PATHOGENESIS AND CURRENT METHODS OF TREATMENT OF SECONDARY UVEITIC GLAUCOMA. A REVIEW.

Secondary uveitic glaucoma is a serious sight-threatening complication of intraocular inflammation (uveitis). It develops in approximately 10-20% of patients with uveitis (although this figure may be higher depending on the type of inflammation). It is more commonly associated with chronic forms of uveitis, especially anterior uveitis. Elevation of intraocular pressure (IOP) and the development of secondary glaucoma arise as a direct or indirect consequence of uveitis, and may develop further in association with therapy for intraocular inflammation. Several types of uveitic glaucoma are distinguished according to the mechanism of development: open-angle secondary glaucoma (including steroid-induced secondary glaucoma), angle-closure secondary glaucoma, and a combination of both. It is necessary to determine the pathogenesis of uveitis and target the treatment of the inflammatory process according to it. Subsequently, it is necessary to determine the type of secondary glaucoma, which influences the choice of therapy. Compensation for IOP should be achieved as quickly as possible, before irreversible damage to the optic nerve and visual field occurs. In the first instance, we choose conservative pharmacological therapy. However, this therapy fails more often in secondary uveitic glaucoma than in primary open-angle glaucoma. For this reason, surgical or laser therapy is necessary for refractory glaucoma. Trabeculectomy remains the gold standard in surgical therapy for secondary uveitic glaucoma, but other surgical techniques can also be used (Ahmed drainage implants, goniotomy in the paediatric population, surgical iridectomy, and synechiae for angle closure etc.). The choice of method is individualised according to the clinical findings of the patient and previous ocular procedures. However, the main factor influencing the success and efficacy of filtration surgery is adequate therapy and control of the intraocular inflammatory process.

MICROBIOME AND UVEITIDES. A REVIEW.

Microorganisms inhabiting all surfaces of mucous membranes and skin and forming a complex ecosystem with the host is called microbiota. The term microbiome is used for the aggregate genome of microbiota. The microbiota plays important role in the mechanisms of number of physiological and pathological processes, especially of the hosts immune system. The origin and course of autoimmune diseases not only of the digestive tract, but also of the distant organs, including the eye, are significantly influenced by intestinal microbiota. The role of microbiota and its changes (dysbiosis) in the etiopathogenesis of uveitis has so far been studied mainly in experimental models. Reduction of severity of non-infectious intraocular inflammation in germ-free mice or in conventional mice treated with broad-spectrum antibiotics was observed in both the induced experimental autoimmune uveitis model (EAU) and the spontaneous R161H model. Studies have confirmed that autoreactive T cell activation occurs in the intestinal wall in the absence of retinal antigen. Recent experiments focused on the effect of probiotic administration on the composition of intestinal microbiota and on the course of autoimmune uveitis. Our study group demonstrated significant prophylactic effect of the administration of the probiotic Escherichia coli Nissle 1917 on the intensity of inflammation in EAU. To date, only a few studies have been published investigating intestinal dysbiosis in patients with uveitis (e.g., in Behcets disease or Vogt-Koyanagi-Harada syndrome). The results of preclinical studies will be presumably used in clinical practice, mainly in the sense of prophylaxis and therapy, such as change in the lifestyle, diet and especially the therapeutic use of probiotics or the transfer of faecal microbiota.

IMMUNE-MEDIATED INTRAOCULAR INFLAMMATION. A REVIEW.

