Uveitis is an inflammation of the uvea, the middle layer of the eye that includes the iris, ciliary body, and choroid. The causes of uveitis are diverse and complex, involving a range of factors that can be broadly categorized into infectious, autoimmune, traumatic, and idiopathic origins.
One of the primary causes of uveitis is **autoimmune and inflammatory disorders**. In these cases, the body’s immune system mistakenly attacks its own eye tissues, leading to inflammation. This autoimmune response can be isolated to the eye or part of a systemic condition affecting multiple organs. Diseases such as ankylosing spondylitis, psoriatic arthritis, and other HLA-B27 associated conditions are commonly linked to uveitis. These genetic predispositions can trigger inflammation when combined with environmental factors or infections, through a process called molecular mimicry, where the immune system confuses eye proteins with infectious agents.
Infectious causes are another major category. Various microorganisms can directly infect the eye or trigger an immune response that results in uveitis. Common infectious agents include viruses like herpes simplex and herpes zoster, bacteria such as tuberculosis and syphilis, fungi, and parasites. These infections can cause localized inflammation or systemic illness that manifests in the eye. For example, herpes viruses can cause recurrent anterior uveitis, often requiring antiviral treatment to control the inflammation.
Trauma to the eye, including surgical procedures like cataract surgery, can also lead to uveitis. Postoperative inflammation may occur due to the eye’s response to surgical trauma or retained lens material, which can provoke an immune reaction. This type of uveitis is often called rebound iritis when inflammation flares up after tapering off steroid treatment post-surgery. In such cases, inadequate control of inflammation or infection can worsen the condition.
Other systemic diseases can cause uveitis as part of their broader inflammatory effects. Conditions like sarcoidosis, vasculitis, and relapsing polychondritis involve widespread inflammation that can include the uveal tract. These diseases often present with additional symptoms such as joint pain, skin changes, or organ involvement, which help in diagnosing the underlying cause of uveitis.
Sometimes, uveitis occurs without a clearly identifiable cause, termed idiopathic uveitis. In these cases, despite thorough investigation, no systemic disease or infection is found. It is believed that genetic factors, environmental triggers, and subtle immune dysregulation may play roles in these cases.
Medications can rarely induce uveitis as an adverse reaction. Certain drugs may trigger inflammation either through direct toxicity or by altering immune responses. This cause is less common but important to consider, especially if uveitis develops shortly after starting a new medication.
The pathophysiology of uveitis involves immune cells infiltrating the uveal tissues, releasing inflammatory mediators that cause redness, pain, light sensitivity, and vision changes. The inflammation can affect different parts of the uvea, leading to classifications such as anterior uveitis (iris and ciliary body), intermediate uveitis (pars plana and peripheral retina), posterior uveitis (choroid and retina), or panuveitis (all layers). Each type may have different causes and clinical features.
In summary, uveitis is caused by a complex interplay of genetic predisposition, immune system dysfunction, infections, trauma, systemic inflammatory diseases, and sometimes unknown factors. Understanding the cause is crucial for effective treatment, which often involves controlling inflammation with steroids or immunosuppressive drugs and addressing any underlying infection or systemic condition.
