title: Acute bilateral phrenic neuropathy following treatment with adalimumab.
abstract: The recombinant human IgG1 monoclonal antibody specific for human TNF-a adalimumab (Humira) has been recently introduced for the treatment of moderate/severe psoriasis. Neurological diseases have been rarely described as adverse events of anti-TNF agents. A case of acute respiratory failure due to diaphragmatic weakness following adalimumab therapy for psoriasis is described. A 65-year-old female patient presented with jaundice followed 2 days later by severe dyspnea and tachypnea which worsened when patient was lying flat, 1 week after the fourth dose of adalimumab. Isoniazid and vitamin B6 were co-administered with adalimumab. A symmetric elevation of diaphragms was shown on radiography and fluoroscopy. A pulmonary restrictive defect with a prominent decline of forced vital capacity (FVC) when the patient was on supine position was recorded. In the absence of specific limb electrophysiological abnormalities, acute bilateral symmetric phrenic neuropathy was diagnosed. The patient was a borderline candidate for mechanical ventilation for 3 weeks. Conservative treatment with oxygen was administered and both respiratory and liver disorder resolved 4 weeks following admission. A causal relationship of phrenal neuropathy with adalimumab is herein discussed.
authors: 2nd Department of Medicine, University of Athens Medical School, Hippokration General Hospital, 40 Konstantinoupoleos Street, 16342 Athens, Greece. alexopou@ath.forthnet.gr
authors: Alexandra
authors: A
authors: Alexopoulou
authors: John
authors: J
authors: Koskinas
authors: Aspasia
authors: A
authors: Soultati
authors: Panayiotis
authors: P
authors: Katsaounis
authors: Konstantin
authors: K
authors: Kilidireas
authors: Constantin
authors: C
authors: Papageorgiou
authors: Christina
authors: C
authors: Antoniou
authors: Andreas
authors: A
authors: Katsambas
authors: Athanasios
authors: A
authors: Archimandritis
mesh_terms: D000208:Acute Disease; D000068879:Adalimumab; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D061067:Antibodies, Monoclonal, Humanized; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000503:physiopathology; D004359:Drug Therapy, Combination; D004417:Dyspnea / Q000139:chemically induced / Q000503:physiopathology / Q000628:therapy; D005260:Female; D006801:Humans; D007538:Isoniazid / Q000009:adverse effects; D007565:Jaundice / Q000139:chemically induced; D020422:Mononeuropathies / Q000139:chemically induced* / Q000503:physiopathology; D010791:Phrenic Nerve / Q000187:drug effects* / Q000503:physiopathology; D011565:Psoriasis / Q000188:drug therapy; D012129:Respiratory Function Tests; D012131:Respiratory Insufficiency / Q000139:chemically induced* / Q000503:physiopathology / Q000628:therapy; D016896:Treatment Outcome; D025101:Vitamin B 6 / Q000008:administration & dosage
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D025101:Vitamin B 6; D000068879:Adalimumab; D007538:Isoniazid