Immune mediated inflammatory diseases are categorized into autoimmune and autoinflammatory. Autoimmune etiology is represented by autoreactive lymphocytes or autoantibodies, e.g. primary Sjögrens syndrome or rheumatoid arthritis. Ocular specific diseases with presumed autoimmune origin are sympathetic ophthalmia or birdshot chorioretinopathy. Autoinflammatory diseases are caused by mutations in regulatory genes for specific immunity. Hereditary periodic fevers represent monogenic autoinflammatory diseases; eye specific is Blau syndrome also named sarcoidosis with early onset. This article reviews the actual knowledge about immune mediated uveitides, their immunological mechanisms and the possible trigger role of infection in autoimmune inflammation. Immune privilege provides a protection of the eye against any strong immune reaction to foreign antigen, based on physical, immune, humoral and molecular mechanisms. Antigens hidden within the eye are revealed in case of damage of hematoretinal barrier caused by infection or mechanical insult. These ocular antigens have not been set as tolerable during the development and immune reaction is initiated subsequently. Current studies demonstrate that uveogenic trigger might be generated by own microbiome, particularly when dysregulated, so called dysbiosis. There is a known association between idiopathic inflammatory bowel disease with ankylosing spondylitis and anterior uveitis in humans. Intensive research is focused on microbiome and immune mediated inflammatory disease to influence therapeutically the intestinal microbiome. The animal models are used to study the immunopathological mechanisms of uveitis and the new therapeutic strategies, because of relatively low incidence of immune mediated uveitis in humans.

Acute elevation of intraocular pressure in patient with hyperlipidemic myeloma.

PURPOSE: To introduce a rare case of patient with hyperlipidemic myeloma and ocular manifestation in form of masquerade syndrome with acute elevation of intraocular pressure (IOP) and hyperviscous retinopathy. RESULTS: 55-year-old man with newly diagnosed hyperlipidemic myeloma and hyperviscous syndrome was acutely referred to our glaucoma outpatient clinic due to problems with his left eye: sudden pain, blurred vision, redness of the eye and IOP of 44 mm Hg. We excluded attack of angle closure glaucoma and found presence of whitish material in the anterior chamber and blood obstructing the iridocorneal angle. Glaucoma therapy was initiated and lavage of the anterior chamber of the left eye with sampling of the aqueous humour for biochemical and cytological examination was performed. Identification of trace amount of cryoprotein in the samples of humour proved diagnosis of masquerade syndrome. Finding of the hyperviscous retinopathy and nonperfusion of wide peripheral areas of retina in both eyes was indicated to laser coagulation of these areas. The patient underwent in the meantime three times plasmapheresis, four cycles of biological therapy and autologous stem cell transplantation reaching complete remission of the myeloma. Local and systemic therapy led to significant clinical finding improvement on the anterior segment and fundus of both eyes. CONCLUSIONS: Masquerade syndrome can be complicated by acute elevation of IOP. Diagnostic lavage of the anterior chamber, local therapy, systemic therapy and close interdisciplinary cooperation contributed to right diagnosis, IOP normalisation, ocular and general condition improvement.

Recommendations for the Management of Uveitis Associated With Juvenile Idiopathic Arthritis: The Czech and Slovak adaptation of SHARE Initiative.

Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease in children and uveitis is its most important extra-articular manifestation. Evidence-based recommendations are available only to a limited extent and therefore JIA associated uveitis management is mostly based on physicians experience. Consequently, treatment practices differ widely, both nationally and internationally. Therefore, an effort to optimize and publish recommendations for the care of children and young adults with rheumatic diseases was launched in 2012 as part of the international project SHARE (Single Hub and Access Point for Pediatric Rheumatology in Europe) to facilitate clinical practice for paediatricians and (paediatric) rheumatologists. The aim of this work was to translate published international SHARE recommendations for the diagnosis and treatment of JIA associated uveitis and to adapt them for use in the Czech and Slovak Republics. International recommendations were developed according to the standard methodology of the European League against Rheumatism (EULAR) by a group of nine experienced paediatric rheumatologists and three experts in ophthalmology. It was based on a systematic literature review and evaluated in the form of an online survey and subsequently discussed using a nominal group technique. Recommendations were accepted if > 80% agreement was reached (including all three ophthalmologists). A total of 22 SHARE recommendations were accepted: 3 on diagnosis, 5 on disease activity assessment, 12 on treatment and 2 on future recommendations. Translation of the original text was updated and modified with data specific to the czech and slovak health care systems and supplemented with a proposal for a protocol of ophthalmological dispensarization of paediatric JIA patients and a treatment algorithm for JIA associated uveitis. Conclusion: The aim of the SHARE initiative is to improve and standardize care for paediatric patients with rheumatic diseases across Europe. Therefore, recommendations for the diagnosis and treatment of JIA-associated uveitis have been formulated based on the evidence and agreement of leading European experts in this field.

