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azathioprine (azathioprine, Salix / Azasan / Azasan)

✓ Approved

Salix · 小分子 · 小分子

什么是 azathioprine？

azathioprine 是一种小分子，由Salix研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名azathioprine, Salix, Azasan, Azasan
公司Salix
药物类别小分子
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Salix

治疗适应症

azathioprine 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Immune system disordersSolid organ transplant rejection✓ Approved

相关研究文献

PubMedCrohn's & colitis 3602026-10-25

Prevalence and impact of Thiopurine S-methyltransferase (TPMT) and Nudix hydrolase 15 (NUDT15) polymorphisms on the occurrence of myelosuppression in Thai patients with inflammatory bowel disease receiving thiopurine therapy.

Phoojaroenchanachai Rujirada R, Chaemsupaphan Thanaboon T, Sattayalertyanyong Onuma O, Subdee Nichcha N et al.

Thiopurine-induced myelosuppression (TIM) is an important side effect influenced by 2 main genetic polymorphisms, thiopurine-S-methyltransferase (TPMT) and NUDT15. The data on Southeast Asian inflammatory bowel disease (IBD) patients remain limited. Our study aimed to determine the relationship between TPMT and NUDT15 polymorphisms and TIM following thiopurine treatment in Thai patients with IBD. We performed a retrospective cohort study of IBD patients receiving azathioprine with active follow-up at the IBD clinic. TPMT and NUDT15 polymorphisms were checked. Medical records were reviewed for TIM occurrence and its genetic associations. A total of 124 IBD patients (73 Crohn's disease, 51 ulcerative colitis; mean age 46.9 years) were included. Initial azathioprine dosing was 0.87 mg/kg/day, titrated to 1.54 mg/kg/day. TPMT variants were found in 6 patients (4.8%; 5 heterozygous and 1 homozygous) and NUDT15 variants in 21 patients (16.9%; 20 heterozygous and 1 homozygous). Over a 7.6-year follow-up, TIM occurred in 12 patients (9.7%). TIM rate was not significantly different among TPMT polymorphisms (wild-type 9.3%, heterozygous 20%, homozygous 0%), but was significantly different among NUDT15 polymorphisms (7.8% wild-type and heterozygous/homozygous 19%). The cumulative rates of TIM at 6, 12, and 60 months were 2.1%, 3.2%, and 7.2% in wild type and 0%, 5%, and 10% in NUDT15 heterozygous mutation. The only participant with a homozygous mutation developed TIM within the first month. NUDT15 polymorphisms are more common than TPMT variants in this study and are significantly associated with TIM. Pre-treatment genotyping may be considered, taking into account local mutation prevalence, test availability, and cost-effectiveness.

PMID 42927292
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PubMedCNS neuroscience & therapeutics2026-10-25

Efficacy and Safety of Multidisciplinary Sandwich Regimen in AQP4-IgG+ NMOSD With Preconception B-Cell Depletion During Perigravidity.

Xiao Li L, Lu Gengxin G, Gao Qian Q, Wan Feiyan F et al.

Neuromyelitis optica spectrum disorder (NMOSD) predominantly affects women of childbearing age, accompanied by markedly elevated relapse risks during pregnancy and postpartum periods, bringing great challenges to perigravid management. At present, there is no standardized gestational therapeutic regimen for NMOSD worldwide, and data on perigravid application of B-cell depleting agents including rituximab and inebilizumab remain limited. For patients exposed to B-cell depleting agents before conception, balancing disease control and fetal safety is an urgent clinical problem to be solved. This multicenter prospective cohort study aimed to evaluate the efficacy and safety of a three-stage multidisciplinary "sandwich" management regimen in AQP4-IgG-positive pregnant women with NMOSD exposed to B-cell depleting agents before conception. Maternal disease activity, pregnancy outcomes, neonatal conditions, and offspring growth and developmental characteristics within the first year of life were analyzed. A total of 8 AQP4-IgG-positive pregnant women with NMOSD who received B-cell depleting agents within 9 months prior to conception were enrolled from multiple centers between January 2022 and October 2024, including 3 patients treated with inebilizumab and 5 patients treated with rituximab. All subjects received a unified three-stage intervention: B-cell depleting agents were discontinued upon confirmed pregnancy; low-dose azathioprine combined with low-dose glucocorticoids was administered during gestation; B-cell depleting agents were reinitiated at 2 weeks postpartum. Multidisciplinary teams consisting of neurology, obstetrics, clinical pharmacy, and neonatology departments conducted full-cycle monitoring and follow-up. Primary observation indicators included maternal relapse events, Expanded Disability Status Scale (EDSS) scores, B-cell counts, gestational complications, gestational age at delivery, neonatal physical indicators, Apgar scores, congenital malformations, as well as offspring growth and neurodevelopment and vaccination safety from birth to 1 year of age. All subjects achieved term live births without severe obstetric complications. Seven patients remained relapse-free throughout pregnancy and postpartum period with stable or improved EDSS scores; one patient discontinued all medications during gestation and suffered a relapse at 1 month postpartum. Neonatal physical indicators and Apgar scores were generally normal, one neonate presented mild hypospadias and two developed transient neonatal abnormalities; neonatal B-cell counts at birth and 1 month of age were within normal ranges. One-year follow-up showed normal physical and neurodevelopment in all offspring with safe vaccination procedures. For AQP4-IgG-positive pregnant women with NMOSD exposed to B-cell depleting agents before conception, the multidisciplinary "sandwich" regimen featuring B-cell depletion before conception and postpartum plus gestational bridging therapy with low-dose azathioprine combined with glucocorticoids is safe and effective, reduces disease relapse risk and yields favorable overall maternal and fetal outcomes. This regimen may serve as a promising perigravid management strategy that warrants further validation in larger cohorts.

