Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. The quality of the evidence for treating the oral ulcers associated with<unk> , however, is poor. High-dose corticosteroid therapy is often used for severe<unk>  manifestations. Anti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the<unk> . Another Anti-TNF agent, etanercept, may be useful in people with mainly skin and mucosal symptoms. Apremilast may also be used to treat oral ulcers associated with<unk> . Interferon alpha-2a may also be an effective alternative treatment, particularly for the genital and oral ulcers as well as ocular lesions. Azathioprine, when used in combination with interferon alpha-2b also shows promise, and colchicine can be useful for treating some genital ulcers, erythema nodosum, and arthritis. Benzathine‐penicillin may also reduce new arthritic attacks. Thalidomide has also been used due to its immune-modifying effect. Dapsone and rebamipide have been shown, in small studies, to have beneficial results for mucocutaneous lesions. Given its rarity, the optimal treatment for acute optic neuropathy in<unk>  has not been established. Early identification and treatment are essential. Response to ciclosporin, periocular triamcinolone, and IV methylprednisone followed by oral prednisone has been reported although relapses leading to irreversible visual loss may occur even with treatment. Immunosuppressants such as interferon-alpha and tumour necrosis factor antagonists may improve though not completely reverse symptoms of ocular<unk> , which may progress over time despite treatment. When symptoms are limited to the anterior chamber of the eye prognosis is improved. Posterior involvement, particularly optic nerve involvement, is a poor prognostic indicator. Secondary optic nerve atrophy is frequently irreversible. Lumbar puncture or surgical treatment may be required to prevent optic atrophy in cases of intracranial hypertension refractory to treatment with immunomodulators and steroids. IVIG could be a treatment for severe or complicated cases. Surgery Surgical treatment of arterial manifestations of<unk>  bears many pitfalls since the obliterative endarteritis of vasa vasorum causes thickening of the medial layer and splitting of elastin fibers. Therefore, anastomotic pseudoaneurysms are likely to form, as well as pseudoaneurysms at the site of the puncture in case of angiography or endovascular treatment; furthermore, early graft occlusion may occur. For these reasons, invasive treatment should not be performed in the acute and active phases of the<unk>  when inflammation is at its peak. The evaluation of<unk> 's activity is usually based on relapsing symptoms, ESR (erythrocyte sedimentation rate), and serum levels of CRP (C‐reactive protein). Endovascular treatment can be an effective and safe alternative to open surgery, with less postoperative complications, faster recovery time, and reduced need for intensive care, while offering patency rates and procedural success rates comparable with those of surgery. This notwithstanding, long‐term results of endovascular treatment in<unk>  are still to be determined.
Behçet's disease
Stevens–Johnson syndrome
Chilaiditi syndrome
Reactive arthritis
Coats' disease
Febrile neutrophilic dermatosis
Sever's disease
Lhermitte's sign