Azathioprine

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Article initiated by:
Raeesah.Ahsan, Romy Bejjani, MD, Priyanka.Bhatnagar, Erin Flynn, Agni Kakouri MD, MBA, Andreas Theocharis, MD, Ally.Toyos
All contributors:
Raeesah.Ahsan, Romy Bejjani, MD, Priyanka.Bhatnagar, Erin Flynn, Andreas Theocharis, MD, Ally.Toyos, Agni Kakouri MD, MBA
Assigned editor:
Review:
Assigned status Update Pending
.


Azathioprine (AZA) is a systemic thiopurine antimetabolite used as a corticosteroid-sparing immunomodulatory agent for selected noninfectious ocular inflammatory diseases, including uveitis, scleritis, and ocular mucous membrane pemphigoid/ocular cicatricial pemphigoid.[1][2][3] It is generally considered a conventional non-biologic systemic immunomodulatory agent and may be used when inflammation is inadequately controlled with corticosteroids alone, when corticosteroid-related adverse effects are significant, or when long-term disease control is anticipated and a corticosteroid-sparing strategy is required.[2]

Medical Therapy

Description

Azathioprine is a prodrug of 6-mercaptopurine and is classified clinically as an antimetabolite immunosuppressant (thiopurine).[3] Its immunomodulatory effects are mediated through interference with purine metabolism and nucleic acid synthesis, resulting in suppression of T- and B-lymphocyte proliferation and reduced immune activation. This underlies its use as a systemic corticosteroid-sparing agent in chronic inflammatory diseases, including ocular inflammation.[3][4]

Within systemic immunomodulatory therapy for uveitis, AZA is often considered alongside other conventional antimetabolites (e.g., methotrexate and mycophenolate mofetil).[1] Comparative cohort analyses suggest AZA can be effective but may have higher treatment-limiting side effects than some alternative antimetabolites in ocular inflammation.[5] Separately, AZA is currently approved as an adjunctive therapy for the prevention of renal transplant rejection and for the treatment of active rheumatoid arthritis (RA).[6]

Patient Selection

Azathioprine is appropriate for patients with noninfectious ocular inflammatory diseases requiring corticosteroid-sparing immunosuppression, including those with chronic or recurrent inflammation inadequately controlled with corticosteroids alone, significant corticosteroid-related adverse effects, or requiring long-term disease control.[1]

Current practice patterns generally favor methotrexate over azathioprine as the preferred first-line conventional agent overall, although azathioprine remains a useful option in selected patients.[7] In current uveitis practice, azathioprine remains particularly relevant in Behcet uveitis and has also shown activity in selected pediatric series, including juvenile idiopathic arthritis-associated uveitis.[2][7][8][9][10]

In the largest ophthalmic cohort, azathioprine was found to be moderately effective as a corticosteroid-sparing agent for ocular inflammatory disease, but treatment success often required several months and treatment-limiting adverse effects were not uncommon.[2]

Indications

In ophthalmology, azathioprine is used typically off-label as a systemic corticosteroid-sparing agent for noninfectious ocular inflammation, including:

  • Noninfectious uveitis (anterior, intermediate, posterior or panuveitis), particularly when disease is chronic, recurrent, vision-threatening, or requires systemic corticosteroids beyond what is considered acceptable for long-term use.[1][2][3]
  • Behcet disease uveitis/retinal vasculitis, where azathioprine benefits on both ocular and systemic outcomes.[9][11][12]
  • Scleritis.[2][5]
  • Ocular mucous membrane pemphigoid/ocular cicatricial pemphigoid, where systemic immunosuppression is used to limit progressive conjunctival cicatrization and vision-threatening surface disease.[2][13][14]
  • Selected pediatric indications (e.g., refractory or steroid-dependent juvenile idiopathic arthritis-associated uveitis) when other conventional agents are inadequate or not tolerated.[8]

Historically, azathioprine has also been reported in older ophthalmic literature for chronic iridocyclitis and other autoimmune uveitis phenotypes, though contemporary use is typically guided by broader uveitis immunomodulatory frameworks and modern safety monitoring expectations.[15]


More recently, retrospective ophthalmic data have suggested that azathioprine may be an effective first-line adjunct to systemic corticosteroids in acute Vogt-Koyanagi-Harada disease, although the available evidence remains limited and retrospective.[16] A 2024 comparative study in non-anterior sarcoidosis-associated uveitis provides useful contemporary context for azathioprine’s place among conventional agents, but does not establish it as the preferred drug.[17]

Contraindications

Azathioprine is contraindicated in patients with known hypersensitivity to azathioprine, 6-mercaptopurine, or any component of the formulation.

