The evaluation of sleep quality and response to anti-tumor necrosis factor α therapy in rheumatoid arthritis patients

Poor sleep quality (SQ) is increasingly recognized as giving rise to decreased quality of life, and raising pain perception. Our aim is to evaluate the SQ in rheumatoid arthritis (RA) patients treated with anti-tumor necrosis factor alpha (anti-TNF-α) therapy. This was a prospective observational and open-label study of RA patients. A total of 35 patients with RA were enrolled in this study. Of the 35 patients, 22 had high disease activity (DA), and 13 were in remission. High DA group was initiated an anti TNF-α therapy. Clinical and objective parameters of SQ were assessed by using the Pittsburgh Sleep Quality Index (PSQI) and polysomnography (PSG). The total PSQI score and the frequency of poor SQ were high in 60 % of the RA patients. The median PSQI score was significantly higher in the high DA group than in the remission group (P = 0.026). Following an anti-TNF-α therapy initiation, significant improvements were observed in the high DA group by PSQI test (P = 0.012). However, no statistically significant difference was found by PSG (P > 0.05). Although an improvement in DA with anti-TNF-alpha therapy did not provide an amelioration in laboratory parameters, we found a significant improvement in SQ by subjective PSQI test. These findings may support that sleep disorders in RA are likely to be associated with a complex pathophysiology.     

A predictive model for remission and low disease activity in patients with established rheumatoid arthritis receiving TNF blockers

The objective of this study was to identify predictors for remission or low disease activity (LDA) in established rheumatoid arthritis (RA) at 12 months of anti-TNF-α therapy. We have performed a prospective observational study in 90 consecutive patients with active RA receiving TNF-α inhibitors. Baseline and standard assessments were done every 3 months, including individual parameters (clinical and biological) and composite activity scores (28-joint disease activity score, DAS28). The primary outcome measure was DAS28-based EULAR response criteria. The multivariate logistic regression was used to analyze the association between disease activity and several RA baseline characteristics. Of the RA, 78.8 % was classified as good responders based on the EULAR-DAS28 criteria, 44.4 % RA achieving remission (DAS28?≤?2.6) and 34.4 %, LDA (DAS28?≤?3.2). Parameters associated with an increased likelihood of remission and LDA were initial DAS28-erythrocyte sedimentation rate ≤7 (odds ratio (OR) 3.3, 95 % confidence interval (CI) 2.03–5.81; OR 1.8, 95 % CI 1.09–6.68), Health Assessment Questionnaire Disability Index ≤?2 (OR 7.0, 95 % CI 1.56–31.91; OR 1.3, 95 % CI 1.03–5.79), C-reactive protein level ≤20 mg/l (OR 1.5, 95 % CI 0.29–8.22; OR 0.5, 95 % CI0.08–2.97), rheumatoid factor ≤20 IU/ml (OR 18.9, 95 % CI 10.79–38.36; OR 32.9, 95 % CI 4.03–269), anti-cyclic citrullinated peptide antibodies ≤40 IU/ml (OR 3.5, 95 % CI 0.67–18.19; OR 1.2, 95 % CI 1.02–1.59), concurrent prednisolone (OR 0.2, 95 % CI 0.05–0.36; OR 0.2, 95 % CI 0.06–0.63), methotrexate or leflunomide (OR 1.6, 95 % CI 1.2–13.53; OR 2.9, 95 % CI 1.20–4.36). A predictive matrix for remission and LDA in established active RA patients receiving TNF-α inhibitors was proposed. Further studies are necessary to confirm the value of such matrix in particular RA settings, leading to optimization of the use of anti-TNF-α therapy.     

Severe Multiple Sclerosis Manifesting upon GnRH Agonist Therapy for Uterine Fibroids

This case concerned a 39-year-old woman diagnosed with uterine fibroids. Upon initiation of gonadotropin-releasing hormone (GnRH) agonist therapy, she experienced various neurological deficits but did not seek medical attention because of gradual spontaneous symptom improvement. Upon completing four courses of GnRH agonist therapy, she began experiencing severe neurological symptoms and was diagnosed with multiple sclerosis (MS). Although her symptoms improved with steroid pulse therapy, serious sequelae remained. GnRH agonist therapy can exacerbate the disease activity of MS; therefore, awareness of the potential emergence of neurological symptoms during GnRH agonist therapy is important.     

