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At least 1 million new cases of nonmelanoma skin cancer (NMSC) are diagnosed in the United States each year and the incidence is increasing. A higher incidence of NMSC in organ transplant recipients on immunosuppression has been documented for some time, and recent studies indicate that patients with inflammatory bowel disease (IBD), particularly those treated with immunosuppressive medications, might also be at higher risk for this condition. In this review we summarize recent data evaluating the associations between immunomodulators, antitumor necrosis factor-α biologic agents and NMSC in patients with IBD and other autoimmune conditions such as rheumatoid arthritis. We also offer recommendations for prevention of NMSC in these populations. (Inflamm Bowel Dis 2011;)

With the increasingly widespread use of immunosuppressive and biologic agents for the treatment of Crohn's disease and ulcerative colitis come concerns about potential long-term consequences of such therapies. Disentangling the potential confounding effects of the underlying disease, its extent, severity, duration, and behavior, and concomitant medical therapy has proven to be exceedingly difficult. Unlike the case in rheumatoid arthritis, the overwhelming preponderance of population-based evidence suggests that a diagnosis of inflammatory bowel disease (IBD) is not associated with an increased relative risk of lymphoma. However, well-designed studies that evaluate the potential modifying effect of IBD severity have yet to be performed. Although the results from hospital- and population-based studies have conflicted, the results of a recent meta-analysis suggest that patients receiving purine analogs for the treatment of IBD have a lymphoma risk ≈4-fold higher than expected. Analyses of lymphoma risk in patients receiving biologic agents directed against tumor necrosis factor-alpha are confounded by concomitant use of immunosuppressive agents in most of these patients. Nevertheless, there may be a small but real risk of lymphoma associated with these therapies. Although the relative risk of lymphoma may be elevated in association with some of the medical therapies used in the treatment of IBD, this absolute risk is low. Weighing the potential risk of lymphoma associated with select medical therapies against the risk of undertreating IBD will help physicians and patients to make more informed decisions pertaining to the medical management of IBD.

Over the last 10 years, biologic treatment with the antitumor necrosis factor (anti-TNF) antibodies has dramatically changed the therapeutic approach in pediatric patients with inflammatory bowel disease (IBD). Currently, infliximab and adalimumab are the only anti-TNF drugs that have been approved for use in refractory pediatric Crohn’s disease (CD) and infliximab the only anti-TNF agent for use in refractory pediatric ulcerative colitis (UC). According to the current treatment recommendations, anti-TNF therapy is indicated for moderate and severe pediatric IBD when remission is not achieved using conventional treatment or conventional therapy is not tolerated by the patients. Despite the demonstrated efficacy of anti-TNF drugs in pediatric IBD patients, the potential development of serious adverse events, such as severe immune reactions, infections, and malignancies, limit the possibility of a wider use of anti-TNF drugs. Moreover, a substantial percentage of patients gradually develop non-responsiveness to these therapeutics, due to generation of antibodies against anti-TNF antibodies. Therefore, treatment of pediatric IBD patients with biologics should be undertaken in specialized tertiary medical centers, which are specially qualified for this purpose.

Background. To present a case of anti-TNFα drug-induced lupus (DIL) in a patient with rheumatoid arthritis (RA) and progressive respiratory complications. Materials and Methods: Review of clinical records and multidisciplinary follow-up. Results: A 60-year-old female smoker with a history of GERD, bronchial asthma, and OSAS was diagnosed with RA in 2022 due to polyarthritis (ANA 1:320, low-titer RF, negative ACPA). After failure of methotrexate, abatacept and tocilizumab, etanercept was initiated. In April 2024, purpuric lesions appeared on the upper back and chest, associated with resting dyspnea and a right-sided pleural effusion on chest X-ray, initially treated as parapneumonic. In May 2024, the patient was hospitalized for a widespread maculopapular rash and active arthritis (SDAI 39.3). Laboratory tests showed elevated ESR and CRP, ANA 1:1280, positive anti-dsDNA, anti-histone, and anti-nucleosome antibodies. ENA, ANCA and antiphospholipid antibodies were negative. Skin biopsy was consistent with a drug-induced toxic-allergic rash. Chest CT revealed post-inflammatory bibasal atelectasis. A diagnosis of etanercept-induced DIL was made based on clinical and serological criteria. The biologic was discontinued and steroid therapy, azithromycin, and antihistamines were started, with subsequent cutaneous improvement. However, dyspnea persisted with bilateral pleural effusion and severe mixed ventilatory syndrome requiring nocturnal CPAP. In September 2024, due to anti-dsDNA normalization and ongoing arthritis (with previous methotrexate failure), filgotinib 200 mg/day was started, achieving good cutaneous and joint response (SDAI 12.1 at 3 months). In December 2024, the patient was rehospitalized for acute type I respiratory failure due to worsening bilateral pleural effusion, treated with oxygen therapy, nebulization bronchodilator therapy and levofloxacin. In March 2025, due to residual debilitating dyspnea, medical cannabis was initiated. Discussion. Anti-TNFα DIL occurs in 0.1–0.5% of treated patients, more frequently in elderly women. Clinical features are variable: cutaneous involvement is present in up to 80% of cases. Diagnostic criteria include drug exposure, compatible clinical manifestations, positive ANA/anti-dsDNA, and improvement after discontinuation. The recurrent, antibiotic-resistant nature of pleural effusions suggests possible immune-mediated etiology. Early recognition is crucial to prevent systemic progression. Filgotinib has shown efficacy in controlling both articular and cutaneous disease activity, representing a valuable therapeutic alternative. The use of medical cannabis for refractory dyspnea highlights the importance of personalized, symptom-oriented approaches. Conclusions. This case illustrates the complex management of RA complicated by etanercept-induced DIL. Persistent respiratory manifestations, steroid-related complications, and intolerance to conventional DMARDs require a multidisciplinary, patient-tailored approach, emphasizing early DIL recognition and the selection of safe and effective alternative therapies.

