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Infliximab-abda

Author: Shamma Aboobacker Author: Preeti Patel Editor: Ahmad M. Al Aboud Updated: 7/6/2025 9:28:27 PM

Indications

Infliximab (IFX) is a biologic agent targeting tumor necrosis factor alpha (TNF-α), an immune mediator involved in various pathological processes. Infliximab-abda is a biosimilar of infliximab. Anti-TNF-α agents have been administered since 1998; however, their first use in dermatology dates back to 2002, when they were introduced to treat psoriasis.[1] Knight et al discovered the first anti-TNF therapy: a chimeric monoclonal antibody, now known as infliximab. This early form of infliximab comprised a 25% to 30% murine fusion or antigen-binding variable segment and a 70% to 75% human IgG antibody constant segment.[2] The first trial of IFX was conducted in 1994 on patients with rheumatoid arthritis, yielding marked clinical improvement compared to the placebo.[3][4]

FDA-Approved Indications

  • Crohn disease, including pediatric Crohn disease (CD) [5][6]
  • Ulcerative colitis, including pediatric ulcerative colitis [7][8]
  • Rheumatoid arthritis [9]
  • Ankylosing spondylitis [10]
  • Psoriatic arthritis [11]
  • Plaque psoriasis [12]
  • Juvenile idiopathic arthritis [13]

Crohn's disease: Moderate-to-severe, active Crohn disease is an indication for induction and maintenance of clinical remission. An inadequate response to conventional therapy serves as an indication for starting infliximab in such cases. Pediatric patients aged 6 and older with moderate-to-severe disease who fail to respond to conventional treatment are candidates for infliximab. The American Association of Gastroenterology recommends TNF-α inhibitors, including infliximab, for adult patients with moderate or severe CD for induction and maintenance of remission. For patients with active perianal fistulas, infliximab is strongly recommended over no treatment for induction and maintenance of fistula remission.[14]

Ulcerative colitis: Infliximab is prescribed to induce and maintain clinical remission and eliminate corticosteroid therapy in those showing inadequate response. Pediatric patients aged 6 and older are suitable for this mode of treatment.

Rheumatoid arthritis: Patients undergoing infliximab therapy for moderate-to-severe disease have reported inhibition of joint damage progression and improved physical strength.

Psoriasis: The following types of psoriasis benefit from infliximab therapy:

  • Chronic plaque psoriasis or stable psoriasis of moderate-to-severe involvement
  • Recalcitrant psoriasis
  • Unstable psoriasis
  • Generalized pustular psoriasis or von Zumbusch pustular psoriasis
  • Psoriatic arthritis
  • The American Academy of Dermatology (AAD) and the National Psoriasis Foundation (NPF) recommend infliximab as a monotherapy option for moderate-to-severe plaque psoriasis in adults, including cases involving the palms, soles, nails, and scalp. Infliximab is also suitable for subtypes like pustular or erythrodermic psoriasis. For patients with psoriatic arthritis, infliximab is effective in preventing joint damage and improving symptoms.[15]

Off-label Uses

  • Systemic diseases
    • Systemic lupus erythematosus-associated glomerulonephritis
    • Systemic sclerosis
    • Dermatomyositis
    • Sjogren syndrome
    • Adult-onset Still disease
    • Chronic obstructive pulmonary disease
    • Polymyalgia rheumatica
    • Granulomatosis with polyangiitis [16]
    • Giant cell arteritis [17]
    • Cardiac sarcoidosis [18]
    • Idiopathic membranous nephropathy [19]
  • Ocular diseases 
    • Grave disease ophthalmopathy
    • Idiopathic scleritis
    • Cystoid macular edema (uveitic and diabetic)
    • Age-related macular degeneration
    • Idiopathic uveitis or scleritis [20][21]
  • Dermatological diseases
    • Pemphigoid
    • Aphthous stomatitis
    • Subcorneal pustular dermatosis
    • Atopic dermatitis
    • Toxic epidermal necrolysis
    • SAPHO syndrome
    • Pityriasis rubra pilaris
    • Eosinophilic fasciitis
    • Panniculitis
    • Hidradenitis suppurativa [22]
    • Pyoderma gangrenosum [23]
    • Behcet syndrome [24]
    • Acne fulminans [25]

The United States and Canadian Hidradenitis Suppurativa Foundations recommend infliximab for the treatment of moderate-to-severe disease; however, dose-ranging studies are needed to determine the optimal dosage for effective management.[22] The American College of Rheumatology suggests that in adults with active ankylosing spondylitis who have not responded adequately to treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), treatment with tumor necrosis factor inhibitors, including infliximab, is recommended.[26]

Mechanism of Action

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Mechanism of Action

Infliximab, a TNF-α inhibitor, acts by blocking TNF-α, a proinflammatory, pleiotropic cytokine that is particularly involved in defense mechanisms. Nevertheless, the role of TNF-α varies depending on its concentration, as low levels confer a protective effect, while high amounts exhibit a pathogenic role.[27] TNF-α exists in 2 forms: soluble and transmembrane, both of which are biologically active via TNF receptors (TNFR) Type 1 and Type 2.[28]

The protective role in infection is the most important effect of TNF-α. Interestingly, TNF-α is involved in attaining resistance to infectious agents and has a pathogenic role in septic shock. TNF-α produces anti-inflammatory effects by signaling via TNFR Type 2. The explanation is that TNF-α promotes resistance by activating polymorphonuclear leukocytes and platelets, while enhancing the cytotoxic action of macrophages and natural killer cells, thereby stimulating the immune system.[29] In particular, studying the concept in patients with meningococcal disease revealed high levels of TNF-α in the serum, which coincided with its cytotoxic effect.[30][31]

Another role of TNF-α is resistance to tumors, which occurs due to the cytotoxic effect of TNF-α, leading to cell lysis or apoptosis. Fiers et al studied the impact of TNF-α on tumors in animal models and found that TNF-α acts directly on the tumor cells, particularly in the presence of interferon.[32] Additionally, TNF-α is known to exert proinflammatory effects on the vascular endothelium, resulting in hemorrhagic necrosis.[28] The biological effects are beneficial in various host responses. However, TNF-α has been found to exert pathogenic roles in certain instances.