Severe Guillain–Barré syndrome in a patient receiving anti-TNF therapy. Consequence or coincidence. A case-based review

The adverse effects of anti-tumour necrosis factor alpha (TNFα) drugs include an increase in the risk of infections, congestive heart failure, lupus-like syndrome, and the onset or worsening of various demyelinating diseases such as, multiple sclerosis, optic neuritis, and Guillain–Barrè syndrome (GBS), among others. We describe the case of a patient who developed GBS while she was on treatment with adalimumab. A 50-year-old woman with rheumatoid arthritis (RA) was admitted to the hospital due to progressive severe bilateral symmetric weakness of the legs, which quickly extended to the upper limbs and to the respiratory muscles. Adalimumab was started 13 months before. GBS was diagnosed and the anti-TNFα therapy discontinued. The serological test for Campylobacter jejuni was positive. She required invasive mechanical ventilatory support for 9 months. Twelve months later, the patient was using a wheelchair following a rehabilitation programme, and at 24 months she was walking a few steps with assistive devices. The relevant literature on the relationship between GBS and anti-TNFα is reviewed. Twenty three cases of GBS occurring during anti-TNFα therapy have been reported so far in the literature. In several cases, there was no clear temporal association, more than half had a possible previous infection, and in two cases the drug was reintroduced without recurrence of GBS. Our case, which is best explained by C. jejuni infection, as well as some of the cases described are probably not a direct result of anti-TNFα treatment, but an accidental coincidence. We also discuss the potential therapeutic options after anti-TNFα discontinuation.     

Good response to infliximab in a patient with deep vein thrombosis associated with Behçet disease

Vascular involvement is a lethal complication in Behçet disease. It is often refractory to conventional therapy such as steroids and immunosuppressants in addition to anticoagulants. We describe here successful treatment with the anti-tumor necrosis factor-alpha (anti-TNF-α) antibody, infliximab, in a patient with Behçet disease presenting with deep vein thrombosis. A 60-year-old man with Behçet disease complained of edema and pain in the lower extremities. Computed tomography revealed a thrombosis extending from the popliteal vein to the inferior vena cava at the level of the renal vein and which recurred despite combination therapy of steroid and immunosuppressants such as cyclosporine, azathioprine, and methotrexate. The patient was then administered infliximab (5 mg/kg) in weeks 0 and 2 and every 4 weeks thereafter. Clinical and laboratory findings improved after the infliximab therapy. Computed tomography of the abdomen and lower extremities showed a reduction of the thrombosis. No severe adverse events occurred during the clinical course. Although further studies are needed to confirm the efficacy and safety of its use, anti-TNF-α antibody may be worth considering as treatment for refractory venous thrombosis in patients with Behçet disease.

     

Interleukin-17 gene expression in patients with rheumatoid arthritis

Abstract

Interleukin-17 is a proinflammatory cytokine. Recent animal studies have shown that IL-17 plays a role in the initiation and progression of arthritis. However, whether IL-17 has a prominent role in human rheumatoid arthritis (RA) or not remains unclear. Here we investigated the role of IL-17 in patients with RA. cDNA was prepared from knee joint synovial tissues of RA (n = 11) and osteoarthritic (OA, n = 10) patients and PBMC of RA (n = 52) and healthy subjects (n = 34). IL-17 gene expression level was measured by real-time PCR, and was compared with various clinical parameters. IL-17 gene expression in synovial tissues of RA was similar to that in OA. IL-17 gene expression level in PBMC of RA patients was significantly higher than in the control. The response (changes in DAS) to two-week treatment with anti-TNF-α blockers (infliximab or etanercept) did not correlate with changes in IL-17 gene expression levels. The IL-17/TNF-α gene expression ratio at baseline (before treatment) tended to be lower in responders to the treatment. Expression of IL-17 gene in PBMC may be associated with the inflammatory process of RA. IL-17/TNF-α expression ratio is a potentially suitable marker of response to anti-TNF-α therapy.     

Esclerosis múltiple como efecto adverso de los agentes antifactor de necrosis tumoral alfa: una complicación infrecuente pero relevante de infliximab en la enfermedad de Crohn

Anti-tumor necrosis factor alpha (TNF-α) agents have been a great advantage in the treatment of inflammatory bowel disease. The safety profile of these agents is well-known and they can be considered safe when properly used. In clinical practice, the most important adverse events are infections. Other adverse effects are also possible but are much less frequent. However, because of the widespread use of these drugs, these uncommon adverse effects may also occur in clinical practice. We report one of these infrequent adverse events, multiple sclerosis, which is rare but important because of its severity. When neurological symptoms appear during treatment with anti-TNF-α, multiple sclerosis must be ruled out. The diagnosis and therapeutic management of this entity, led by a neurologist with our collaboration, required permanent cessation of anti-TNF-α therapy. Azathioprine, interferon, and even natalizumab, may be used as alternatives in patients who require therapy.     

