Abstract
Tuberculous uveitis continues to be a diagnostic challenge, mainly due to its heterogeneous clinical manifestations but also the limitations of currently available diagnostic tools. There is often a substantial delay until a correct diagnosis is made which may influence the visual prognosis of these patients. However, there have been substantial experimental and clinical advances in the understanding of the pathogenesis of this disease as well as in the diagnosis and therapeutic management of these patients. The main aim of this review is to summarize these advances and their implications in clinical practice.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
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Tuberculous uveitis (TBU) is the most frequent clinical manifestation of ocular tuberculosis (TB).
Ocular TB may be secondary to direct invasion of ocular tissues by tubercular bacilli and/or hypersensitivity reaction to mycobacterial antigens in the eye.
Retinal pigment epithelium is the reservoir of Mycobacterium tuberculosis bacilli in a latent status. However, identification and amplification of its DNA does not necessarily imply the existence of a direct invasion of ocular tissues since the genome of M. tuberculosis may persist in the macrophages and may initiate an immune-mediated inflammatory response resulting in granulomatous hypersensitivity.
Most frequent clinical signs of TBU are choroidal tubercles, vitritis and retinal vasculitis. It has been reported an increased number of cases with multifocal and geographical choroiditis called ‘multifocal serpiginoid choroiditis’. However, TBU still has heterogeneous clinical manifestations with no pathognomonic signs.
Diagnosis of TBU is presumptive in most cases (presumed TBU) because of the difficulties regarding isolation and identification of the pathogen. A compatible clinical picture, systemic evidence of active or latent TB and absence of a better diagnostic hypothesis are enough for a presumptive diagnosis and therapeutic testing with anti-TB treatment.
IFN-γ release assays improve some limitations associated to tuberculin skin test increasing its specificity, particularly in immunocompromised patients. The use of both tests in suspected cases of TBU is mandatory.
Anti-TB treatment achieves clinical improvement after some weeks of its initiation with a significant reduction of recurrences if long-lasting regimens (>9 months) are used. A positive response to therapeutic testing is of high diagnostic value in many cases.
The simultaneous use of steroids may limit the injuries caused by immune-mediated mechanisms over ocular tissues.
Notes
TB: Tuberculosis.
Data taken from Citation[45].