Drug Database
AZ

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

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

PubMedIntestinal research2026-09-10

Development of liver cirrhosis during azathioprine therapy for inflammatory bowel disease.

Park Jihye J, Lee Jae Seung JS, Kim Mi Na MN, Park Soo Jung SJ et al.

PMID 42717573
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PubMedFrontiers in medicine2026-09-10

Diagnostic challenge of GAD65-associated autoimmune encephalitis mimicking post-traumatic complications in an older adult: a case report.

Huang Xiuqing X, Zhang Qile Q, Huang Li L, Xu Jian J

Glutamic acid decarboxylase 65 (GAD65) antibody-associated autoimmune encephalitis is an uncommon immune-mediated neurological disorder with heterogeneous neuropsychiatric manifestations. Diagnosis is particularly challenging in older adults when symptoms of recent traumatic brain injury (TBI) overlap with structural or metabolic conditions. We report a 79-year-old man who developed recurrent headache, progressive confusion, abnormal behavior, poor oral intake, intermittent myoclonic jerks, and low-grade fever after TBI complicated by chronic subdural hematoma. Initial laboratory testing revealed hyponatremia, and the working diagnosis was post-traumatic brain syndrome with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although serum sodium was corrected and nocturnal agitation partially improved, persistent daytime confusion, cognitive impairment, behavioral abnormalities, and low-grade fever prompted further investigation. Cerebrospinal fluid (CSF) analysis showed mild inflammatory changes with pleocytosis and elevated protein. CSF metagenomic next-generation sequencing (mNGS) and paraneoplastic antibody testing were negative, whereas the autoimmune encephalitis panel was positive for GAD65 antibody at a titer of 1:32. Whole-body positron emission tomography-computed tomography (PET-CT) did not reveal malignancy. The diagnosis was therefore revised to GAD65 antibody-associated autoimmune encephalitis. Because high-dose corticosteroids were considered unsuitable owing to his history of gastric ulcer and previous gastrointestinal bleeding, he was treated with intravenous immunoglobulin (IVIG) at a total dose of 2 g/kg divided over 3 consecutive days followed by oral azathioprine 50 mg daily. His fever resolved within 1 week, and his mental status and responsiveness gradually improved. At 6-month follow-up, he had achieved near-baseline mental status, was able to walk with a cane, and was almost fully independent in daily activities, without relapse or serious treatment-related adverse events. This case highlights the diagnostic difficulty of recognizing autoimmune encephalitis after TBI. The clinical overlap between post- traumatic syndrome and immune-mediated brain injury often delays diagnosis, emphasizing the value of targeted CSF autoantibody testing in atypical cases. Traumatic brain injury may obscure the onset of GAD65-associated autoimmune encephalitis. Early recognition and a corticosteroid-sparing immunotherapy strategy (IVIG and azathioprine) can yield favorable outcomes in elderly patients with medical comorbidities.

PMID 42718506
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PubMedLupus2026-09-09

Global prevalence and associated factors of metabolic syndrome in patients with systemic lupus erythematosus: A systematic review and meta-analysis.

Samethadka Nayak Sandeep S, Ghodous Shahriar S, Keetha Narsimha Rao NR, Gurram Anoop A et al.

