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PubMedDate not supplied

[Clinical chorioretinal aspects of systemic immune vasculitis. I. General aspects].

The eye, due to its rich vascularity, is frequently involved, directly or not, in the systemic immune vascular pathology. For a better understanding of the ocular clinical syndrome, the paper discusses the etiologic and pathogenic factors, and their influence on the characteristics of chorioretinal changes. The etiologic factors are classified according to the predominance of the lesions of the choroidal or retinal vessels. The pathogeny of the chorioretinal changes is correlated with the histopathologic lesion (fibrinoid necrosis) and its involvement in the "choriocapillaris complex-brush membrane-EPR". Clinical chorioretinal syndrome, irrespective of its etiology, induces several retinal and choroidal changes having varied as a function of the evolution stage.

Chorioretinitis↗
PubMed1999

Retinopathy in systemic lupus erythematosus: pathogenesis and approach to therapy.

The starting point in the assessment of SLE-retinopathy is the clinical examination by ophthalmoscopy and retinal fluorescein angiography. It is noted that two major clinical forms of retinopathy may occur in SLE; (1st) the "classic" type characterized by cotton-wool spots with or without intraretinal hemorrhages, and (2nd) the thrombosis of larger retinal blood vessels, such as central or branch arteries/veins. However, a well-defined pathogenetic classification of SLE-retinopathy has still not been proposed as yet. A practical classification based on the pathogenesis could be of aid to commence a more appropriate treatment. The aims of this paper are; (1st) to focus on the most implicate mechanisms of retinal vascular disease in SLE, (2nd) to mention the most common features associated with the different forms of retinopathy, and finally (3rd) to assess the prevalence of retinopathy in SLE. In our opinion, it seems that two major types of retinopathy exist in SLE: firstly, the Hughes' retinopathy due to antiphospholipid-induced retinal vascular thrombosis, for which anticoagulation is the best treatment, and secondly, the "classic" retinopathy in which at least two major causes could be associated; vasculitis and accelerated atherosclerosis. In patients with "classic" retinopathy, the most appropriate treatment still needs to be established. If "classic" retinopathy is due to vasculitis, immunosuppressive drugs should be administered, while if atherosclerosis play an etiologic role, a prophylaxis with antioxidants or the use of low-dose aspirin should be assessed.

Adolescent↗
PubMed1995

A combination of livedo racemosa, occlusion of cerebral blood vessels, and nephropathy: kidney involvement in Sneddon's syndrome.

A 59-year-old woman with retinal vein thrombosis and livedo racemosa had hematuria (4+) and proteinuria (1.7 g/day). Skin biopsy showed swollen blood vessel walls with infiltration of mononuclear cells, which were compatible with livedo racemosa (vasculitis). Magnetic resonance imaging (MRI) of the brain demonstrated multiple lacunar infarctions in the basal ganglia and white matter. Renal biopsy showed that small round cells had infiltrated into the interstitium, and a reticular structure was observed in the glomerular hilus. An amorphous substance composed of a single cell was present in the glomerular capillary lumen. Immunofluorescent study demonstrated the deposition of only IgA, in a segmental pattern differing from the diffuse global mesangial pattern seen in IgA nephropathy. After combined therapy including 40 mg/day prednisolone, 50 mg/day cyclophosphamide, antiplatelet drug, and anticoagulant was started, proteinuria and hematuria improved to 0.5 g/day and 2+, respectively, at the time of discharge. Sneddon's syndrome is a rare entity characterized by livedo racemosa and cerebrovascular lesions. In our patient with livedo racemosa, occlusion of cerebral blood vessels, and nephropathy with segmental immunoglobulin A (IgA) deposition, no antiphospholipid antibodies were detected on routine examination. Dermatologists, neurologists, psychiatrists, and nephrologists should be aware of the existence of Sneddon's syndrome with nephropathy (LI-O-N).

Antibodies, Antiphospholipid↗
PubMed1998

Nerve biopsy in patients with AIDS.

Patients with AIDS can present clinical involvement of the peripheral nervous system due to different causes. In the present work, it was studied the histopathological changes in sural nerve biopsy of fifteen patients with AIDS with this clinical involvement. It was observed the presence of a polyarteritis nodosa-like vasculitis of small arteries with fibrinoid necrosis in the sural nerve of 3 patients, one of them associated to polyradiculitis due to cytomegalovirus infection (CMV). Six patients presented mild axonal loss by light microscopy. Three other patients had a more important axonal neuropathy with myelin ovoids by teasing. By the electron microscopy in these patients were observed some fibers with axonal damage. The other three patients had normal sural nerves. We concluded that sural nerve biopsy may be important in peripheral neuropathies or myelo-radiculo-polyneuropathies in AIDS especially to search for nerve vasculitis, because it can change the therapeutic approach.

Acquired Immunodeficiency Syndrome↗
PubMed2001

[Ophthalmological diagnosis in systemic vasculitis].

