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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 66 (1988), S. 914-919 
    ISSN: 1432-1440
    Keywords: Erythropoietin ; Hypertension ; Erythropoietin ; Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Wirksamkeit von rekombinantem humanem Erythropoietin (rhEpo) bei der Korrektur der Anämie des terminal niereninsuffizienten dialysepflichtigen Patienten ist in mehreren Studien belegt. Eine deutliche Verbesserung der physischen Leistungsfähigkeit konnte durch ergometrische Untersuchungen dokumentiert werden. Neben seltenen Shunt-Thrombosen ist die einzige relevante unerwünschte Wirkung von rhEpo die Entwicklung oder Aggravierung einer Hypertonie bei etwa 30% der behandelten Patienten. Bei ca. 2% der Patienten kam es zur hypertensiven Enzephalopathie mit zentralnervöser Symptomatik. Als Ursache für diese Hypertonie-Entwicklung ist ein Anstieg des peripheren Widerstands anzunehmen. Belege dafür sind Messungen des regionalen Blutflusses mit Plethysmographie vor und nach Anämie-Korrektur mit rhEpo. Ursache für den Widerstandsanstieg wiederum dürfte eine Zunahme der Vollblutviskosität und eine Abnahme der peripheren hypoxiebedingten Vasodilatation sein. Zur Prävention der hypertensiven Komplikationen bei rhEpo-Therapie werden eine langsame Hämatokrit-Korrektur über 12–16 Wochen und eine Begrenzung des Ziel-Hämatokrits auf 30–35 Vol. % bei strikter Blutdruck- und Volumenkontrolle empfohlen.
    Notes: Summary Recombinant human erythropoietin (rhEpo) has been demonstrated in several studies to be effective in correcting the anemia of regular dialysis patients. This was accompanied by a significant improvement of the physical work capacity shown by exercise testing. The main side effect of rhEpo treatment has been the development or aggravation of hypertension in approximately 30% of the treated patients. In 2% hypertensive encephalopathy and convulsions occured. Data obtained by measurements of regional blood flow indicate the peripheral resistance did increase probably due to rise of blood viscosity and reversal of preexisting hypoxic vasodilatation. To avoid hypertensive complications anemia should be corrected slowly over a period of 12–16 weeks. Target hematocrit should not exceed 30–35 vol. %. Blood pressure and volume status should be monitored closely.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 70 (1992), S. S120 
    ISSN: 1432-1440
    Keywords: Hypertension ; Kidney ; Antihypertensive drugs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antihypertensive therapy influences kidney function by different mechanisms depending on the mode of action of the drug used. The GFR is improved by calcium entry blockers and ACE inhibitors, unaffected by vasodilators, α-blockers and centrally acting sympatholytics and impaired by β-blockers. The same is true for renal blood flow and is due to changes of renal vascular resistance. Renal sodium excretion is impaired mostly by vasodilators, by α-blockers, sympatholytics and β-blockers; in contrast, calcium entry blockers and ACE inhibitors acutely induce natriuresis. The RAAS is stimulated by vasodilators, unaffected by α-blockers and sympatholytics and suppressed by β-blockers. Plasma catecholamines are stimulated by vasodilators and suppressed by centrally acting sympatholytics and unaffected by the others. Induction of acute renal functional impairment is reported for ACE inhibitors under conditions of compromised renal perfusion pressure such as in renal artery stenosis. These data from the literature reviewed are supported by our own experimental data on sodium balance under different drugs and micropuncture data in experimental renal artery stenosis. To achieve effective antihypertensive treatment with a low profile of side effects, careful monitoring of renal function seems to be mandatory.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Intensivmedizin und Notfallmedizin 35 (1998), S. 332-336 
    ISSN: 1435-1420
    Keywords: Key words Schmidt's syndrome ; Addison disease ; Addisonian crisis ; Diabetes mellitus type I (IDDM) ; Autoimmune thyreoiditis ; Autoimmune polyglandular syndrome (APS) ; Schlüsselwörter Schmidt-Syndrom ; Morbus Addison ; Addison-Krise ; Diabetes mellitus Typ I (IDDM) ; Autoimmunthyreoiditis ; Auto-immunes Polyglanduläres Syndrom (APS)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das Zusammentreffen von Nebennierenrinden- und Schilddrüseninsuffizienz wird in der Literatur als Schmidt-Syndrom bezeichnet. Bei 2/3 dieser Patienten findet man einen koexistenten Diabetes mellitus Typ I. Da in der Gruppe der Diabetiker das Auftreten von pluriglandulären Erkrankungen beschrieben ist, sollte ein Krankheitsprozeß mit auffälliger Adynamie, Erbrechen, Bauchschmerzen, Exiskkose und Hypotonie auch an das gleichzeitige Vorliegen eines M. Addison denken lassen. Zusätzlich ist das frühzeitige Erkennen einer beginnenden Addison-Krise sehr wichtig, da trotz Intensivmedizin dieses Krankheitsbild mit einer hohen Letalität behaftet ist.
    Notes: Summary The coexistance of thyroid- and adrenocortical insufficiency is known as Schmidt's syndrome. In two-thirds of these patients you find also diabetes mellitus. In the group of diabetic patients one sees pluriglandular endocrine dysfunction more often than in non-diabetic patients. Therefore, one should be aware of a coexisting Addision's disease in diabetic patients who are complaining of tireness, weakness, vomiting, abdominal pain, and circulatory disturbances. It is very important to detect this combination as early as possible, because the lethality of an Addisionian crisis is still high.
    Type of Medium: Electronic Resource
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