Anterior uveitis, an inflammation of the anterior part of the uvea (iris, ciliary body), is the most common form of uveitis (58–90%; [1, 2]). It can be differentiated according to various characteristics such as the time course, the appearance, or the cause. Clinical signs of acute uveitis include ciliary injection, anterior chamber cells, Tyndall effect, and miosis, which predisposes to posterior synechiae formation. In addition, complications such as macular edema, glaucoma, or cataract may occur in the course of the disease. For the correct therapy, it is important to know the etiology or at least to exclude some important causes of uveitis that require specific therapies. A detailed medical history and specific diagnostic measures such as blood sampling or chest X‑ray can exclude or confirm the most important and frequent differential diagnoses. Nevertheless, in 20–50% of patients no cause can be found and these cases are classified as idiopathic [3]. The most common non-infectious cause is a positive HLA-B27 status, which is often associated with systemic diseases such as axial spondyloarthritis or inflammatory bowel disease. Therapy consists of local and/or oral cortisone therapy or long-term cortisone-sparing immunosuppression, depending on the course of the disease. Infectious anterior uveitis is often caused by certain viruses (herpesvirus, cytomegalovirus) or bacteria such as Borrelia or Treponema pallidum. Depending on the causative agent, treatment comprises antibiotics or antiviral drugs. In addition, topical or oral cortisone can be administered to suppress the inflammation. Special types of uveitis such as Fuchs uveitis or Posner–Schlossmann syndrome are pathognomonic and can be diagnosed clinically.
