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 and vomiting may potentially be porphyrinogenic through reduction in carbohydrate intake.

An acute cytokine release syndrome occurs in most patients, and because of this it is often given with steroids, paracetamol and antihistamins. Typical clinical manifestations of the cytokine release syndrome include high fever (77 % of patients), chills or rigors, headache, tremor, nausea, vomiting, diarrhoea, myalgia, generalised weakness, tachycardia and hypertension. 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 such as nausea and vomiting may also be potentially porphyrinogenic through reduction in carbohydrate intake.

Muromonab-CD3 is an antibody protein and is not metabolized by cytochrome P450 enzymes. No pharmacokinetic porphyrinogenic effects are suspected.

Muromonab-CD3 is a murine monoclonal antibody to the T3 (CD3) antigen of human T-lymphocytes.

Muromonab-CD3 is used in the treatment of acute allograft rejection in organ transplant recipients. It is administered as intravenous injections.

Mechanisms for elimination of monoclonal antibodies are not well documented but are reported to include proteolysis by the liver and the reticuloendothelial system, target-mediated elimination and nonspecific endocytosis (Keizer 2010). Secondary PXR/CAR inhibition via the initial heavy release of pro-inflammatory cytokines is probable.