IMMUNE-MEDIATED INTRAOCULAR INFLAMMATION. A REVIEW.

Immune mediated inflammatory diseases are categorized into autoimmune and autoinflammatory. Autoimmune etiology is represented by autoreactive lymphocytes or autoantibodies, e.g. primary Sjögrens syndrome or rheumatoid arthritis. Ocular specific diseases with presumed autoimmune origin are sympathetic ophthalmia or birdshot chorioretinopathy. Autoinflammatory diseases are caused by mutations in regulatory genes for specific immunity. Hereditary periodic fevers represent monogenic autoinflammatory diseases; eye specific is Blau syndrome also named sarcoidosis with early onset. This article reviews the actual knowledge about immune mediated uveitides, their immunological mechanisms and the possible trigger role of infection in autoimmune inflammation. Immune privilege provides a protection of the eye against any strong immune reaction to foreign antigen, based on physical, immune, humoral and molecular mechanisms. Antigens hidden within the eye are revealed in case of damage of hematoretinal barrier caused by infection or mechanical insult. These ocular antigens have not been set as tolerable during the development and immune reaction is initiated subsequently. Current studies demonstrate that uveogenic trigger might be generated by own microbiome, particularly when dysregulated, so called dysbiosis. There is a known association between idiopathic inflammatory bowel disease with ankylosing spondylitis and anterior uveitis in humans. Intensive research is focused on microbiome and immune mediated inflammatory disease to influence therapeutically the intestinal microbiome. The animal models are used to study the immunopathological mechanisms of uveitis and the new therapeutic strategies, because of relatively low incidence of immune mediated uveitis in humans.

IMMUNE-MEDIATED INTRAOCULAR INFLAMMATION. A REVIEW.

Immune mediated inflammatory diseases are categorized into autoimmune and autoinflammatory. Autoimmune etiology is represented by autoreactive lymphocytes or autoantibodies, e.g. primary Sjögrens syndrome or rheumatoid arthritis. Ocular specific diseases with presumed autoimmune origin are sympathetic ophthalmia or birdshot chorioretinopathy. Autoinflammatory diseases are caused by mutations in regulatory genes for specific immunity. Hereditary periodic fevers represent monogenic autoinflammatory diseases; eye specific is Blau syndrome also named sarcoidosis with early onset. This article reviews the actual knowledge about immune mediated uveitides, their immunological mechanisms and the possible trigger role of infection in autoimmune inflammation. Immune privilege provides a protection of the eye against any strong immune reaction to foreign antigen, based on physical, immune, humoral and molecular mechanisms. Antigens hidden within the eye are revealed in case of damage of hematoretinal barrier caused by infection or mechanical insult. These ocular antigens have not been set as tolerable during the development and immune reaction is initiated subsequently. Current studies demonstrate that uveogenic trigger might be generated by own microbiome, particularly when dysregulated, so called dysbiosis. There is a known association between idiopathic inflammatory bowel disease with ankylosing spondylitis and anterior uveitis in humans. Intensive research is focused on microbiome and immune mediated inflammatory disease to influence therapeutically the intestinal microbiome. The animal models are used to study the immunopathological mechanisms of uveitis and the new therapeutic strategies, because of relatively low incidence of immune mediated uveitis in humans.

IMMUNE-MEDIATED INTRAOCULAR INFLAMMATION. A REVIEW.

Immune mediated inflammatory diseases are categorized into autoimmune and autoinflammatory. Autoimmune etiology is represented by autoreactive lymphocytes or autoantibodies, e.g. primary Sjögrens syndrome or rheumatoid arthritis. Ocular specific diseases with presumed autoimmune origin are sympathetic ophthalmia or birdshot chorioretinopathy. Autoinflammatory diseases are caused by mutations in regulatory genes for specific immunity. Hereditary periodic fevers represent monogenic autoinflammatory diseases; eye specific is Blau syndrome also named sarcoidosis with early onset. This article reviews the actual knowledge about immune mediated uveitides, their immunological mechanisms and the possible trigger role of infection in autoimmune inflammation. Immune privilege provides a protection of the eye against any strong immune reaction to foreign antigen, based on physical, immune, humoral and molecular mechanisms. Antigens hidden within the eye are revealed in case of damage of hematoretinal barrier caused by infection or mechanical insult. These ocular antigens have not been set as tolerable during the development and immune reaction is initiated subsequently. Current studies demonstrate that uveogenic trigger might be generated by own microbiome, particularly when dysregulated, so called dysbiosis. There is a known association between idiopathic inflammatory bowel disease with ankylosing spondylitis and anterior uveitis in humans. Intensive research is focused on microbiome and immune mediated inflammatory disease to influence therapeutically the intestinal microbiome. The animal models are used to study the immunopathological mechanisms of uveitis and the new therapeutic strategies, because of relatively low incidence of immune mediated uveitis in humans.

