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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a patient with systemic lupus erythematosis and renal involvement and who developed visual impairment in the absence of hypertension and anti-cardiolipin antibodies. This was attributed to occlusive vascular disease and choroidal infarction in the context of active lupus. Complete and irreversible blindness developed rapidly despite treatment and the patient died of cerebral haemorrhage 2 months after discharge.
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PMID:Irreversible blindness in systemic lupus erythematosis. 840 6

On the whole, diabetic microangiopathy can be understood as the clinical renal-retinal syndrome. About 10% of all diabetics die of end-stage renal failure, more frequent in IDDM. With an incidence of 14% diabetic retinopathy is one of the major causes of blindness in adulthood. In the non-proliferative state, the pathological changes are limited to the retina, whereas the alterations affect both retina and vitreous in the proliferative state. Photocoagulation is the treatment of choice. If photocoagulatory treatment is not possible because of cataract, vitreous surgery (pars-plana vitrectomy) could improve visual prognosis. The clinical features hypertension, proteinuria and finally renal failure define the term "diabetic nephropathy". The increased intraglomerular pressure is the main pathological alteration of incipient nephropathy. Microalbuminuria essentially determines the prognosis: in IDDM it concerns the incidence of a manifest nephropathy, in NIDDM the excessively increased incidence of cardiovascular mortality. Sonographically, the kidneys are large with bright and wide parenchyma. Along with the development of end-stage renal disease the kidney size diminishes. According to Mogensen, nephropathy is divided into five stages: Stage 1, the early stage, is defined by hypertrophy and hyperfiltration. Stage 2 shows incipient structural changes without any clinical findings. Stage 3 is characterised by persistent microalbuminuria. Stage 4 leads to increasing renal failure and stage 5 to end-stage renal disease and the necessity of dialysis treatment. Incipient nephropathy demands a strict treatment of both hypertension and diabetes. In the meantime, ACE inhibitors are the treatment of choice. In case of dialysis treatment continuous ambulant peritoneal dialysis (CAPD) is usually preferred.
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PMID:[Diabetic microangiopathy]. 847 38

Some epidemiological aspects of drug-treated intraocular hypertension in Belgium were established in 1992 from questionnaires filled in by 1513 patients who attended a sample of 209 pharmacies open to the public. The mean age of the patients was 67 years (range: 3-95). After standardization for age, the prevalence of diabetes mellitus among patients was found to be 1.7 times higher than in the general population. Family history of glaucoma and/or blindness was reported by 28% of the patients. Beta-blocker eye drops were used by 96% of the sample. An ophthalmologist was consulted more than four times a year by 24% of the patients who had been drug-treated for less than one year; the proportion, however, decreases to 11% for those treated for at least five years. The annual consumed dose of eye drops containing parasympathomimetics, beta-blockers, and epinephrine or dipivefrine was 12.4, 13.6, and 12.3 bottles, respectively, and that of ointments containing parasympathomimetics was 9.9 tubes. From these results and using sales figures, the prevalence of drug-treated intraocular hypertension was found to be 77 per 10,000 inhabitants (95% CI: 31-123).
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PMID:Results of an epidemiological study on drug-treated intraocular hypertension in Belgium. 862 2

Bardet-Biedl syndrome is a rare autosomal recessive disease characterized by dysphormic extremities, retinal dystrophy, obesity, hypogenitalism in males, and renal structural abnormalities. Because the clinical outcome of these patients is not well known, 21 families with Bardet-Biedl syndrome (BBS) were studied to determine the natural history of the disease. In a prospective cohort study, 38 patients with the syndrome and 58 unaffected siblings were identified. Patients were studied in 1987 and again in 1993. Age of onset of blindness, hypertension, diabetes, renal impairment, and death was determined. The prevalence of obesity, gonadal dysfunction, and renal structural abnormalities was assessed. All but 5 BBS patients (86%) were legally blind, 26% being blind by the age of 13 years and 50% by 18 years. Eighty-eight percent were above the 90th percentile for height and weight. Twenty-five (66%) patients had hypertension, 25% of BBS patients by age 26 years, and 50% by age 34 years, whereas in the unaffected group, 25% had hypertension by age 49 years (P < 0.0001). Twelve (32%) BBS patients developed diabetes mellitus, compared with none of the unaffected group. Only 2 patients were insulin dependent. Twenty-five percent of BBS patients had diabetes by the age of 35 years. In 12 women of reproductive age, 1 (8%) had primary gonadal failure. In 10 men, 4 had primary testicular failure. Nine (25%) patients developed renal impairment, with 25% of the BBS group affected by the age of 48 years. Imaging procedures of the kidney were performed in 25 patients with normal renal function. Whereas fetal lobulation and calyceal cysts/diverticula/clubbing were characteristic, occurring in 96% of patients, 20% (n = 5) had diffuse and 4% (n = 1) focal cortical loss. Eight patients with BBS died, 3 with end-stage renal failure and 3 with chronic renal failure. On life-table analysis, 25% of BBS patients had died by 44 years, whereas at that age 98% of unaffected siblings were still alive (P < 0.0001). Bardet-Biedl syndrome has an adverse prognosis, with early onset of blindness, obesity, hypertension, and diabetes mellitus. Renal impairment is frequent and an important cause of death. Survival is substantially reduced.
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PMID:The importance of renal impairment in the natural history of Bardet-Biedl syndrome. 865 Dec 40