PMID 42924580
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PubMedCase reports in dermatology2026-10-25

Apremilast in Persistent Mucocutaneous Erythema Multiforme: A Case Report - Expanding the Therapeutic Evidence.

Fernández Esparcia Pedro José PJ, González García Andrés A, Baracaldo Santamaría Daniela D, Moreno García Del Real Carmen C et al.

Persistent erythema multiforme (EM) is a rare and poorly defined variant of EM characterized by prolonged mucocutaneous involv ent and limited therapeutic options. Evidence regarding its management is scarce. Apremilast has shown efficacy in isolated reports of other EM subtypes, suggesting a potential role in refractory cases. We present the case of a 45-year-old woman with recurrent EM who subsequently developed prolonged, continuously active mucocutaneous disease lasting 6 years. The disease was refractory or intolerant to multiple therapies, including antivirals, corticosteroids, colchicine, dapsone, hydroxychloroquine, azathioprine, and biologic agents. Extensive clinical, histopathological, immunological, and systemic evaluation supported the diagnosis of EM and did not identify an underlying condition. Apremilast (30 mg twice daily) was initiated resulting in progressive improvement, with complete resolution of oral involvement within 3 months. After 1 year of follow-up, the patient remains in sustained clinical remission with good tolerability and no significant adverse effects. This case adds to the limited evidence supporting the potential use of apremilast in difficult-to-treat EM with prolonged mucocutaneous activity. Although the rapid and sustained response observed in this patient is encouraging, further studies are needed to determine the efficacy, optimal treatment duration, and long-term safety of apremilast in this setting.

PMID 42927400
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PubMedFrontiers in pediatrics2026-10-25

Treatment of idiopathic pulmonary hemosiderosis in children: a systematic review.

Liu PengCheng P, Lei ZhiChao Z

Idiopathic pulmonary hemosiderosis (IPH) is a rare disease characterized by recurrent diffuse alveolar hemorrhage in children. Corticosteroids are the conventional first-line treatment, and immunosuppressive agents also constitute a mainstay of management. However, evidence is derived almost entirely from small observational studies, and no standardized recommendations exist. We systematically searched PubMed, Embase, Web of Science, the Cochrane Central Register of Controlled Trials, and Chinese databases (CNKI and Wanfang) from inception to 24 September 2026, with no language restrictions. Studies reporting treatment for IPH in children (0-18 years) were included; a narrative synthesis was performed. A total of 149 studies were included. Corticosteroids were the first-line treatment, with 78.7% of the 494 children with IPH or undetermined etiology in the largest multicenter cohort (n = 567) receiving corticosteroid monotherapy. The overall relapse rate ranged from approximately 35% to 60% across small single-center cohorts, most commonly triggered by respiratory infections and corticosteroid tapering. Immunosuppressive agents, including azathioprine, hydroxychloroquine, cyclophosphamide, leflunomide, and 6-mercaptopurine, were added for refractory, steroid-dependent, or relapsing disease. Biological agents such as rituximab also emerged as promising steroid-sparing options. Adjunctive therapies included intravenous immunoglobulin, ECMO, arterial embolization, and iron chelation. In a single-center IPH cohort of 41 children, mortality was 27.3% (6 of 22 children followed). Corticosteroids remain the cornerstone of pediatric IPH treatment, with immunosuppressive or biologic agents reserved for refractory disease. Given the absence of high-quality evidence, multicenter prospective studies with standardized protocols are urgently needed. https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420261486860, PROSPERO CRD420261486860.