Ocular Manifestations of Granulomatosis with Polyangiitis.

Granulomatosis with polyangiitis (GPA), formerly known as Wegeners granulomatosis, is an autoimmune vasculitis of small vessels, presenting as necrotizing granulomatous inflammation especially of the upper and lower respiratory tract and necrotizing glomerulonephritis. GPA affects more often Caucasians in northern states, predominantly is affected the age-range group of 50 - 60 years. GPA may affect any organ; the eye symptoms are stated in the range of 16-78 %. The eye symptoms are very variable, and in up to 27 % they are the first sign of undiagnosed GPA. The etiology of GPA was not until now explained. Anti-neutrophil cytoplasmic antibodies (ANCA) play important role in the pathogenesis of this disease. GPA is ranked among ANCA associated vasculitis. The GPA is diagnosed on the basis of clinical signs and symptoms of systemic vasculitis, laboratory and histological tests and imaging studies. Immunomodulative therapy made a contribution to the improvement of GPA prognosis in the last decades; biological treatment reaches the prominence of the GPA treatment procedures. Good collaboration with other specialties is necessary for the early diagnosis and treatment of this life and vision threating disease. The ophthalmologist in the collaboration with specialists of other medical branches may take an important part in the GPA diagnostics, monitoring of the diseases course, or adverse affects of the medication. This paper pays attention to the eye symptoms of the GPA; the literature is supplemented with own photographs of GPA eye symptoms in patients followed up at the Department of Ophthalmology, First medical faculty, Charles University and General Faculty Hospital in Prague, Czech Republic, E.U. Key words: Granulomatosis with polyangiitis (GPA), orbit, scleritis, peripheral ulcerative keratitis (PUK), immunomodulation.

Metronidazole Attenuates the Intensity of Inflammation in Experimental Autoimmune Uveitis.

Autoimmune uveitis is a serious sightthreatening disease that in many cases fails to respond to conventional immunosuppressive or biological therapy. Experimental models used in research allow more detailed study of pathogenesis of the autoimmune process and testing new therapeutic strategies. Recent results show that infection can trigger autoimmune diseases, and some commensal microorganisms are essential in causing disease activity. The aim of this work was to assess the effect of broadspectrum antibiotics - combination of metronidazole and ciprofloxacin or metronidazole alone - on the intensity of intraocular inflammation in experimental autoimmune uveitis (EAU). EAU was induced in mouse strain C57BL/6J by interphotoreceptor retinoid- binding protein in complete Freund's adjuvant and pertussis toxin. The grade of uveitis was assessed clinically and histologically in haematoxylin and eosin- stained tissues. Lymphocytes and macrophages were detected in cryosections using the immunoperoxidase method with antibodies. The therapy was commenced one week before EAU induction and continued throughout the experiment. In addition, metronidazole treatment was also started two weeks before EAU induction. Antibiotics significantly reduced the intensity of uveitis compared to the control group (P < 0.05). The effects of combination of ciprofloxacin and metronidazole and of metronidazole alone were similar when the therapy started one week before EAU induction (P < 0.05). Metronidazole commenced two weeks before EAU induction and throughout the experiment suppressed the intensity of EAU with even higher statistical significance (P < 0.0001). It can be assumed that the high protective effect of metronidazole on EAU intensity may be due not only to its antimicrobial effect, but also to its immunomodulatory activity.

[TATTOO-ASSOCIATED UVEITIS]. / UVEITIDA ASOCIOVANÁ S TETOVÁNÍM.