BackgroundSystemic lupus erythematosus (SLE) is characterized by chronic systemic inflammation, frequent corticosteroid exposure, and heightened cardiometabolic vulnerability. Metabolic syndrome (MetS) has become a clinically significant comorbidity among individuals with SLE. We performed an updated systematic review and meta-analysis to better understand the prevalence and identify the factors associated with the occurrence of MetS in SLE.MethodsPubMed, Scopus, and Web of Science were systematically searched through January 4, 2026 to identify observational studies reporting the prevalence of MetS among individuals with SLE. Random-effects meta-analytic models were applied to calculate pooled prevalence estimates and evaluate the associations with potential risk factors.ResultsThe overall pooled prevalence of MetS in patients with SLE was estimated at 0.27 (95% CI: 0.24-0.30). Sex-stratified analyses showed a prevalence of 0.36 (95% CI: 0.25-0.47) in male patients and 0.27 (95% CI: 0.23-0.30) in female patients. Across continents, the highest prevalence was observed in Africa (0.36, 95% CI: 0.30-0.41), followed by South America (0.32, 95% CI: 0.24-0.40), Asia (0.27, 95% CI: 0.22-0.32), Europe (0.23, 95% CI: 0.18-0.28), and North America (0.21, 95% CI: 0.14-0.30). Regarding medication use, hydroxychloroquine was associated with a significantly reduced risk of MetS (OR = 0.66, 95% CI: 0.52-0.83; P < 0.01), whereas cyclophosphamide (OR = 1.39, 95% CI: 1.06-1.81; P = 0.02), azathioprine (OR = 1.25, 95% CI: 1.00-1.55; P = 0.04), and mycophenolate mofetil (OR = 1.13, 95% CI: 1.03-1.23; P = 0.01) were each associated with a significant increased risk of MetS. No significant associations were found for steroids (OR = 1.34, 95% CI: 0.97-1.83; P = 0.07), methotrexate (OR = 1.07, 95% CI: 0.78-1.47; P = 0.84), or cyclosporine use (OR = 1.19, 95% CI: 0.64-2.21; P = 0.33). The analysis also identified several risk factors for MetS in SLE patients. Patients with MetS were older (Hedges' g = 0.47; P < 0.01), had higher BMI (Hedges' g = 0.88; P < 0.01), and higher total cholesterol (Hedges' g = 0.39; P < 0.01) and LDL levels (Hedges' g = 0.41; P < 0.01) than those without MetS.ConclusionMetS is prevalent among individuals with SLE and is influenced by demographic, clinical, and treatment-related factors. These findings highlight the need for targeted monitoring and management strategies to reduce the cardiometabolic risk in this population.

PMID 42712258
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PubMedThe American journal of case reports2026-09-08

Vogt-Koyanagi-Harada Disease Presenting With Progressive Visual Loss and Multisystem Involvement: A Case Report.

Elshweikh Samah A SA, Almutairi Atheer G AG, Thalib Husna Irfan HI, Alolayan Reema Waleed RW et al.

BACKGROUND Vogt-Koyanagi-Harada (VKH) disease is a rare autoimmune disorder targeting melanocyte-rich tissues that often presents with bilateral ocular inflammation and multisystem involvement. Early manifestations, such as headache and optic disc edema, can mimic other conditions, leading to diagnostic delays. Clinician awareness is essential, particularly in high-risk populations, to ensure timely intervention. CASE REPORT We report the case of a 55-year-old Indian man who presented with a 20-day history of progressive bilateral visual loss, headache, and hearing impairment. Ophthalmologic examination revealed hand motion vision in both eyes, anterior chamber inflammation, disc edema, and serous retinal detachments. Spectral-domain optical coherence tomography confirmed neurosensory detachment and disc edema, whereas B-scan ultrasonography demonstrated pronounced choroidal thickening. Brain and orbital magnetic resonance imaging revealed bilateral focal nodular choroidal lesions. Laboratory investigations excluded infectious, malignant, and systemic inflammatory etiologies. A diagnosis of VKH disease was established based on the clinical presentation, multimodal imaging findings, and revised diagnostic criteria. The patient was treated with high-dose intravenous methylprednisolone followed by a prolonged oral taper; azathioprine was initiated early as a steroid-sparing agent to prevent relapse. CONCLUSIONS This case underscores the importance of prompt ophthalmologic evaluation and multimodal imaging in the diagnosis of VKH disease. Early initiation of intensive immunosuppressive therapy may help limit inflammatory progression and reduce long-term complications.

PMID 42706706
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PubMedOcular immunology and inflammation2026-09-07

Cilioretinal-Sparing Central Retinal Artery Occlusion in a Child with Adenosine Deaminase 2 (ADA2) Deficiency.

Sharma Arpit A, Rajan Renu P RP, V Muthukrishnan M, Kannan Naresh B NB et al.

