Anti-tumor necrosis factor-alpha induced lupus (ATIL) represents a major diagnostic and therapeutic challenge. Most cases of ATIL are caused by infliximab, followed by etanercept and adalimumab. Symptoms can range from common, mild cutaneous lesions to rare, serious pleural or pericardial effusions, deep venous thrombosis, life-threatening pneumonitis, and neuritis. Constitutional symptoms often present in association with positive autoantibody serology. Diagnosis can be considered if there is a temporal relationship between symptoms and anti-tumor necrosis factor-α (TNF- α) therapy and at least one serologic and one non-serologic American College of Rheumatology criteria. Since it is contraindicated to use anti-TNF-α drugs in patients with systemic lupus erythematosus, it is recommended to perform a thorough immunological screening in any patient with polyarthritis to assure accurate diagnosis. In addition, prior to anti- TNF therapy, baseline immunological investigations (including antinuclear antibodies) should be performed, and there should be close follow up to assess the development of lupus manifestations. The main approach in the treatment of ATIL is withdrawal of the offending drug. Traditional therapy with corticosteroids and immunosuppressive agents may be required to achieve full resolution of lupus symptoms. In this review, we discuss the pathogenesis, clinical manifestations, and management of ATIL.

BackgroundEven after achieving tremendous advances in diagnosis and treatment of rheumatoid arthritis (RA), many of the patients undergo delays in diagnosis and initiation of treatment, which leads to worsening of the condition and poor prognosis.ObjectiveThe objective of this study was to perform a literature review to quantify the lag times in diagnosis and treatment of RA and study the reported factors associated with it.MethodsThe authors searched literature published until September 2016 in electronic full-text and abstract databases and hand-searched the suitable articles.ResultsThe weighted average of median lag time from symptom onset to therapy was 11.79 months (12 studies, 5,512 patients, range 3.6–24.0 months). Lag1 was 3.14 months (onset of symptoms to first physician consultant; 12 studies, 6,055 patients, range 0–5.7 months); lag2 was 2.13 months (physician visit to RA specialist referral; 13 studies, 34,767 patients, range 0.5–6.6 months); lag3 was 2.91 months (consultation with rheumatologist to diagnosis; 3 studies, 563 patients, range 0–5 months), lag4 was 2.14 months (diagnosis to initiation of disease-modifying antirheumatic drug therapy; 5 studies, 30,685 patients, range 0–2.2 months). Numerous patient-and physician-related factors like gender, ethnicity, primary care physician knowledge of the condition, availability of diagnostics, and so on were responsible for the delays.ConclusionThis review estimated the delay times and identified the main factors for delay in RA patients in diagnosis and initiation of treatment. A most plausible solution to this is coordinated effort by the rheumatology and primary care physicians.

No abstract

Failure of patients to be seen by rheumatologists at RA onset delayed diagnosis and treatment. Thus, RA diagnosis can be accelerated by encouraging early referral to rheumatologists.

The primary objective of this study is to describe the demographics and clinical characteristics of patients with Poncet's disease (PD) in the Makkah region in Saudi Arabia, where tuberculosis is on the rise. The secondary objective is conducting a PD systematic literature review to compare our findings. We studied seven patients who presented with arthritis within the first 3 years from diagnosis of active tuberculosis in two centers in the Makkah region: King Faisal Specialist Hospital and King Fahad Hospital in Jeddah from January 2005 to December 2011. We conducted a literature review on PD in multiple biomedical/pharmaceutical databases up to December 2011. We detected a new pattern of reactive arthritis associated with tuberculosis (TB). We identified this as PD or tuberculous rheumatism, which is a sterile reactive arthritis that can emerge during any stage of acute TB infection. Seven cases of Poncet's disease were identified in our study. The most common presentation was extrapulmonary with involvement of multiple sites. Six out of seven patients developed arthritis after initiation of anti-TB drugs; one patient developed polyarthritis after completion of anti-TB medication. Asymmetrical polyarthritis was the most common presentation and the resolution of the arthritis was with symptomatic treatment and continuation of anti-TB drugs except in one case. PD may manifest in a variable pattern during the course of active tuberculous infection. Physicians should be aware of this rare complication associated with a common disease to prevent delay in diagnosis and initiation of appropriate treatment.