The clinical case of tattoo-associated uveitis was first described by Lubeck and Epstein in 1952. Uveitis is accompanied by induration and hyperemia of tattoo skin, which can precede, follow or manifest simultaneously with uveitis. The diagnosis is determined on clinical grounds after exclusion of other causes. Uveitis is usually bilateral, chronic and vision impairment is variable. Tattoo-associated uveitis should be remembered in differential diagnosis due to the growing interest in tattoo.Key words: uveitis, tattoo, masquerade syndrome.

[The Clinical Signs of Experimental Autoimmune Uveitis]. / Klinické projevy experimentální autoimunitní uveitidy.

INTRODUCTION: Autoimmune uveitis is a sight threatening disease which in many cases fails to respond to conventional immunosuppressive or biological therapy. The research in experimental models of autoimmune uveitis helps to find new therapeutical strategies. The aim of this study is to present the clinical and histological signs of experimental autoimmune uveitis (EAU) in mice. METHODS: EAU was induced in C57BL/6 mice by subcutaneous application of IRBP (interphotoreceptor retinoid binding protein) in complete Freunds adjuvant and intraperitoneal application of pertussis toxin. Clinical evaluation of uveitis was performed in vivo using special imaging system with otoscope. Histological evaluation of uveitis was performed at day 35 post induction of EAU on hematoxylin and eosin stained frozen sections. Clinical and histological grading was used to assess the inflammation intensity of EAU. RESULTS: The intensity of inflammation is depicted on representative fundus images and histological images of retina at day 35 post induction. CONCLUSION: The model of EAU is robust and reproducible and allows us to study the immunopathological mechanisms of inflammation and its regulation. The inflammatory signs in our model are similar to findings of posterior uveitis of autoimmune etiology in humans, thus we may apply our experimental results in human medicine.

Mycophenolate mofetil and cyclophosphamide treatments suppress inflammation intensity in an experimental model of autoimmune uveitis.

In human, autoimmune uveitis is a leading cause of visual disability and ranks with diabetic retinopathy as a major source of blind registrations in developed countries. Since most cases of non-infectious uveitis are considered to be autoimmune or at least immune-mediated, the management of such patients has rested on appropriate immunosuppression. Some patients, however, despite maximal immunotherapy, fail to respond or are seriously intolerant of the drug therapies. Since its establishment 20 years ago, the model of experimental autoimmune uveoretinitis has served as a useful template for novel therapeutic approaches. The aim of our study was to compare the efficacy of mycophenolate mofetil and cyclophosphamide and golimumab treatment in the mouse model of experimental autoimmune uveitis. The intensity of intraocular inflammation was evaluated histologically in the treatment and control groups. Experimental autoimmune uveitis has been induced in mouse strain C57BL/6 by subcutaneous application of interphotoreceptor retinoid binding protein in complete Freund's adjuvant and pertussis toxin. The treatment was commenced on the day of uveitis induction. Cyclophosphamide was applied intraperitoneally in a single dose (100 mg/kg), mycophenolate mofetil intraperitoneally daily (30 mg/kg or 50 mg/kg), golimumab subcutaneously weekly (70 mg/kg). Sham intraperitoneal injection of a placebo (aqua pro injectione) and untreated mice with experimental autoimmune uveitis served as controls. The results show statistically significant suppression of experimental uveitis both with mycophenolate mofetil and with cyclophosphamide, and thus support its use in human medicine.

[Retinitis pigmentosa mimicking uveitis. A case report]. / Benigní maskující syndrom u pacientky s retinitis pigmentosa.