Asthma unmasked with tumor necrosis factor-α-blocking drugs

We report five cases of asthma unmasked by anti-tumor necrosis factor (TNF)-α-blocking drugs. Asthma symptoms appeared within an average of 4 months (range 1-24 months) after starting the anti-TNF-α treatment for inflammatory disease. The patients did not appear to be predisposed to asthma except for one patient who had asthma during childhood. Four patients stopped anti-TNF-α-blocking drugs with an improvement of symptoms within 1 to 5 months. In the patient with a history of childhood asthma, respiratory symptoms recurred when another anti-TNF-α therapy was started. Asthma control was achieved with inhaled steroids, allowing anti-TNF-α treatment to continue. The biotherapy was maintained for the fifth patient in association with inhaled steroids. The pathophysiologic mechanisms are unknown but are probably more complex than the T helper 1/T helper 2 imbalance suggested in the literature, and further studies are required.     

SAPHO Syndrome: Current Developments and Approaches to Clinical Treatment

SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) is a rare autoimmune disease which, due to its clinical presentation and symptoms, is often misdiagnosed and unrecognized. Its main features are prominent inflammatory cutaneous and articular manifestations. Treatments with immunosuppressive drugs have been used for the management of SAPHO with variable results. To date, the use of anti-TNF-α agents has proved to be an effective alternative to conventional treatment for unresponsive or refractory SAPHO cases. TNF-α is a pro-inflammatory cytokine and pivotal regulator of other cytokines, including IL-1 β, IL-6, and IL-8, involved in inflammation, acute-phase response induction, and chemotaxis. IL-1 inhibition strategies with anakinra have shown efficacy as first and second lines of treatment. In this review, we will describe the main characteristics of biological drugs currently used for SAPHO syndrome. We also describe some of the promising therapeutic effects of ustekinumab, an antibody against the p40 subunit of IL-12 and IL-23, after failure of multiple drugs including anti-TNF-α and anakinra. We discuss the use and impact of the new anti-IL-1 antagonists involved in the IL-17 blockade, in particular for the most difficult-to-treat SAPHO cases.     

Effect of TNF-α Blockade in Gingival Crevicular Fluid on Periodontal Condition of Patients with Rheumatoid Arthritis

Background: Periodontitis and rheumatoid arthritis (RA) share a number of clinical and pathologic features, one of which is the presence of the tumor necrosis factor alpha (TNF-α)-induced bone resorption that is involved in the pathogenesis of both. Objectives: To investigate the effect of TNF-α blockade on periodontal conditions in patients with active RA. Method: The periodontal statuses of 36 patients (26 females, 10 males) diagnosed with active RA were evaluated both before and after anti-TNF-α therapy. Gingival index, bleeding on probing (BOP), probing pocket depth (PPD), oral hygiene index (OHI), and levels of TNF-α in gingival crevicular fluid (GCF) were measured at the baseline and 6 weeks after the treatment. Wilcoxon signed ranked test was used for statistical analyses. Results: Based on OHI (p=0.860), the level of plaque control did not change during the study period, but there was a significant reduction in gingival inflammation based on the mean BOP (p=0.049) and GI (p=0.036) before and after 6 weeks of anti-TNF-α therapy. The mean PPD index did not significantly differ at the baseline and 6 weeks after treatment (p=0.126). Conclusion: Anti-TNF-α therapy might have a desirable effect on periodontal conditions and might reduce TNF-α level in GCF of patients with RA.     

Impact of 24 months of anti-TNF therapy versus methotrexate on body weight in patients with rheumatoid arthritis: a prospective observational study

Clinical Rheumatology - To evaluate the impact of anti-TNF-α therapy on the body weight of rheumatoid arthritis (RA) patients following 24 months of treatment. Data were collected on...     