The role of TNF-α in inflammatory diseases was identified in 1988, when increased TNF-α expression was found in the synovial fluid of patients with rheumatoid arthritis, making it the prototypical disease associated with TNF-α. The discovery of increased TNFR expression in active diseases confirmed this finding. Furthermore, the quantity of shed receptors correlates with disease activity. The evidence suggests that TNF-α regulates proinflammatory cytokines and has a central role in inflammatory processes.[33]

Another disease linked with TNF-α is psoriasis. Studies have shown increased expression of TNF-α in psoriatic skin lesions. The study confirmed this by investigating the peripheral blood mononuclear cells for TNF-α mRNA expression and revealed increased expression in patients with psoriasis compared to healthy controls.[28][34]

Infliximab acts by binding to both soluble and membrane-bound forms of TNF. Binding with TNF-α is found to be stable with high affinity, thereby neutralizing its action. Additionally, it causes apoptosis of cells that release TNF-α, alters cytokine secretion, and upregulates p38 MAP kinase, which is involved in the downward signaling of TNF-α. Binding triggers intracellular signaling, complement-mediated cell lysis, and a decrease in cytokine production.[35]

The effect of intracellular signaling triggers a variety of responses, including the reduction of cytokines, an increase in vascular permeability, a decrease in adhesion molecule expression, and the inactivation of cell lines.[36][37][38] Another response is the delayed recruitment of immune cells to sites of inflammation. However, this excludes the regulatory T-cells that play a beneficial role in immune responses and leads to their increased expression.[39][40][41]

Pharmacokinetics

Absorption: Infliximab is administered intravenously, achieving complete systemic bioavailability.

Distribution: The volume of distribution studies suggests that infliximab is primarily confined to the vascular compartment.

Metabolism: Infliximab is a chimeric IgG1 monoclonal antibody composed of human constant and murine variable regions. This drug is metabolized through proteolytic catabolism into small peptides and amino acids, consistent with the metabolic pathways of endogenous immunoglobulins.

Excretion: Elimination occurs predominantly via the reticuloendothelial system. The median terminal half-life ranges from 7.7 to 9.5 days. Serum concentrations decline in a log-linear fashion. No systemic accumulation has been reported with repeat dosing at 4 or 8-week intervals. Anti-infliximab antibodies significantly increase clearance, often leading to undetectable trough concentrations.

Administration

Available Dosage Forms and Strengths 

Infliximab-abda is available as a 100 mg lyophilized drug powder in a 20 mL vial. Each vial is reconstituted with 10 mL sterile distilled water using a 21-gauge needle, followed by gentle stirring to dissolve the powder. The vial is kept aside for 5 minutes, and the solution is dissolved in 250 mL of 0.9% sodium chloride intravenous solution.[42]

Adult Dosing

Before infliximab infusion, pretreatment with loratadine or cetirizine (0.5 mg/kg; max 25 mg), hydrocortisone (4 mg/kg; max 200 mg), and acetaminophen (15 mg/kg; max 1 g) 30 to 60 minutes before infusion is necessary for mitigating infusion reactions that may occur.[43] Infliximab is prepared as an intravenous infusion, ranging from 3 to 10 mg/kg, with the most common dose of 5 mg/kg. Infliximab has a half-life of 7 to 12 days and a low elimination rate. Therefore, the dosing schedule repeats at weeks 2, 6, and every 8 weeks thereafter.[44] The administration of infliximab should commence within 3 hours after dilution and should be completed over 2 to 3 hours. Monitoring vital signs, including temperature, pulse, blood pressure, and respiratory rate, is crucial for one hour post-infusion.

FDA-approved indications with dosages

  • Psoriasis and psoriatic arthritis: For psoriasis and psoriatic arthritis, infliximab is administered at 5 mg/kg at weeks 0, 2, and 6, followed by every 8 weeks.
  • Rheumatoid arthritis: For rheumatoid arthritis, infliximab is given at 3 mg/kg at weeks 0, 2, and 6, followed by every 8 weeks. Based on the response, the dose may be increased to 10 mg/kg and administered every 4 weeks.
  • Ankylosing spondylitis: The recommended dose for ankylosing spondylitis is 5 mg/kg at weeks 0, 2, and 6, followed by every 6 to 8 weeks.
  • Crohn disease and ulcerative colitis: For Crohn disease and ulcerative colitis, infliximab is administered at 5 mg/kg at weeks 0, 2, and 6, followed by every 8 weeks. Depending on the response, doses may be increased to 10 mg/kg.[45]

Specific Patient Populations

Hepatic impairment: Discontinue infliximab if there is significant transaminitis or increased bilirubin levels.[46]

Renal impairment: The manufacturer's labeling does not provide a dose adjustment for patients with renal impairment. Use with caution.

Pregnancy considerations: According to the joint guidelines established by the American Academy of Dermatology and the National Psoriasis Foundation (AAD-NPF), TNF-α inhibitors are considered safe for use during pregnancy. Furthermore, TNF-α inhibitors are considered safe for men who are attempting conception with their partners. Due to the potential for drug delivery to the fetus, it is essential to consider neonates and infants as immunosuppressed for a duration of at least 1 to 3 months, depending on the specific TNF inhibitor utilized, following the postpartum period of mothers who have been treated with TNF inhibitors. There exists a heightened theoretical risk associated with the use of these medications during the third trimester of pregnancy, attributed to the transplacental transfer of TNF-α inhibitors.[15]

Breastfeeding considerations: Infliximab is typically either absent or present at only trace levels in human milk, with negligible oral bioavailability in nursing infants. Clinical follow-ups of infants exposed in utero and via breastfeeding have demonstrated normal development and no reported adverse effects. While minimal concentrations identified in some samples raise theoretical concerns, levels are insufficient to suggest risk of systemic immunosuppression. In mothers with inflammatory bowel disease, anti–tumor necrosis factor therapy has been associated with reduced concentrations of TNF and IP-10 in early postpartum milk. Continued postpartum use in women treated during pregnancy does not appear to extend infliximab clearance in the infant. Consensus supports the use of infliximab during lactation. Postponing therapy until 2 weeks after delivery may further reduce infant exposure.[47] AAD-NPF suggests that infants may be immunocompromised for 1 to 3 months after birth.[15]

Pediatric patients: Infliximab is approved for use in patients aged 6 to 17 years for the induction and maintenance of remission in Crohn disease (CD) and ulcerative colitis (UC) after an inadequate response to conventional therapy. The effect of administering infliximab to children younger than 6 years for these indications has not been established. In pediatric CD, infliximab has shown efficacy in combination with immunosuppressants in patients 6 and older, though long-term safety (>1 year) remains unconfirmed.

Older patients: No significant differences in safety or efficacy have been noted between older and younger adult patients treated with infliximab. However, severe adverse reactions and infections are more common in older adults, so close monitoring is advised in this population.