It should also generally be avoided, or used only with extreme caution, in the following settings:

  • Baseline severe cytopenias or significant hepatic dysfunction where adding a myelosuppressive/hepatotoxic agent poses high risk (clinical judgment; coordinate with internal medicine/rheumatology).[6][18][19][20]
  • Patients with absent TPMT or absent NUDT15 function (e.g., homozygous loss-of-function) because of increased risk of profound, potentially life-threatening myelosuppression with standard thiopurine dosing.[4][21] Contemporary guidance recommends avoiding thiopurines or using extreme dose reductions only in exceptional circumstances with specialized oversight.[4]
  • Clinically significant active infection, where additional immunosuppression would be unsafe (clinical judgment).[1]
  • Concurrent use with xanthine oxidase inhibitors, such as allopurinol, without dose reduction. Coadministration with febuxostat is generally avoided because of the risk of severe toxicity.[22]
  • Prior severe hypersensitivity reaction to azathioprine.[23]
  • Pre-existing hepatotoxicity, because liver dysfunction may occur during treatment. Regular monitoring of liver enzymes is required.[6][20]


Use of AZA during pregnancy is not generally contraindicated. It may be continued with specialist supervision and individualized risk/benefit assessment.[24]

Clinical Pharmacology

Azathioprine is a prodrug that is well absorbed after oral administration and is rapidly converted to 6-mercaptopurine (6-MP), which is subsequently metabolized to 6-thioguanine nucleotides (6-TGNs), the active metabolites responsible for the immunosuppressive effects of thiopurines through incorporation into DNA and suppression of lymphocyte proliferation, as well as for their toxic effects.[3][4] Inactivation occurs primarily through thiopurine S-methyltransferase (TPMT) mediated methylation and xanthine oxidase–mediated oxidation. NUDT15 (nudix hydrolase 15) also catabolizes active thioguanine triphosphates downstream. Both azathioprine and 6-MP are rapidly cleared from blood, and the elimination half-life of 6-MP is less than 2 hours.[6]

A major practical point for ophthalmologists is that thiopurines have substantial inter-patient variability in metabolism and toxicity risk.[4][21] Two enzymes are central to this variability:

  • TPMT: reduced activity raises the risk of excessive active metabolite exposure and severe myelosuppression with standard dosing.[4]
  • NUDT15: decreased function also predisposes to thiopurine toxicity, including severe myelosuppression; allele frequencies vary by ancestry, supporting a low threshold for either genotype- or phenotype-informed prescribing in diverse populations.[4]


Pharmacogenetic dosing recommendations are published and periodically updated by the Clinical Pharmacogenetics Implementation Consortium[21] and provide starting-dose frameworks based on TPMT and NUDT15 genotypes/phenotypes, emphasizing that genotype-informed dosing reduces (but does not eliminate) the need for ongoing laboratory monitoring.[4]

Genetic polymorphisms in TPMT and NUDT15 significantly influence toxicity risk.[21] Variant frequencies differ by ancestry, and reduced activity of either enzyme increases the risk of severe thiopurine-related myelosuppression.[6] For ophthalmic practice, the key point is that genotype-informed dosing can reduce, but does not eliminate, toxicity risk.[6][21]

Warnings/Precautions

General

Regular laboratory monitoring is indicated with azathioprine.[6] The major preventable harms are hematologic toxicity and hepatotoxicity.[6] Azathioprine may cause dose-dependent, reversible bone marrow suppression, including leukopenia/neutropenia, thrombocytopenia, and anemia, and these complications can be abrupt and severe even when pre-treatment TPMT/NUDT15 assessment has been performed.[4][6][18]