Pre-eclampsia (PE) and eclampsia is the leading cause of maternal death in the UK and a major cause of perinatal morbidity and mortality. PE is predominantly a disorder of first pregnancy. There is a genetic component. PE is a syndrome without a defined cause. The variability with which it presents, and the speed with which it progresses, make it hard to diagnose. High blood pressure and proteinuria, with or without oedema, are classic symptoms but it may also present in an unusual way, eg as jaundice; as proteinuria with normal blood pressure; as intra-uterine growth retardation; as abdominal pain. The placenta becomes "sick" because of restricted blood flow from the mother; an unknown factor causes disturbances to spread throughout the mother's circulation which may lead to blindness, strokes, liver rupture and death. Delivery of the placenta is the only effective treatment, but preventive options being explored include aspirin and calcium supplements.
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PMID:Update on the "sick placenta syndrome". Pre-eclampsia: still a difficult disease. 868 Jan 54

A 6.5-year-old child who received a shunt at 3 weeks of age for triventricular hydrocephalus related to his congenital toxoplasmosis developed symptoms of intracranial hypertension and papilloedema. Computed tomographic scan demonstrated slit ventricles. The shunt device was shown to be patent on isotope transit study. Spontaneously the cranial sutures widened and headaches disappeared, but loss of vision occurred and did not reverse despite optic nerve sheath fenestration. We suspect that a rapid drop in intracranial pressure played a role in the pathogenesis of our patient's blindness. This possible complication should be taken into account when calvarial expansion is planned in a patient with an intracranial hypertension syndrome with papilloedema in the presence of slit ventricles and a patent shunt.
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PMID:Cranial disjunction and visual failure in a slit ventricle syndrome with patent shunt. 873 5

Cyclosporin A (CsA) has been shown to be useful in the prophylaxis of acute graft-versus-host-disease (GVHD). However, this immunosuppressive agent produces multiple side-effects including nephrotoxicity, hypertension, hypertricosis, gum hyperplasia, infections, and neurotoxicity. We report a retrospective analysis of neurotoxicity in 625 recipients transplanted for thalassemia and given CsA as part of GVHD prophylaxis. Neurotoxicity consisted in mental status changes, tremor, headache (grade 1), visual disturbance and cortical blindness (grade 2) and seizures and coma (grade 3). The overall toxicity was 28.8% and the incidence of convulsions was 10.1%. Neurological findings were reversible after temporary reduction or discontinuation of CsA. Class 3 patients, when prepared with protocol 6 (Bu 14 + Cy 200 and CsA for GVHD) or when they developed acute GVHD, had the highest risk of convulsions. Age, sex, different conditioning regimens, different anticonvulsive prophylaxis, liver damage due to iron-overload and/or to chronic inflammation did not influence the occurrence of CsA-related CNS toxicity. The occurrence of acute GVHD with concomitant use of high-dose corticosteroids is the single significant predisposing factor in the occurrence of convulsions. Grades 1 and 2 of neurotoxicity occurred earlier and were not influenced even by acute GVHD.
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PMID:CsA-associated neurotoxicity and ineffective prophylaxis with clonazepam in patients transplanted for thalassemia major: analysis of risk factors. 883 9

This case documents acquired reversible cortical blindness as a complication of hypertension secondary to acute glomerulonephritis and emphasizes the importance of recognizing this complication in children. The etiology of the cortical blindness is felt to be secondary to ischemia with edema from arterial spasm. Results of a CT scan of the head and lack of clinical sequelae support this assertion.
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PMID:Cortical blindness as a complication of acute glomerulonephritis. 907 54

A boy presented with hypertension, seizures, lethargy, headache, and occipital blindness. He improved with antihypertensive therapy. Other reported children with a similar distinctive clinical condition are compared with adults with a syndrome termed reversible posterior leukoencephalopathy. Because both gray and white matter are involved, we suggest that the name be changed to occipital-parietal encephalopathy syndrome.
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PMID:Occipital-parietal encephalopathy: a new name for an old syndrome. 930 87

Transient blindness of cortical origin associated with gestational (pregnancy induced) hypertension is a terrifying and unusual experience in obstetric practice. Two cases encountered in our centre at the University of Ilorin Teaching Hospital (UITH) Ilorin, Nigeria are presented. One case occurred in pregnancy and the other in early puerperium. The two patients were Nigerians. The possible aetiology and pathophysiology of this very rare condition are discussed.
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PMID:Transient cortical blindness in gestational hypertension: report of two cases. 910 99


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