Abstract Background Several studies have reported the surgical outcomes of inflammatory bowel disease (IBD) patients exposed to vedolizumab (VDZ) preoperatively, with conflicting results. This meta-analysis aims to evaluate the risk of postoperative complications in IBD patients preoperatively exposed to VDZ in comparison with patients exposed to anti-tumor necrosis factor (anti-TNF) treatment or no biologic therapy. Methods A systematic review with a meta-analysis of the existing literature was conducted. The main outcomes included the odds of developing overall postoperative complications, infectious complications, surgical site infections, need for repeat surgery, and major postoperative complications, as defined by the Clavien-Dindo criteria. Results Four studies were included in the meta-analysis. The risk of all postoperative complications was not significantly different between IBD patients exposed preoperatively to VDZ vs anti-TNFs (odds ratio [OR], 0.64; 95% confidence interval [CI], 0.21-1.88). In patients with ulcerative colitis (UC), the OR for complications was significantly lower in VDZ-exposed as opposed to anti-TNF-exposed patients (OR, 0.35; 95% CI, 0.14-0.85); the comparison was insignificant in Crohn's disease. There were no significant differences in the risk of infectious complications, surgical site infections, need for reoperation, or major surgical complications in patients exposed to VDZ vs anti-TNFs. There were no significant differences in outcomes when comparing patients exposed to VDZ with those not given biologic therapy. Conclusions This meta-analysis did not detect an increased risk of postoperative complications with preoperative VDZ exposure; the risk of overall complications may be lower in UC patients in comparison with those with anti-TNF exposure. These results merit further verification in future studies.

Macrophages contribute to the pathogenesis of rheumatoid arthritis (RA). They can display different states of activation or \"polarization,\" notably the so-called inflammatory \"M1\" and the various alternative \"M2\" polarizations, characterized by distinct functions. Data regarding the effects of RA anti-cytokine biological disease-modifying anti-rheumatic drugs (bDMARDs) on macrophage polarization are scarce. We aimed to assess modulation of macrophage polarization by bDMARDs targeting pro-inflammatory cytokines in RA. We generated monocyte derived macrophages using blood samples from 20 RA patients with active RA and 30 healthy controls. We evaluated the impact on M1 inflammatory macrophages of: etanercept (ETA), adalimumab (ADA), certolizumab (CZP), tocilizumab (TCZ), and rituximab (RTX). We assessed the impact on macrophage polarization using flow cytometry and RTqPCR to study the expression of surface markers and perform functional studies of cytokine production, phagocytosis, and negative feedback control of inflammation. Among evaluated bDMARDs, anti-TNF agents modulated the polarization of inflammatory macrophages by decreasing inflammatory surface markers (CD40, CD80) and favoring alternative markers (CD16, CD163, MerTK). Anti-TNF agents also induced alternative functions in macrophages activated in inflammatory condition with (i) the inhibition of inflammatory cytokines (TNF, IL-6, IL-12), (ii) an increase in phagocytosis. These findings were mechanistically related to an increase in early IL-10 production, responsible for higher negative feedback control of inflammation involving SOCS3 and Gas6. This IL-10 effect was STAT3-dependent. Anti-TNF agents not only inhibit inflammatory functions of macrophages, but also favor resolution of inflammation through polarization toward alternative features specifically involving the IL-10/STAT3 axis.

