Vogt-Koyanagi-Harada syndrome

Vogt-Koyanagi-Harada Syndrome Vogt-Koyanagi-Harada syndrome is an acute diffuse uveitis with specific systemic symptoms characterized by: 1 sudden uveitis; 2 whitening of eyebrows and hair, baldness and vitiligo Damage; 3 headache, dizziness, nausea and other nervous system manifestations; 4 tinnitus, deafness and dizziness and other symptoms of the inner ear. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population Mode of infection: non-infectious Complications: retinopathy, optic discitis

The cause of Vogt-Koyanagi-Harada syndrome

(1) Causes of the disease

The etiology of Vogt-Koyanagi-Harada syndrome is not fully understood, mainly related to autoimmune response and infection factors.

(two) pathogenesis

The pathogenesis of this disease is still not very clear, it may be caused by the combination of cellular immunity and humoral immunity.

1. Cellular immunity causes tissue damage. This damage is mediated by lymphocytes. Experiments have confirmed that the lymphocytes of patients with this disease are sensitized by melanocyte surface antigens, and sensitized lymphocytes attack melanin as a target cell. That is to say, melanocytes are both antigens of immune response and target cells damaged by sensitized lymphocytes. Antibodies against various components of the pigment membrane have been detected from patients, and the most important antibodies are A melanocyte surface antigen antibody that destroys melanocytes by an anti-dependent cell-mediated cytotoxic mechanism, indicating that it is autoimmune caused by humoral immunity.

According to Sugiura, the disease is a melanocyte-specific autoimmune disease. The antigen that induces this autoimmunity is located on the surface of melanocytes. In normal people, because the antibody immunosurveillance system works, immune-active cells do not occur on themselves. The immune attack of melanocytes, this state is called immune tolerance, and in this disease, the immune tolerance to autologous melanocytes may be terminated by two factors:

1 immune surveillance system function primary disorder;

2 Some changes have occurred in melanocytes, and the antigenicity of the cell surface has been modified.

2. The role of immunogenetics in pathogenesis Many autoimmune diseases are known to be closely related to human leukocyte antigen (HLA). Sugiura has detected HLA-A, B, and D locus antigens in a group of patients, resulting in HLA- The frequency of BW54 antigen was 45.2%, that of the control group was 13.2%; that of LD-Wa antigen was 66.7%, and that of the control group was 16%; the relative risk of HLA-BW54 was 4.9, and that of LD-Wa was 10.5. The incidence rate is 4.9 times and 10.5 times that of non-carriers. HLA-BW54 and LD-Wa are HLA-B and D site antigens respectively. These two antigens are not found in whites, so they are considered to be unique to people in the Far East. The antigen is more common in Japanese and Oriental people, but less common in European and American whites. This also indicates that the disease is closely related to immunogenetics. Ohno also confirmed that the relative risk of DR4 and MT3 in patients with this disease increased by 15.2 times compared with the control. 74.5 times, this disease, like other autoimmune diseases, is also closely related to HLA-D (DR) site antigen (MT3). All cases with D (DR) site antigen are positive for MT3. , indicating that the disease is highly related to immunogenetic factors, and that DR4 and MT3 are also Japanese and Far East. The unique antigen, Volgo-Koyanagi-Harada syndrome and HLA related effects.

3. Pathology The typical pathological change of this disease is choroidal histology: the lesion is a nodular granuloma lesion formed by lymphocytes, plasma cells surrounding epithelioid cells and multinucleated giant cells, no necrotic lesions in the center, epithelial-like The cells are large cells with clear cytoplasm, containing more organelles, lysosomes and phagosomes. Melanin particles are visible in the phagosome, and there are Delen-Fuchs nodules protruding into the choroid. The nodule is composed of degenerated retinal pigment epithelial cells and epithelioid cells. The pathological changes of the iris ciliary body are essentially the same as the choroidal changes, and are lesions composed of epithelioid cells, lymphocytes and plasma cells. Lymphocyte mitotic signs are sometimes seen, but epithelial-like cells are less visible in the choroid than in the choroid.

Corneal epithelial melanocytes and melanin particles are reduced, while Langhan cells are increased. Normal Langhan cells are only found in the superficial layer, and the disease can also be seen in the basal layer.