Adverse Effects

Various adverse effects associated with the administration of infliximab-abda are discussed below.[48][49][50][49]

Infectious risk

  • Tuberculosis
  • Deep mycoses (eg, histoplasmosis, coccidioidomycosis, blastomycosis, aspergillosis, and candidiasis)
  • Listeriosis and pneumocystosis
  • Pneumonia
  • Abscess
  • Cellulitis
  • Skin ulcers
  • Pyelonephritis

Infusion reactions

  • Immediate: Anaphylaxis
  • Delayed
    • Myalgia
    • Arthralgia
    • Fever and chills
    • Pruritus
    • Edema
    • Urticaria and flushing

Gastrointestinal 

  • Dysphagia
  • Nausea
  • Abdominal pain
  • Diarrhea
  • Dyspepsia

Other

  • Sore throat
  • Flu-like syndrome
  • Headache
  • Vertigo
  • Hepatotoxicity
  • Lupus-like syndrome
  • Serum sickness
  • Congestive heart failure
  • Hypotension
  • Demyelinating disease
  • Lymphoma and other malignancies (eg, hepatosplenic T-cell lymphoma)
  • Cytopenias
  • Optic neuritis

Drug-Drug Interactions

Combination with other biological products: Combining infliximab with other biologics is not recommended to treat the same conditions. Clinical studies of other tumor necrosis factor (TNF) blockers, such as anakinra or abatacept, in combination with infliximab have shown an increased risk of serious infections without additional clinical benefit. Given the nature of adverse reactions associated with these combinations, similar toxicities may be observed when combining anakinra or abatacept with other TNF inhibitors. Therefore, infliximab should not be combined with anakinra or abatacept. Concomitant use of tocilizumab with biologic disease-modifying antirheumatic drugs (DMARDs), including infliximab, should be avoided due to the potential for increased immunosuppression and a heightened risk of infection.

Cytochrome P450 substrates: Chronic inflammation can suppress the formation of cytochrome P450 (CYP450) enzymes due to elevated cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), and interferon (IFN). Consequently, for molecules that antagonize cytokine activity, such as infliximab, CYP450 enzyme activity may be normalized. Monitoring the therapeutic effect or drug concentration is recommended when initiating or discontinuing infliximab in patients using CYP450 substrates with a narrow therapeutic index, such as warfarin, cyclosporine, or theophylline. Dosage adjustments may be necessary.

Live vaccines: Live vaccines should not be administered concurrently with infliximab. Infants exposed to infliximab in utero should not be given live vaccines for at least 6 months following birth.[51]

Contraindications

The absolute contraindications for the use of biologics include the conditions below.[42]

  • Presence of active infections, more importantly, latent or active tuberculosis, Hepatitis B, C, and HIV
  • Hypersensitivity to murine products or infliximab
  • Recent FDA contraindication: the use of infliximab-abda at doses >5 mg/kg in moderate or severe heart failure

Relative contraindications include:

  • PUVA sessions
  • Premalignant conditions
  • Demyelinating disease (eg, Guillain-Barre syndrome)
  • Optic neuritis
  • Multiple sclerosis
  • Pregnancy and lactation
  • Fever
  • Jaundice or marked liver enzyme elevations
  • Stricturing disease

Box Warnings

  • Severe infections: Treatment with infliximab is associated with an increased risk of serious infections, including those resulting in hospitalization or death. This risk is particularly elevated in patients receiving concomitant immunosuppressive agents such as methotrexate or systemic corticosteroids. Infliximab should be discontinued in patients who develop severe infections or sepsis. Infections caused by Legionella pneumophila and Listeria monocytogenes have been reported, along with invasive fungal infections, such as Histoplasma capsulatum, Coccidioides immitis, Candida species, Aspergillus species, Blastomyces dermatitidis, and Pneumocystis jirovecii. These fungal infections can present with disseminated symptoms, and diagnostic testing for fungal antigens or antibodies may yield false-negative results in active cases. Empiric antifungal treatment should be considered in patients at risk for invasive fungal disease who present with systemic illness.
  • Tuberculosis: Active tuberculosis, particularly reactivation of latent Mycobacterium tuberculosis, is another serious risk associated with infliximab. Tuberculosis may present as disseminated or extrapulmonary disease. All patients should undergo testing for latent Mycobacterium tuberculosis infection before starting infliximab and should be monitored throughout therapy. Treatment for latent tuberculosis should be initiated before infliximab use.
  • Malignancies: Malignancies, including lymphoma and other neoplasms, have been reported in pediatric and adolescent patients treated with tumor necrosis factor (TNF) inhibitors, including infliximab. Hepatosplenic T-cell lymphoma (HSTCL), a rare and aggressive malignancy, has been reported postmarketing in patients receiving TNF inhibitors. These cases were often fatal and predominantly occurred in male adolescents and young adults with Crohn disease or ulcerative colitis who had received simultaneous therapy with azathioprine or 6-mercaptopurine. The descriptions of warnings and precautions are provided below.

Warning and Precautions

  • Hepatosplenic T-cell Lymphoma (HSTCL): This rare, aggressive, and fatal lymphoma has been reported with TNF blockers (including infliximab), mainly in young males with Crohn disease or ulcerative colitis on azathioprine or 6-mercaptopurine.[52][53]
  • Skin cancer: Merkel cell carcinoma and melanoma have been reported; periodic skin exams are recommended, especially in patients with risk factors.[54]
  • Cervical cancer: An increased risk of cervical cancer has been observed in women with rheumatoid arthritis on infliximab, especially those older than 60; a causal link has not been excluded; continue periodic screening.[55]
  • Lymphomas: Infliximab may increase the risk of lymphomas and leukemia. However, inflammatory bowel disease and rheumatoid arthritis are independent risk factors for leukemia/lymphoma.
  • Other malignancies: Some TNF blockers may increase the risk of other malignancies. Exercise caution in patients with COPD (smokers). Monitor patients with psoriasis for nonmelanoma skin cancers, especially those who have received prior phototherapy. The role of TNF blockers is unknown. Exercise caution in patients with a previous malignancy or if one develops during treatment.
  • Hepatitis B virus reactivation: Reactivation can occur in HBV carriers, sometimes with fatal outcomes. Test patients before starting infliximab; a positive test requires specialist consultation. Monitor carriers closely during and after therapy. Discontinue infliximab if HBV reactivates and initiate antiviral therapy. Clinicians should exercise caution when restarting infliximab.[56]
  • Hepatotoxicity: Severe liver reactions, some fatal or requiring transplant, have been reported; monitor liver function and discontinue infliximab for jaundice or significantly elevated liver enzymes.[46]
  • Heart failure: Infliximab at doses >5 mg/kg is contraindicated in moderate or severe heart failure; it may cause new or worsening heart failure. Monitor patients with mild heart failure or those with moderate or severe heart failure receiving ≤5 mg/kg closely; discontinue infliximab if symptoms worsen.[57]
  • Hematologic reactions: Low blood cell counts have been reported. Exercise caution in patients with blood disorders. Advise patients to seek immediate medical attention for signs and symptoms of blood disorders or infection. Consider stopping infliximab.
  • Hypersensitivity: Hypersensitivity reactions, including severe manifestations, may occur during or following the infusion or upon re-administration. Therefore, it is critical to have treatment readily available, as re-administration after a period without treatment may escalate the risk of infusion reactions. A study indicates that high levels of CRP are a risk factor for infusion reactions.[58]
  • Cardiovascular and cerebrovascular reactions: Serious events have been reported during or within 24 hours of infusion. Monitor patients closely during infusion and discontinue if a severe reaction occurs.
  • Concurrent administration with other biological products: Concurrent use is not recommended due to the potential for increased infection risk.
  • Switching between biological DMARDs: Exercise caution due to the potential for increased infection risk from overlapping biological activity.
  • Neurologic reactions: Infliximab has been linked to CNS vasculitis, seizures, and new or worsening demyelinating disorders; exercise caution in patients with these disorders and consider discontinuing infliximab if they develop.[59][50]
  • Autoimmunity: Infliximab may cause autoantibody formation and a lupus-like syndrome; discontinue treatment if suggestive symptoms develop.[60]
  • Vaccinations and use of live vaccines or therapeutic infectious agents: Update vaccinations before starting infliximab; avoid live vaccines concurrently. Fatal disseminated BCG infection has been reported in an exposed infant. Wait at least 6 months after birth before giving live vaccines to infants exposed in utero. Avoid concurrent use of therapeutic infectious agents.[61][62]

