Effects of Subcutaneous Methotrexate in Patients with Refractory Uveitis and Chorioretinitis.

PURPOSE: Methotrexate (MTX) is an immunosuppressive agent used to treat noninfectious inflammatory eye conditions and is generally administered orally for ocular inflammatory diseases. When used in rheumatological diseases, subcutaneous administration has been reported to show higher efficacy than oral administration. Therefore, this study aimed to evaluate the effect of subcutaneous MTX in patients with refractory uveitis or choroiditis who did not respond to other immunosuppressive agents. METHODS: A retrospective case series study was performed between January and December 2018. Patients with uveitis or chorioretinitis who showed little to no treatment response for 6 months or more with conventional immunosuppressive agents were treated with MTX, administered subcutaneously. After 6 months of treatment, patients were evaluated to determine whether complete suppression of inflammation sustained for ≥28 days was achieved in both eyes and whether improvement can be confirmed by fluorescein angiography (FAG). RESULTS: Subcutaneous MTX treatment was performed on 18 patients: 11 had intermediate uveitis and seven had posterior uveitis. In the intermediate uveitis patient group, five patients (50% of the group excluding one patient who dropped out) showed improvement in FAG and three patients (30%) showed complete suppression of inflammation. In the posterior uveitis group, two out of seven patients (excluding two patients who dropped out) showed an improvement, two patients in the group showed little change, and one patient showed aggravation of FAG findings. CONCLUSIONS: The study confirmed that in patients with uveitis or chorioretinitis who had a refractory response to treatment with other immunosuppressive agents, subcutaneous MTX showed improved treatment efficacy.

Central serous chorioretinopathy resulting in altered vision and color perception after glenohumeral corticosteroid injection.

Complications from shoulder corticosteroid injections are uncommon. This article presents a case of altered color perception and visual disturbances in a 29-year-old male active duty Navy SEAL following an intra-articular glenohumeral corticosteroid injection, previously unreported in the orthopedic literature. The corticosteroid injection was administered for the treatment of right-shoulder stiffness occurring approximately 3 months following an arthroscopic superior labrum anterior-posterior (SLAP) repair and subacromial decompression of the ipsilateral shoulder. The patient experienced immediate relief after the injection. Seven days later, however, he began to notice visual disturbances with color and image distortion of his right eye. He also developed a papular, nonpruritic rash on his upper trunk that eventually extended down his legs. He was diagnosed by an ophthalmologist as having central serous chorioretinopathy, a condition in which serous fluid accumulates in the subretinal space of the eye, causing detachment of the retina from the underlying retinal pigment epithelium. The reaction spontaneously resolved within approximately 10 to 12 weeks without treatment. Although intra-articular corticosteroid injections are frequently performed with a low rate of complication, clinicians should be familiar with this rare yet distressing condition. Furthermore, patients with increased production of endogenous corticosteroids (eg, those with Cushing's syndrome, type A personality, hypertension, or obstructive sleep apnea) should be warned of the potential of chorioretinopathy after an intra-articular corticosteroid injection.

[Retinochoroidopathy after intravitreal anti-VEGF treatment]. / Retinochoroidopathie nach intravitrealer Anti-VEGF-Behandlung.

A 74-year-old man presented with persistent metamorphopsias of the right eye 2 weeks after intravitreal injection of bevacizumab to treat choroidal neovascularization due to exudative age-related macular degeneration. The diagnosis reached was retinochoroiditis as an occult manifestation of sarcoidosis, possibly resulting from an intravitreal injection of bevacizumab. The patient received a prescription for 100 mg Ultralan to be taken daily for 3 days and then tapered in 3 day steps. During the further course no deterioration of the condition was observed.

[Iatrogenic central serous chorioretinopathy during glucocorticoid therapy for temporal arteritis]. / Baisse de l'acuité visuelle chez une patiente traitée par corticoïdes pour maladie de Horton : choriorétinopathie séreuse centrale iatrogène.