CBC and liver function testing should be performed frequently early after initiation or dose escalation and periodically thereafter, with closer monitoring in higher-risk patients.[20]

Other commonly reported adverse effects include gastrointestinal intolerance (nausea, vomiting, and diarrhea), hepatotoxicity, pancreatitis, and increased susceptibility to infections due to immunosuppression.[6][19] While long-term thiopurine therapy has been linked to malignancy in some non-ophthalmic settings, available ophthalmology-specific data have not shown a clear azathioprine-associated increase in malignancy risk, though a modest excess risk with systemic immunosuppression overall has been reported in at least one cohort.[25][26][27][28]

Patients with deficiency of TPMT or NUDT15 are at increased risk of severe myelosuppression and may require dose adjustments or alternative therapy.[4]

Before treatment is initiated, baseline evaluation generally includes CBC with differential, liver function testing, and consideration of TPMT and NUDT15 assessment where available, with additional systemic evaluation guided by the patient’s comorbidities and co-managing clinicians.[1][4][6]

Information for Patients

Patients receiving azathioprine should be counseled that it is an immunomodulatory medication and that:

  • Benefits often require time on therapy and may be paired with corticosteroid tapering strategies rather than immediate symptom relief.[2][3]
  • Regular blood testing (including CBC and LFT) is a core part of safe use, and symptoms such as fever, unexpected bruising/bleeding, severe sore throat, jaundice, dark urine, or profound fatigue should prompt urgent evaluation for infection or cytopenia/hepatotoxicity.[6][18][20]
  • Sudden systemic symptoms soon after initiation (e.g., fever, malaise, rash, arthralgia) can reflect azathioprine hypersensitivity.[23]

Ophthalmology-specific studies have not shown increased cancer or overall mortality with azathioprine use in ocular inflammatory disease cohorts.[26][27][28] Nevertheless, because chronic immunosuppression may increase the risk of nonmelanoma skin cancer, particularly in highly sun-exposed patients, counseling regarding sun protection and consideration of periodic skin surveillance are reasonable.[25]


Patients should notify their provider of all concomitant medications, as certain drugs may require dose adjustment or avoidance. Azathioprine use in pregnancy should be discussed with a healthcare provider. Patients should not discontinue therapy without medical guidance, as this may lead to recurrence of ocular inflammation.

Drug Interactions

Several interactions are important because they may involve medications prescribed by other clinicians (primary care, rheumatology, gastroenterology), and they can substantially increase toxicity risk.

  • Allopurinol (xanthine oxidase inhibition) can markedly increase thiopurine toxicity risk; ophthalmology-focused reviews recommend reducing azathioprine dose (e.g., to ~25% of typical dose) when co-administered, with close monitoring.[3][22] Concomitant use with febuxostat is not recommended.[6]
  • Warfarin: evidence supports an inhibitory interaction in which azathioprine reduces warfarin anticoagulant effect, implying the need for closer INR monitoring when doses change or therapy is initiated/stopped.[29]


Additional interactions may further increase the risk of hematologic toxicity. Co-administration with angiotensin-converting enzyme (ACE) inhibitors, aminosalicylates (e.g. sulphasalazine or mesalazine) and other myelosuppressive agents can increase hematologic toxicity risk.[4][6][21] These interactions warrant careful monitoring of blood counts and consideration of dose adjustment when used concurrently.