Monitoring

Baseline Monitoring

  • Complete blood count and hemogram
  • Erythrocyte sedimentation rate or C-reactive protein
  • Liver function test
  • Renal function test and urinalysis
  • Serum electrolytes
  • Anti-nuclear and anti-dsDNA antibodies
  • Screening for hepatitis and HIV infection
  • Chest x-ray
  • Tuberculin skin testing or interferon-gamma release assay test
  • Pregnancy test in females of childbearing age

If indicated, serology for varicella zoster and measles may be obtained.

Ongoing Monitoring

Response to treatment can be evaluated by respective assessment scores, including the Psoriasis Area and Severity Index (PASI), the Dermatology Life Quality Index (DLQI), the Pediatric Crohn Disease Activity Index (PCDAI), the Pediatric Ulcerative Colitis Activity Index (PUCAI), and the Inflammatory Bowel Disease Questionnaire (IBDQ) at 3 months initially and subsequently every 6 months.[63][64]

A complete blood count and hemogram should be repeated at 3 months and every 6 months thereafter. Liver function tests, renal function tests, serum electrolytes, and urinalysis are evaluated at 3 months and every 6 months.[65][66]

Toxicity

Signs and Symptoms of Overdose

Overuse of infliximab leads to prolonged TNF-α inhibition, thereby increasing the risk of infections. This furthermore poses deleterious effects on pregnancy and lactation by impairing the newborn’s defense mechanisms. Since TNF-α is involved in embryogenesis and organogenesis, a deleterious effect on embryo and fetal development is postulated. Another toxic effect of infliximab is the carcinogenic potential resulting from reports of malignancies in children, adolescents, and young adults receiving infliximab over a median of 30 sessions. This hypothesis comes from the finding that TNF-α causes tumoral hemorrhagic necrosis and is therefore used as a treatment for selective tumors.[67] 

Management of Overdose

There is no antidote for infliximab. In case of overdose, it is recommended that the patient be monitored for any signs or symptoms of adverse reactions or effects/precautions listed above. Symptomatic treatment should be initiated immediately.

Enhancing Healthcare Team Outcomes

The primary drawback with biologic therapy is the necessity for lifelong or long-term treatment, the failure of which can lead to incomplete resolution or recurrences. Combination with other agents, such as methotrexate, can enhance the efficacy and response.[68]

Live vaccines and contact with infectious agents should be avoided during infliximab therapy due to the markedly depressed immunity that can result in disseminated infections.[69] A history of latent or active tuberculosis with no confirmation of complete therapy or recent travel to a country with a high incidence of tuberculosis may warrant a course of empiric anti-tubercular treatment. Avoidance of concomitant therapy with anakinra and abatacept is essential due to the increased risk of severe infections.[70] 

Primary care physicians and advanced practice providers evaluate patients for infliximab and initiate baseline screening. Nurses educate, prepare, administer infusions, monitor vital signs and reactions, and escalate concerns as needed. Pharmacists verify dosing, ensure proper preparation, and check for drug interactions. Internists play a crucial role in the comprehensive care of hospitalized patients with multiple comorbidities. Gastroenterologists manage infliximab therapy for inflammatory bowel disease, adjusting doses as needed. Rheumatologists and dermatologists collaborate on therapy for arthritis and psoriasis, assess disease progression, and guide biologic treatment. Consultation with an infectious disease specialist is required for fungal infections, tuberculosis, or HBV reactivation. Oncologists evaluate cancer risk and recurrence, guiding therapeutic decisions. Critical care specialists manage rare overdoses or severe reactions, providing intensive care as needed. As described above, an interprofessional team approach and communication among physicians, advanced practice providers, pharmacists, and nurses are crucial to decreasing potential adverse effects and improving patient outcomes related to infliximab therapy.

References

[1]

Cordoro KM, Feldman SR. TNF-alpha inhibitors in dermatology. Skin therapy letter. 2007 Sep:12(7):4-6     [PubMed PMID: 17940711]

Level 3 (low-level) evidence

[2]

Knight DM, Trinh H, Le J, Siegel S, Shealy D, McDonough M, Scallon B, Moore MA, Vilcek J, Daddona P. Construction and initial characterization of a mouse-human chimeric anti-TNF antibody. Molecular immunology. 1993 Nov:30(16):1443-53     [PubMed PMID: 8232330]

Level 3 (low-level) evidence

[3]

Maini RN, Breedveld FC, Kalden JR, Smolen JS, Davis D, Macfarlane JD, Antoni C, Leeb B, Elliott MJ, Woody JN, Schaible TF, Feldmann M. Therapeutic efficacy of multiple intravenous infusions of anti-tumor necrosis factor alpha monoclonal antibody combined with low-dose weekly methotrexate in rheumatoid arthritis. Arthritis and rheumatism. 1998 Sep:41(9):1552-63     [PubMed PMID: 9751087]

Level 1 (high-level) evidence

[4]

Lichtenstein GR, Soonasra A, Latymer M, Singh S, Feagan BG. Systematic review: effectiveness and safety of switching between originator infliximab and biosimilar infliximab in patients with inflammatory bowel disease. Expert opinion on biological therapy. 2024 Jul:24(7):691-708. doi: 10.1080/14712598.2024.2378090. Epub 2024 Jul 18     [PubMed PMID: 38979696]

Level 1 (high-level) evidence

[5]

Chetwood JD, Tran Y, Subramanian S, Smith PJ, Iborra M, Buisson A, Paramsothy S, Leong RW. Intravenous Versus Subcutaneous Infliximab in Inflammatory Bowel Disease: A Systematic Review and Meta-analysis. Journal of Crohn's & colitis. 2024 Sep 3:18(9):1440-1449. doi: 10.1093/ecco-jcc/jjae059. Epub     [PubMed PMID: 38656784]