INTRODUCTION: Visual complications of temporal arteritis are frequent and serious. Their risk prompts glucocorticoid therapy, but this treatment may also cause ophthalmologic troubles. EXEGESIS: A sudden and isolated monocular visual blur, occurring in a 66 years old woman after 4 month of glucocorticoid treatment for temporal arteritis, revealed a case of iatrogenic central serous chorioretinopathy. The diagnosis of this disease is established by fluorescein angiography and its functional prognosis is excellent. Tapering the doses of glucocorticoids, as fast as the underlying disease allows, hastens visual recovery. CONCLUSION: When the treatment of temporal arteritis is commenced for more than a month, new visual complications are rare. Central serous chorioretinopathy induced by glucocorticoids belongs to the diagnoses that should be evoked in this case, especially if there is no clinical manifestation of arteritis and no inflammatory markers.

[Central serous chorioretinopathy and systemic diseases report of 2 cases associated with corticotherapy]. / Choriorétinopathie séreuse centrale et maladies systémiques: deux cas observés sous corticothérapie.

INTRODUCTION: Central serous chorioretinopathy is an uncommon retinal disease, whose pathogenesis is largely unknown. It is characterized by an accumulation of subretinal fluid at the posterior pole of the fundus, creating a circumscribed area of serous retinal detachment. It manifests generally as a visual loss or an abnormal colour vision. It is often idiopathic but may also be associated with numerous pathological situations, with frequent exposure to corticosteroids. EXEGESIS: We report on two patients with central serous chorioretinopathy. The first female patient had been treated with steroids for a systemic lupus erythematosus for fifteen years, and the second male patient had been treated with steroids for an idiopathic hypereosinophilic syndrome for a few months. Visual loss led to a diagnosis of central serous chorioretinopathy. Lowering of steroids doses was followed by a clinical improvement in both cases. CONCLUSION: Similarly to cataract or glaucoma, central serous chorioretinopathy belongs to the potential ocular side-effect of steroid treatment, and thus deserves to be known by internists.

[Ocular manifestation in amiodarone toxicity--case report]. / Manifestari oculare ale toxicitatii amiodaronei--caz clinic.

The authors present the case of a patient having both toxic keratopathy and maculopathy after a medication with amiodarone. Some of the ocular damages are irreversible, even while amiodarone medication is stopped, which recommends the screening as an efficient tracking method for ocular reversible injuries, avoiding major loss of visual function.

Corticosteroid-induced modulation of acute syphilitic posterior placoid chorioretinitis.

PURPOSE: To report a case of corticosteroid-induced modulation of acute syphilitic posterior placoid chorioretinitis. DESIGN: Interventional case report. METHOD: A 38-year-old homosexual male who presented with a unilateral uveitis secondary to syphilis developed large placoid macular lesions after treatment with oral prednisone that resolved when the corticosteroids were discontinued. RESULTS: A cause-and-effect relationship was demonstrated between oral prednisone and the appearance of acute syphilitic posterior placoid chorioretinitis. CONCLUSIONS: The clinical appearance of posterior placoid chorioretinitis in syphilis may be modulated by the immune status of the patient.

Corticosteroid-induced central serous chorioretinopathy in patients with ocular inflammatory disorders.

BACKGROUND: Development of central serous chorioretinopathy (CSC) following the administration of corticosteroids by diverse routes is a well-known fact. We report acute visual loss after the use of systemic corticosteroids in three patients with long-standing ocular inflammatory disorders in whom CSC could initially be misinterpreted as a worsening of the primary inflammatory condition. METHODS: We analyzed the clinical findings and the fluorescein and indocyanine green (ICG) angiographic signs in those three patients. RESULTS: The first patient had birdshot chorioretinopathy with minimal functional impairment for several years without treatment. When visual acuity and fields deteriorated, systemic corticosteroids were administered resulting in improved inflammatory and functional parameters during the first 2 months. Subsequently, the visual acuity of his left eye decreased due to CSC. The second patient had Vogt-Koyanagi-Harada disease with five episodes of acute inflammation. She was treated each time with systemic corticosteroids, but thrice her visual acuity deteriorated, caused by CSC. The third patient presented with scleritis of his right eye related to relapsing polychondritis. Massive oral corticosteroids were given, soon followed by the development of CSC in the right eye. Fluorescein and ICG angiographic signs were typical for CSC in all three patients. Cyclosporine was introduced in the two first patients and cyclophosphamide in the third patient, in parallel with tapering of oral corticosteroids. Progressive regression of CSC occurred in all three patients. CONCLUSION: The potentially deleterious effects of corticosteroids, favoring CSC, are well-known. They should be borne in mind when an unexpected clinical and angiographic evolution compatible with CSC develops in an uveitis patient treated with corticosteroids.

