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  • 1
    ISSN: 1432-1238
    Keywords: Key words Hypoxia ; Ischemia ; Acute phase proteins ; Cardiac arrest ; Infections
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: Inflammation and hypoxia are frequently associated, but their interaction is poorly understood. In vitro studies have shown that hypoxia stimulates the genes of acute phase proteins (APP) and cytokines known to induce APP. We decided to determine kinetics and potential determinants of an acute phase response after cardiac arrest and to assess whether isolated moderate hypoxia can induce APP in humans in vivo. Design: Prospective, observational study in patients and human experiment. Setting: Tertiary care university hospital. Patients and participants: 22 patients after primarily successful cardiopulmonary resuscitation (CPR) and 7 healthy volunteers. Interventions: None in patients; exposure of volunteers to simulated altitude (460 torr/6 h). Results: Following CPR, type-1 APP (C-reactive protein, α1-acidglycoprotein, serum amyloid A) and type-2 APP (haptoglobin, α1-antitrypsin) increased consistently within 1–2 days and the ’negative' APP transferrin was downregulated. This APP response occurred irrespective of the cause of arrest, the estimated time of anoxia, clinical course or patient outcome and was not different in patients with and without infectious complications. Exposure of healthy volunteers to less severe but more prolonged hypoxia did not induce APP, although a time dependent increase of serum erythropoietin (EPO) was measurable under these conditions, indicating the activation of oxygen dependent gene expression. Conclusions: (i) A marked acute phase response occurs regularly after cardiac arrest, but within the complexity of this situation the severity of hypoxia is not a predominant determinant of this response. (ii) Despite in vitro evidence for similarities in the oxygen dependent regulation of APP and EPO production, the oxygen sensitivity of these proteins in vivo is different. (iii) Measurements of APP are not revealing regarding infectious complications in the early phase after CPR.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-2451
    Keywords: Secondary hyperparathyroidism ; Total parathyroidectomy ; Autotransplantation ; Transplantation tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 41 Patienten mit chronisch globaler Niereninsuffizienz und sekundärem Hyperparathyreoidismus wurde eine totale Parathyreoidektomie und Autotransplantation von Epithelkörperchengewebe in die fistelfreie Unterarmmuskulatur durchgeführt. Innerhalb von 7–33 Monaten entwickelten 5 Patienten ein Transplantatrezidiv im Unterarm. Die morphologischen und klinischen Aspekte des Transplantathyperparathyreoidismus rücken die Regenerate im Unterarm in die Nachbarschaft eines malignen Wachstums. Bei Abwägung der Erfolge und der Risiken dieses Verfahrens nach 5jähriger Beobachtung kann die Autotransplantation beim sekundären Hyperparathyreoidismus nicht empfohlen werden. Ausschlaggebend ist die hierfür zwar morphologisch vorerst nicht nachgewiesene, aber durchaus vorstellbare Entwicklung eines Transplantatcarcinoms.
    Notes: Summary The results of clinical and morphologic studies performed in 41 patients with chronic, renal failure and secondary hyperparathyroidism, who had total parathyroidectomy and autotransplantation of parathyroid tissue into the forearm muscle are presented. In five cases, 7–33 months after autotransplantation we found transplantation tumors developing in the forearm. Explanted grafts showed invasive growth of parathyroid tissue in the adjacent structures, into the musculature and blood vessels. The increased incidence of mitosis otherwise seen as evidence of malignant neoplasia of parathyroid tumors, indicated atypical focal proliferation of the transplanted tissue. This is justification for not performing transplantations any more in the treatment of renal osteodystrophy.
    Type of Medium: Electronic Resource
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