PURPOSE: To describe a case report of a 23-year-old patient with retinitis pigmentosa (RP) misdiagnosed as uveitis. METHODS: A comprehensive eye examination including automated visual field assessment, contrast sensitivity, colour vision discrimination, ultrasound examination (US), spectral domain optical coherence tomography (SD-OCT) and full-field electroretinography (ERG) was performed in a patient diagnosed elsewhere as having intermediate uveitis because of the observation of a cellular reaction in the anterior chamber, bilateral cystoid macular oedema and suspected left optic disc swelling. RESULTS: The patient reported nyctalopia. The best corrected visual acuity in both eyes was 6/12. Concentric visual field constriction was detected bilaterally (less than 25 degrees in the right eye and 15 degrees in the left eye). Fundus examination revealed a few pigment clumps and cystoid macular edema in both eyes confirmed by SD-OCT. Contrast sensitivity was decreased to 1,20 in the right and 0,9 in the left. No colour vision disturbance was present. The B scan ultrasound showed left optic disc drusen. Rod ERG responses were bilaterally not detectable and cone ERGs were abnormally reduced. Based on the examination results, a diagnosis of nonsyndromic RP was made. CONCLUSION: Clinicians should be aware of various manifestations of RP, including mild inflammation, to avoid possible confusin with uveitis.

[Cytomegalovirus retinitis in HIV negative patients - retrospective study]. / Cytomegalovirová retinitida u HIV negativních pacientu - retrospektivní studie.

AIM: To evaluate own experience with the diagnosis and treatment of cytomegalovirus (CMV) retinitis in HIV negative patients with immunodeficiency. METHODS: Retrospective study and case reports. RESULTS: In the Centre for diagnosis and treatment of Uveitis 1869 patients with uveitis we have examined from June 2003 to June 2012. CMV retinitis was diagnosed in 7 patients (1 woman and 6 men) according to the typical clinical findings and history of immunodeficiency. In 2 atypical findings was the diagnosis confirmed by determination of DNA pathogen in vitreous sample (a patient with non-Hodgkin lymphoma) or by positive serology (CMV in leukocytes - indolent form of CMV retinitis in a patient with systemic lupus erythematosus). In 8 cases we found fulminant form, in 1 case indolent form of CMV retinitis. The average age of patients was 39,1 years (18-51 years old), ratio of men to women 6 : 3. In 6 of 9 cases we noticed bilateral retinitis. The average period of observation in our study was 15,8 months (1-48 months). Five of our patients underwent bone marrow transplantation, 2 patients were treated with systemic immunosuppressive drugs (colitis ulcerosa, systemic lupus erythematosus) and 2 patients had chemotherapy for lymphoma. The initiation or modification of treatment (gancyklovir p.o./i.v., foscarnet i.v.) was consulted and coordinated with others specialists. After initiation of treatment we followed-up 7 patients. In 4 eyes of 3 patients (31 %) the improvement of visual acuity was documented, in 5 eyes of 5 patients (38 %) the visual acuity was stabilized. The worsening of vision in 4 eyes of 3 patients (31 %) was caused by complications without any connection to virostatic therapy. All of our patients, who underwent bone marrow transplantation, died within 12 months since the diagnosis of CMV retinitis was determined. CONCLUSION: The diagnosis of CMV retinitis only in 9 cases (0,48% of all uveitic patients) confirms the rare occurrence of this retinitis. The important tool to the diagnosis of CMV retinitis is the history of immunodeficiency. In an atypical findings, the analysis of intraocular fluids or serological tests could help to the final diagnosis. The occurrence of CMV retinitis signify a very unfavourable prognosis for patients who underwent bone marrow transplantation and these patients died within 12 months since CMV retinitis has been diagnosed. The management of the therapy requires close interdisciplinary cooperation.

[Eye and inflammatory bowel diseases]. / Oko a idiopatické strevní zánety.

AIM: To point out the wide range of ocular features of inflammatory bowel diseases (IBD), focusing on uveitis. METHODS: A retrospective study. RESULTS: In the Centre for diagnosis and therapy of uveitis of our Ophthalmology Department, we have in years 2003-2010 followed in total 18 patients with intraocular inflammation associated with IBD: anterior uveitis (14), vasculitis (1), panuveitis (1), infectious uveitis as a secondary complication of systemic immunosuppressive therapy (2). The most often diagnosis was mild to moderate recurrent acute anterior uveitis. We have noticed more severe course of uveitis in patients with the HLA B27 positivity. Part of this paper consists of an overview of other ocular manifestations of IBD and current available therapeutical strategies. CONCLUSION: Ocular manifestations of IBD can be a valuable signal of the activity of the primary disease. The knowledge of the ocular manifestations of these systemic diseases and of possible complications is required for successful interdisciplinary care of patients with IBD. While local treatment is fully in hands of an ophthalmologist, the form and extent of the systemic treatment is necessary to coordinate with gastroenterologists.