Ocular manifestations of systemic vasculitides are extraordinarily pleomorph and have been described for many decades. In the introduction the special interaction of the immune system and the eye is outlined. Thereafter diagnostic procedures of patients suffering from systemic vasculitides are shown from an ophthalmological view point. Many examples, which show multiple possibilities of ocular manifestations on systemic vasculitides, are given. With regard to the anatomy of the eye, a review is given on the involvement of the 1) outer eye and a tear film, 2) lacrimal duct diseases, 3) diseases of the lid, 4) diseases of conjunctiva, 5) diseases of sclera, 6) diseases of the cornea, 7) diseases of the lens, 8) intraocular inflammation, 9) retinal affections, 10) optic nerve inflammation, and 11) orbiota involvement. Frequencies of these structures involved in the various systemic vasculitides are outlined. Principally every systemic vasculitis can induce every eye manifestation; however, larger patient groups show characteristic features of eye manifestations in systemic vasculitides. Special reference is given to Wegener's granulomatosis, giant-cell arteritis and Behcet vasculitis.

Diagnosis, Differential↗
PubMed1987

Choroidal involvement in systemic necrotizing vasculitis.

Wegener's granulomatosis and lymphomatosis are systemic necrotizing vasculitides of unknown cause. We report similar involvement of the choriocapillaris in these two diseases. A presumed choriocapillaritis caused ischemia and infarction of the choriocapillaris-retinal pigment epithelium-outer neurosensory retina complex. Systemic corticosteroid and immunosuppressive agents were successful in controlling systemic disease and preserving useful vision. At the time of this study, one patient had not had a recurrence for 12 years, and the other patient had been asymptomatic for seven years.

Adult↗
PubMed2004

[Fundus quiz 2003].

6 cases with pathognomonic fundus pathologies are presented and discussed using multiple-choice questions.

Adult↗
PubMed1999

Compound heterozygosity for one novel and one recurrent mutation in a Thai patient with severe protein S deficiency.

Homozygous or compound heterozygous protein S (PS) deficiency is a very rare disorder in the anticoagulant system, that can lead to life-threatening thrombotic complications shortly after birth. This report describes the results of the genetic analysis of the PROS 1 genes in a Thai girl patient. She was reported in 1990 as the first case with homozygous PS deficiency and neonatal purpura fulminans. In the present report, we identified the mutations in this patient by direct sequencing of PCR products representing all 15 exons of the PROS 1 gene and their flanking intronic regions. The patient turned out to be compound heterozygous for two null mutations. One allele contained a novel sequence variation, an A-insertion in an A5-tract covering codon 146 and 147, that results in a frameshift and a stop codon (TAA) at position 155. The other allele contained a nonsense mutation in exon 12 by a transition at codon 410 CGA (Arg) to TGA (stop). Cosegregation of PS deficiency with these two genetic defects was observed in her family.

Alleles↗
PubMed1975

Retinal microangiopathy in systemic lupus erythematosus.

We performed complete ocular examination, including fluorescein angiography of the fundus, in 50 ambulatory patients with moderately active or inactive systemic lupus erythematosus; none had ocular symptoms. One patient had drusen and two patients had increased intraocular pressures with disk cupping attributable to orally administered corticosteroids. No patient had detectable abnormalities by ophthalmoscopic examination. Despite this apparently normal condition, fluorescein angiography revealed single or multiple microaneurysms in nine patients (13 eyes) and retinal capillary dilatations with leakage of fluorescein in six patients (six eyes). Both abnormalities occurred in two patients. These capillary changes in moderately ill patients with lupus erythematosus are probably the residue of previous acute vasculitis, perhaps due to immune-complex deposition.

Aneurysm↗
PubMed1985

[Hypereosinophilic syndrome with ocular involvement].

The authors report a case of idiopathic hypereosinophilia with Löffler endocarditis in a 19 year old male. Retinal arteriolar occlusions were observed in the pre-equatorial region and documented by angiography. Histologic examination of the globes showed obliteration of the arterioles by a fibrinous coagulum without signs of vasculitis. Clinical data appears to suggest an embolic origin of the occlusions rather than thrombosis in situ.

Adult↗
PubMedDate not supplied

Behçet's disease.

Behçet's disease is characterized by three primary components: iridocyclitis (historically with hypopyon), aphthous lesions in the mouth, and ulceration of the genitalia. Erythema nodosum, arthropathy and thrombophlebitis often accompany these manifestations, but the ocular symptoms may be the most important and serious manifestations of the disease. Central nervous system involvement, most often due to necrotizing vasculitis, may be the most protean manifestation of the disease, leading to death. The frequency of ocular manifestations is 70-85% in patients with the disease; the underlying disease mechanism in all organ systems is an occlusive vasculitis. Although the most common ocular symptom is that of anterior uveitis, often with hypopyon as a very late sign, the presence of necrotizing retinal vascular lesions is well known and often obscured by the severity of the anterior reaction. Definitions, incidence, clinical characteristics, differential diagnosis, and management of Behçet's ocular disease are discussed, as are the interrelationships of the different organ manifestations. The ophthalmologist should be familiar with the full spectrum of disease presentation since he or she may be the first physician to encounter the Behçet's patient.

