Certolizumab pegol
- PDF / 175,747 Bytes
- 1 Pages / 595.245 x 841.846 pts (A4) Page_size
- 28 Downloads / 148 Views
1 ★S
First report of hypocomplementemic urticarial vasculitis: case report An adult woman [exact age not stated] developed hypocomplementemic urticarial vasculitis during treatment with certolizumab pegol for rheumatoid arthritis (RA). The woman was diagnosed with RA in 1991 during her early 20s. Subsequently, in 2010, she presented due to advanced RA. Laboratory tests were strongly positive for anticitrullinated protein antibody. Also, she occasionally developed urticaria, which was relieved by short-term unspecified steroids and antihistamines. The laboratory and immunological findings were suggestive of concurrent systemic lupus erythematosus (SLE). However, characteristic skin manifestations and organ complications were not observed. Arthralgia in her finger and ankle persisted despite methotrexate and etanercept. Consequently, prednisolone was started, and etanercept was switched to adalimumab followed by golimumab. However, both were not effective. She received tocilizumab, tacrolimus and abatacept. However, these were discontinued due to leucocytopenia, liver dysfunction and secondary failure. In 2016, abatacept was changed to SC certolizumab pegol 400mg, administered after 2 and 4 weeks and every 4 weeks thereafter, while she had moderate RA disease activity administered. Her RA disease activity improved. Subsequently, the dose of certolizumab pegol was reduced to 200mg. The dose of methotrexate was gradually decreased; and eventually, discontinued. The dose of prednisolone was increased. Approximately after 3 years of certolizumab pegol initiation, she developed urticaria. The woman was treated with unspecified antihistamines, but she was refractory to the treatment. Additionally, wheal-like erythematous plaques persisted for a few days, which were complicated by post-inflammatory pigmentation developed on her legs five months thereafter. Consequently, unspecified antihistamines and corticosteroids was started. Microscopic examination of the affected lesion revealed erythrocyte extravasation, inflammatory infiltrates comprising neutrophils and eosinophils, and leucocytoclasia. Immunofluorescence staining exhibited deposition of IgA, IgM and C3c in the vessel walls. The serum CH50 (total complement activity) level was low, which was indicative of hypocomplementemic urticarial vasculitis. Test for anti-cardiolipin antibody IgG was positive, which was included as a classification criterion for SLE. The presence of chronic urticarial exanthema, arthralgia/arthritis, hypocomplementemia and histological evidence of leucocytoclastic vasculitis led to the diagnosis of hypocomplementemic urticarial vasculitis. She did not experience any visual disturbances or abdominal pain and did not show any signs of renal dysfunction or haematuria/proteinuria. Markers for hepatitis-B and C were absent. Based on her clinical course and laboratory findings, the possibility of hypocomplementemic urticarial vasculitis secondary to certolizumab pegol was considered. Her treatment with certolizumab pegol was discontinued, and the do
Data Loading...
