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Ocular Involvement in Sarcoidosis

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Ocular Involvement in Sarcoidosis 110 Br J Ophthalmol 2000;84:110–116 Br J Ophthalmol: first published as 10.1136/bjo.84.1.110 on 1 January 2000. Downloaded from PERSPECTIVE Ocular involvement in sarcoidosis Aniki Rothova Sarcoidosis is a chronic multisystemic granulomatous dis- molecular techniques and a causal role in the aetiology of order thought to result from an exaggerated cellular sarcoidosis was proposed.16 17 Conflicting results have been immune response to a variety of self antigens or non-self obtained from the studies assessing the aetiological role of antigens.1 The aetiology of sarcoidosis is unknown, which mycobacterial infection in the pathogenesis of sarcoidosis might be in part related to the diverse manifestations of the and the discrepancies were attributed to diVerent sensitivi- disease and the absence of approved diagnostic criteria. ties of the diagnostic procedures.18 19 The nested polymer- Although specific inhalation antigens have been put ase chain reaction (PCR), a procedure more sensitive than forward as possible triggers, no study has yet proved a con- the standard PCR protocol, has failed to identify sistent relation with a causative agent.2 Genetic factors sequences specific for Mycobacterium tuberculosis complex might also be involved since familial incidence in certain in sarcoidosis, whereas positive results were found in biop- populations as high as 19% has been noted and, further, sies from patients with active tuberculosis.20 21 Polymerase specific HLA associations have been connected with chain reactions of 123 bp fragment of IS6110 have shown disease susceptibility and outcome—for example, HLA-B8 the absence of M tuberculosis DNA in lymph nodes and and DR-3 with Löfgren’s syndrome (acute systemic lung biopsies from patients with sarcoidosis and suggest disease with fever, polyarthritis, erythema nodosum, and that M tuberculosis does not have a pathogenic role in favourable prognosis).34The infectious agents, specifically sarcoidosis in most patients.22 By molecular techniques, mycobacteria and more recently herpesvirus 8, have also atypical mycobacteria, Corynebacterium acnes, and Propioni- been implicated.56 Sarcoidosis has only sporadically been bacterium DNA have also been identified in sarcoid granu- reported in AIDS and has occasionally been described lomas and a link with sarcoidosis has been proposed.23 24 during the immune recovery with the highly active antiret- Whether these bacteria induce some cases of sarcoidosis by roviral therapy.78 The evidence that disease might be of an allergic mechanism has not yet been elucidated. environmental or infectious origin is supported by occupa- Presumably, in response to antigen exposure, exuberant tional clustering (medical nurses, fire fighters) and by the cellular immune response occurs in target organs, and 9–11 transmission of the disease from transplanted organs. leads to the development of granulomas. Granulomas con- The genetic and environmental influences cannot be sist of epitheloid and multinucleated giant cells (aggre- adequately evaluated in small samples of patients; a large gated macrophages), abundant CD4 positive T cells and, http://bjo.bmj.com/ study addressing the phenotyping diVerences and various usually in the periphery of the granuloma, to some extent environmental data is lacking however. So far, only CD8 positive T cells and B cells may be encountered.25 26 T interesting disease patterns in families and inconclusive lymphocytes in aVected organs are of T helper 1 allelic associations for diVerent populations have been phenotype and produce interferon ã and interleukin 2, reported. Therefore, sarcoidosis might represent an abnor- which subsequently lead to the production of tumour mal immune response directed against one or more possi- necrosis factor and interleukin 6 by macrophages, and ble antigens in an individual with a hereditary or acquired thereby cause a cascade of inflammatory changes, on September 27, 2021 by guest. Protected copyright. abnormality of the immune system. culminating in fibrosis. Fibrosis of the granulomas induces organ destruction and loss of function. The very high ratios Epidemiology of T helper to T suppresser cells have been reported for Sarcoidosis occurs worldwide but is predominant in various organs aVected by sarcoidosis, including the eye.26 certain ethnic and racial groups (for example, US blacks, Epitheloid cell granulomas are not pathognomonic for sar- Scandinavian and Irish white people).12 Black patients coidosis, and other causes of granulomatous inflammation present typically with more severe and acute disease (for example, Wegener’s disease) as well as the presence of whereas the white patients usually have asymptomatic and infectious agents (fungi or mycobacteria) and foreign bod- chronic disease.13 14 The frequency of sarcoidosis is ies (beryllium, organic dusts) should be sought.1 Probably reported to be low in various parts of the world14 15;itisnot secondary laboratory abnormalities include depressed cel- known whether this low frequency of sarcoidosis is genuine lular immunity to other antigens (resulting in cutaneous or whether it represents an underdiagnosis owing to the anergy), hyperglobulinaemia caused by overstimulated B frequent occurrence of subclinical course, similarity with lymphocytes, and hypercalcaemia. other diseases, or absence of firm diagnostic criteria. So far, the search for the associations between HLA related genes and sarcoidosis has revealed that the most Pathogenesis common allele associated with the susceptibility to Sarcoidosis is characterised by the formation of non- sarcoidosis has been HLA-B8.27 The present studies, using caseating granulomas in aVected organs. Three types of the DNA sequence analysis rather than serological typing, agents are known to cause epitheloid cell granulomas— support the hypothesis that the major genetic factors con- infectious organisms (bacteria and fungi), products of trolling the development of sarcoidosis are located within plants and animals (pollen, proteins), and metallic the DRB1 locus in the HLA class II region.28 29 Several compounds (beryllium, zirconium). In sarcoid granulo- studies on genetic polymorphism have shown the potential mas, the presence of mycobacterial DNA was identified by to predict the clinical course of the disease.28 Although the Ocular involvement in sarcoidosis 111 HLA class II genotyping was associated with disease sarcoidosis at a very early age.37 Childhood sarcoidosis Br J Ophthalmol: first published as 10.1136/bjo.84.1.110 on 1 January 2000. Downloaded from outcome in Scandinavian patients (HLA-DR 14 and 15 might be misdiagnosed because of its rarity and resem- were associated with chronic sarcoidosis and HLA-DR 17 blance to juvenile chronic arthritis. Autosomal, dominantly with non-chronic forms of sarcoidosis), in other popula- inherited Blau syndrome (familial granulomatous inflam- tions other alleles were responsible for the susceptibility matory arthritis, uveitis and rash, and camptodactylia) is and course of the disease.30 31 characterised by multiorgan inflammation and may strongly resemble sarcoidosis; however, the typical pulmo- Clinical manifestations nary involvement is absent.39–41 The course of sarcoidosis ranges from asymptomatic to severe and even lethal disease. The clinical manifestations and severity of the disease vary widely and are strongly Diagnostic methods associated with racial and ethnic factors: acute and more In the absence of the known causative agent, the diagnosis severe disease is typical of black patients, whereas of sarcoidosis remains mainly a diagnosis of exclusion. asymptomatic and chronic disease is more frequent in Since there are no definitive diagnostic serological or whites.12 In all races, however, mortality remains similar.32 radiological tests, the presence of non-caseating granulo- Although the overall prognosis is relatively benign, many mas on tissue biopsy together with compatible clinical fea- patients develop some organ dysfunction. Factors associ- tures is usually considered as a proof of the diagnosis of ated with poor outcome include black race, late onset, and sarcoidosis. However, even in cases with tissue biopsy con- disease persisting for longer than 6 months, involvement of sistent with the presence of sarcoidosis, other possible more than three organs, and stage III of pulmonary disease causes of granulomatous diseases should be evaluated. (parenchymal infiltrates without adenopathy).133 Sar- Although biopsy is not pathognomonic, tissue examination coidosis aVects people of all ages with the peak age of onset is essential to diVerentiate sarcoidosis from infections or in the third decade.13 malignancies. Tissue biopsy might be obtained from lung, The disease aVects predominantly the lungs and skin, lymph node, or other aVected organs. Undirected thoracic lymph nodes, skin, and eyes and might have either biopsies yielded less positive results compared with those self limited or chronic course. Although the manifestations obtained from overtly aVected organs; this was also of sarcoidosis may be widespread, as a result of the reported for conjunctival granuloma or lacrimal gland frequent manifestations in lungs and lymph nodes, most biopsy.42–44 The analysis of fluids and cells obtained by patients will have some respiratory problems.13 The major- bronchoalveolar lavage, including CD4/CD8 ratio, is not ity of patients have constitutional symptoms such as fever, specific enough for the definitive diagnosis of sarcoidosis.45 malaise, fatigue, and weight loss. Frequently
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