To report cilioretinal-sparing central retinal artery occlusion (CRAO) in a child with adenosine deaminase 2 (ADA2) deficiency and polyarteritis nodosa-like systemic vasculitis. This retrospective case report was based on clinical records, retinal imaging, automated visual field testing, systemic evaluation, and genetic testing. An 11-year-old girl first presented with intermittent exotropia and a normal fundus. Eight months later, she developed fever, weight loss, post-prandial abdominal pain, vasculitic rash, and hypertensive urgency. Her elder brother was also diagnosed with severe hypertension. Skin biopsy revealed medium-vessel vasculitis, raising suspicion for monogenic polyarteritis nodosa-like vasculitis. ADA2 testing was initiated, and she began treatment with oral prednisolone and azathioprine. Twelve months after her initial ophthalmic visit, she maintained best-corrected visual acuity of 20/20 in both eyes but showed a neuroretinitis-like appearance in the left eye, including subtle optic disc margin blurring, sectoral retinal whitening, perivascular sheathing, and peripapillary exudation. One week later, she reported a grey central field disturbance. Visual acuity remained 20/20, but automated perimetry revealed a dense paracentral scotoma. At this time, genetic testing confirmed a homozygous pathogenic ADA2 variant in both siblings. Fundus examination and optical coherence tomography identified CRAO with cilioretinal artery territory sparing. She was treated with intravenous methylprednisolone, blood pressure management, and adalimumab. At 6 months, visual acuity remained stable, with persistent paracentral field loss and structural sequelae of CRAO. ADA2 deficiency should be considered in children with retinal arterial occlusion, especially when systemic vasculitis, severe hypertension, or sibling involvement is present.

PMID 42703705
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PubMedRheumatology and therapy2026-09-05

Updates on the Evaluation of Lupus Arthritis.

Tang Wei W, Nordmann-Gomes Alberto A, Khalili Leila L, Rosas Giovanna G et al.

Lupus arthritis is the most common manifestation of systemic lupus erythematosus (SLE), affecting up to 95% of patients. Clinical presentations range from inflammatory arthralgia and non-deforming non-erosive (NDNE) synovitis to Jaccoud arthropathy and erosive arthritis, reflecting substantial clinical heterogeneity. Despite its high prevalence, widely used outcome measures lack the granularity to distinguish between these phenotypes or accurately quantify disease severity. This narrative review integrates clinical phenotypes, serologic biomarkers, imaging advances, and emerging therapies to provide a framework for evaluating lupus arthritis. Besides distinct clinical phenotypes, we propose a conceptual hypothesis-generating model describing the evolution of lupus arthritis. In an early, preclinical stage, genetically predisposed individuals may develop pathogenic autoantibodies and alterations in the gut microbiome that can lead to increased inflammation within the synovium. The intermediate stage is characterized by progressive leukocyte accumulation within the joint space, leading to clinical symptoms and early abnormalities on imaging including joint effusions, synovitis, and tenosynovitis. In the late stage, persistent inflammation results in clinically evident joint damage, including synovial hypertrophy, joint capsular swelling, and bone erosions. Biomarkers such as anti-citrullinated protein antibodies (ACPAs), anti-carbamylated protein (anti-carP) antibodies, interleukin (IL)-6, IL-17, and metalloproteinases may help identify patients at risk for erosive or deforming disease and those prone to rapid progression. Advances in imaging technologies including musculoskeletal ultrasound (MSK-US), MRI, and optical tomography may enable earlier detection before clinical manifestations or physical exam findings, creating opportunities for earlier intervention. Therapeutically, hydroxychloroquine (HCQ) remains the foundation of treatment. Belimumab and anifrolumab are US Food and Drug Administration (FDA)-approved biologics now recommended as standard of care for persistent disease, alongside conventional immunosuppressants such as methotrexate, mycophenolate, or azathioprine when indicated. Additional targeted therapies including obinutuzumab and Janus kinase (JAK) inhibitors are closely following behind. Chimeric antigen receptor T cell (CAR-T) represents a promising approach that may transform the future management of SLE.

PMID 42698059
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