Carcinogenesis/Mutagenesis/Impairment of Fertility

Cancer risk counseling in ocular inflammation should be evidence-informed and nuanced. A focused assessment of malignancy risk literature extrapolated to ocular inflammation suggests that azathioprine likely does not increase overall cancer risk to a detectable degree in non-transplant settings, although immunosuppression generally may increase skin cancer risk in sun-exposed patients, supporting counseling on sun protection and skin surveillance when appropriate.[25][26]

In the SITE ocular inflammation cohort mortality analysis, patients who used azathioprine had overall and cancer mortality similar to patients who never received immunosuppressive therapy, after multivariable adjustment. As with any observational analysis, residual confounding and differing risk profiles among drug classes remain relevant considerations.[27]

Extended follow-up of SITE participants using National Death Index linkage likewise found no increase in overall or cancer mortality with antimetabolites, with similar findings reported for azathioprine individually, while also noting that mortality data do not exclude the possibility of rare or non-lethal cancers.[28]

Regarding fertility/reproductive outcomes, contemporary rheumatology recommendations consider azathioprine among synthetic DMARDs compatible with pregnancy (and address use across pregnancy, lactation, and male patients), supporting its continued role when maternal disease control requires it.[24]

Pregnancy

Pregnancy counseling should distinguish drug effect from underlying systemic inflammatory disease activity, which itself can influence pregnancy outcomes.

  • Contemporary recommendations consider azathioprine compatible with pregnancy when clinically indicated and when pregnancy-compatible disease control is required.[24][30][31]
  • Population-based studies have reported mixed findings, with some analyses noting associations with preterm birth, lower birth weight, and, in some cohorts, congenital malformations. However, these findings are difficult to disentangle from confounding by underlying maternal disease severity and activity.[32][33][34]


The practical takeaway is that pregnancy decisions should be individualized, ideally coordinated with maternal-fetal medicine and the prescribing specialist, balancing the maternal and ocular/systemic risks of uncontrolled inflammation against the potential fetal and obstetric risks described in the broader literature.

Nursing Mothers

Regarding nursing mothers, multiple studies evaluating thiopurine metabolite transfer into breast milk and short-term infant outcomes suggest low exposure and no clear signal of significant short-term harm in typical dosing contexts, supporting breastfeeding in many cases with appropriate counseling and follow-up.

  • In lactation pharmacokinetic work, most measurable 6-MP in breast milk was excreted within the first hours after maternal dosing, and estimated infant exposure was very low in that study’s calculations.[35]
  • Additional observational data have reported no significant immediate clinical risk signals in breastfed infants of mothers taking azathioprine, while noting the need for continued monitoring and long-term assessment in the literature.[36]
  • An obstetric review concluded breastfeeding should not automatically be withheld for mothers receiving azathioprine, based on available evidence and risk assessment.[37]


To summarize, very small or undetectable amounts of thiopurine metabolites have been found in breast milk or infant samples in reported series. Available evidence suggests low infant exposure, and azathioprine is generally considered compatible with breastfeeding when clinically indicated.[24][30][35][36][37]

Pediatric Use

Azathioprine has been used in pediatric ocular inflammatory disease, although methotrexate is often favored first-line in juvenile idiopathic arthritis-associated uveitis and escalation strategies vary by center. In a retrospective multicenter study of children with JIA-associated uveitis refractory to other therapies, azathioprine was evaluated for achieving uveitis inactivity and steroid-sparing outcomes, supporting its role as an option in selected pediatric cases under specialist oversight and structured monitoring.[8]

Adverse Reactions

Although AZA is used as a steroid-sparing immunomodulatory agent, its use is limited by potentially serious systemic toxicity. The most clinically important adverse effects are bone marrow suppression, gastrointestinal intolerance, hepatotoxicity, and an increased risk of infection.[6] The frequency and severity of these adverse effects vary with dose, duration of therapy, underlying disease, and concomitant treatment, and many of the most severe toxicity data come from transplant and other non-ophthalmic populations.

