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. Side effects like nausea, vomiting and diarrhoea may potentially be porphyrinogenic through reduction in carbohydrate intake.

Infections are common in patients using immunosuppressant drugs. Since infections might trigger an acute porphyric attack, vigilance regarding signs and symptoms of an infection and/ or a porphyric attack is recommended. Common adverse reactions of pirfenidone that can be confused with an acute porphyric attack are nausea, diarrhoea, vomiting and abdominal pains. These side effects may potentially be porphyrinogenic if leading to a decrease in carbohydrate intake.

Pirfenidone is a CYP1A2 substrate and is not suspected to be an inducer or a mechanism-based inhibitor of CYP enzymes.

Pyridinone

Pirfenidone has antifibrotic and anti-inflammatory properties and is used in the treatment of adult patients with mild to moderate Idiopathic Pulmonary Fibrosis (IPF). It is administered orally.

Pirfenidone is primarily metabolized by CYP1A2 (70-80 %) and to a lesser extent via CYP2C9, 2C19, 2D6, and 2E1 (SPC). The major metabolite is 5-carboxy-pirfenidone, and about 80 % of pirfenidone is excreted in the urine as this metabolite. Less than 1 % is excreted as unchanged metabolite. Interaction studies have shown that co-administration of pirfenidone and various CYP1A2 inhibitors (e.g. fluvoxamine, ciprofloxacine) resulted in a 2-4 fold increase in the plasma concentration of pirfenidone depending on the inhibitor. Co-administration with a CYP1A2 inducer (e.g. smoking) resulted in a decrease in plasma concentration of pirfenidone (SPC). This indicates that pirfenidone is a CYP1A2 substrate. Pirfenidone is not suspected to be an inducer or a mechanism-based inhibitor of CYP enzymes.