SUMMARY Plasma hyperviscosity is a striking abnormality in patients suffering from subcortical arteriosclerotic encephalopathy (SAE) and is thought to perpetuate the chronic ischaemic demyelinating process of the periventricular white matter. Ancrod, a defibrinating enzyme, was given to 10 patients with SAE in an attempt to reduce plasma fibrinogen, which would thus normalise hyperviscosity. This was paralleled by a significant improvement of the initially abnormal retinal arteriovenous passage time, as well as a significant augmentation of the C02-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrence of strokes during a 6 month observation period or improvement of various audiological parameters. The findings indicate that hyperviscosity in patients with SAE is merely an epiphenomenon. A potentially reversible, chronic penumbral state of the brain tissue apparently does not exist in SAE.
Impaired red cell deformability has been found in patients suffering from chronic peripheral vascular disorders, the implication being that microcirculatory blood flow is hindered and tissue hypoxaemia is aggravated. Measurement of erythrocyte deformability by a standard filtration technique for whole blood was carried out in 40 young healthy persons, in 25 untreated patients with peripheral occlusive arterial disease and in 25 patients with matching vascular disease, before and after a 6-weeks' oral treatment with 400 mg pentoxifylline 4-times daily. The filtration rates were significantly lower in the patient groups compared to those of healthy volunteers. After the oral administration of pentoxifylline, a significant increase in filtration rates was observed pointing to an improvement in erythrocyte deformability. The findings suggest that by improving erythrocyte deformability pentoxifylline positively influences the microcirculatory blood fluidity, an important factor for efficient therapy in peripheral arterial occlusive disease.
Survival of patients with systemic lupus erythematosus has increased with corticosteroid therapy. However, adverse effects of corticosteroid therapy on cardiovascular structures, such as scarring and shrinking of affected valves, are not well known. We report the case of a 19-year-old patient who developed severe mitral insufficiency within a few weeks after high-dosage corticosteroid therapy had been instituted for an acute relapse of systemic lupus erythematosus. The rapid development of severe mitral regurgitation was documented by sequential colour Doppler echocardiography.
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