The aim of this study was to evaluate the reliability, content, and quality of videos for patients available on YouTube for learning how to self-administer subcutaneous anti-tumour necrosis factor (TNF) injections. We searched for the terms Humira injection, Enbrel injection, Simponi injection, and Cimzia injection. Videos were categorised as useful information, misleading information, useful patient opinion, and misleading patient opinion by two physicians. Videos were rated for quality on a 5-point global quality scale (GQS; 1 = poor quality, 5 = excellent quality) and reliability and content using the 5-point DISCERN scale (higher scores represent greater reliability and more comprehensive videos). Of the 142 English videos, 24 (16.9%) videos were classified as useful information, 6 (4.2%) as misleading information, 47 (33.1%) as useful patient opinion, and 65 (45.8%) as misleading patient opinion. Useful videos were the most comprehensive and had the highest reliability and quality scores. The useful information and useful patient opinion videos had the highest numbers of views per day (median 8.32, IQR: 3.40–14.28 and 5.46, IQR: 3.06–14.44), as compared with 2.32, IQR: 1.63–6.26 for misleading information videos and 2.15, IQR: 1.17–7.43 for misleading patient opinion videos (p = 0.001). Almost all (91.5%) misleading videos were uploaded by individual users. There are a substantial number of English-language YouTube videos, with high quality, and rich content and reliability that can be sources of information on proper technique of anti-TNF self-injections. Physicians should direct patients to the reliable resources of information and educate them in online resource assessment, thereby improving treatment outcomes.

Monogenic autoinflammatory diseases are rare conditions caused by genetic abnormalities affecting the innate immunity. Previous therapeutic strategies had been mainly based on results from retrospective studies and physicians' experience. However, during the last years, the significant improvement in their genetic and pathogenic knowledge has been accompanied by a remarkable progress in their management. The relatively recent identification of the inflammasome as the crucial pathogenic mechanism causing an aberrant production of interleukin 1β (IL-1β) in the most frequent monogenic autoinflammatory diseases led to the introduction of anti-IL-1 agents and other biologic drugs as part of the previously limited therapeutic armamentarium available. Advances in the treatment of autoinflammatory diseases have been favored by the use of new biologic agents and the performance of a notable number of randomized clinical trials exploring the efficacy and safety of these agents. Clinical trials have contributed to increase the level of evidence and provided more robust therapeutic recommendations. This review analyzes the treatment of the most frequent monogenic autoinflammatory diseases, namely, familial Mediterranean fever, tumor necrosis factor receptor-associated periodic fever syndrome, hyperimmunoglobulin D syndrome/mevalonate kinase deficiency, and cryopyrin-associated periodic syndromes, together with periodic fever with aphthous stomatitis, pharyngitis, and cervical adenitis syndrome, which is the most common polygenic autoinflammatory disease in children, also occurring in adult patients. Finally, based on the available expert consensus recommendations and the highest level of evidence of the published studies, a practical evidence-based guideline for the treatment of these autoinflammatory diseases is proposed.

[This corrects the article DOI: 10.3389/fphar.2021.752879.].

The use of biological agents and immunomodulators for inflammatory bowel disease (IBD) has remarkably improved disease management in the current era but at the same time has increased the risk of infectious complications. Patients with IBD on corticosteroids, immunomodulators, and biological agents are considered immunocompromised and are at risk for opportunistic infections. These are infections caused by organisms that take advantage of a weakened immune system, and cause disease, when they ordinarily would cause mild illness or no disease in an immunocompetent host. Risk factors for opportunistic infections include malnutrition, older age, congenital immunodeficiency, HIV infection, chronic diseases, and use of corticosteroids, immunomodulators, and anti–tumor necrosis factor alpha therapy. Apart from immunosuppressive medications and older age, there is only indirect evidence for above risk factors contributing directly to opportunistic infection risk in patients with IBD. Opportunistic infections in patients with IBD include viral infections (herpes viruses, human papillomavirus, influenza virus, and JC virus), bacterial infections (tuberculosis, nocardiosis, Clostridium difficile infection, pneumococcal infection, legionellosis, and listeriosis), fungal infections (histoplasmosis, cryptococcosis, Pneumocystis jirovecii infection, aspergillosis, and candidiasis), and parasite infections (Strongyloides stercoralis). Although these infections lead to high morbidity and mortality, only a minority of patients with IBD develop opportunistic infections. Currently, we lack a test to accurately predict patients at risk of opportunistic infection, and future research needs to focus on biomarkers or predictive models for risk stratification. Until such a test is developed, we need to screen, prevent, diagnose, and treat opportunistic infections in all patients with IBD in a timely manner.