Level 1 (high-level) evidence

[6]

Vuijk SA, Jongsma MME, Hoeven BM, Cozijnsen MA, van Pieterson M, de Meij TGJ, Norbruis OF, Groeneweg M, Wolters VM, van Wering H, Hummel T, Stapelbroek J, van der Feen C, van Rheenen PF, van Wijk MP, Teklenburg S, Rizopoulos D, Poley MJ, Escher JC, de Ridder L. Randomised clinical trial: First-line infliximab biosimilar is cost-effective compared to conventional treatment in paediatric Crohn's disease. Alimentary pharmacology & therapeutics. 2024 Jun:59(12):1510-1520. doi: 10.1111/apt.18000. Epub 2024 Apr 21     [PubMed PMID: 38644588]

Level 1 (high-level) evidence

[7]

Choy MC, Li Wai Suen CFD, Con D, Boyd K, Pena R, Burrell K, Rosella O, Proud D, Brouwer R, Gorelik A, Liew D, Connell WR, Wright EK, Taylor KM, Pudipeddi A, Sawers M, Christensen B, Ng W, Begun J, Radford-Smith G, Garg M, Martin N, van Langenberg DR, Ding NS, Beswick L, Leong RW, Sparrow MP, De Cruz P. Intensified versus standard dose infliximab induction therapy for steroid-refractory acute severe ulcerative colitis (PREDICT-UC): an open-label, multicentre, randomised controlled trial. The lancet. Gastroenterology & hepatology. 2024 Nov:9(11):981-996. doi: 10.1016/S2468-1253(24)00200-0. Epub 2024 Sep 2     [PubMed PMID: 39236736]

Level 1 (high-level) evidence

[8]

Ananthakrishnan AN, Murad MH, Scott FI, Agrawal M, Haydek JP, Limketkai BN, Loftus EV Jr, Singh S. Comparative Efficacy of Advanced Therapies for Management of Moderate-to-Severe Ulcerative Colitis: 2024 American Gastroenterological Association Evidence Synthesis. Gastroenterology. 2024 Dec:167(7):1460-1482. doi: 10.1053/j.gastro.2024.07.046. Epub 2024 Oct 18     [PubMed PMID: 39425738]

Level 2 (mid-level) evidence

[9]

Khan D, Ahmed N, Muhammad A, Shah KU, Mir M, Rehman AU. A macromolecule infliximab loaded reverse nanomicelles-based transdermal hydrogel: An innovative approach against rheumatoid arthritis. Biomaterials advances. 2025 Feb:167():214093. doi: 10.1016/j.bioadv.2024.214093. Epub 2024 Oct 30     [PubMed PMID: 39492133]

Level 3 (low-level) evidence

[10]

Zouris G, Evangelopoulos DS, Benetos IS, Vlamis J. The Use of TNF-α Inhibitors in Active Ankylosing Spondylitis Treatment. Cureus. 2024 Jun:16(6):e61500. doi: 10.7759/cureus.61500. Epub 2024 Jun 1     [PubMed PMID: 38952586]

[11]

Kerschbaumer A, Smolen JS, Ferreira RJO, Bertheussen H, Baraliakos X, Aletaha D, McGonagle DG, van der Heijde D, McInnes IB, Esbensen BA, Winthrop KL, Boehncke WH, Schoones JW, Gossec L. Efficacy and safety of pharmacological treatment of psoriatic arthritis: a systematic literature research informing the 2023 update of the EULAR recommendations for the management of psoriatic arthritis. Annals of the rheumatic diseases. 2024 May 15:83(6):760-774. doi: 10.1136/ard-2024-225534. Epub 2024 May 15     [PubMed PMID: 38503473]

Level 1 (high-level) evidence

[12]

Ismail O, Jaber K, Jaber Y, Froukh U, Younis A, Albdour K, Momani Y, Almaani N. Short term efficacy of biological treatment for moderate-to-severe plaque psoriasis: a systematic review and network meta-analysis. Archives of dermatological research... 2024 Oct 18:316(10):699. doi: 10.1007/s00403-024-03398-y. Epub 2024 Oct 18     [PubMed PMID: 39424649]

Level 1 (high-level) evidence

[13]

Steeland S, Libert C, Vandenbroucke RE. A New Venue of TNF Targeting. International journal of molecular sciences. 2018 May 11:19(5):. doi: 10.3390/ijms19051442. Epub 2018 May 11     [PubMed PMID: 29751683]

[14]

Feuerstein JD, Ho EY, Shmidt E, Singh H, Falck-Ytter Y, Sultan S, Terdiman JP, American Gastroenterological Association Institute Clinical Guidelines Committee. AGA Clinical Practice Guidelines on the Medical Management of Moderate to Severe Luminal and Perianal Fistulizing Crohn's Disease. Gastroenterology. 2021 Jun:160(7):2496-2508. doi: 10.1053/j.gastro.2021.04.022. Epub     [PubMed PMID: 34051983]

Level 1 (high-level) evidence

[15]

Menter A, Strober BE, Kaplan DH, Kivelevitch D, Prater EF, Stoff B, Armstrong AW, Connor C, Cordoro KM, Davis DMR, Elewski BE, Gelfand JM, Gordon KB, Gottlieb AB, Kavanaugh A, Kiselica M, Korman NJ, Kroshinsky D, Lebwohl M, Leonardi CL, Lichten J, Lim HW, Mehta NN, Paller AS, Parra SL, Pathy AL, Rupani RN, Siegel M, Wong EB, Wu JJ, Hariharan V, Elmets CA. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with biologics. Journal of the American Academy of Dermatology. 2019 Apr:80(4):1029-1072. doi: 10.1016/j.jaad.2018.11.057. Epub 2019 Feb 13     [PubMed PMID: 30772098]

[16]

Valor-Méndez L, Kleyer A, Rech J, Manger B, Schett G. Sustained clinical remission under infliximab/rituximab combination therapy in a patient with granulomatosis with polyangiitis. Auto- immunity highlights. 2021 Mar 6:12(1):5. doi: 10.1186/s13317-020-00147-9. Epub 2021 Mar 6     [PubMed PMID: 33676553]

[17]

Hoffman GS, Cid MC, Rendt-Zagar KE, Merkel PA, Weyand CM, Stone JH, Salvarani C, Xu W, Visvanathan S, Rahman MU, Infliximab-GCA Study Group. Infliximab for maintenance of glucocorticosteroid-induced remission of giant cell arteritis: a randomized trial. Annals of internal medicine. 2007 May 1:146(9):621-30     [PubMed PMID: 17470830]

Level 1 (high-level) evidence

[18]

Ahmed R, Okafor J, Khattar R, Azzu A, Baksi J, Wechalekar K, Sharma R, Wells A, Kouranos V. The role of infliximab in treating refractory cardiac sarcoidosis. Case series and systematic review of literature. Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG. 2024 Jun 28:41(2):e2024013. doi: 10.36141/svdld.v41i2.14484. Epub 2024 Jun 28     [PubMed PMID: 38940716]