PMID 42923410
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PubMedJournal of thrombosis and thrombolysis2026-10-25

Thiopurines and vitamin K antagonist resistance: warfarin inhibits thiopurine S-methyltransferase.

Bayoumy A B AB, Russell D A DA, Zandbergen A A M AAM, Totah R A RA

Vitamin K antagonists (VKAs) inhibit vitamin K epoxide reductase, reducing the synthesis of vitamin K-dependent clotting factors and increasing bleeding risk. Thiopurines, such as azathioprine (AZA) and 6-mercaptopurine (MP), are immunosuppressants commonly used in inflammatory bowel disease and other immune-mediated disorders. Case reports suggest a dose-dependent relationship between thiopurines and reduced INR levels, potentially contributing to VKA resistance. We present a case of a female patient with Sjögren's disease, Factor V Leiden thrombophilia and intermediate thiopurine S-methyltransferase (TPMT) metabolism who experienced VKA resistance associated with high 6-thioguanine nucleotide (6-TGN) levels. Despite phenprocoumon therapy, therapeutic INR levels were not maintained after multiple higher dosages (37.5 mg per week) of phenprocoumon which were much higher than patients' regular dose (15 mg/week). After reducing AZA dosage, her 6-TGN levels decreased significantly, and therapeutic INR was restored, suggesting a direct relationship between elevated 6-TGN levels and VKA resistance. An in vitro inhibition assay showed that warfarin inhibits TPMT, which could have contributed to higher 6-TGN levels. Potential mechanisms for thiopurine-induced VKA resistance include increased prothrombin activity, but may also theoretically be caused by alterations in gut microbiota reducing vitamin K synthesis, and interference with enzymes like VKORC1. Literature highlights cases where thiopurines lowered INR, leading to thrombotic events, particularly in female patients, suggesting a potential hormonal influence. Other cases also described that stopping thiopurines led to high INR levels, which led to bleeding. This case underscores the need for therapeutic drug monitoring in patients using both VKAs and thiopurines. Gender-specific factors may further contribute to VKA resistance and warrant additional research. Clinicians should remain vigilant in managing this complex interaction to optimize patient outcomes.

PMID 42927566
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PubMedReports (MDPI)2026-10-25

A Rare Association of Turner Syndrome, Celiac Disease, and Ulcerative Colitis in a Pediatric Patient: A Case Report.

Rogalidou Maria M, Dimakou Konstantina K, Stefanaki Kalliopi K, Botsa Evanthia E et al.

Background and Clinical Significance: Turner syndrome is associated with an increased prevalence of autoimmune disorders, particularly celiac disease, and is also associated with impaired bone health. The coexistence of Turner syndrome, celiac disease, and ulcerative colitis is rare and represents a challenging clinical scenario requiring multidisciplinary management; Case Presentation: We report the case of a 7-year-old girl referred for short stature who was diagnosed with celiac disease based on positive serology and duodenal histology (Marsh 3a/3c). Cytogenetic analysis revealed 46,X,i(X)(q10) Turner syndrome. Despite strict adherence to a gluten-free diet, persistent growth impairment led to initiation of recombinant human growth hormone therapy. At 14 years of age, she developed bloody diarrhea, weight loss, iron-deficiency anemia, and elevated inflammatory markers. Colonoscopy and histology confirmed extensive ulcerative colitis. During follow-up, dual-energy X-ray absorptiometry demonstrated reduced bone mineral density (lumbar spine Z-score -2.7; whole-body Z-score -2.5). At 16 years of age, treatment with azathioprine and 5-aminosalicylic acid was complicated by pancreatitis, with recurrence of pancreatic enzyme elevation following sequential drug reintroduction, leading to discontinuation of both agents. Infliximab therapy was subsequently initiated, resulting in sustained clinical, endoscopic, and near-complete histological remission. The patient was later transitioned to adult multidisciplinary care; Conclusions: The coexistence of Turner syndrome, celiac disease, ulcerative colitis, and low bone mineral density is an exceptionally rare combination of genetic susceptibility, autoimmunity, and chronic inflammation. This case highlights the importance of lifelong multidisciplinary surveillance in patients with Turner syndrome, including monitoring for additional autoimmune disorders, growth impairment, and skeletal complications.

PMID 42924774
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