The pathological changes of the skin are the same as those of the corneal epithelium, that is, the melanocytes and melanin particles are reduced, and the Langhans cells are increased. This cell is also found in the basal layer. A small amount of lymphocytes and mild inflammatory cell infiltration are found in the epidermis. There are no melanocytes in the body, but melanocytes derived from the mother's plaque can be seen in the hips of the Mongolian plaque, and melanocytes are fused with lymphocytes, which is exactly the same as seen in the pigmented membrane. Intradermal cells infiltrate very lightly, no epithelial-like cells are formed, and occasionally lymphocytes infiltrate with epithelioid cells. In addition to Langhan cells, there are cells identical to rod-shaped granule cells. The cells have active migratory and phagocytic functions.

According to the observed characteristics of melanocytes, they can be divided into superficial and deep types. The melanocytes in the pigmented membrane, meninges, inner ear and dermis belong to the deep type, while the corneal epithelium and melanocytes in the epidermis belong to the superficial type. The characteristics of the two types of melanocytes are significantly different, that is, the deep melanocytes lose the function of synthesizing melanin. Under electron microscope, the cell wall of this type of cells is thin and the basement membrane is incomplete. On the contrary, superficial melanocytes have active melanin synthesis. Function, the cell membrane has no deep basement membrane features.

Vogt-Koyanagi-Harada syndrome prevention

Every effort to avoid provoking the body's immune response is the key to preventing autoimmune diseases.

1. Eliminate and reduce or avoid the disease factors, improve the living environment, develop good living habits, prevent infection, pay attention to food hygiene, and rational diet.

2. Insist on exercising, increase the body's ability to resist disease, do not over-fatigue, excessive consumption, quit smoking and alcohol.

Vogt-Koyanagi-Harada syndrome complications Complications retinopathy optic discitis

The occurrence of complications is related to the duration of uveitis and the frequency of recurrence. The longer the duration of inflammation, the higher the frequency of recurrence, the more prone to complications. In addition, it is related to the application of glucocorticoids. Glucocorticoid eye drops are easy to cause glucocorticoid glaucoma and cataract.

The most common complication of Vogt-Koyanagi-Harada disease is complicated cataract, secondary glaucoma (Table 4), in addition to the subretinal neovascular membrane, macular hole, proliferative retinopathy, etc. Some scholars The change of the sunset-like fundus is also classified as a complication.

1. The granulomatous anterior uveitis of the complicated cataract Vogt-Koyanagihara disease is often recurrent, which is prone to cause post-iris adhesion, and the blood-water barrier function is very significant in such patients. The changes in aqueous components often give the lens The metabolism has adverse effects, so complicated cataract is a common complication. It is reported to have an incidence of 10.5% to 40.4%. The cataract caused by this disease is mainly characterized by opacity of the posterior capsule of the lens. Cataract, anterior cortical opacity, etc.

2. Secondary glaucoma Secondary glaucoma is a common complication of Vogt-Koyanagi field disease, the incidence rate is 6% to 45%. Secondary glaucoma caused by Vogt-Koyanagi field disease can be seen after uveitis At any time, but most of the recurrence of anterior uveitis, its occurrence is related to post-irisal adhesion, pupillary block, occlusion of the anterior chamber, trabecular mesh inflammation, occlusion of inflammatory trabecular meshwork and long-term application of glucocorticoids. The glaucoma caused by this syndrome is mostly caused by complete posterior adhesion of the iris or most or complete adhesion of the anterior chamber. Some patients with complete posterior adhesion of the iris may be accompanied by iris neovascularization. This neovascularization can be used for traffic and intraocular pressure in the anterior and posterior chambers. It can disappear completely after falling.

It is worth noting that a small number of patients with Vogt-Koyanagi Harada can develop acute angle-closure glaucoma. This kind of complication can occur in the prodromal phase, and it can also occur with uveitis. Some patients use acute angle-closure glaucoma as the comprehensive The initial eye manifestations of the sign, the patient showed a sudden increase or slow increase in intraocular pressure, shallow anterior chamber, may also be associated with anterior chamber flash, or with choroiditis, chorioretinitis, optic discitis and neuroretinitis After systemic treatment with glucocorticoids, the angle of the anterior chamber is open, and it is speculated that the acute inflammatory edema of the ciliary body causes the lens iris to move forward, resulting in the closure of the angle of the anterior chamber, causing acute angle-closure glaucoma , the intraocular pressure caused by this syndrome. Elevation can be transient.