Level 1 (high-level) evidence

[19]

Sfikakis PP. The first decade of biologic TNF antagonists in clinical practice: lessons learned, unresolved issues and future directions. Current directions in autoimmunity. 2010:11():180-210. doi: 10.1159/000289205. Epub 2010 Feb 18     [PubMed PMID: 20173395]

Level 3 (low-level) evidence

[20]

Kruh JN, Yang P, Suelves AM, Foster CS. Infliximab for the treatment of refractory noninfectious Uveitis: a study of 88 patients with long-term follow-up. Ophthalmology. 2014 Jan:121(1):358-364. doi: 10.1016/j.ophtha.2013.07.019. Epub 2013 Sep 4     [PubMed PMID: 24011995]

[21]

Ishikawa T, Nishimura K, Okamoto N, Akamine K, Inoue N, Irabu H, Kato K, Keino H, Kojima M, Kubo H, Maruyama K, Mizuta M, Shabana K, Shimizu M, Sugita Y, Takakuwa Y, Takanashi S, Takase H, Umebayashi H, Umezawa N, Yamanishi S, Yamazaki K, Yashiro M, Yasumi T, Mori M. Efficacy and safety of tumor necrosis factor inhibitors for systemic juvenile idiopathic arthritis: A systematic review. Modern rheumatology. 2024 Dec 25:35(1):174-184. doi: 10.1093/mr/roae050. Epub     [PubMed PMID: 38795057]

Level 1 (high-level) evidence

[22]

Alikhan A, Sayed C, Alavi A, Alhusayen R, Brassard A, Burkhart C, Crowell K, Eisen DB, Gottlieb AB, Hamzavi I, Hazen PG, Jaleel T, Kimball AB, Kirby J, Lowes MA, Micheletti R, Miller A, Naik HB, Orgill D, Poulin Y. North American clinical management guidelines for hidradenitis suppurativa: A publication from the United States and Canadian Hidradenitis Suppurativa Foundations: Part II: Topical, intralesional, and systemic medical management. Journal of the American Academy of Dermatology. 2019 Jul:81(1):91-101. doi: 10.1016/j.jaad.2019.02.068. Epub 2019 Mar 11     [PubMed PMID: 30872149]

[23]

Salehzadeh F, Mohammadikebar Y, Enteshary A, Ghanbarpour O, Mirzarahimi M. Infliximab in treatment of idiopathic refractory childhood pyoderma gangrenosum (PG). Biologics : targets & therapy. 2019:13():97-99. doi: 10.2147/BTT.S203753. Epub 2019 May 27     [PubMed PMID: 31239637]

[24]

Saadoun D, Maalouf G, Vieira M, Trad S, Lazaro E, Sacre K, Plessier A, Sené T, Koné-Paut I, Noel N, Mekinian A, Lambert M, Ribeiro E, Mirault T, Mele N, Dellal A, Fain O, Melki I, Chiche L, Gaudric J, Redheuil A, Maillart E, Ghembaza A, Desbois AC, Mirouse A, Domont F, Leroux G, Ferfar Y, Rigolet A, Viallard JF, Vautier M, Resche-Rigon M, Cacoub P. Infliximab versus Cyclophosphamide for Severe Behçet's Syndrome. NEJM evidence. 2024 Nov:3(11):EVIDoa2300354. doi: 10.1056/EVIDoa2300354. Epub 2024 Oct 22     [PubMed PMID: 39437137]

[25]

Dall'oglio F, Puglisi DF, Nasca MR, Micali G. Acne fulminans. Giornale italiano di dermatologia e venereologia : organo ufficiale, Societa italiana di dermatologia e sifilografia. 2020 Dec:155(6):711-718. doi: 10.23736/S0392-0488.20.06711-5. Epub 2020 Oct 21     [PubMed PMID: 33084268]

[26]

Ward MM, Deodhar A, Gensler LS, Dubreuil M, Yu D, Khan MA, Haroon N, Borenstein D, Wang R, Biehl A, Fang MA, Louie G, Majithia V, Ng B, Bigham R, Pianin M, Shah AA, Sullivan N, Turgunbaev M, Oristaglio J, Turner A, Maksymowych WP, Caplan L. 2019 Update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network Recommendations for the Treatment of Ankylosing Spondylitis and Nonradiographic Axial Spondyloarthritis. Arthritis & rheumatology (Hoboken, N.J.). 2019 Oct:71(10):1599-1613. doi: 10.1002/art.41042. Epub 2019 Aug 22     [PubMed PMID: 31436036]

[27]

Tracey D, Klareskog L, Sasso EH, Salfeld JG, Tak PP. Tumor necrosis factor antagonist mechanisms of action: a comprehensive review. Pharmacology & therapeutics. 2008 Feb:117(2):244-79     [PubMed PMID: 18155297]

Level 3 (low-level) evidence

[28]

Schottelius AJ, Moldawer LL, Dinarello CA, Asadullah K, Sterry W, Edwards CK 3rd. Biology of tumor necrosis factor-alpha- implications for psoriasis. Experimental dermatology. 2004 Apr:13(4):193-222     [PubMed PMID: 15086336]

Level 3 (low-level) evidence

[29]

Wong M, Ziring D, Korin Y, Desai S, Kim S, Lin J, Gjertson D, Braun J, Reed E, Singh RR. TNFalpha blockade in human diseases: mechanisms and future directions. Clinical immunology (Orlando, Fla.). 2008 Feb:126(2):121-36     [PubMed PMID: 17916444]

Level 3 (low-level) evidence

[30]

Esposito E, Cuzzocrea S. TNF-alpha as a therapeutic target in inflammatory diseases, ischemia-reperfusion injury and trauma. Current medicinal chemistry. 2009:16(24):3152-67     [PubMed PMID: 19689289]

[31]

Waage A, Halstensen A, Espevik T. Association between tumour necrosis factor in serum and fatal outcome in patients with meningococcal disease. Lancet (London, England). 1987 Feb 14:1(8529):355-7     [PubMed PMID: 2880163]

[32]

Fiers W. Tumor necrosis factor. Characterization at the molecular, cellular and in vivo level. FEBS letters. 1991 Jul 22:285(2):199-212     [PubMed PMID: 1649771]

Level 3 (low-level) evidence

[33]

Feldmann M. Development of anti-TNF therapy for rheumatoid arthritis. Nature reviews. Immunology. 2002 May:2(5):364-71. doi: 10.1038/nri802. Epub     [PubMed PMID: 12033742]

[34]

