The approved dosing of tocilizumab for GCA is 162 mg administered subcutaneously every week; however, for both cost and adherence reasons, we elected to treat her with IV tocilizumab. We used the higher dose of 8 mg/kg rather than 4 mg/kg in hopes of enhancing the steroid-sparing effect, because she was having severe steroid side effects.
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Explore This IssueNovember 2018
It should be noted that IV tocilizumab is FDA approved thus far only for rheumatoid arthritis. The recommended monitoring parameters for tocilizumab are to check neutrophils, platelets and ALT/AST prior to therapy and again at four to eight weeks after the start of therapy, and every three months thereafter.
Well-recognized adverse effects of tocilizumab include mild transaminitis in up to 36% of patients, with severe transaminitis occurring only 1–2% of the time, in addition to mild neutropenia in up to 7% of patients. Our patient’s labs were incidentally checked one week after she received tocilizumab, and she was found to have severe grade 4 transaminitis (in the 4,000s) and severe grade 4 neutropenia with an ANC of 0, requiring hospitalization and discontinuation of tocilizumab.
During the patient’s hospitalization, an arterial thrombus was unexpectedly found on venous Doppler. The patient also experienced other thrombotic phenomena, including an acute cerebrovascular accident (CVA) and recurrent lower extremity DVTs. GCA has been shown to increase the risk of CVA, myocardial infarction (MI) and peripheral vascular disease (PVD).4
A study published in Arthritis & Rheumatism by Schmidt et al. examined 33 patients with newly diagnosed GCA using ultrasound exams of the abdominal aorta and 15 peripheral arteries and revealed that 30% had characteristic findings of inflammation (hypoechoic wall thickening or halo sign) in arteries other than the temporal arteries and 12% had abnormalities in the arteries of the lower extremities.5
A study published in Arthritis & Rheumatology by Blockmans et al. performed 18F fluorodeoxyglucose (FDG) positron emission tomography (PET) scans on 35 patients with GCA and found vascular FDG uptake in 83%. The most common site of FDG uptake was in the subclavian arteries (74%), while lower extremity uptake was noted in 37%.6 In our case, the patient’s hypercoagulable state was multifactorial; immobilization and recurrent hospitalizations likely played a role in her recurrent DVTs. The patient’s CVA and arterial thrombus may have been directly caused by smoldering inflammation from GCA.
We decided to treat the patient with abatacept based on a randomized controlled trial published in Arthritis & Rheumatism by Langford et al. that showed improvement in the ability to wean prednisone in GCA patients treated with abatacept.7 Fortunately, this has allowed us to wean the patient’s prednisone to 3 mg daily without recurrent symptoms or further complications.