Biomedical subjects

J Steurer

Publications and source records attributed to J Steurer.

114 records · Page 7Linked to original sources

PubMed1981

Platelet aggregation and beta-thromboglobulin levels in nephrotic patients with and without thrombosis.

Platelet aggregation and beta-thromboglobulin levels were studied in 17 patients with the nephrotic syndrome. Thrombosis or thromboembolic complications occurred in 4 of these patients with serum albumin levels below 2 g/100 ml. Pathologic platelet aggregation assessed by estimating alpha 2-angle values derived from platelet aggregation curves was seen in the 4 patients with thromboembolic complications (alpha 2-angle 69.5 degrees +/- 10.1 degrees), whereas patients without thrombosis showed normal alpha 2-angle values (less than 30 degrees) with only one exception. In addition, patients with thromboembolic complications demonstrated significantly elevated beta-thromboglobulin levels, when compared with those not having thrombosis or thromboembolic complications (76.8 +/- 14.3 ng/ml vs 44.8 +/- 8.6 ng/ml, P less than 0.001). The decrease in serum albumin concentration showed an inverse relationship with both, alpha 2-angle values (r = -0.82, P less than 0.001) and beta-thromboglobulin levels (r = -0.83, P less than 0.001) indicating a regulatory role of serum albumin in platelet aggregation. We conclude, that altered platelet aggregation as well as hypercoagulability may be involved in the pathogenesis of thrombosis and thromboembolic complications in the course of the nephrotic syndrome.

Adult↗

PubMed1980

[Incidence of proteinuria and nephrotic syndrome in renal vein occlusion caused by a tumor].

A retrospective study was conducted in 13 patients with phlebographically diagnosed tumor-induced renal vein occlusion to evaluate the incidence and extent of proteinuria and/or nephrotic syndrome. In 5 patients minimal proteinuria was found, but in none of the patients were the criteria of nephrotic syndrome fulfilled. These data can be used as additional evidence that renal vein occlusion is not the cause of nephrotic syndrome. They underline the hypothesis that, in cases of nephrotic syndrome associated with renal vein occlusion, the thrombic occlusion of the renal vein is a complication of the excessive renal protein loss and developing hypercoagulability.

Aged↗

PubMed1979

[Goldenhar syndrome].

The basic features of Goldenhar syndrome are preauricular appendices, epibulbar dermoids, vertebral and cardiac anomalies, and hypoplasia of the lungs. The syndrome appears to be caused by early damage during the first or second month of embryonic development. Prognosis is most often determined by the underlying heart disease. In the present study a 24-year-old female student is reported who exhibited a preauricular appendix on the right side, severe thoracic scoliosis, aplasia of the middle and lower lobes of the right lung, dextropositio cordis and an atrial septal defect with severe pulmonary hypertension. Cineangiocardiography revealed a mitral valve prolapse with slight mitral regurgitation and a dilated right ventricle with severe tricuspid regurgitation. Left and right ventricular function was slightly to moderately reduced. Selective coronary arteriography revealed a coronary fistula from an atrial branch of the left coronary artery to the right atrium. Symptomatic therapy with digitalis, anticoagulation and repeated venesection was initiated because of the severe hemodynamic findings. However, the patient developed syncope at increasingly frequent intervals and died 3 months after the initial examination.

Adult↗

PubMed1978

[The oto-vertebral syndrome].

The oto-vertebral syndrome is a rare combination of malformations of the ears, spinal anomalies, and congenital heart disease. The syndrome appears to be caused by early embryonic exogenous damage during the 6th or 7th week of embryonic development. The case is reported of a 28-year-old man with bilateral aplasia of the external ear, bilateral aplasia of the ear canal, hypoplasia of the mandibula, severe thoracic scoliosis, and ventricular septal defect with pulmonary hypertension. He was admitted with dyspnea on exertion, syncope, and severe cyanosis. Cardiac catheterization revealed severe pulmonary hypertension with moderate right-to-left and slightly left-to-right shunt (Eisenmenger syndrome). Right and left ventricular function, as evaluated by angiocardiography, was slightly reduced. Because of the severe hemodynamic alterations, symptomatic therapy with digitalis, repeated venesection, and anticoagulation was initiated.

Abnormalities, Multiple↗

PubMedDate not supplied

Local blood flux in skin and muscle during voluntary hyperventilation in healthy controls and patients with hyperventilation syndrome.

Laser Doppler fluxmetry was used to analyze local blood flux in the anterior tibial muscle and the skin of the calf simultaneously during 3 min of hyperventilation. Examinations were performed in 10 controls and 10 patients with a hyperventilation syndrome in order to evaluate a possible different vascular response to the provocation test. During hyperventilation, mean muscle blood flux increased in both groups. In controls, flux augmented from 23.4 +/- 12.3 arbitrary units (AU) to 51.6 +/- 28.3 AU (p < 0.05) and in patients from 21.6 +/- 10.8 AU to 45.0 +/- 26.4 AU (p < 0.05). The changes of skin blood flux during hyperventilation were not significant. The flux response did not differ significantly in controls and patients. Using the laser Doppler technique we were able to confirm muscular vasodilatation previously reported during short-term hyperventilation. Possible mechanisms include release of vasoactive substances and/or a stimulation of the autonomic nervous system.

Adult↗

PubMedDate not supplied

Hyperventilation enhances transcapillary diffusion of sodium fluorescein.

Voluntary hyperventilation (HV) provokes hemoconcentration due to a loss of fluid from the intravascular space. In 10 healthy male volunteers the hypothesis was tested whether HV increases transcapillary fluid shift into the interstitial compartment. For this purpose, fluorescent light intensity (FLI) alterations after intravenous injection of sodium fluorescein (Na fluorescein) before and during 3 min of HV were determined. Concomitantly, temperature and microvascular skin flux (laser Doppler fluxmetry, LDF) were recorded continuously. Hematocrit and serum proteins, as markers of hemoconcentration, increased significantly from 41.2 +/- 2.3 to 42.7 +/- 2.0% (p = 0.0023) and from 69.5 +/- 3.4 to 72.9 +/- 3.0 g/l (p = 0.0005, respectively). Skin temperature and LDF showed no changes during HV compared to baseline levels. Interstitial FLI indicating transcapillary diffusion of Na fluorescein was significantly higher (p < 0.001) during HV compared to the values recorded during the baseline period. The exact mechanism of enhanced transcapillary diffusion of Na fluorescein is not known. The distinct increase in FLI without a significant change in microvascular skin flux suggests an HV-induced increase in capillary pressure or an enhancement in capillary permeability for water and small solutes.

Adult↗