MEASUREMENT OF ENDOGENOUS CORTISOL PRODUCTION IN PATIENTS ON LONG TERM STEROIDS FOR ? TUBERCULOUS ADRENAL DISEASE October 07, 2016

MEASUREMENT OF ENDOGENOUS CORTISOL PRODUCTION IN PATIENTS ON LONG TERM STEROIDS FOR ? TUBERCULOUS ADRENAL DISEASE   October 07, 2016
QUESTION--I have a 56 year old male patient who was treated for  Adrenal crisis in December 2014. Investigations done at that time elsewhere were suggestive of right adrenal mass and adrenal biopsy revealed granulomatous tissue. As Tuberculosis is one of the most common cause of granulomatous lesion in our country (India), he was treated with Antituberculous treatment and put on steroid replacement ( prednisolone 20 mg and Fludrocortisone 0.1 mg daily).
He has now presented to me with signs and symptoms of overreplacement. Type 2 DM , HT, obesity and water retenton, low potassium. I  am tapering the dose of prednisolone and the fludrocortiosne with clinical monitoring.
However my question is - how common is for the adrenal glands to recover if it was tuberculosis adrenalitis. How do I check for endogenous steroid production in this situation? (as long term oral steroids would any way have suppressed the adrenal axis) I am reluctant to stop steroids completely in view of past history of adrenal crisis. What is the best option to proceed in this scenario?
I personally was thinking of following two options:
1) to slowly taper prednisolone to 7.5 mg over next 4 weeks and then switch to Dexamethone 1 mg . I could then do the Synacthen test to check for endogenous steroid production.
or 2) to switch to hydrocortisone once Prednisolone 7.5 mg dose reached. Then omit the evening and morning dose of hydrocortisone and do the Synacthen test. I would be glad if you could advise. purvi mehta [mailto:drpcmehta@hotmail.com]
RESPONSE--Thanks, an interesting question. In brief, either option is quite reasonable. I note that he was placed on quite a high dose of prednisolone, which originally was appropriate as (1) patients with active TB have often been placed on pharmacological doses of 'steroids' for a brief initiation period, and (2) I assume he was on a rifampicin regime which induces liver enzymes and increase steroid requirements. However, over a longer period this dose could quite clearly cause adrenal suppression, as you suggest.
I usually tail down the prednisolone to 5mg once daily, then check a 9am cortisol 24h after the last dose: if this is readily detectable, stop the prednisolone and perform a short Synacthen test (using 0.25mg). If it is very low or undetectable, switch to hydrocortisone 10/5/5 and then see if this can be titrated downwards. Note that normative values for the Synacthen test are very assay dependent (Sbardella et al, Clinical Endocrinology, 2016, abstract on-line).
Regards,  Ashley Grossman, MD