Uyemura K, Yamamura M, Fivenson DF, Modlin RL, Nickoloff BJ. The cytokine network in lesional and lesion-free psoriatic skin is characterized by a T-helper type 1 cell-mediated response. The Journal of investigative dermatology. 1993 Nov:101(5):701-5     [PubMed PMID: 7693825]

[35]

Mitoma H, Horiuchi T, Tsukamoto H, Ueda N. Molecular mechanisms of action of anti-TNF-α agents - Comparison among therapeutic TNF-α antagonists. Cytokine. 2018 Jan:101():56-63. doi: 10.1016/j.cyto.2016.08.014. Epub 2016 Aug 24     [PubMed PMID: 27567553]

[36]

Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM. Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis. The Journal of clinical investigation. 2003 Mar:111(6):821-31     [PubMed PMID: 12639988]

[37]

Charles P, Elliott MJ, Davis D, Potter A, Kalden JR, Antoni C, Breedveld FC, Smolen JS, Eberl G, deWoody K, Feldmann M, Maini RN. Regulation of cytokines, cytokine inhibitors, and acute-phase proteins following anti-TNF-alpha therapy in rheumatoid arthritis. Journal of immunology (Baltimore, Md. : 1950). 1999 Aug 1:163(3):1521-8     [PubMed PMID: 10415055]

Level 1 (high-level) evidence

[38]

Danese S, Sans M, Scaldaferri F, Sgambato A, Rutella S, Cittadini A, Piqué JM, Panes J, Katz JA, Gasbarrini A, Fiocchi C. TNF-alpha blockade down-regulates the CD40/CD40L pathway in the mucosal microcirculation: a novel anti-inflammatory mechanism of infliximab in Crohn's disease. Journal of immunology (Baltimore, Md. : 1950). 2006 Feb 15:176(4):2617-24     [PubMed PMID: 16456024]

Level 1 (high-level) evidence

[39]

Souto-Carneiro MM, Mahadevan V, Takada K, Fritsch-Stork R, Nanki T, Brown M, Fleisher TA, Wilson M, Goldbach-Mansky R, Lipsky PE. Alterations in peripheral blood memory B cells in patients with active rheumatoid arthritis are dependent on the action of tumour necrosis factor. Arthritis research & therapy. 2009:11(3):R84. doi: 10.1186/ar2718. Epub 2009 Jun 5     [PubMed PMID: 19500335]

Level 2 (mid-level) evidence

[40]

Leipe J, Skapenko A, Lipsky PE, Schulze-Koops H. Regulatory T cells in rheumatoid arthritis. Arthritis research & therapy. 2005:7(3):93     [PubMed PMID: 15899057]

[41]

Bayry J, Lacroix-Desmazes S, Dasgupta S, Kazatchkine MD, Kaveri SV. Efficacy of regulatory T-cell immunotherapy: are inflammatory cytokines key determinants? Nature reviews. Immunology. 2008 Jan:8(1):1p following 86; author reply 1p following 86     [PubMed PMID: 18049489]

Level 3 (low-level) evidence

[42]

Hanauer SB, Feagan BG, Lichtenstein GR, Mayer LF, Schreiber S, Colombel JF, Rachmilewitz D, Wolf DC, Olson A, Bao W, Rutgeerts P, ACCENT I Study Group. Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial. Lancet (London, England). 2002 May 4:359(9317):1541-9     [PubMed PMID: 12047962]

Level 1 (high-level) evidence

[43]

Wasserman MJ, Weber DA, Guthrie JA, Bykerk VP, Lee P, Keystone EC. Infusion-related reactions to infliximab in patients with rheumatoid arthritis in a clinical practice setting: relationship to dose, antihistamine pretreatment, and infusion number. The Journal of rheumatology. 2004 Oct:31(10):1912-7     [PubMed PMID: 15468353]

[44]

Rajagopalan M, Mital A. Biologics use in Indian psoriasis patients. Indian dermatology online journal. 2016 Nov-Dec:7(6):489-497     [PubMed PMID: 27990383]

[45]

Monaco C, Nanchahal J, Taylor P, Feldmann M. Anti-TNF therapy: past, present and future. International immunology. 2015 Jan:27(1):55-62. doi: 10.1093/intimm/dxu102. Epub 2014 Nov 19     [PubMed PMID: 25411043]

Level 3 (low-level) evidence

[46]

. Infliximab. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. 2012:():     [PubMed PMID: 31643528]

[47]

. Infliximab. Drugs and Lactation Database (LactMed®). 2006:():     [PubMed PMID: 30000410]

[48]

Aygun D, Sahin S, Adrovic A, Barut K, Cokugras H, Camcıoglu Y, Kasapcopur O. The frequency of infections in patients with juvenile idiopathic arthritis on biologic agents: 1-year prospective study. Clinical rheumatology. 2019 Apr:38(4):1025-1030. doi: 10.1007/s10067-018-4367-9. Epub 2018 Nov 17     [PubMed PMID: 30448935]

[49]

Kerbleski JF, Gottlieb AB. Dermatological complications and safety of anti-TNF treatments. Gut. 2009 Aug:58(8):1033-9. doi: 10.1136/gut.2008.163683. Epub     [PubMed PMID: 19592682]

[50]

Kaltsonoudis E, Zikou AK, Voulgari PV, Konitsiotis S, Argyropoulou MI, Drosos AA. Neurological adverse events in patients receiving anti-TNF therapy: a prospective imaging and electrophysiological study. Arthritis research & therapy. 2014 Jun 17:16(3):R125. doi: 10.1186/ar4582. Epub 2014 Jun 17     [PubMed PMID: 24938855]

[51]

Selinger CP, Bel Kok K, Limdi JK, Kent A, Cooney R, Nelson-Piercy C. Live vaccinations for infants exposed to maternal infliximab in utero and via breast milk - the need for nuanced decision making. BMJ open gastroenterology. 2022 Oct:9(1):. doi: 10.1136/bmjgast-2022-001029. Epub     [PubMed PMID: 36216381]

[52]

Chang M, Frohlinger M, Williams N, George L. A Rare Presentation of a Devastating Disease: Hepatosplenic T-Cell Lymphoma in Crohn's Disease Without Thiopurine Exposure. ACG case reports journal. 2025 May:12(5):e01695. doi: 10.14309/crj.0000000000001695. Epub 2025 May 8     [PubMed PMID: 40343217]

Level 3 (low-level) evidence

[53]

Kotlyar DS, Osterman MT, Diamond RH, Porter D, Blonski WC, Wasik M, Sampat S, Mendizabal M, Lin MV, Lichtenstein GR. A systematic review of factors that contribute to hepatosplenic T-cell lymphoma in patients with inflammatory bowel disease. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2011 Jan:9(1):36-41.e1. doi: 10.1016/j.cgh.2010.09.016. Epub 2010 Oct 1     [PubMed PMID: 20888436]

Level 1 (high-level) evidence

[54]

