Interferon alfa-2a 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 alfa-2a, 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 alfa-2a might therefore protect against attacks of acute porphyria. However, very common side effects such as anorexia, diarrhoea, nausea and vomiting are potentially porphyrogenic through reduction in caloric intake. Interaction studies performed on pegylated interferon alfa-2a show no effect on CYP3A4, 2C9, 2D6 or 2C19 activities.

Interferon alfa-2a is a cytokine glycoprotein produced by a method based on recombinant DNA technology using bacteria as host cells.

Interferon alfa-2a is a cytokine with antiviral, antiproliferative and immunomodulating effects. It is used in chronic hepatitis B and chronic hepatitis C, AIDS-related Kaposis sarcoma, hairy-cell leukemia, chronic myeloid leukemia, follicular lymphoma, cutaneous T-cell lymphoma, stadium II malignant melanoma, and renal cell carcinoma. It is administered subcutaneously. In recurrent chronic hepatitis C it is administered in combination with ribavirin. Common adverse reactions of interferon alfa-2a are that can be confused with an acute porphyric attack are muscle pain, fatigue, diarrhoea, nausea and vomiting. Common side effects such as anorexia, diarrhoea, nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Interferon alfa-2a is mainly eliminated by the kidneys. Interaction studies performed on pegylated interferon alfa-2a show no effect on CYP3A4, 2C9, 2D6 or 2C19 activities, but it has shown to have inhibitory effects on CYP1A2 activity (SPC, pegasys). Inflammation suppresses the expression of several hepatic transporters and detoxifying CYPs including CYP3A4 (Aitken, 2005; Moreau, 2008).