Certolizumab-induced lichenoid eruption in a patient with rheumatoid arthritis

2021 ◽  
Vol 14 (12) ◽  
pp. e245875
Author(s):  
Anuj Kunadia ◽  
Kenneth Shulman ◽  
Naveed Sami

Certolizumab is a monoclonal antibody against tumour necrosis factor-alpha (TNF-α) commonly used in rheumatologic conditions such as rheumatoid arthritis. Skin rashes are an uncommon side effect with few cases of lichenoid drug eruption reported in the literature. We describe a patient with rheumatoid arthritis who presented 6 weeks after initiating certolizumab pegol. Physical examination showed pink-to-violaceous papules on her upper and lower extremities. Biopsy confirmed a lichenoid drug eruption. The medication was discontinued and she was treated with topical steroids and a calcineurin inhibitor, with resolution of her lesions. Clinicians should be cognizant of such adverse reactions to TNF-α inhibitors and keep drug-induced lichenoid eruptions on the differential. Lichenoid eruptions induced by certolizumab pegol may affect the skin and/or mucous membranes. While most cases occur within weeks to months of starting therapy, eruptions may occur years after treatment initiation, underscoring the importance of a thorough review of medications.

2012 ◽  
Vol 19 (5) ◽  
pp. 699-703 ◽  
Author(s):  
Eric Assier ◽  
Luca Semerano ◽  
Emilie Duvallet ◽  
Laure Delavallée ◽  
Emilie Bernier ◽  
...  

ABSTRACTTumor necrosis factor alpha (TNF-α) blockade is an effective treatment for patients with TNF-α-dependent chronic inflammatory diseases, such as rheumatoid arthritis, Crohn's disease, and psoriasis. TNF-α kinoid, a heterocomplex of human TNF-α and keyhole limpet hemocyanin (KLH) (TNF-K), is an active immunotherapy targeting TNF-α. Since the TNF-K approach is an active immunization, and patients receiving this therapy also receive immunosuppressant treatment, we evaluated the effect of some immunosuppressive drugs on the generation of anti-TNF-α antibodies produced during TNF-K treatment. BALB/c mice were injected intramuscularly with TNF-K in ISA 51 adjuvant. Mice were also injected intraperitoneally with one of the following: phosphate-buffered saline, cyclophosphamide, methylprednisolone, or methotrexate. Anti-TNF-α and anti-KLH antibody levels were assessed by enzyme-linked immunosorbent assay and the anti-TNF-α neutralizing capacity of sera by L929 bioassay. Our results showed that current treatments used in rheumatoid arthritis, such as methylprednisolone and methotrexate, do not significantly alter anti-TNF-α antibody production after TNF-K immunization. In contrast, the administration of cyclophosphamide (200 mg/kg) after immunization significantly reduced anti-TNF-α antibody titers and their neutralizing capacity.


2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Ashley Fonseca ◽  
Julee Sunny ◽  
Lina M. Felipez

Crohn’s disease (CD) is a chronic inflammatory disease that can be associated with intestinal and extraintestinal manifestations. Some patients are treated with infliximab, an antitumor necrosis factor-alpha (TNF-α) agent, to help them achieve and maintain clinical and biochemical remission. However, some patients with CD can present severe adverse effects such as drug-induced lupus and rarely present with pleural space and pericardium involvement. We report a case of an 18-year-old Hispanic male with CD who acquired anti-TNF-α-induced lupus after infliximab therapy presenting with pleural effusion and pericarditis. The patient presented with a 2-week history of pleuritic chest pain. Initial laboratory workup was remarkable for leukocytosis and increased inflammatory markers. Imaging and cardiovascular studies were consistent with pericarditis and pleural effusions. Serositis was initially thought to be reactive secondary to the current Mycoplasma pneumoniae infection. He was treated with colchicine 0.6 mg PO TID for six weeks and azithromycin 500 mg PO for seven days. Pain improved after discharge but resurfaced on the day of infliximab infusion. Imaging and cardiovascular studies demonstrated the persistence of pleural effusions and pericarditis. Ultrasound-guided thoracentesis was consistent with exudative pleural effusions. Rheumatological workup was remarkable for increased antihistone antibodies, consistent with drug-induced lupus. Infliximab-induced pericarditis and pleural effusions are rarely reported in the literature. It is thought that infliximab may have a proinflammatory activity or have a delayed type III hypersensitivity reaction. The first line of therapy of anti-TNF-α-induced lupus is the withdrawal of the offending drug. Our patient is unique as few cases of anti-TNF-α-induced pleural effusion and pericarditis in CD are reported. After discontinuing the offending drug, ustekinumab was started, and maintaining a steroid and colchicine regimen, the patient’s chest pain improved. Antihistone antibodies have returned to normal one month after starting ustekinumab.


