasani, Boyle, Greig, Dalakos, Browning, Thompson, andBuchanan, 1967). Much work has been done on the influence of the regimen of corticosteroid administration on this suppression. Harter, Reddy, and Thorn (1963) have presented evidence that administration of oral corticosteroid in a single dose given every other day leads to substantially less adrenal suppression than that which occurs with a regimen giving divided doses of corticosteroid over the same period. The doses used in this study were not physiological; that is to say patients received doses of prednisone or prednisolone-equivalent ranging from 20 to 40 mg. daily. Grant, Forsham, and DiRaimondo (1965) have shown that a daily morning dose of 8 mg. Triamcinolone administered to normal subjects over a period of 8 days does not lead to lasting adrenal suppression. Nichols, Nugent, and Tyler (1965) have demonstrated virtually complete suppression of the secretion of cortisol by the adrenal gland for a period of 24 hours following the administration of a physiological dose of corticosteroid (0 5 mg. dexamethasone) given at midnight. The same amount given at 8 a.m. or 4 p.m. caused only temporary suppression of cortisol secretion.In the present study we have compared the effect of two regimens of corticosteroid administration on *Present Address: Senior Clinical Research Associate in Pharmacology,

Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review

“…A summary of these groups is presented in Table 1 , while a condensed version of the data extraction table can be seen in Supplementary File 3 . There were thirteen RCTs [19] , [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] with random allocation and blinding maintained throughout; the remaining 60 studies were classified as observational studies [12] , [13] , [14] , [15] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , [66] , [67] , [68] , [69] , [70] , [71] , [72] , [73] , [74] , [75] , [76] , [77] , [78] , [79] , [80] , [81] …”

Recovery of hypothalamo‐pituitary‐adrenal function in the rat after prolonged treatment with betamethasone

“…Thus, minimal HPA disturbance would probably follow multiple small doses of steroid spaced so that there is no cumulative effect. Such treatment might be preferable to alternate day therapy which does not always give good symptom relief, although effects on the endocrine system are reduced (Ackerman & Nolan, 1968;Harter, Reddy & Thorn, 1963;Jasani, Boyle, Carson-Dick, Williamson, Taylor & Watson-Buchanan, 1968).…”

A Controlled Transfer from Oral Corticosteroids to Corticotrophin in Bronchial Asthma

“…The transfer of patients from corticosteroids to corticotrophin should be controlled and an easy and reliable test of adrenocortical function is desirable. Many methods have been employed (McGill et al , 1967; Hedner and Einerth, 1963; Krieger et al , 1968; Bacon et al , 1968; Jasani et al , 1968; Robinson et al , 1962; Wood et al , 1965). These all involve parenteral administration of corticotrophin in some form.…”