[Central serous chorioretinopathy and systemic steroid therapy]. / Choriorétinite séreuse centrale et corticothérapie systémique. A propos de 14 cas.

BACKGROUND: The manifestations of the ocular toxicity of systemic corticosteroids include posterior subcapsular cataracts and glaucoma. We describe 14 cases of serous detachment of the macula due to central serous chorioretinopathy in patients given long-term steroid therapy, which may be another potential ocular side effect of corticosteroid. CASES REPORT: The 14 (9 men and 5 women) patients were aged from 39 to 55 year old. Their systemic diseases were allergic thrombopenic purpura, optic neuritis, kidney or heart transplant, Churg and Strauss vasculitis, facial palsy, rheumatoid arthritis, systemic lupus and a kidney tumor. None of the patients had hypertension. RESULTS: Serous detachment occurred between 6 days and 10 years after the start of steroid treatment. The higher the doses, the earlier the onset of ocular disease. All patients were symptomatic, with rapid onset of blurred vision. Serous detachment was bilateral in two cases. The fluorescein angiographic finding was in most cases a single small focal hyperfluorescent leak from the retinal pigment epithelium which appeared early in the angiogram and increased in size and intensity. No diffuse degradation of the retinal pigment epithelium was seen on the fluorescein angiogram. Five patients underwent laser photocoagulation of the leaking area followed by resorption of subretinal fluid. In other patients, the symptoms disappeared as the doses of steroid were reduced. CONCLUSION: The pathogenesis of central serous chorioretinopathy remains unclear and is controversial. Corticosteroids are known to worsen the prognosis of idiopathic central serous chorioretinopathy, and serous detachment has been reported after renal transplantation. In most of these cases, chorioretinopathy was combined with diffuse leakage from the choriocapillaris. We discuss the relationship between steroid therapy and focal leakage as seen in idiopathic central serous chorioretinopathy. In conclusion, we describe 14 cases of central serous retinopathy whose clinical and fluorescein angiography were fairly typical, without obvious diffuse degradation of the retinal pigment epithelium. All these patients had been given long-term steroid therapy for various diseases.

Ornithine aminotransferase, a potential target for the treatment of hyperammonemias.

Ornithine-delta-aminotransferase (OAT) (EC 2.6.1.13) is a pyridoxal-5' phosphate dependent mitochondrial matrix enzyme. It controls the L-ornithine (Orn) level in tissues by catalysing the transfer of the delta-amino group of Orn to 2-oxoglutarate. The products of this reaction are L-glutamate-gamma-semialdehyde and L-glutamate. Among the compounds known to inhibit (or inactivate) OAT, only L-canaline and (SS)-5-(fluoromethyl)ornithine [(SS)-5FMOrn] are selective for OAT. Treatment of laboratory animals with 5FMOrn causes a dramatic accumulation of Orn in most tissues and organs, and the enhanced formation of urea due to saturation of ornithine:carbamoyltransferase with its substrate. The enhancement of urea formation by increased endogenous levels of Orn is comparable with that produced by large doses of Orn and arginine, a treatment known to enhance the detoxification of ammonia. However, protection to lethal doses of ammonium salts by exogenous Orn is rapidly fading. In contrast, inactivation of OAT by a small dose of 5FMOrn renders a long-lasting protective effect against various forms of hyperammonemic states. Among these the reduction of ammonia concentrations in blood and tissues, and the reduction of the pathologic excretion of orotic acid to normal levels in mice with hereditary defects of the urea cycle, were most impressive. In human hereditary OAT deficiency the elevated intraocular concentrations of Orn are considered to be a cause of gyrate atrophy. This is presumably the reason, why OAT has not been considered as a therapeutically useful target. Chronic inactivation of OAT by repeated administration of 5FMOrn, caused elevated intraocular Orn concentrations, but this treatment had no effect on the function and histology of the visual system, or the behaviour of adult mice. The confirmation of this and related observations in higher species will show, whether OAT inactivation has potentials in the treatment of hyperammonemic states.