3. Subretinal neovascular membrane and proliferative lesions The subretinal neovascular membrane is a relatively rare complication of Vogt-Koyanagi field disease, which occurs mainly in patients with choroidal inflammation who are not timely controlled and recurrent, with an incidence of 0.96. %36%, although it is not as common as complicated cataract, its visual function damage is much greater than that of complicated cataract. Moorthy et al. observed 130 cases of 65 patients, and 12 cases had subretinal neovascular membranes. The time of occurrence was 14.5 months after the onset of uveitis. Statistical analysis of some parameters revealed that the occurrence of this lesion was not related to race, gender, age, etc., but with chronic or recurrent inflammation (P < 0.001). Significant anterior segment inflammation (P < 0.01) and extensive retinal pigment epithelial changes (P < 0.05) were closely related.

The subretinal proliferative membrane is white colloidal, and may have a bulge due to subretinal hemorrhage during the active phase. The subretinal neovascular membrane occurs mostly in the optic disc and the macular area (Fig. 1, 2), and may also occur in the peripheral part. The paravertebral disc and the macular area are the prone areas of the subretinal neovascular membrane. The reason may be related to the occurrence of inflammatory lesions in this syndrome. Inflammation of the Bruch membrane and choroidal capillaries can lead to the choroid and outer layer. Retinal ischemia, which stimulates the proliferation of choroidal capillary endothelial cells, causes the formation of subretinal neovascular membranes, and the lower peripheral part is also a frequent site of inflammatory lesions, and the underlying subretinal neovascular membrane is not common, which may be related to this site. Concealed and emerging neovascular membranes have little effect on visual acuity and are not related to factors such as people's attention.

Vogt-Koyanagi-Harada Syndrome Symptoms Common Symptoms Photophobia, tears, retinal edema, hawthorn, or eve, fundus, retinal detachment, ciliary congestion

Vogt-Koyanagi-Harada syndrome check

1. Lumbar puncture lumbar puncture and cerebrospinal fluid examination is a useful auxiliary laboratory test, but it is not widely used in clinical applications, because in most patients, according to medical history, clinical examination and fluorescein fundus angiography The diagnosis can be confirmed. The cerebrospinal fluid changes in patients are mainly caused by lymphocytosis. In about 80% of patients, cerebrospinal fluid lymphocytosis occurs within 1 week after inflammation, and 97% of patients have such changes in 1 to 3 weeks. Cerebrospinal fluid lymphocytosis usually disappears within 8 weeks. When inflammation recurs, cerebrospinal fluid lymphocytosis usually does not occur. Therefore, this examination has not been diagnosed for patients with chronic prolonged uvitis and recurrent uveitis. value.

2. Immunological examination Vogt-Koyanagi-Harada disease can cause a variety of immunological abnormalities, such as anti-uveal membrane in serum, anti-photoreceptor extracellular domain, anti-retinal S antigen, anti-Müller cell and other antibodies, serum IgD levels in patients The level of -interferon is also elevated, but these changes are not specific, so it is of little significance in determining the diagnosis. HLA antigen-type examination of patients shows that HLA-DR4, HLA-DRw53 antigen is positive, and there is a diagnosis. Helped.

3. Fluorescein fundus angiography Fluorescein fundus angiography is of great value in the diagnosis of Vogt-Koyanagi-Harada disease. The changes in angiography can be very different at different stages of the disease.

(1) Fluorescein angiographic changes in the acute phase of uveitis: during the period of uveitis, usually called the acute phase of inflammation (actually including the posterior uveitis and anterior uveal age), Fluorescein fundus angiography is mainly characterized by multiple punctate strong fluorescence at the level of retinal pigment epithelium. These fluorescent spots gradually enlarge and cause fluorescein to enter the subretinal fluid and retinal pigment epithelial fluid. The strong fluorescent spot is located in the choroidal inflammation site. The dye comes from the choroidal capillaries and enters the subretinal space, delineating the contour of the multifocal retinal neuroepithelial detachment. Another characteristic of the uveitis is the appearance of radial choroidal vaginal dark bands and bright bands, which are caused by swollen choroid Caused by wrinkles; in addition, optic disc leakage is also a common change, occasionally seeing macular edema, focal retinal vasodilation and leakage.

