Systemic infection with Alaria americana (Trematoda).
(1/2352)
Alaria americana is a trematode, the adult of which is found in mammalian carnivores. The first case of disseminated human infection by the mesocercarial stage of this worm occurred in a 24-year-old man. The infection possibly was acquired by the eating of inadequately cooked frogs, which are intermediate hosts of the worm. The diagnosis was made during life by lung biopsy and confirmed at autopsy. The mesocercariae were present in the stomach wall, lymph nodes, liver, myocardium, pancreas and surrounding adipose tissue, spleen, kidney, lungs, brain and spinal cord. There was no host reaction to the parasites. Granulomas were present in the stomach wall, lymph nodes and liver, but the worms were not identified in them. Hypersensitivity vasculitis and a bleeding diathesis due to disseminated intravascular coagulation and a circulating anticoagulant caused his death 8 days after the onset of his illness. (+info)
Study of an epidemic of venoocclusive disease in India.
(2/2352)
Twenty-five cases of rapidly developing ascites occurring in an epidemic form were observed in a tribal district in Central India during August 1972-May 1973. Eleven of the patients died. Six patients were brought to hospital and studied for periods of two to 17 months. Necropsy was performed on one patient who died. The clinical features suggested an outflow tract obstruction such as a Budd-Chiari-like syndrome or venoocclusive disease. Radiographic and haemodynamic studies demonstrated a combination of post and perisinusoidal blocks. Liver dysfunction was indicated by the presence of a marked bromsulphthalein retention and mild to moderate hypoalbuminaemia. Histological examination of the liver biopsies showed changes that ranged from centrizonal haemorrhagic necrosis to an extensive centrilobular fibrosis associated with central vein occlusion. The disease was apparently caused by a food toxin, and the possible nature of this is discussed. (+info)
Prevalence of angiographic atherosclerotic renal artery disease and its relationship to the anatomical extent of peripheral vascular atherosclerosis.
(3/2352)
BACKGROUND: Recognition of the possible presence of atherosclerotic renal artery disease (ARAD) is important because of its progressive nature, and because of the potential for precipitating an acute deterioration in renal function by administration of angiotensin-converting enzyme inhibitors. The aim of this study was to identify the prevalence of ARAD in patients undergoing peripheral angiography and its relationship to the extent of their peripheral vascular disease (PVD). METHODS: The reports of the 218 patients who underwent peripheral angiography to investigate PVD in one centre in a calendar year, and in whom it was possible to image the renal arteries, were analysed retrospectively. The presence of atherosclerotic disease in the renal, aortic, iliac, femoral and distal areas was recorded for each patient. RESULTS: The prevalence of ARAD was 79/218 (36.2%). The greater the number of atherosclerotic areas of the arterial tree, the higher the prevalence of ARAD. Patients with aortic disease and bilateral iliac, femoral and distal vessel disease had the highest incidence of ARAD 19/38 (50%). The incidence of ARAD in those with femoral artery atherosclerosis was significantly higher than in those without femoral artery atherosclerosis (42.1% compared with 9.7%, P=0.001 chi2). There was no significant difference in those groups with or without iliac and distal disease. None of the 11 patients with normal femoral and iliac arteries had ARAD. CONCLUSIONS: Renal artery atherosclerosis is a common occurrence in patients with PVD. If extensive PVD is recognized during aortography, a high flush should be considered to examine the renal arteries, if they are not included in the main study. (+info)
Relief of obstructive pelvic venous symptoms with endoluminal stenting.
(4/2352)
PURPOSE: To select patients for percutaneous transluminal stenting of chronic postthrombotic pelvic venous obstructions (CPPVO), we evaluated the clinical symptoms in a cohort of candidates and in a series of successfully treated patients. METHODS: The symptoms of 42 patients (39 women) with CPPVO (38 left iliac; average history, 18 years) were recorded, and the venous anatomy was studied by means of duplex scanning, subtraction venography, and computed tomography or magnetic resonance imaging. Successfully stented patients were controlled by means of duplex scanning and assessment of symptoms. RESULTS: The typical symptoms of CPPVO were reported spontaneously by 24% of patients and uncovered by means of a targeted interview in an additional 47%. Of 42 patients, 15 had venous claudication, four had neurogenic claudication (caused by dilated veins in the spinal canal that arise from the collateral circulation), and 11 had both symptoms. Twelve patients had no specific symptoms. Placement of a stent was found to be technically feasible in 25 patients (60%), was attempted in 14 patients, and was primarily successful in 12 patients. One stent occluded within the first week. All other stents were fully patent after a mean of 15 months (range, 1 to 43 months). Satisfaction was high in the patients who had the typical symptoms, but low in those who lacked them. CONCLUSION: Venous claudication and neurogenic claudication caused by venous collaterals in the spinal canal are typical clinical features of CPPVO. We recommend searching for these symptoms, because recanalization by means of stenting is often feasible and rewarding. (+info)
Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis.
