Patients on immunosuppressive therapy have an increased risk of infections. Since infections have a potential to trigger acute porphyric attacks vigilance is motivated regarding signs or symptoms of infection and/or possible symptoms of a porphyric attack. Diarrhoea is a very common side effect that may potentially be porphyrinogenic through reduction in carbohydrate intake.

Infections are common in patients using immunosuppressants and since infections might trigger an acute porphyric attack, vigilance regarding signs and symptoms of an infection and/ or a porphyric attack is recommended. Diarrhoea is a very common side effect that can be potentially porphyrinogenic through reduction in carbohydrate intake.

Fingolimod is mainly metabolized by CYP4F2, and has little or no capacity to inhibit or induce expression of CYP enzymes.

Fingolimod is a sphingosine 1-phosphate receptor modulator

Fingolimod is used in the treatment of relapsing forms of multiple sclerosis. It is administered orally.

Fingolimod is biotransformed by reversible stereoselective phosphorylation to the pharmacologically active (S)-enantiomer of fingolimod-phosphate, by oxidative biotransformation mainly via the cytochrome P450 4F2 isoenzyme and subsequent fatty acid-like degradation to inactive metabolites, and by formation of pharmacologically inactive non-polar ceramide analogs of fingolimod. Fingolimod is primarily metabolized via human CYP4F2 with a minor contribution of CYP2D6, 2E1, 3A4, and 4F12. (FDA) Co-administration of fingolimod with ciclosporin did not elicit any change in the ciclosporin or fingolimod exposure. Also, co-administration of fingolimod with oral contraceptives (ethinylestradiol and levonorgestrel) did not elicit any change in oral contraceptive exposure. Fingolimod has little or no capacity to inhibit or induce expression of CYP enzymes (SPC, David 2012).