Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 15 P70

SFEBES2008 Poster Presentations Clinical practice/governance and case reports (86 abstracts)

Lithium blocks the mineralocorticoid action of fludrocortisone in Addison’s disease both for replacement and in the treatment of Addisonian crisis

Malcolm Prentice 1 & Gerald Russell 2


1Department of Endocrinology, Mayday University Hospital, Croydon, UK; 2The Priory Hospital, Kent, UK.


A 44-year-old Caucasian female eight years previously had been diagnosed auto immune Addison’s disease and started on replacement with hydrocortisone 30 mg daily in divided doses and fludrocortisone 0.1 mg was started on lithium carbonate. One month later when her lithium level was 1.0 mmol/l she was noted to have a sodium of 129 mmol/l, potassium of 5.2 mmol/l and fludrocortisone was increased to 0.3 mg om. Over the next year as her lithium dose was increased as her renin rose to a peak of 36 pmol/ml per h, with a potassium of 5.8 mmol/l her fludrocortisone was increased maximum of 0.6 mg which maintained her with a sodium of 143 mmol/l, potassium of 4.2 mmol/l, renin of 7.1 pmol/ml per h. Throughout therapy she remained normotensive. Her lithium level was between 0.4 and 1.0 mmol/l throughout. Hydrocortisone replacement requirements were unchanged.

After 2 years she was changed with overlap from Lithium to Carbamazepine. Ten days later she presented in Addisonian crisis and lithium toxicity precipitated by adverse reaction to carbamazepine. She required fludrocortisone 0.6 mg om orally in addition to hydrocortisone 400 mg i.v. daily and i.v. saline. She was discharged off all psychotropics on fludrocortisone 0.1 mg in addition to her standard hydrocortisone replacement.

There has been one previous report of 1) of inhibition by lithium carbonate of the action of fludrocortisone in the distal renal tubule. We present the first case report of a patient on increasing lithium therapy requiring increased doses of fludrocortisone in an apparently dose dependant fashion suggestive of competitive inhibition by lithium both for maintenance and in the treatment of Addisonian crisis. Other less toxic mood stabilisers than lithium are now available and should be considered for Addisonian patients. In an Addisonian patient or other patients on fludrocrtisone requiring lithium close joint care with an endocrinologist with frequent monitoring is essential.

References

1. Stewart PM et al. Clin Endocrinol 1987 27 (1) 63–68.

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