(2) fluorescein fundus angiography changes in the recurrence of anterior uveitis: in the recurrence of anterior uveitis, inflammation in the posterior segment of the eye is generally chronic inflammation and mild inflammation, and inflammatory exudation can be absorbed. Typical angiographic changes were worm-like fluorescence appearance and window-like defects, and diffuse retinal pigment epithelial lesions showed a strong or weak fluorescence change in the salt-and-salt (Fig. 3). In addition, punctate staining and strong fluorescence of the optic disc were observed. Hemorrhage obscures fluorescence, the petal-like strong fluorescence caused by macular edema, and occasionally the localized strong fluorescence caused by pigment epithelial detachment.

4. Indocyanine green fundus angiography The changes of indocyanine green angiography in Vogt-Koyanagi-Harada vary greatly with the course of the disease.

(1) acute phase of uveitis: in the acute phase of uveitis (post-uvitis period and anterior uveal age), changes in indocyanine green fundus angiography have weak fluorescent dark spots, focally strong fluorescent choroidal vascular changes And optic disc staining.

1 weak fluorescent dark spots: three types of weak fluorescent dark spots can appear in this syndrome:

A. In the early stage of angiography, the flaky weak fluorescent dark area has a blurred edge. As the contrast time prolongs, the weak fluorescent black spot gradually becomes shallow or disappears, and segmental choroidal vasodilation occurs, and the fluorescence segmentation is enhanced;

B. The weak fluorescence region of the late fusion appears as a plurality of circular weak fluorescence regions or irregular weak fluorescence regions, which can roughly delineate the boundary of neuroepithelial detachment;

C. Multiple weak fluorescent spots scattered throughout the fundus. Such weak fluorescent black spots can appear in the early stage of angiography, and the size is relatively consistent. Some weak fluorescent black spots merge into a large weak fluorescent area, but the fluorescence can be strong or weak. Etc. Some areas have focal strong fluorescence.

2 Focal strong fluorescence: This focal strong fluorescence usually appears after a few minutes of contrast or in the middle of contrast, located between the edge of the weak fluorescent area or the weak fluorescent area, representing the active choroidal inflammation area.

3 choroidal vascular changes: choroidal vascular changes mainly include vascular segmental dilatation (Fig. 4), vascular wall staining and leakage; vortex veins can also be affected, manifested as dilatation and blurred edges, these changes are most obvious within a few minutes of contrast.

4 optic disc staining: This staining is mainly seen in patients with obvious involvement of the optic disc, the intensity is generally lower than that of fluorescein fundus angiography, the staining is not so uniform, and the optic disc as a whole is weakly fluorescent.

5 Other changes: When the retinal detachment is seen, the retinal blood vessels are not at the same level as the non-disengaged area, and the choroidal blood vessels in the detached area are blurred and the boundary is unclear.

(2) Changes in the chronic phase and recurrence of uveitis (recurrent phase of anterior uveitis): overall, in the recurrence of anterior uveitis, indocyanine green angiography changes are not as typical as acute phase changes, in choroidal activity In the case of sexual inflammation, weak fluorescent spots, focal strong fluorescence and the aforementioned choroidal vascular changes are still visible.

5. Ultrasound examination Although the diagnosis of Vogt-Koyanagi-Harada is mostly based on clinical examination and fluorescein fundus angiography, patients often have post-iris adhesions, which are difficult to expand. In addition, some patients may have obvious Lens opacity, which can affect the visibility of the fundus, ultrasound examination provides important evidence for diagnosis in these patients. Foster et al. recently described ocular ultrasound changes in this syndrome, including:

1 diffuse posterior choroid with low to moderate reflex thickening;

2 exudative retinal detachment is limited to the posterior pole or below;

3 a certain degree of vitreous opacity, without the posterior detachment of the vitreous;

4 posterior sclera or superficial sclera thickening.

Ultrasound changes in Vogt-Koyanagi-Harada should be differentiated from changes caused by other diseases:

1 posterior scleritis (see differential diagnosis);

2 benign reactive lymphoid hyperplasia, this disease can appear iris, ciliary body and choroidal diffuse lymphocytic infiltration, causing anterior uveitis, exudative retinal detachment and changes in retinal pigment epithelium, but 90% of patients are single Side involvement, and inflammation can also extend to the posterior bulbar tissue, and ultra-reflective choroidal thickening is found by ultrasonography;

3 diffuse choroidal malignant lymphoma and other tumors, this disease is rare, the results of ultrasound examination is similar to the change of this syndrome, there is low-reflective choroidal thickening, but most patients with monocular involvement, in the eyes of lymphoma or leukemia, Choroidal thickening as small as 1 to 2 mm can also be detected by ultrasonography, but Kincaid et al. believe that this syndrome and choroidal infiltration of tumors are sometimes difficult to identify in ultrasound examination.