  • Myelosuppression may present with leukopenia, thrombocytopenia, anemia, or pancytopenia, and can occur even after therapy has been established. Patients with reduced or absent TPMT or NUDT15 activity are at substantially increased risk of severe or life-threatening toxicity. Reducing the dose or withdrawing the drug temporarily may reverse these toxicities.[4][6][21]
  • Serious bacterial, viral, fungal, protozoal, and opportunistic infections, including reactivation of latent infections, may occur during azathioprine therapy. Infection may also occur secondary to bone marrow suppression or leukopenia.
  • Gastrointestinal intolerance is common. Nausea and vomiting may occur within the first few months of therapy and may be reduced by dividing the dose and/or administering it after meals. In some patients these symptoms may be accompanied by diarrhea, fever, malaise, and myalgias.[6]
    • Hypersensitivity pancreatitis and hepatotoxicity may occur following azathioprine use. Hepatotoxicity may present with elevations in alkaline phosphatase, bilirubin, and/or transaminases and is often reversible after dose reduction or drug interruption. Periodic liver function monitoring is indicated for early detection.[6]
    • Hepatic veno-occlusive disease is another potential adverse event which is rare but life-threatening, and has been associated with chronic administration of azathioprine. It has been reported mainly in transplant patients and in one patient with panuveitis. Azathioprine should be permanently discontinued in any patient if hepatic veno-occlusive disease is suspected.[6]
  • Other low-frequency adverse reactions include rash, alopecia, fever, arthralgias, diarrhea, steatorrhea, negative nitrogen balance, reversible interstitial pneumonitis, Sweet syndrome, and hepatosplenic T-cell lymphoma.[6]

Dosage and Administration

Ophthalmology-specific review literature commonly describes weight-based oral dosing with titration and laboratory monitoring:

  • A typical starting approach is 2–3 mg/kg/day orally, adjusted to clinical response and tolerability, with baseline CBC/differential, LFTs, and TPMT testing prior to initiation. Patients with low/absent TPMT activity should not receive standard dosing regimens, and concomitant allopurinol necessitates substantial dose reduction (e.g., to ~25% of typical dose) with close surveillance.[3][4][6]


Genotype/phenotype-guided dosing:

  • CPIC genotype-based guidance provides starting-dose recommendations by TPMT phenotype (and similarly for NUDT15), including reduced starting doses for intermediate metabolizers and avoidance or extreme reduction for poor metabolizers, reinforcing that steady-state takes time after dose adjustments and that careful titration is required.[4][21]


Duration in ocular inflammatory disease:

  • Many uveitis treatment frameworks emphasize maintaining systemic immunomodulation long enough to reduce relapse risk. Ophthalmology literature commonly discusses prolonged treatment courses aimed at durable remission before attempting taper/discontinuation, with decision-making individualized by the uveitis phenotype and systemic disease context.[1][3]


Patients should be counseled that clinical benefit with azathioprine is typically expected within 4–12 weeks, although in some patients a longer interval may be required.[38] Corticosteroid tapering should generally be aligned with inflammatory control rather than attempted too quickly.[2]


Patients with absent TPMT or NUDT15 activity generally require an alternative therapy or major dose reduction, whereas intermediate metabolizers usually require reduced starting doses and careful laboratory monitoring.


Patients with renal dysfunction may require lower doses because of delayed clearance of azathioprine and its metabolites.[6]

Overdosage

Large overdoses of azathioprine may cause severe gastrointestinal toxicity, infection, bleeding, and delayed bone marrow suppression. Management is primarily supportive, with close clinical and laboratory monitoring because myelosuppression may be delayed and clinically significant.[18][20]

How Supplied

Azathioprine is administered systemically, most commonly orally. Formulation details should be confirmed from the relevant product label and pharmacy resources (e.g., tablet vs compounded liquid in pediatrics).[6]

Patient’s Instructions for Use

Key counseling points:

  • Monitor and communicate:
    • Emphasize the need for scheduled blood tests and rapid reporting of systemic symptoms suggestive of cytopenia or infection (fever, sore throat, easy bruising, unusual bleeding).[18][20]
    • Encourage coordination between ophthalmology and the clinician co-managing systemic immunosuppression (often rheumatology, uveitis specialist, gastroenterology, or internal medicine), consistent with consensus guidance stressing shared decision-making and safety monitoring for noninfectious uveitis.[1]
  • Avoid dangerous co-medication changes:
    • Patients should inform prescribers before starting or stopping xanthine oxidase inhibitors (e.g. allopurinol) or anticoagulants (e.g., warfarin) due to clinically meaningful interaction risk.[6][29]
  • Pregnancy and lactation:
    • Counsel patients of childbearing potential to discuss pregnancy planning early. Current guidance considers azathioprine compatible with pregnancy when clinically needed for disease control, but population studies have reported mixed associations that may be confounded by underlying disease severity. Management should be individualized with appropriate specialists.[24][30][31][33]
    • For breastfeeding, available data support low infant exposure in typical dosing contexts and do not mandate avoidance of breastfeeding in all cases; counseling should be individualized.[24][30][35][36][37]
  • Skin protection:
    • Discuss sun-protective behaviors and skin surveillance as appropriate, consistent with immunosuppression counseling and malignancy risk discussions in ocular-inflammation-focused evidence assessments.[25]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Dick AD, Rosenbaum JT, Al-Dhibi HA, et al. Guidance on Noncorticosteroid Systemic Immunomodulatory Therapy in Noninfectious Uveitis. Ophthalmology. 2018;125(5):757-773. doi:10.1016/j.ophtha.2017.11.017
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Pasadhika S, Kempen JH, Newcomb CW, et al. Azathioprine for Ocular Inflammatory Diseases. Am J Ophthalmol. 2009;148(4):500-509.e2. doi:10.1016/j.ajo.2009.05.008
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Castiblanco C, Foster CS. Review of Systemic Immunosuppression for Autoimmune Uveitis. Ophthalmol Ther. 2014;3(1-2):17-36. doi:10.1007/s40123-014-0023-x
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 Maillard M, Schwab M, Whirl‐Carrillo M, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for Thiopurine Dosing Based on TPMT and NUDT15 Genotypes: 2025 Update. Clin Pharmacol Ther. Published online January 31, 2026:cpt.70209. doi:10.1002/cpt.70209
  5. ↑ 5.0 5.1 Galor A, Jabs DA, Leder HA, et al. Comparison of Antimetabolite Drugs as Corticosteroid-Sparing Therapy for Noninfectious Ocular Inflammation. Ophthalmology. 2008;115(10):1826-1832. doi:10.1016/j.ophtha.2008.04.026
  6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 6.16 6.17 6.18 6.19 6.20 6.21 6.22 6.23 IMURAN (azathioprine) prescribing information. U.S. Food and Drug Administration. 2024. Accessed March 17, 2026. https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/017391s018lbl.pdf
  7. ↑ 7.0 7.1 Branford JA, Bodaghi B, Ferreira LB, et al. Use of immunomodulatory treatment for non-infectious uveitis: an International Ocular Inflammation Society report of real-world practice. Br J Ophthalmol. 2025;109(4):482-489. doi:10.1136/bjo-2024-326239
