Adalimumab is a fully humanised monoclonal antibody against TNF- purported to be less immunogenic with a safer side effect profile. ankylosing spondylitis (AS), juvenile idiopathic arthritis (JIA) and inflammatory bowel disease (IBD). They are also rarely used as third-line therapy in the treatment of sarcoidosis.1 However, these brokers have a variety of serious adverse effects including infection, reactivation of tuberculosis (TB) and immunogenicity. Induction of Lexibulin dihydrochloride autoantibodies, particularly antinuclear antibodies, is usually a relatively common side effect post treatment, but the development of drug-induced lupus with overt clinical manifestations remains rare. Its recognition is usually a challenge in a patient population where its symptoms may mimic a flare of their underlying disease, associated autoimmune conditions or overlap syndromes. Adalimumab is usually a fully humanised monoclonal antibody against TNF- purported to be less immunogenic with a safer side effect profile. Here we describe a case of anti-TNF-induced lupus (ATIL) secondary to adalimumab therapy. Case presentation A 61-year-old man presented to the emergency department of Cork University Hospital in Ireland with a 4-week history of exertional dyspnoea, Lexibulin dihydrochloride chest tightness and poor exercise Lexibulin dihydrochloride tolerance. He also reported anorexia and involuntary weight loss of 6?kg in 2?months. He had a background of AS diagnosed 20?years earlier for which he was treated with adalimumab for the past 2?years. He had previously failed to respond to two different non-steroidal anti-inflammatory drugs (NSAIDs) including ibuprofen and diclofenac. No trial of sulfasalazine was attempted, as it is usually no longer a mandatory pretreatment in this group. 2 Prior to start of adalimumab 40?mg every alternate week, the patient had negative testing for latent TB contamination including Quantiferon and Mantoux assessments along with a normal chest X-ray (CXR) as per the American College of Rheumatology (ACR) guidelines.3 He had been recently treated for recurrent lower respiratory tract infections (LRTI) by his primary care physician. He had a CXR at the time, which showed a small right pleural effusion with patchy atelectasis. His adalimumab had been temporarily withheld for 4?weeks and he was treated with antibiotics. He was an active smoker with a 50-pack year history and he consumed 12 units of alcohol per week. He was a former army engineer. There was no known history of asbestos exposure or other risk factors for respiratory disease. On examination, he was tachypnoic with a respiratory rate (RR) of 28 breaths per minute and his oxygen saturations were reduced at 92% on room air. He was apyrexial. His blood pressure (BP) was 101/59?mm?Hg and his heart rate (HR) was 82?bpm. Auscultation of his chest elicited reduced air entry bibasally with inspiratory coarse crackles. Investigations Arterial blood gas (ABG) showed a pH of 7.47, pCO2 of 4.6?kPa, pO2 of 7.7?kPa, SO2 of 91.5% and HCO3 of 25.5 (normal ranges: pH 7.35C7.45, pCO2 4.5C6?kPa, pO2 11C15kPa, sO2 94C100%, HCO3 22C28?mmol/L), consistent with type 1 respiratory failure. Collected sputum and blood cultures were all sterile. The patient’s white cell count (WCC) was 11.3109/L (normal range: 4.0C11.0109/L) with a differential of 9.28109/L neutrophils (normal range: 1.4C6.6109/L) and 1.37109/L lymphocytes (normal range: 0.9C3.2109/L). He had a normochromic normocytic anaemia with a haemoglobin (Hb) level of 12.3?g/dL (normal range: 14C17.4?g/dL). Lexibulin dihydrochloride Direct Coombs test was not performed as there was no evidence of haemolysis. The patient’s platelets were 331109/L (normal range: 140C440109/L). His C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were both elevated at 116.1?mg/L (normal range: 0C5?mg/L) and 68?mm/h (normal range: 0C10?mm/h), respectively. His renal and liver function tests were unremarkable. There were bilateral pleural effusions and bibasal consolidation on his CXR (physique 1). Open in a separate window Figure?1 Bilateral effusions and consolidation on chest X-ray. Ultrasound-guided left pleural drainage was performed, with fluid analysis showing a pH of 7.24, glucose 4?mmol/L (serum 6.5?mmol/L), total protein 53?g/L (serum total protein 62?g/L), lactate dehydrogenase 2737?U/L and 7390 white cells/cm2 with 70% neutrophils. No organisms were produced after 48?h incubation. There were no acid-fast bacilli seen and the TB culture was LIFR unfavorable. The cytology showed degenerating lymphocytes, polymorphs and eosinophils. At this time, the.