[Central serous chorioretinopathy in systemic therapy with corticosteroids]. / Zentrale seröse Chorioretinopathie unter systemischer Therapie mit Kortikosteroiden.

PURPOSE: To describe retinal pigment epithelial changes associated with systemic corticosteroid treatment. METHODS: We report on five patients who developed maculopathy during treatment with systemic corticosteroids. A thorough ophthalmologic examination including perimetry, fundus photography, and fluorescein angiography was performed. RESULTS: Three patients displayed focal and two patients showed diffuse retinal pigment epithelial changes comparable to the acute and chronic form of central serous chorioretinopathy, respectively. Four of five patients had a complete visual recovery after decrease or cessation of treatment with corticosteroids. CONCLUSION: These five patients provide further evidence that systemic treatment with corticosteroids may damage the posterior blood-retinal barrier, leading to central serous chorioretinopathy. Visual acuity may increase after reduction of the dosage or cessation of treatment with corticosteroids. Patients on systemic corticosteroid treatment should be informed about possible symptoms of central serous chorioretinopathy in order to prevent irreversible visual loss.

Recurrent ocular toxoplasmosis in patients treated with systemic corticosteroids.

PURPOSE: The authors discuss a possible relationship between systematic corticosteroid use and reactivation of ocular toxoplasmosis. METHODS: Patients were identified who developed foci of recurrent toxoplasmic retinochoroiditis while being treated with systemic corticosteroids. Case histories were reviewed retrospectively. RESULTS: During a 10-year interval, three patients were identified at the University of California, Los Angeles, who had been receiving systemic corticosteroid therapy (dose range, 0.27-1.23 mg/kg/day) when they developed recurrent toxoplasmic retinochoroiditis. Disease occurred at intervals of 20 days to approximately 1 year after start of corticosteroid therapy. Lesions were typical in appearance, course, and manner in which they responded to antimicrobial therapy. CONCLUSION: Recurrent toxoplasmosis in patients receiving corticosteroid therapy probably is uncommon. These cases do not confirm a causal relationship between corticosteroid use and initiation of disease recurrence.

Chorioretinitis caused by synthetic absorbable sutures.

Two cases of chorioretinitis were caused by polymer material from the suture (Dexon) used in squint surgery. The lesions were macula edema, granulomatous uveitis and capillary occlusions on the ocular fundus located in the operated area. To confirm the cause of this injury, an immunological investigation was performed. Macrophage block and an incomplete adjuvant were necessary to lead delayed hypersensitivity against the synthetic polymer polyglycolic acid (PGA). The mice showed a strong reaction as hyperemia and swelling on their experimental footpads after the injection of PGA. Histologically the footpad accumulated a large quantity of lymphocytes in the swollen tissue but the control footpad had no reaction.

Rhodopsin-induced experimental autoimmune uveoretinitis in monkeys.

We present the first evidence that purified rhodopsin can induce experimental autoimmune uveoretinitis (EAU) in monkeys. Injection of a highly purified lipid-free rhodopsin preparation provokes severe chorioretinitis with concomitant anterior uveitis. The onset of disease is earlier, its frequency is higher, and the inflammation is considerably more severe than in EAU induced under similar conditions by opsin. The first inflammatory cells are observed in the ciliary body and pars plana. Within a few days the inflammation extends into the anterior chamber, choroid, and retina. Retinitis predominates in the central area, while chorioretinitis is observed in the periphery, both accompanied by damage to and elimination of the photoreceptor cells. The monkeys develop high cellular and humoral immune responses against rhodopsin and opsin. The cellular response maximum just precedes the onset of EAU. This may indicate that cellular immunity has an important role in the pathogenesis of rhodopsin-induced EAU.

Ultrasonic chorioretinopathy: a chloroquine vs control study.

High frequency ultrasound was used to produce chorioretinal lesions in two groups of pigmented rabbits. The control group received no medications. The other group was treated with subretinotoxic doses of chloroquine. Our experiment showed that the untreated group developed focal chorioretinal lesions and ricochet lesions at lower energies than did the chloroquinated group. We postulated that chloroquine, a melanin binding drug, altered melanin's ability to process ultrasonic energy by sonic-thermal conversion. This work suggests that chloroquine, even in subretinotoxic doses, may still exert an effect on the retina by chemically binding melanin and preventing its function as an energy transport system.