Matsuura-Otsuki Yuki, Hanafusa Takaaki, Yokozeki Hiroo, Watanabe Kyoko
aDepartment of Dermatology, Shonan Fujisawa Tokushukai Hospital, Fujisawa, Japan.
bDepartment of Dermatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Case Rep Dermatol. 2017 May 22;9(2):26-29. doi: 10.1159/000458405. eCollection 2017 May-Aug.
A 42-year-old Japanese man presented with persistent headache during treatment for psoriatic arthritis (PsA) with infliximab. Treatment with infliximab was initiated 3 years before and the psoriatic skin lesions with arthritis were well controlled. However, after 21 doses of infliximab, the skin lesions and joint pain exacerbated and became intractable. Ten days after the dosage of infliximab was increased, the patient experienced headache and nausea with high fever. He had scaly, well-circumscribed erythemas on his trunk, extremities, and deformed nails. He also had swelling and pain in multiple joints. His complete blood and differential leukocyte counts were normal. The level of C-reactive protein was 16.66 mg/dL, whereas anti-infliximab antibodies were absent. Nuchal rigidity was absent and there were no abnormal neurological findings; however, jolt test results were positive. Results from magnetic resonance imaging were normal, whereas those from cerebrospinal fluid (CSF) examination were almost normal. The CSF contained mononuclear cells and was negative for bacteriological cultures, India ink staining, and polymerase chain reaction amplification of herpesvirus group DNA. Headache and nausea improved 2 months after infliximab was discontinued. The patient failed to respond to infliximab treatment for PsA, and we diagnosed infliximab-induced aseptic meningitis. Infliximab was discontinued and treatment with ustekinumab and methotrexate was initiated. Thereafter, the psoriatic skin lesion and joint pain gradually improved. Infliximab-induced aseptic meningitis may be a differential diagnosis when symptoms of meningitis develop during infliximab administration.
一名42岁的日本男性在使用英夫利昔单抗治疗银屑病关节炎(PsA)期间出现持续性头痛。英夫利昔单抗治疗于3年前开始,银屑病皮肤病变伴关节炎得到了良好控制。然而,在使用21剂英夫利昔单抗后,皮肤病变和关节疼痛加剧且变得难以治疗。在英夫利昔单抗剂量增加10天后,患者出现头痛、恶心并伴有高热。他的躯干、四肢有边界清晰的鳞屑性红斑,指甲变形。他还存在多个关节的肿胀和疼痛。他的全血细胞计数和白细胞分类计数正常。C反应蛋白水平为16.66mg/dL,而不存在抗英夫利昔单抗抗体。无颈项强直,无异常神经系统体征;然而,轻推试验结果为阳性。磁共振成像结果正常,而脑脊液(CSF)检查结果几乎正常。脑脊液中含有单核细胞,细菌培养、墨汁染色及疱疹病毒组DNA的聚合酶链反应扩增均为阴性。停用英夫利昔单抗2个月后,头痛和恶心症状改善。该患者对英夫利昔单抗治疗PsA无反应,我们诊断为英夫利昔单抗诱导的无菌性脑膜炎。停用英夫利昔单抗并开始使用乌司奴单抗和甲氨蝶呤治疗。此后,银屑病皮肤病变和关节疼痛逐渐改善。当在英夫利昔单抗给药期间出现脑膜炎症状时,英夫利昔单抗诱导的无菌性脑膜炎可能是一种鉴别诊断。