This question arises from your (correct) understanding that administration of exogenous (i.e. not produced by the body) glucocorticoids (GCs) can suppress the body’s ability to produce its own GCs in the adrenal glands. In order to understand the answer, a little background is necessary.
Why does the body become unable to produce cortisone?
As in many endocrine systems, negative feedback maintains homeostasis. Exogenous GCs exert negative feedback on the hypothalamic-pituitary-adrenal (HPA) axis (a series of hormones starting in the hypothalamus) that normally stimulates GC production in the adrenals. This negative feedback is almost immediately reversible. However, with extended administration of exogenous GCs, the lack of stimulation via the HPA axis leads to atrophy of the adrenal gland, and it becomes unable to produce the horomone even when the feedback suppression is removed. Your question is, how much exogenous GC is required to produce this effect?
It’s a very practical question because it affects how doctors prescribe steroids. If adrenal suppression is expected, they must be tapered slowly. If not, a “burst” can be administered and then immediately stopped. Because it’s such a practical question, people thought to study it quite a while ago, and the relevant literature is mostly pretty old (relative to most biomedical data, at least). (See below.)
The time required to achieve suppression depends upon:
- the dose;
- the length of time administered; and
- factors unique to each patient, probably resulting from (ultimately genetic) differences in their rates of GC metabolism.
Who is likely to be suppressed: some general guidelines
Not suppressed
- GC treatment (any dose) for less than three weeks.
- Treatment with less than 10 mg total daily dose (prednisone equivalents) for any time period.
Suppressed
- Oral GC treatment of >20 mg prednisone daily (or equivalent) for >3 weeks
- Any patient with clinical Cushing’s syndrome (see this answer for description)
Uncertain suppression: The degree of suppression in this intermediate group is related to individual metabolism parameters that are not (yet!) established in a way that can be measured and used clinically.
- Less than 20 mg prednisone daily (or equivalent) for >3 weeks.
- Any dose for >3 weeks administered every other day.
The rule of thumb I learned (which is fairly conservative): >10 mg for >3 weeks requires tapering.
In those patients who fall into the uncertain category, there is something called a "cosyntropin stimulation test” that helps make the distinction. In this test, a doctor administers a hormone (cosyntropin, a.k.a. ACTH) that stimulates the adrenal gland and measures plasma cortisol concentrations to see if it responds appropriately.
I’ve been talking in prednisone “equivalents.” There are steroid equivalent converters around. In general, prednisolone and prednisone have a 1:1 dosing relationship.
The answer to your question, then, is no. Seven days is a common prescription for a steroid “burst”, and tapering is generally considered to be unnecessary.
Ackerman GL, Nolsn CM. Adrenocortical responsiveness after alternate-day corticosteroid therapy. N Engl J Med. 1968;278(8):405.
Christy NP. Corticosteroid withdrawal. In: Current Therapy in Endocrinology and Metabolism, 3rd Ed, Bardin CW (Ed), BC Decker, New York 1988. p.113.
Danowski, et al. Probabilities of pituitary-adrenal responsiveness after steroid therapy. Ann Intern Med. 1964;61:11.
Myles AB, Bacon PA, Daly JR. Single daily dose corticosteroid treatment. Effect on adrenal function and therapeutic efficacy in various diseases. Ann Rheum Dis. 1971;30(2):149.