Challenges in diagnosing latent tuberculosis infection in patients treated with tumor necrosis factor antagonists

Reactivation of latent tuberculosis infection (LTBI) is well recognized as an adverse event associated with anti-tumor necrosis factor-α (anti-TNF-α) therapy. The strengths and weaknesses of current techniques for detecting LTBI in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) and psoriasis have not been fully examined. T cell hyporesponsiveness due to immunosuppression caused by illness or drugs, referred to as anergy, may produce false-negative tuberculin skin test (TST) and interferon-γ release assay (IGRA) results. The literature suggests that anergy may influence screening performance of TST and IGRA tests in candidates for anti-TNF-α therapy. Conversely, the potential for false-positive TST and IGRA results must be considered, as treatment for LTBI may be associated with significant morbidity. This review examines the reliability issues related to LTBI diagnostic testing and provides practical direction to help prevent LTBI reactivation and facilitate successful anti-TNF-α treatment.     

Tumor necrosis factor-α -308 polymorphism in North Indian rheumatoid arthritis patients and association with mRNA and serum TNF-α

Rheumatoid arthritis (RA) is a severely disabling chronic autoimmune disorder that leads to progressive inflammation of the joints and surrounding tissues. TNF-α, a potent proinflammatory cytokine, plays a pivotal role in the pathogenesis of RA. The endogenous formation of TNF-α may be influenced by TNF-α promoter polymorphisms. Hence, the present study was designed to explore any possible association between genetic polymorphism of TNF-α -308 G/A, messenger RNA (mRNA) expression, serum levels of TNF-α, and inflammatory markers in North Indian RA patients. A total of 214 controls and 187 RA patients were recruited according to the revised American College of Rheumatology 2010 criteria. TNF-α -308 G/A genetic polymorphism within promoter region was analyzed by using PCR-RFLP. Levels of inflammatory markers and serum TNF-α were estimated by ELISA. The mRNA expression of TNF-α gene was measured by quantitative real-time PCR. Higher levels of autoantibodies (RF and anti-CCP) were present in RA patients as compared to controls. We found a positive and significant correlation of circulating TNF-α levels with RF (r = 0.18), anti-CCP (r = 0.16), and mRNA expression of TNF-α gene (r = 0.57) in RA patients. The mRNA expression levels of TNF-α was 4.5-fold higher in patients with RA as compared to controls. The heterozygous mutant variants (G/A) and homozygous mutant variants (A/A) were found to be significantly associated with RA as compared to control (OR = 1.52 and 3.02, respectively). Our observations illustrated a significant association of allele -308 A TNF-α with progression of RA. Significant and positive correlation of TNF-α levels with mRNA expression and inflammatory marker levels suggests that serum TNF-α may be a susceptibility marker for RA.     

Successful treatment using cyclosporine in a patient with rhupus complicated by aplastic anemia: a case report and review of the literature

Systemic lupus erythematosus (SLE) co-morbid with rheumatoid arthritis (RA) is known as 'Rhupus syndrome' and is estimated to be present in between 0.01 and 2% of SLE and RA patients. The occurrence of aplastic anaemia in a patient with rhupus is very rare and a treatment for this condition has not been reported. A 52-year-old woman presented complaining of nausea and dizziness during the preceding month. She had been treated for rheumatoid arthritis for 16 years. At the time of presentation, she had a malar rash, multiple arthritis, pancytopenia, pleural effusion, proteinuria, and positive anti-nuclear and anti-dsDNA antibodies. A kidney biopsy revealed ISN/RPS class IV-G (A) lupus nephritis. Bone marrow aspiration and biopsy showed aplastic anaemia with no evidence of viral infection. The patient was successfully treated using cyclosporine and prednisolone and she remained symptom-free at the one-and-a-half-year follow-up. To our knowledge, this is the first report of a successful treatment using cyclosporine in a patient with rhupus complicated by aplastic anaemia.     

Subclinical cardiovascular target organ damage manifestations of ankylosing spondylitis in young adult patients

Aim

Although it is known that ankylosing spondylitis (AS) is associated with cardiovascular complications, the extent of these complications has not been clearly demonstrated in young adult patients. We have therefore investigated myocardial diastolic functions, carotid intima-media thickness (CIMT), and aortic elastic properties of young adult patients diagnosed with AS.

Method

Sixty-six AS patients and 21 age/gender-matched healthy subjects were enrolled in the study. Spectral and tissue Doppler echocardiography, CIMT, aortic strain and distensibility, and serum B-type natriuretic peptide values were compared with disease activity indexes of AS, including the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and the role of other variables, such as anti-tumor necrosis factor-alpha (anti-TNF-α) treatment, lipid parameters, erythrocyte sedimentation rate, and C-reactive protein.