  8. ↑ 8.0 8.1 8.2 Goebel JC, Roesel M, Heinz C, Michels H, Ganser G, Heiligenhaus A. Azathioprine as a treatment option for uveitis in patients with juvenile idiopathic arthritis. Br J Ophthalmol. 2011;95(2):209-213. doi:10.1136/bjo.2009.173542
  9. ↑ 9.0 9.1 Yazici H, Pazarli H, Barnes CG, et al. A Controlled Trial of Azathioprine in Behçet’s Syndrome. N Engl J Med. 1990;322(5):281-285. doi:10.1056/NEJM199002013220501
  10. ↑ Pilly B, Heath G, Tschuor P, Lightman S, Gale RP. Overview and recent developments in the medical management of paediatric uveitis. Expert Opin Pharmacother. 2013;14(13):1787-1795. doi:10.1517/14656566.2013.816677
  11. ↑ Hamuryudan V, Özyazgan Y, Hizli N, et al. Azathioprine in Behçet’s syndrome. Effects on long‐term prognosis. Arthritis Rheum. 1997;40(4):769-774. doi:10.1002/art.1780400425
  12. ↑ Saadoun D, Bodaghi B, Cacoub P. Behçet’s Syndrome. Ingelfinger JR, ed. N Engl J Med. 2024;390(7):640-651. doi:10.1056/NEJMra2305712
  13. ↑ Mondino BJ, Brown SI. Immunosuppressive Therapy in Ocular Cicatricial Pemphigoid. Am J Ophthalmol. 1983;96(4):453-459. doi:10.1016/S0002-9394(14)77908-5
  14. ↑ Miserocchi E, Baltatzis S, Roque MR, Ahmed AR, Foster CS. The effect of treatment and its related side effects in patients with severe ocular cicatricial pemphigoid. Ophthalmology. 2002;109(1):111-118. doi:10.1016/S0161-6420(01)00863-6
  15. ↑ Mathews JD, Crawford BA, Bignell JL, Mackay IR. Azathioprine in active chronic iridocyclitis. A double-blind controlled trial. Br J Ophthalmol. 1969;53(5):327-330. doi:10.1136/bjo.53.5.327
  16. ↑ Parchand SM, Saraogi T, Chatterjee S, Gangwe A, Agrawal D, Agrawal D. Efficacy of azathioprine as a first-line therapy in new onset of acute Vogt-Koyanagi-Harada disease in the Indian population. Saudi J Ophthalmol. 2025;39(1):65-70. doi:10.4103/sjopt.sjopt_200_23
  17. ↑ Leclercq M, Sève P, Biard L, et al. Methotrexate versus conventional disease-modifying antirheumatic drugs in the treatment of non-anterior sarcoidosis-associated uveitis. Br J Ophthalmol. 2025;109(1):34-40. doi:10.1136/bjo-2024-325163
  18. ↑ 18.0 18.1 18.2 18.3 18.4 Connell WR, Kamm MA, Ritchie JK, Lennard-Jones JE. Bone marrow toxicity caused by azathioprine in inflammatory bowel disease: 27 years of experience. Gut. 1993;34(8):1081-1085. doi:10.1136/gut.34.8.1081
  19. ↑ 19.0 19.1 Gisbert JP, González-Lama Y, Maté J. Thiopurine-Induced Liver Injury in Patients With Inflammatory Bowel Disease: A Systematic Review. Am J Gastroenterol. 2007;102(7):1518-1527. doi:10.1111/j.1572-0241.2007.01187.x
  20. ↑ 20.0 20.1 20.2 20.3 20.4 20.5 Wallace TM, Veldhuyzen Van Zanten SJ. Frequency of Use and Standards of Care for the Use of Azathioprine and 6-Mercaptopurine in Treatment of Inflammatory Bowel Disease: A Systematic Review of the Literature and a Survey of Canadian Gastroenterologists. Can J Gastroenterol. 2001;15(1):21-28. doi:10.1155/2001/518192
  21. ↑ 21.0 21.1 21.2 21.3 21.4 21.5 21.6 21.7 Azathioprine. ClinPGx. Accessed March 17, 2026. https://www.clinpgx.org/drug/PA448515
  22. ↑ 22.0 22.1 Raman GV, Sharman VL, Lee HA. Azathioprine and allopurinol: a potentially dangerous combination. J Intern Med. 1990;228(1):69-71. doi:10.1111/j.1365-2796.1990.tb00195.x
  23. ↑ 23.0 23.1 Hessels AC, Sanders JSF, Van De Ven AAJM, et al. Azathioprine Hypersensitivity Syndrome in a Cohort of Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Patients. J Allergy Clin Immunol Pract. 2019;7(3):1004-1009. doi:10.1016/j.jaip.2018.10.018