Adolescent↗
PubMedDate not supplied

Central retinal vein occlusion associated with hemodialysis.

Central retinal vein occlusion (CRVO) occurred in 3 of 15 maintenance hemodialysis patients over a two-week period. There have been no previous reports of this ophthalmologic catastrophe observed in the dialysis setting. Lupus nephritis, Henoch-Schönlein purpura and nephrosclerosis constituted the patients' major underlying diseases. Moderate hypertension was also present. Impaired vision of the left eye noted 24 to 36 hours following dialysis was the presenting symptom in all cases. Findings included decreased visual acuity, retinal vein engorgement, hemorrhage, and disc edema. All three patients subsequently lost the vision in their left eye (two received anticoagulation therapy). With the exception of hypertension, there were no known underlying predisposing conditions present. Although we are unable to offer a definite explanation for these unusual cases of CRVO, we feel a hypercoagulable state may have been responsible. Because our three cases occurred during a two-week period, some transient unidentified procoagulant factor associated with hemodialysis could have been present.

Adolescent↗
PubMed1998

The clinico-ophthalmological spectrum of antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is a hypercoagulable disorder with highly variable symptomatology including ocular manifestations. Antiphospholipid antibodies (aPL) are the serologic markers of this clinical entity. Our aim was to note the main associated ocular features of APS and elucidate which pathogenic mechanisms may participate. Retinal vascular thrombosis and different neuro-ophthalmologic manifestations, such as optic neuropathy and amaurosis fugax, may be considered as the ocular hallmarks of this syndrome. Ocular features due to aPL-induced thrombosis should be treated with anticoagulant drugs. Conversely, for the treatment of ocular features due to immunological mechanisms such as vasculitis, immunosuppressive regimes seem to be more appropriate.

Animals↗
PubMed1998

Acute blindness associated with monoclonal gammopathy induced by Ehrlichia canis infection.

Ehrlichia canis infection was diagnosed in a Labrador retriever presented with a primary complaint of acute blindness. Ocular signs on admission included bilateral hyphema, retinal haemorrhage and retinal detachment. Serum protein electrophoresis results revealed monoclonal gammopathy. This report discusses and suggests the pathogenesis of ocular bleeding in canine monocytic ehrlichiosis. Blood hyperviscosity, elevation in oncotic pressure, vasculitis, thrombocytopenia and platelet dysfunction are all proposed to be important factors in the pathogenesis of acute blindness in canine monocytic ehrlichiosis.

Acute Disease↗
PubMed2000

Familial thrombophilia and retinal vein occlusion.

PURPOSE: To perform a pilot study on the prevalence of familial thrombophilia in all cases of retinal vein occlusion with no known risk factors. METHODS: Over the 1 year study period 71 patients presented with a new diagnosis of retinal vein occlusion (age 28-90 years). Fifty-five (77%) were excluded because of local predisposing factors. The remaining 16 (23%) had a full risk factor history taken and blood investigations of rheological factors and thrombophilia including tests for the factor V Leiden mutation, prothrombin G20210A allele and hyper-homocystinemia. RESULTS: Of those with no local predisposing factors, 3 patients had antiphospholipid antibodies, 3 had raised fibrinogen levels, 4 had hyper-homocystinemia and 1 was heterozygous for the Leiden mutation. Other lifestyle risk factors such as obesity, smoking and a positive family history of venous thrombosis were not uncommon. No patient had the prothrombin G20210A variant. CONCLUSIONS: It seems likely that several risk factors, both genetic and acquired, need to be present for thrombosis to occur. In investigating a new patient with a retinal vein occlusion one should test for hypertension, glaucoma and diabetes mellitus. Estimation of plasma viscosity and a full blood count are cheap investigations which may reveal neoplasia or vasculitis, and lipid levels should be estimated. In a young patient or one with an unexpected vein occlusion and a personal or family history of thrombosis, a hypercoagulable state may rarely be identified. This additional testing should include testing for antiphospholipid antibodies and a full thrombophilia screen including the factor V Leiden mutation, homocysteine and the prothrombin variant as part of a clinical trial. Until the role of these markers in thrombosis is better defined in relation to causation of retinal vein occlusion and treatment has been shown to improve outcome, we can not recommend them for routine testing. If a hereditary defect is found, referral should be made to a hematologist and consideration given to anticoagulation and screening of family members to prevent further thrombotic episodes. Retinal vein occlusions are multifactorial in origin except in rare cases.

Adult↗