[Malignant masquerade syndromes]. / Maligní maskující syndromy.

PURPOSE: To evaluate our experience with the diagnosis and treatment of malignant masquerade syndromes. METHODS: A retrospective study of 46 patients treated for malignant masquerade syndromes at our Department for Diagnosis and Treatment of Uveitis, 1st Faculty of Medicine in Prague, between 1995 and 2008, was performed. RESULTS: Eighty-nine patients with masquerade syndromes (7.2%) from all 1233 patients with uveitis were included. Malignant masquerade syndromes were recognized in 46 patients (22 females and 24 males, mean age 55 years). The most frequent cause of malignant masquerade syndromes was intraocular non-Hodgkin lymphoma (26 patients). The primary diagnosis was idiopathic uveitis in many cases. The most valuable diagnostic procedure was analysis of intraocular fluids. CONCLUSION: Diagnosis of masquerade syndromes should be considered in all patients with idiopathic corticosteroid-resistant chronic uveitis. Timely diagnosis and treatment may in case of malignant masquerade syndromes improve prognosis and sometimes gain control over this potentially lethal disease.

[Current therapeutic approach in non-infectious uveitis]. / Soucasné prístupy k lécbe neinfekcních uveitid.

The aim of this paper is to summarize current therapeutic approach in non-infectious uveitis. It focuses on different immunosuppressive/immunomodulatory treatment modalities and address' its adverse effects.

[Benign masquerade syndromes in differential diagnosis of uveitis]. / Benigní maskující syndromy v diferenciální diagnostice uveitid.

PURPOSE: To present our experience with the diagnosis of benign masquerade syndromes, to evaluate the prevalence, clinical features and diagnostic tests. METHODS: A retrospective study of 42 patients treated for benign uveitis masquerade syndromes at our Department for DIAGNOSIS AND TREATMENT OF UVEITIS: 1st Faculty of Medicine in Prague, between 1996 and 2006, was performed. RESULTS: Seventy-nine patients with masquerade syndromes (7.1%) from all 1112 patients with uveitis were included. Malign masquerade syndromes were recognized in 37 patients (19 females and 18 males, mean age 55 years) and benign masquerade syndromes in 42 patients (23 females and 19 males, mean age 33.7 years). The most frequent cause of benign masquerade syndromes was a group of vascular anomalies (22 patients). The primary diagnosis was infectious or idiopathic uveitis in many cases.The most valuable diagnostic procedures were fluorescein angiography and analysis of intraocular fluids. CONCLUSION: Diagnosis of masquerade syndromes should be considered in all patients with idiopathic corticosteroid-resistant chronic uveitis. Timely diagnosis and treatment may improve the prognosis of masquerade syndromes.

Effect of certain immunosuppressants on non-specific immunity cells in murine corneal grafts: study on early phases after transplantation.

The aim of our study was to evaluate the efficacy of FK506, mycophenolate mofetil (MM) and aminoguanidine (AMG) on infiltration of macrophages (MPHs), neutrophils (NPHs) and dendritic cells (DC) into corneal grafts during the early phases after transplantation (Tx). Tx was performed in mice (C57BL/10 to BALB/c). Therapy included FK506 (0.2 mg/kg), MM (30 mg/kg) or AMG (0.1 g/kg), started at the day of Tx and was injected i.p. daily. Corneas were excised on the third and seventh day after Tx. Immunohistological evaluation using antibodies against MPHs, NPHs and DC was performed and corneal grafts were assessed in the periphery and in central part of the cornea separately. On the third day after Tx, a massive infiltration of MPHs and NPHs into corneal grafts was revealed; the DC infiltration was lower in all treated groups. Treatment with FK506 and MM led to a significant reduction of NPHs in the centers of the grafts, but not of MPHs. In contrast, AMG significantly reduced MPHs migration into allografts on the third day after Tx, whereas NPHs infiltration has not been attenuated. However, immunosuppressants had no influence on the infiltration of DC during early phases after Tx.