Results

Both mitral early diastolic flow speed (mE) and late diastolic flow speed (mA) scores were lower among patients than among the control subjects (p = 0.015 and p = 0.035, respectively). The Em ratio of the patients was remarkably lower than that of the control subjects (p = 0.044). BASDAI scores of >4 were used to identify patients with more active disease. The mA and mE/mA ratios were significantly different between patients with a BASDAI score of >4 and those with a BASDAI score of <4 (p = 0.026 and p = 0.021, respectively). While aortic elasticity were not significantly different between the groups, AS patients treated with anti-TNF-α had significantly improved aortic strain and distensibility values (p = 0.022 and p = 0.014, respectively) compared to those treated with non-steroidal anti-inflammatory drugs (NSAIDs).

Conclusion

Myocardial diastolic functions were significantly deteriorated in the AS patients, and disease activity and myocardial diastolic functions were associated. An interesting finding was that patients receiving anti-TNF-α had better aortic elasticity than those treated with NSAIDs.     

Efficacy and safety of an anti-CD<Subscript>20</Subscript> monoclonal antibody (Reditux™) for the treatment of patients with moderate to severe rheumatoid arthritis following the failure of conventional synthetic disease-modifying anti-rheumatic drugs

Rituximab (anti-CD₂₀ monoclonal antibody) has shown to improve symptoms in rheumatoid arthritis (RA) patients with inadequate response to conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs). An anti-CD₂₀ monoclonal antibody (Reditux?) developed by Dr. Reddy’s Laboratories, India, is currently approved for use both in rheumatology and oncology patients. This retrospective report evaluates the efficacy and safety data from the real-world use of Reditux? over a 6-month period in Indian patients with RA. All consecutive moderate to severe RA patients who failed therapy with at least two DMARDs including methotrexate (MTX) for 6 months, TNFα inhibitor naive, and willing to take Reditux? were included. They were prescribed two doses of 1 g Reditux?, at least 15 days apart, with continued stable doses of methotrexate. Efficacy and safety after 24 weeks relative to baseline was assessed using various health assessment variables. A total of 39 patients (mean age of 46 years; 67.5 % females) treated with Reditux? were evaluated. Statistically significant differences were observed in mean changes of DAS28-CRP, DAS28-ESR, SDAI, HAQ and Patient Global Assessment scores from baseline to 24 weeks (p?<?0.0001 for all). Average steroid use per week also significantly reduced at 24 weeks (p?=?0.0002). There was no significant gender difference. Mean changes in SDAI, HAQ and Patient Global Assessment scores for patients on steroids were significantly different from those not on steroids (p?<?0.05 for all). At 24 weeks, 97 % of patients achieved ACR20 response demonstrating the efficacy of Reditux? treatment. The treatment was well tolerated by patients without any clinically relevant serious adverse events over 24 weeks. Though limited by number of patients and retrospective in nature, this analysis serves as a real-world evidence of efficacy and safety of Dr. Reddy’s rituximab (Reditux?) in the treatment of csDMARD-failed patients with RA over a 6-month period.     

Reduction of plasma IL-6 but not TNF-α by methotrexate in patients with early rheumatoid arthritis: a potential biomarker for radiographic progression

Objective

To determine the effect of methotrexate (MTX) on plasma levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α and to investigate their associations with clinical and radiographic responses in patients with early rheumatoid arthritis (RA).

Methods

Sixty-two untreated RA patients with the disease duration of ≤36 months in whom MTX was initiated were consecutively identified in our prospective RA cohort and included in this study. Concomitant use of prednisolone and synthetic disease-modifying anti-rheumatic drugs with MTX was allowed, but patients who used biological agents were excluded. Plasma IL-6 and TNF-α levels were measured at the time of diagnosis (baseline) and 1 year later. The relationships of the clinical and radiographic data with plasma levels of IL-6 and TNF-α were analyzed.

Results

The median age of the patients was 57 years, 49 patients were female, and the median disease duration was 3 months. Forty-six (74.2 %) patients were anti-cyclic citrullinated protein antibody-positive. Serum C-reactive protein (CRP), plasma IL-6, and DAS28 decreased significantly (p <0.001) after MTX treatment, but plasma TNF-α did not. Radiographic progression was significantly correlated with disease activity score and plasma IL-6 levels but not with CRP or TNF-α after MTX treatment. Patients with plasma IL-6 level above 4.03 pg/ml showed clinically relevant radiographic progression with a sensitivity of 91.7 % and a specificity of 88.0 %.