6. Electrophysiological examination Electroencephalogram (EOG) and electroretinogram (ERG) examinations are not specific in the diagnosis of Vogt-Koyanagi-Harada disease, but may be observed in patients with refractive media opacity or follow-up observation. In a certain sense, the EOG amplitude decreases in the prodromal phase and uveitis. In the chronic phase, the EOG amplitude gradually recovers. As the disease progresses, the L/D ratio of the patient decreases significantly. In the less than 1.8, the group below 5 years is 6.9%, 26% in the 5-10 years group, 87% in the 10 years and above group, the response of the resting potential in the inflammatory active phase is still normal, and when the retinal pigment epithelium depigmentation in the chronic phase, the retinal pigment epithelium penetrates. The sensitivity of pressure change is reduced. It has been found that ERG exhibits a, b wave amplitude is reduced during the onset period, and can be maintained for a long period of time. It gradually recovers in the chronic phase and chronic relapse. The longer the course of disease, the more the ERG changer The higher the proportion, the lower the disease duration of 5 years, 55% showed that the b-wave amplitude of dark-adapted ERG decreased, and in patients over 10 years, the b-wave decreased, and the flash ERG amplitude was less than 40V in patients less than 5 years. 9.7%, 60% of those over 10 years %.

Ultrasound biomicroscope (UBM) is an ultrasonography method used in recent years for the examination of the structure and disease of the anterior segment of the eye. It not only has a good evaluation of iris lesions, Accurate evaluation of the ciliary body and nearby structural changes that are not easily observed by the general method is also performed. Although the Vogt-Koyanagi-Harada disease mainly involves the choroid in the early stage, the iris ciliary body is often involved, showing the iris front. After adhesion, posterior chamber fibrinous exudation, sometimes posterior chamber fibrinous exudate can divide the posterior chamber into several posterior chambers (Fig. 5), ciliary body edema, thickening, inflammatory exudate can be seen nearby. The detachment of the ciliary body can still be observed in individual patients, and such detachment can sometimes extend to the peripheral portion, causing choroidal detachment.

Diagnosis and identification of Vogt-Xiaoliu-Harada syndrome

Diagnostic criteria

Mainly relying on medical history and anterior and posterior examination of the eye, young or middle-aged people, both eyes have a simultaneous or short-term uveitis, have or have meningeal irritation, no other eye or systemic symptoms and signs, you can Make a preliminary diagnosis, such as the patient's first onset, and the course of disease is 1 to 8 weeks, cerebrospinal fluid examination has lymphocytes, increased protein content, the diagnosis can be determined, such as uveitis repeatedly, and there are inner ear hearing impairment and skin When the hair turns white (all or one of them, two), the diagnosis is more in doubt, but not all of the cases can see the above typical changes. The following tests have certain reference value.

In the acute phase of H-type inflammation, FFA can be characterized by multiple focal fluorescein in the retinal pigment epithelial layer. The fluorescence is located in the choroidal lesion and rapidly enters the subepithelial layer of the retinal pigment epithelium, which is continuously enlarged and enhanced to make the pigment epithelium under the pigment. And the neuroepithelial exudate staining, outlines the detachment zone of the multifocal retinal two layers, ICGA is seen by the choroidal swelling wrinkles and visible radial choroidal vaginal dark band and bright band, after inflammation relief or rest, choroidal and The pigment epithelial pigment is largely lost and free, showing a haze-like fundus. At this time, the FFA is mottled. The pigmentation can be seen in the fluorescence, the fluorescence at the pigmentation is blocked, and the choroidal capillary atrophy is also a weak fluorescence zone.

VK type is severe due to anterior segmental lesions, and can not be used for angiography. Ultrasound can be performed if necessary. The common changes in sonogram are vitreous opacity; posterior choroid, sclera and sclera outer layer thickening; sometimes posterior or lower Retinal detachment.

