Search

Purpose: Cotton wool patch and retinal hemorrhage are common ocular findings in systemic lupus erythematosus(SLE). Immunosuppressive treatment with corticosteroids may modify choroidal and retinal findings. We examined ocular complications, mainly choroidal and retinal pigment epithelium (RPE) changes in patients with SLE., Materials and Methods: Fifty SLE cases[3 males, 47 females, 41 +/- 15 (mean +/- standard deviation) year-old] were examined and treated in the departments of Internal Medicine and Ophthalmology of Osaka University Medical Hospital., Results: Complications included cataract in 16 cases, glaucoma or ocular hypertension in 9 cases, and choroidal and retinal changes in 15 cases. Occlusive retinal vasculitis, retinal pigment epithelial dysfunction, such as pigment epithelial detachment, choroidal neovascularization and multiple posterior pigment epitheliopathy, in 6 cases, and branch retinal vein occlusion in 2 cases were detected as fundus complications. Average time period from the first detection of SLE was 13 years in patients with RPE changes., Conclusion: Long term corticosteroid therapy is probably responsible for the RPE complications.

1) The earliest electroretinographic manifestation of diabetic retina is a selective change in the oscillatory potential (OP), which originates in postsynaptic retinal neuronal circuits. "Diabetic intraretinal neuropathy" precedes angiopathic retinopathy. 2) The peak latency and the amplitude of the OP are significantly correlated with the psychophysical contrast threshold for motion perception (CTMP) measured with our original device. 3) The CTMP is not correlated with the conventional static contrast threshold measured with a commercially available chart (VCTS-6000). 4) The CTMP is beyond the upper limit in nondiabetic control eyes in 135 out of 162 diabetic eyes at stage 0 (no ophthalmoscopic diabetic retinopathy) and all retinopathic eyes at stages AI (11 eyes) and AII (21 eyes). The CTMP test, which is completely non-invasive and easy to perform, could be useful for mass-screening of early diabetic retinal dysfuction. 5) The amplitude of the OP is enhanced by dopamine and nomifensine (a potent dopamine-uptake blocker), and diminished by haloperidol (a potent antagonist to dopamine D1-D2 receptors). Intrinsic dopamine release in the retina would regulate the amplitude of the OP. 6) The intraretinal content of dopamine decreases in streptozotocin (STZ)-induced diabetic rats where the OP amplitude is diminished, and increases in eyes where the OP amplitude is enhanced at the early stage in spontaneously diabetic (OLETF) rats. The changes in the OP amplitude in STZ-induced and OLETF diabetic rats can not be accounted for by the intraretinal content of gamma-aminobutyric acid (GABA), glycine, glutamate, aspartate or taurine. The changes in the OP amplitude in the diabetic retina are at least partly due to dysfunction of dopaminergic retinal neurons. 7) The peak latency prolongation and the amplitude diminution of the OP in STZ-induced diabetic rats are normalized after insulin treatment, while vitreous fluorescein concentration by vitreous fluorophotometry is not restored by insulin. Thus, the OP changes in STZ-induced diabetic rats are not due to STZ toxicity but to diabetes per se, and are not attributable to blood-ocular barrier disruption as revealed by vitreous fluorophotometry. Retinal neuronal dysfunction revealed by the OP changes at the early preretinopathic stage in STZ-induced diabetic rats is reversible after insulin treatment. 8) The OP changes in OLETF rats are prevented by decreasing food intake by 30% to maintain their blood glucose level and body weight normal. Even in highly genetically diabetic animals, diet therapy starting at an early stage of life inhibits the diabetic OP changes. 9) The amplitude of the bicarbonate response from the retinal pigment epithelium diminishes even at the preretinopathic stage, and is significanly correlated with the peak latency and the amplitude of the OP. Diabetic retinal pigment epitheliopathy as well as retinal neuropathy takes place prior to angiopathic retinopathy in the diabetic retina.

We describe two cases of multifocal posterior exudative lesions accompanied by non-rhegmatogenous retinal detachment and massive choroidal detachment. The fluorescein angiogram in both cases showed multiple hyperfluorescent areas in the posterior pole, which resolved following repeated dye-laser photocoagulation. The reported cases are compatible with the clinical features of either multifocal posterior pigment epitheliopathy or uveal effusion, or both. The presence of choroidal detachments and resistance against photocoagulation therapy suggest that the initial lesions occurred in the choroid as well as in the retinal pigment epithelium. We conclude that the two clinical nosologic diseases represent the variable clinical expression of a single disorder.

Multifocal posterior pigment epitheliopathy (MPPE) is a rare complication of systemic lupus erythematosus (SLE) and resistant to treatment. We here report a case of SLE with MPPE, successfully treated with prednisolone (PSL) and laser photocoagulation therapy. A 38-year-old woman, who had suffered from SLE for four years, was admitted to our hospital with the complaints of left hemiparesis, right homonymous hemianopsia, and dysarthria. The findings of MRI suggested her symptoms were caused by cerebrovascular involvement of SLE. The treatment with prednisolone was started at a dose of 100 mg per day. While the dose of PSL was reduced, she began to complain of paresthesia in left face and myodesopsia of left eye. Based upon the result of fluorescein angiogram, the diagnosis of MPPE was made. Since MPPE accompanied exacerbation of neurological manifestation, we considered that MPPE was a symptom of vascular involvement of SLE. MPPE was treated with laser photocoagulation therapy and an increased dosage of PSL, with favorable results. It has not been reported, as far as we concern, that laser photocoagulation therapy is effective for MPPE caused by SLE. This case is important for the pathogenesis and therapy of MPPE with SLE.