(5/2352)
Receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface molecules and engages diverse ligands relevant to distinct pathological processes. One class of RAGE ligands includes glycoxidation products, termed advanced glycation end products, which occur in diabetes, at sites of oxidant stress in tissues, and in renal failure and amyloidoses. RAGE also functions as a signal transduction receptor for amyloid beta peptide, known to accumulate in Alzheimer disease in both affected brain parenchyma and cerebral vasculature. Interaction of RAGE with these ligands enhances receptor expression and initiates a positive feedback loop whereby receptor occupancy triggers increased RAGE expression, thereby perpetuating another wave of cellular activation. Sustained expression of RAGE by critical target cells, including endothelium, smooth muscle cells, mononuclear phagocytes, and neurons, in proximity to these ligands, sets the stage for chronic cellular activation and tissue damage. In a model of accelerated atherosclerosis associated with diabetes in genetically manipulated mice, blockade of cell surface RAGE by infusion of a soluble, truncated form of the receptor completely suppressed enhanced formation of vascular lesions. Amelioration of atherosclerosis in these diabetic/atherosclerotic animals by soluble RAGE occurred in the absence of changes in plasma lipids or glycemia, emphasizing the contribution of a lipid- and glycemia-independent mechanism(s) to atherogenesis, which we postulate to be interaction of RAGE with its ligands. Future studies using mice in which RAGE expression has been genetically manipulated and with selective low molecular weight RAGE inhibitors will be required to definitively assign a critical role for RAGE activation in diabetic vasculopathy. However, sustained receptor expression in a microenvironment with a plethora of ligand makes possible prolonged receptor stimulation, suggesting that interaction of cellular RAGE with its ligands could be a factor contributing to a range of important chronic disorders. (+info)
Chronic retinal vein occlusion in glaucoma.
(6/2352)
Asymptomatic chronic retinal vein occlusion that occurs in chronic simple glaucoma is described. The condition is characterized by marked elevation of retinal vein pressure with collateral vessels and vein loops at the optic disc in cases of central vein occlusion, or retinal veno-venous anastomoses along a horizontal line temporal and nasal to the disc in hemisphere vein occlusion. No patient had visible arterial changes, capillary closure, fluorescein leakage, or haemorrhages. The vein occlusion was not limited to "end stage" glaucoma. The role of increased intraocular pressure and glaucomatous enlargement of the optic cup with retinal vein distortion in the pathogenesis of the condition was stressed. Follow-up of these patients revealed persistence of the retinal vein occlusion shown by elevated retinal vein pressures. This would reduce effective perfusion of the inner retina and optic disc and may affect the long-term visual prognosis. (+info)
Perifoveal vascular leakage and macular oedema after intracapsular cataract extraction.
(7/2352)
Perifoveal capillary leakage of fluorescein was demonstrated in 60 per cent of 50 eyes when angiography was performed two weeks after cataract extraction. Repeat angiography six weeks postoperatively in 17 eyes demonstrated persistence of already established leakage in 11 of 12 eyes and no new leakage in five eyes previously negative. Cystoid macular oedema with visual acuity of less than 20/40 six weeks postoperatively occurred in five eyes (10 per cent). Eyes of patients with vascular disease and those patients of 60 years or older were found to have altered vascular permeability significantly more frequently. Inflammation was no more severe or prevalent in those patients who demonstrated leakage and no inflammation was clinically apparent in 10 of 11 eyes demonstrating dye leakage six weeks postoperatively. We conclude that the constitutional factors of age and vascular disease are of prime importance in causing altered vascular permeability in the early postoperative period after cataract extraction; factors causing sustained leakage with reduction of visual acuity were not demonstrated. (+info)
A prospective study of xenon arc photocoagulation for central retinal vein occlusion.
(8/2352)
Twenty patients with central retinal vein occlusion were randomly divided into two groups in a prospective study to evaluate the effects of xenon are photocoagulation in central retinal vein occlusion. The patients in one group were treated with 360 degrees scatter xenon photocoagulation and the others received no treatment. The average follow-up was 18 months. There were no cases of rubeosis or neovascular glaucoma in the treated group. Two patients in the untreated group developed rubeosis with subsequent neovascular glaucoma. There was no significant difference in the visual prognosis or in fundus neovascularization between the groups. (+info)