Differential diagnosis

Vogt-Koyanagi-Harada disease should be differentiated from types that can cause choroiditis, chorioretinitis, optic discitis, neuroretinitis, total uveitis and recurrent granulomatous anterior uveitis, the most important of which Sensible ophthalmia, sarcoma-like disease, intraocular lymphoma, etc.

1. Sympathetic ophthalmia Sympathetic ophthalmia has many similarities with Vogt-Koyanagi-Harada disease both in clinical manifestations and histology. The most important thing to identify is sympathetic ophthalmia. The patient has a history of penetrating or endoscopic surgery, but some patients are difficult to identify because of a slight penetrating injury or because the injury has been too long (some sympathetic ophthalmia can occur for decades).

2. Acute posterior multifocal squamous pigment epithelial lesions This disease was first reported by Gass in 1968. Patients with sudden central vision loss after viral infection, multiple yellow-white flat squamous lesions in the posterior fundus, these lesions Often spontaneously disappeared with vision recovery, the disease can be confused with Vogt-Koyanagi-Harada disease at the initial onset, but the disease is characterized by diffuse choroiditis, optic discitis, neuroretinitis, and systemic Performance, fluorescein fundus angiography, indocyanine green angiography to help identify.

3. Lumitis caused by Lyme disease This disease is usually characterized by bilateral granulomatous iridocyclitis, and also with intermediate uveitis, occasionally causing bilateral uveitis with exudative retina In addition, patients may have focal neurological signs, such as cranial nerve palsy and optic neuritis. Patients live in forest areas, have a history of bite, fever, arthritis, etc., but Vogt-Koyanagi-Harada The disease usually has a typical progression of uveitis, with typical early diffuse choroiditis, choroidal retinitis and other fundus changes, DalenFuchs nodules in the later stages of the disease, changes in the haema-like fundus and recurrent granulomatous anterior uveitis. Glucocorticoid therapy has a good effect, but the effect on Lyme disease is not certain. According to these characteristics, it is generally easy to distinguish the two.

4. Multifocal and easily dissipative white spot syndrome This syndrome usually occurs in young women, mostly unilateral, characterized by a sudden drop in visual acuity below 0.1, often accompanied by afferent pupillary disorder, and the posterior pole is located. The spotted lesions of the outer retina or retinal pigment epithelium exist in isolation, do not undergo fusion, have the characteristics of easy regression, self-limiting, etc., and the visual acuity can be restored to 0.5-1.0 within 6 weeks. The patient has no anterior chamber inflammation. However, inflammatory cells can appear in the vitreous, no choroidal thickening, and fluorescein fundus angiography can show a strong fluorescent area around the white spot. In the late stage of angiography, the lesion is stained with fluorescein, and can also be stained with optic disc. Occasionally Retinal vascular sheath appears, generally does not recur, according to these characteristics, it is generally easy to distinguish with Vogt-Koyan-Harada disease.

5. Posterior scleritis This disease usually occurs in women, usually bilateral, may have pain, photophobia, red eyes, decreased vision or severe decline, inflammatory cells may appear in the vitreous, ring-shaped mass can be seen in the fundus, choroidal wrinkles Pleated, retinal streaks, optic disc edema, annular choroidal detachment, etc., choroidal thickening can be diffuse or localized, ultrasound examination shows that the choroid is highly reflective thickening, the back of the eyeball becomes flat, the posterior sclera and sclera Tissue thickening and post-balloon tissue edema, Voget-Koyanagi-Harada patients with choroidal thickening and scleral thickening, but diffuse choroiditis, optic discitis, neuroretinitis, chorioretinitis are quite common, and patients There are prodromal symptoms, typical late-seasonal fundus changes, Dalen-Fuchs nodules, and recurrent granulomatous anterior uveitis.

6. Uveal exudation syndrome This syndrome can also cause exudative retinal detachment. Fluorescein fundus angiography shows some fluorescent spots in the subretinal space, and plaque-like fluorescence occurs during recovery. These are similar to Vogt- Koyanagi-Harada disease, but the occurrence of exudative retinal detachment of uveal exudation syndrome is subacute or chronic progressive, generally no inflammatory changes or mild inflammation, although this syndrome can affect both eyes, but Not at the same time, exudative retinal detachment often recovers automatically. The progression of the disease and the lack of inflammation and the absence of skin, hair, and nervous system changes contribute to the differential diagnosis, glaucoma, subretinal neovascularization and other complications. Can affect the patient's visual prognosis.

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