Interferon beta-1a is a recombinant cytokine and fever and flu-like symptoms are very common adverse reactions. Experience seems to be that infection may trigger attacks of acute porphyria. However, infections are not commonly reported in the treatment with interferon beta-1a, and there is no evidence to show that inflammation and fever alone are triggering factors. Chronic inflammatory diseases are not associated with higher incidence of porphyric attacks. Inflammation has also shown to down-regulate the activity and expression of cytochrome P450 enzymes involved in hepatic drug clearance. Through inhibition of ALAS1-induction, interferon beta-1a might therefore protect against attacks of acute porphyria. However, common side effects such as anorexia, nausea, diarrhoea and vomiting are potentially porphyrogenic through reduction in caloric intake.

Interferon beta-1a is a cytokine glycoprotein produced by a method based on recombinant DNA technology using bacteria as host cells.

Interferon beta-1a is used in the treatment of relapsing multiple sclerosis. The mechanism of action is not known. It is administered subcutaneously. Common adverse reactions of interferon beta-1b that can be confused with an acute porphyric attack are nausea, vomiting, depression, insomnia and myalgia. Common side effects such as anorexia, diarrhoea, nausea and vomiting are potentially porphyrogenic through reduction in caloric intake.

Interferon beta-1a is mainly metabolised and excreted by the liver and the kidneys. Probably CYP-inhibing effects. Inflammation suppresses the expression of several hepatic transporters and detoxifying CYPs including CYP3A4 (Aitken, 2005; Moreau, 2008).