Conclusion

In this early RA cohort, we demonstrated a significant (p <0.001) reduction of plasma IL-6, but not TNF-α, during MTX treatment. The post-treatment IL-6 level was a strong indicator of radiographic progression.     

Tumor Necrosis Factor-α Plays an Initiating Role in Extracorporeal Circulation-induced Acute Lung Injury

Background

Despite advances in critical care, the mortality rate for patients with acute lung injury (ALI) remains high. The aim of this study was to test the hypothesis that tumor necrosis factor-α (TNF-α) plays an initiating role in the onset of extracorporeal circulation (ECC)-induced ALI.

Methods

Eight New Zealand rabbits subjected to 1 h of ECC and 40 min of observation after termination of ECC were used for monitoring pulmonary nociceptor activity. Fifty Sprague-Dawley (SD) rats that received 2 h of ECC and 4 h of rest were used to measure the pulmonary function and inflammatory cytokines release, including total cells, neutrophils, and TNF-α in bronchoalveolar lavage (BAL) and white blood cell (WBC) and neutrophils in blood. An additional 40 SD rats were randomized to pretreatment with inhalation of phosphate buffer solution (control group), IgG (IgG inh group), or TNF-α antibody (anti-TNF-α inh group) and venous injection of TNF-α antibody (anti-TNF-α iv group). After 2 h of ECC and 4 h of rest, the arterial blood and BAL fluid were collected for measurement of arterial oxygen pressure (PaO₂) and inflammatory cytokines release. The left-lower-lung tissues of animals were stained with hematoxylin & eosin (H&E).

Results

The results demonstrated that the activities of airway nociceptor and TNF-α release were similarly upregulated at the early stage and in a time-related manner in ECC-induced ALI. Pretreatment with TNF-α antibody inhalation, but not venous injection, improved pulmonary function, inhibited pulmonary inflammation, and attenuated pulmonary histopathological changes after ECC.

Conclusion

We concluded that TNF-α played an important role in the pathogenesis of ALI and acted as an initiating cytokine at the early stage of ECC-induced ALI.     

Is it safe to use anti-TNF-α agents for tuberculosis in children suffering with chronic rheumatic disease?

To determine the incidence of latent tuberculosis infection and evaluate the follow-up protocol of the patients diagnosed with juvenile idiopathic arthritis (JIA) and other chronic rheumatologic diseases treated with anti-TNF-α treatment (etanercept, infliximab, adalimumab) in Turkey, 144 patients were evaluated retrospectively for the development of tuberculosis. Patients were evaluated every 6?months for tuberculosis using history, physical examination, tuberculin skin test (TST), chest radiographs, and, when required, examination of sputum/early morning gastric aspirates for acid-fast bacilli and chest tomography. A tuberculin skin test over 10?mm induration was interpreted as positive. Patients were diagnosed with JIA (n?=?132), enthesitis-related arthritis (ERA; n?=?14), juvenile psoriatic arthritis (JPsA; n?=?4), chronic idiopathic uveitis (n?=?4), and chronic arthritis related to FMF (n?=?8). Mean age was 12.25?±?3.96?years (4.08–19.41?years), mean duration of illness was 5.86?±?3.77?years (0.66–15?years), and the mean duration of anti-TNF-α treatment was 2.41?±?1.47?years (0.6–7?years). Anti-TNF-α agents prescribed were etanercept (n?=?133), infliximab (n?=?30), and adalimumab (n?=?6). When unresponsive to one anti-TNF-α therapy, patients were switched to another. There was no history of contact with individuals having tuberculosis. During follow-up, seven patients (4.8%) with positive TST were given INH prophylaxis. One oligoarticular JIA patient (0.69%) diagnosed with secondary uveitis who had been followed for 5?years and had been using infliximab for 2?years, developed a positive Quantiferon-TB test while on INH prophylaxis. He was started on an anti-tuberculosis drug regimen. In conclusion, anti-TNF-α treatment in children with chronic inflammatory disease is safe. Follow-up every 6?months of children on anti-TNF-α treatment with respect to tuberculosis by the pediatric infectious disease department is important to prevent possible complications.