Author(s):  
Yaldi Rosadi ◽  
Yustin Marinta ◽  
Muthiah Nur Afifah

Background: Orthopedic Surgery in Rheumatoid Arthritis (RA) patients is still controversial between orthopedic surgeons and rheumatologists, mainly due to infection and disease flares. The incidence of postoperative infections may be high due to the immunosuppressive effect of RA medication. Conversely, discontinuance of antirheumatic agents increases the possibility of a disease flare. The objective of our review is to assess the influence of drugs on both incidences.Literature Review: There were 13 studies included in this review. Methotrexate (MTX) is the most common csDMARD option among the included studies. One retrospective study that the incidence of flares tends to be higher among the group of patients who received MTX therapy and stopped more than one week before surgery than the group who did not stop. The use of MTX doses of 5 to 10 mg/week did not show an association with infection or flare incidence. On the use of bDMARD, 37.0% of patients had higher surgical site infection (SSI). Specifically, Tumor Necrosis Factor-alpha (TNF-α) inhibitors significantly (OR: 9.5, 95% CI: 1.0-88.8) increase the incidence of postoperative infections in standard-dose and high-dose, but not significantly in the rate of flares.Summary: csDMARD is recommended for continuous therapy, whereas for bDMARD, although it is recommended for withholding in the perioperative period, the results of the study did not show significant differences. The ideal dosage of medication is by the basic properties of the drug. In comparison, the incidence of flares and infections was significantly higher in biologic than csDMARD.


PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250877
Author(s):  
Ching-Tsai Lin ◽  
Wen-Nan Huang ◽  
Wen-Chan Tsai ◽  
Jun-Peng Chen ◽  
Wei-Ting Hung ◽  
...  

In this study we aimed to identify the predictors of drug survival for biologic and targeted synthetic DMARDs (bDMARDs and tsDMARDs) among patients with rheumatoid arthritis (RA) in a real-world setting. Data from RA patients receiving bDMARDs and tsDMARDs between 2007 and 2019 were extracted from the Taiwan Rheumatology Association Clinical Electronic Registry (TRACER). Patients were categorized into tumor necrosis factor-alpha (TNF-α) inhibitors, non-TNF-α inhibitors, and tofacitinib groups. The primary outcome was 3-year drug retention and the causes of bDMARDs and tsDMARDs discontinuation were recorded. Baseline demographic data before the initiation of bDMARDs and tsDMARDs treatment were analyzed to identify the predictors of 3-year drug survival. A total of 1,270 RA patients were recruited (TNF-α inhibitors: 584; non-TNF-α inhibitors: 535; tofacitinib: 151). The independent protective factors for 3-year drug survival were positive rheumatoid factor (RF) (HR: 0.48, 95% CI: 0.27–0.85, p = 0.013) and biologics-naïve RA (HR: 0.61, 95% CI: 0.39–0.94, p = 0.024). In contrast, positive anti-citrullinated protein antibody (ACPA) (HR: 2.24, 95% CI: 1.32–3.79, p = 0.003) and pre-existing latent tuberculosis (HR: 2.90, 95% CI: 2.06–4.09, p<0.001) were associated with drug discontinuation. RA patients treated with TNF-α inhibitors exhibited better drug retention, especially in the biologics-naïve subgroup (p = 0.037). TNF-α inhibitors were associated with lower cumulative incidence of discontinuation due to inefficacy and adverse events (both p<0.001). Baseline RF and ACPA positivity in abatacept-treated patients were associated with a better 3-year drug survival. However, negative ACPA levels predicted superior drug survival of TNF-α inhibitors and tofacitinib. In conclusion, bio-naïve status predicted better drug survival in TNF-α inhibitors-treated RA patients. RF and ACPA positivity predicted better abatacept drug survival. In contrast, ACPA negativity was associated with superior TNF-α inhibitors and tofacitinib survival.


2013 ◽  
Vol 20 (5) ◽  
pp. 761-764 ◽  
Author(s):  
Pasquale De Nardo ◽  
Rita Bellagamba ◽  
Angela Corpolongo ◽  
Elisa Gentilotti ◽  
Fabrizio Taglietti ◽  
...  

ABSTRACTAnti-tumor necrosis factor alpha (anti-TNF-α) is used in the treatment of rheumatic diseases not responsive to first-line regimens. Data on the safety of anti-TNF-α in HIV-infected patients are scarce and conflicting. We describe a case of septic shock and multiorgan failure that occurred after etanercept initiation and influenza vaccination in an HIV-infected woman with rheumatoid arthritis.


