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MEDICINSKA ISTRAŽIVANJA VOL. 45 / SVESKA 1 / 2011 Figure 7c. Juxtapapillar neovascular membrane in White dot syndrome in the left eye (2003) Figure 7d. The severe form of serpiginous choroidopathy in the left eye, two years after the development of multifocal choroiditis and subretinal neovascularisation (2005) In the observed group of 33 patients with White dot syndrome the results of immunological examinations were within the limits of the normal values, except immune complexes that in 10 patients (30.30%) out of 33 of patients were increased. The minimal value of immune complexes was 0.518, and the maximum was 1.557 IJ. Patients with increased values of immune complexes in the serum had more severe forms of serpiginous choroidopathy and White dot syndrome associated with retinal vasculitis. 36 Discussion White dot syndrome comprises bilateral, chronic, relapsing autoimmune conditions. The diseases of White dot syndrome are classified into this same group due to their main clinical features, including the white dot scattered over the fundus and their common pathogenesis. The diseases classified as White dot syndrome involve the choriocapillaris, pigment epithelium and the exterior layers of the retina.(1,2,4) They should be distinguished from multifocal chorioretinitis of infectious etiology caused by viruses, toxoplasma, and histoplasma and from chorioretinal involvement related to systemic diseases, such as sarcoidosis, Vogt- Koyanagi-Harada syndrome, etc.(5,6,7,8,9,10). Clinical features, evolution and functional damage depend on the involvement of photoreceptors and the pigment epithelium, which are the least significant in APMPPE, while the most severe are expected to be seen in serpiginous and multifocal choroiditis with panuveitis. The angiographic features of these conditions during the early stage of the disease are typical: there is a lack of fluorescence in the areas of lesions during the early angiography stage, followed by subsequent leaking of fluorescein in the same areas. These typical findings suggest that these conditions represent ischemic diseases of choriocapillaris arterioles. (1,2,3). There is a possibility that viruses, certain haptens and other agents, initiate autoimmune response in the setting of the underlying genetic base. (11,12). The fact that the elevated levels of circulating immune complexes have been shown in the significant proportion of these patients (10/33%) suggest that choriocapilaris arterioles may be affected like other vessels in immune complex diseases. Of major concern is the coexistence of APMPPE and retinal vasculities, the ischemic form of the disease, accompanied by neovascularization. (3) White dot syndrome may cause diagnostic dilemma in cases in which the lesions in the fundus are in their advanced stages; on different eyes or even on the same eye of a single patient, lesions pertaining to two or more clinical forms of the disease may be found, e.g. APMPPE and serpiginous choroiditis, or APMPPE and multifocal choroiditis. In addition to that, the disease may alter its presentation during the relapses, as it is shown in case reports: APMPPE evolves towards serpiginous form, while subretinal
MEDICINSKA ISTRAŽIVANJA VOL. 45 / SVESKA 1 / 2011 neovascularization evolves towards multifocal choroiditis, accompanied by subretinal fibrosis. This type of evolution may cause severe functional impairment, and therefore, the appropriate followup and treatment are necessary. It is very difficult References 1. Gass JD. Acute posterior multifocal placoid pigment epitheliopathy. Arch Ophthalmol 1968; 80: 177-185 2. Deutman AF. Acute multifocal ischaemic choroidopathy and the choriocapillaritis. Int Ophthalmol 1983; 6: 155-160. 3. Spaide RF,Yannuzzi LA, Slakter J.Choroidal vasculitis in acute posterior multifocal placoid pigment epitheliopathy. Br J Ophthalmol. 1991; 75: 685-687. 4. Teyssot N, Bodaghi B, Cassoux N, Fardeau C, Le Mer Y, Ullern M, Le Hoang P.Epitheliopathies en plaques, choroidites serpigineuses et multifocales: analyse etiologique et prise en charge therapeurique. J Fr Ophthalmol.2006;29:510-518. 5. Anderson K, Patel KR,Webb L, Dutton GN. Acute posterior multifocal placoid pigment epitheliopathy associated with pulmonary tuberculosis. Nr J Ophthalmol. 1996; 80: 186. 6. Gupta V, Gupta A, Arora S, Bambery P, Dogra MR, Agarwal A. Presumed tubercular serpiginous like choroiditis:clinical presentations and management. Ophthalmology. 2003; 110: 1744-1749. 7. Bodine SR, Marino J, Camisa TJ, Salvate AJ.Multifocal choroiditis with evidence of Lyme disease. Ann Ophthalmol. 1992; 24: 169-173. 37 to distinguish spontaneously resolving from more severe forms of White dot syndrome due to an unpredictable course and relapsing character of the disease. 8. Chiquet C, Germain P, Burillon C, Coudry- Vergne D, Perez M, Paupert-Ravult M, Denis P. Multifocal choroiditis associated with herpes zoster ophthalmicus.Apropos of a case. J Fr Ophthalmol. 1996; 19: 712-715. 9. Priya K,madhavan HN, Reiser BJ, Biswas J, Saptagirish R, Narayana KM, Rao NA. Association of herpes viruses in the aqueous humor of patients with serpiginous Choroiditis apolymerase chain reaction-based study.Ocul Immunol Inflamm. 2002; 10: 253-261. 10. Bodiguel E, Benhamou A, Le Hoang P, Gautier JC. Cerebral infarction,placoid epitheliopathy and sarcoidosis. Rev Neurol. 1992; 148: 746-751. 11. Wolf MD, Folk JC, Panknen CA, Goeken NE. HLA-B7 and HLA-DR2 antigens and acute posterior multifocal placoid pigment epitheliopathy.Arch Ophthalmol. 1990; 108: 698-700. 12. Spaide RF, Skerry JE,Yannuzzi LA, DeRosa JT. Lack of the HLA-DR2 specificity in multifocal choroiditis and panuveitis. Br J Ophthalmol. 1990; 74:536-537. 13. Stanojevic Paovic A. Uveitisi. Medicinski fakultet Univerziteta u Beogradu. 2008;4: 204- 225.
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