Harrison A, Brahs A, Fardos M, Siddiqui F, Walker A, Miller R, Moon S. Merkel cell carcinoma in a young female on infliximab. JAAD case reports. 2022 Sep:27():38-40. doi: 10.1016/j.jdcr.2022.07.003. Epub 2022 Jul 9     [PubMed PMID: 35996443]

Level 3 (low-level) evidence

[55]

Kreijne JE, Goetgebuer RL, Erler NS, De Boer NK, Siebers AG, Dijkstra G, van Kemenade FA, Hoentjen F, Oldenburg B, van der Meulen AE, Ponsioen CIJ, Pierik MJ, van der Woude CJ, de Vries AC, Dutch Initiative on Crohn and Colitis (ICC). Cumulative exposure to immunomodulators increases risk of cervical neoplasia in women with inflammatory bowel disease. Alimentary pharmacology & therapeutics. 2023 Jul:58(2):207-217. doi: 10.1111/apt.17555. Epub 2023 May 23     [PubMed PMID: 37221820]

[56]

Ojiro K, Naganuma M, Ebinuma H, Kunimoto H, Tada S, Ogata H, Iwao Y, Saito H, Hibi T. Reactivation of hepatitis B in a patient with Crohn's disease treated using infliximab. Journal of gastroenterology. 2008:43(5):397-401. doi: 10.1007/s00535-008-2165-x. Epub 2008 Jul 1     [PubMed PMID: 18592158]

[57]

Grillo TG, Almeida LR, Beraldo RF, Marcondes MB, Queiróz DAR, da Silva DL, Quera R, Baima JP, Saad-Hossne R, Sassaki LY. Heart failure as an adverse effect of infliximab for Crohn's disease: A case report and review of the literature. World journal of clinical cases. 2021 Nov 26:9(33):10382-10391. doi: 10.12998/wjcc.v9.i33.10382. Epub     [PubMed PMID: 34904114]

Level 3 (low-level) evidence

[58]

Amemiya T, Suzuki H. Risk factors for infliximab-induced infusion reactions based on a retrospective study of medical information. International journal of clinical pharmacology and therapeutics. 2024 Jul:62(7):307-310. doi: 10.5414/CP204568. Epub     [PubMed PMID: 38726563]

Level 2 (mid-level) evidence

[59]

Baumer FM, Ouahed J, Verhave M, Rivkin MJ. Fatal Central Nervous System Disease Following First Infliximab Infusion in a Child With Inflammatory Bowel Disease. Pediatric neurology. 2016 Apr:57():91-4. doi: 10.1016/j.pediatrneurol.2015.12.017. Epub 2015 Dec 24     [PubMed PMID: 26831951]

[60]

He M, Yang J, Yan S, Shu Q, Liu PC. Conducting a real-world study of Tumor Necrosis factor-alpha inhibitors-induced Systemic Lupus Erythematosus based on the FAERS database. Scientific reports. 2025 Feb 26:15(1):6838. doi: 10.1038/s41598-025-90566-3. Epub 2025 Feb 26     [PubMed PMID: 40000785]

[61]

Cheent K, Nolan J, Shariq S, Kiho L, Pal A, Arnold J. Case Report: Fatal case of disseminated BCG infection in an infant born to a mother taking infliximab for Crohn's disease. Journal of Crohn's & colitis. 2010 Nov:4(5):603-5. doi: 10.1016/j.crohns.2010.05.001. Epub 2010 Jun 9     [PubMed PMID: 21122568]

Level 3 (low-level) evidence

[62]

Yoshida M, Takeuchi I, Shoji K, Miyairi I, Arai K. Bacillus Calmette-Guérin Cervical Lymphadenitis in a 6-Year-Old Boy on Infliximab for Inflammatory Bowel Disease. The Pediatric infectious disease journal. 2020 Sep:39(9):e242-e244. doi: 10.1097/INF.0000000000002712. Epub     [PubMed PMID: 32345827]

[63]

Dotson JL, Crandall WV, Zhang P, Forrest CB, Bailey LC, Colletti RB, Kappelman MD. Feasibility and validity of the pediatric ulcerative colitis activity index in routine clinical practice. Journal of pediatric gastroenterology and nutrition. 2015 Feb:60(2):200-4. doi: 10.1097/MPG.0000000000000568. Epub     [PubMed PMID: 25221935]

Level 2 (mid-level) evidence

[64]

Sexton KA, Walker JR, Targownik LE, Graff LA, Haviva C, Beatie BE, Petty SK, Bernstein MT, Singh H, Miller N, Bernstein CN. The Inflammatory Bowel Disease Symptom Inventory: A Patient-report Scale for Research and Clinical Application. Inflammatory bowel diseases. 2019 Jul 17:25(8):1277-1290. doi: 10.1093/ibd/izz038. Epub     [PubMed PMID: 30918969]

[65]

Archer R, Hock E, Hamilton J, Stevens J, Essat M, Poku E, Clowes M, Pandor A, Stevenson M. Assessing prognosis and prediction of treatment response in early rheumatoid arthritis: systematic reviews. Health technology assessment (Winchester, England). 2018 Nov:22(66):1-294. doi: 10.3310/hta22660. Epub     [PubMed PMID: 30501821]

Level 1 (high-level) evidence

[66]

Svenson M, Geborek P, Saxne T, Bendtzen K. Monitoring patients treated with anti-TNF-alpha biopharmaceuticals: assessing serum infliximab and anti-infliximab antibodies. Rheumatology (Oxford, England). 2007 Dec:46(12):1828-34     [PubMed PMID: 18032541]

Level 2 (mid-level) evidence

[67]

Khanna D, McMahon M, Furst DE. Safety of tumour necrosis factor-alpha antagonists. Drug safety. 2004:27(5):307-24     [PubMed PMID: 15061685]

Level 3 (low-level) evidence

[68]

Barland C, Kerdel FA. Addition of low-dose methotrexate to infliximab in the treatment of a patient with severe, recalcitrant pustular psoriasis. Archives of dermatology. 2003 Jul:139(7):949-50     [PubMed PMID: 12873907]

Level 3 (low-level) evidence

[69]

Heller MM, Wu JJ, Murase JE. Fatal case of disseminated BCG infection after vaccination of an infant with in utero exposure to infliximab. Journal of the American Academy of Dermatology. 2011 Oct:65(4):870. doi: 10.1016/j.jaad.2011.04.030. Epub     [PubMed PMID: 21920245]

Level 3 (low-level) evidence

[70]

Salliot C, Dougados M, Gossec L. Risk of serious infections during rituximab, abatacept and anakinra treatments for rheumatoid arthritis: meta-analyses of randomised placebo-controlled trials. Annals of the rheumatic diseases. 2009 Jan:68(1):25-32. doi: 10.1136/ard.2007.083188. Epub 2008 Jan 18     [PubMed PMID: 18203761]

Level 1 (high-level) evidence