  24. ↑ 24.0 24.1 24.2 24.3 24.4 24.5 Rüegg L, Pluma A, Hamroun S, et al. EULAR recommendations for use of antirheumatic drugs in reproduction, pregnancy, and lactation: 2024 update. Ann Rheum Dis. 2025;84(6):910-926. doi:10.1016/j.ard.2025.02.023
  25. ↑ 25.0 25.1 25.2 25.3 Yates WB, Vajdic CM, Na R, McCluskey PJ, Wakefield D. Malignancy Risk in Patients with Inflammatory Eye Disease Treated with Systemic Immunosuppressive Therapy. Ophthalmology. 2015;122(2):265-273. doi:10.1016/j.ophtha.2014.08.024
  26. ↑ 26.0 26.1 26.2 Kempen JH, Gangaputra S, Daniel E, et al. Long-term Risk of Malignancy Among Patients Treated With Immunosuppressive Agents for Ocular Inflammation: A Critical Assessment of the Evidence. Am J Ophthalmol. 2008;146(6):802-812.e1. doi:10.1016/j.ajo.2008.04.035
  27. ↑ 27.0 27.1 27.2 Kempen JH, Daniel E, Dunn JP, et al. Overall and cancer related mortality among patients with ocular inflammation treated with immunosuppressive drugs: retrospective cohort study. BMJ. 2009;339(jul03 1):b2480-b2480. doi:10.1136/bmj.b2480
  28. ↑ 28.0 28.1 28.2 Kempen JH, Newcomb CW, Washington TL, et al. Use of Immunosuppression and the Risk of Subsequent Overall or Cancer Mortality. Ophthalmology. 2023;130(12):1258-1268. doi:10.1016/j.ophtha.2023.07.023
  29. ↑ 29.0 29.1 Joo Ng H, Crowther MA. Azathioprine and inhibition of the anticoagulant effect of warfarin: Evidence from a case report and a literature review. Am J Geriatr Pharmacother. 2006;4(1):75-77. doi:10.1016/j.amjopharm.2006.03.001
  30. ↑ 30.0 30.1 30.2 30.3 ACOG Committee Opinion No. 776: Immune Modulating Therapies in Pregnancy and Lactation. Obstet Gynecol. 2019;133(4):e287-e295. doi:10.1097/AOG.0000000000003176
  31. ↑ 31.0 31.1 Sammaritano LR, Bermas BL, Chakravarty EE, et al. 2020 American College of Rheumatology Guideline for the Management of Reproductive Health in Rheumatic and Musculoskeletal Diseases. Arthritis Rheumatol. 2020;72(4):529-556. doi:10.1002/art.41191
  32. ↑ Langagergaard V, Pedersen L, Gislum M, Nørgard B, Sørensen HT. Birth outcome in women treated with azathioprine or mercaptopurine during pregnancy: a Danish nationwide cohort study. Aliment Pharmacol Ther. 2007;25(1):73-81. doi:10.1111/j.1365-2036.2006.03162.x
  33. ↑ 33.0 33.1 Cleary BJ, Källén B. Early pregnancy azathioprine use and pregnancy outcomes. Birt Defects Res A Clin Mol Teratol. 2009;85(7):647-654. doi:10.1002/bdra.20583
  34. ↑ Nørgård B, Pedersen L, Fonager K, Rasmussen SN, Sørensen HT. Azathioprine, mercaptopurine and birth outcome: a population‐based cohort study. Aliment Pharmacol Ther. 2003;17(6):827-834. doi:10.1046/j.1365-2036.2003.01537.x
  35. ↑ 35.0 35.1 35.2 Christensen LA, Dahlerup JF, Nielsen MJ, Fallingborg JF, Schmiegelow K. Azathioprine treatment during lactation. Aliment Pharmacol Ther. 2008;28(10):1209-1213. doi:10.1111/j.1365-2036.2008.03843.x
  36. ↑ 36.0 36.1 36.2 Moretti ME, Verjee Z, Ito S, Koren G. Breast-Feeding During Maternal Use of Azathioprine. Ann Pharmacother. 2006;40(12):2269-2272. doi:10.1345/aph.1H152
  37. ↑ 37.0 37.1 37.2 Sau A, Clarke S, Bass J, Kaiser A, Marinaki A, Nelson‐Piercy C. Azathioprine and breastfeeding—is it safe? BJOG Int J Obstet Gynaecol. 2007;114(4):498-501. doi:10.1111/j.1471-0528.2006.01232.x
  38. ↑ Pasadhika S, Rosenbaum JT. Update on the use of systemic biologic agents in the treatment of noninfectious uveitis. Biol Targets Ther. 2014;8:67-81. doi:10.2147/BTT.S41477
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