RMD Open ◽  
2020 ◽  
Vol 6 (1) ◽  
pp. e001032 ◽  
Author(s):  
Przemysław Błyszczuk ◽  
Zoltan Szekanecz

Rheumatoid arthritis (RA) is characterised by a chronic inflammatory condition of the joints, but the comorbidities of RA predominantly contribute to the reduced lifespan associated with this disease. Clinical data indicate that cardiovascular disease is the major comorbidity associated with mortality in RA. In this review, we aimed to describe the pathogenesis of heart failure in RA. First, we emphasised the fundamental differences between ischaemic and non-ischaemic heart diseases and referred to their relevance in excessive cardiovascular-dependent mortality in RA. Second, we highlighted aspects of asymptomatic changes in cardiac tissue and in coronary blood vessels that are commonly found in patients with diagnosed RA. Third, we focused on high-grade systemic inflammation as a key trigger of ischaemic and non-ischaemic heart diseases in RA, and described the implication of conventional and biologic antirheumatic medications on the development and progression of heart disease. In particular, we discussed the roles of tumour necrosis factor-alpha (TNF-α) and anti-TNF-α therapies on the development and progression of ischaemic and non-ischaemic heart diseases in RA.


RMD Open ◽  
2021 ◽  
Vol 7 (1) ◽  
pp. e001399
Author(s):  
Hanzhe Zhang ◽  
Jiajun Wen ◽  
G Caleb Alexander ◽  
Jeffrey R Curtis

ObjectiveTo quantify comparative effectiveness of interleukin (IL)−12/23 antagonist (ustekinumab), IL-17A antagonists (secukinumab and ixekizumab), PDE4 inhibitor (apremilast) and tumour necrosis factor-alpha (TNF-α) inhibitors (infliximab, etanercept, adalimumab, certolizumab pegol and golimumab) for psoriatic arthritis (PsA).MethodsWe adapted a deidentified claims-based algorithm validated for inflammatory arthritis treatments to compare treatments among a retrospective cohort of commercially insured and Medicare Advantage beneficiaries with PsA from October 2013 to April 2019 in the OptumLabs Data Warehouse. Main outcomes include (1) treatment effectiveness, based on: adherence, adding or switching biologic or PDE4, addition of new non-biologic disease-modifying antirheumatic drug, increase in biologic or PDE4 dose or frequency and glucocorticoid use and (2) percentage of each group fulfilling the effectiveness algorithm. We used Poisson regression with robust variance stratified by prior PsA biologic exposure and adjusted for potential confounders.ResultsOf 2730 individuals with PsA, 327 received IL-12/23, 138 IL-17A’s, 624 PDE4 and 1641 TNF-α’s. Effectiveness criteria were fulfilled among 63 (19.3%) IL-12/23 recipients, 40 (29.0%) IL-17A recipients, 160 (25.6%) PDE4 recipients and 530 (32.3%) TNF-α recipients. Among biologic-naïve individuals, IL-12/23 was less effective than TNF-α’s with fully adjusted relative risk (aRR) compared with TNF-α’s of 0.63 (95% CI 0.45 to 0.89). Among biologic-experienced individuals, PDE4 recipients were less effective than TNF-α’s (aRR 0.67, 95% CI 0.46 to 0.96).ConclusionsTNF-α’s appeared more effective than IL-12/23’s for biologic-naïve individuals, and PDE4’s for biologic-experienced individuals. These results may help inform treatment choice for individuals with PsA.


Author(s):  
Natesan Manikandan ◽  
Narasingam Arunagirinathan ◽  
K Priya ◽  
Nallusamy Vijaykanth ◽  
Marimuthu Ragavan Rameshkumar ◽  
...  

ABSTRACTObjective: The present study was aimed to find out the anticyclic citrullinated peptide (CCP) antibody level and expression level Th2 cytokine-liketumor necrosis factor-alpha (TNF-α) in patients with rheumatoid arthritis (RA) from South India.Methods: The patients attending the Arthritis and Rheumatism Care Centre, Vadapalani, Chennai and healthy individuals from the Presidency College,Chennai, were enrolled for this study. The study group included 74 patients with RA and 50 healthy individuals without history of RA. 3-5 ml ofblood samples was aseptically collected using Vacutainer, and the separated serum samples were transported to the Department of Microbiology,Presidency College, Chennai, Tamil Nadu, in cold chain. Anti-CCP antibodies were detected by enzyme-linked immunosorbent assay (ELISA). Serumconcentrations of TNF-α were studied in patients with RA and in healthy controls, using an ELISA method.Results: The results of anti-CCP enzyme immunoassay revealed that out of 74 patients, all were anti-CCP positive, which included 65 femalesand 9 males. Higher levels of anti-CCP (456 IU/ml) were present in the age group between 41 and 50 followed by 21-30 years age group whichshows 335.28 IU/ml of anti-CCP antibody level. The level of serum TNF-α was measured in the range of 4.6-1082.84 pg/ml for RA patients and6.630-459.74 pg/ml for the healthy control group.Conclusion: TNF-α levels were significantly increased in RA patients compared to healthy individuals. A negative correlation was found between antiCCPantibodyand TNF-αlevelin RA patients.Keywords: Rheumatoid arthritis, Tumor necrosis factor-alpha, Enzyme-linked immunosorbent assay, Anticyclic citrullinated peptide antibodies. 


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