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  • Key words Glutaric aciduria type I  (2)
  • Major depressive disorder  (2)
  • Phospholipase A2  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Affective Disorders 6 (1984), S. 265-272 
    ISSN: 0165-0327
    Keywords: Adolescence ; DST ; GH stimulation ; Major depressive disorder ; Puberty ; REM latency
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine , Psychology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Affective Disorders 6 (1984), S. 265-272 
    ISSN: 0165-0327
    Keywords: Adolescence ; DST ; GH stimulation ; Major depressive disorder ; Puberty ; REM latency
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine , Psychology
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 1432-1440
    Keywords: Sepsis ; Shock ; septic ; Glucocorticoids ; Hydrocortisone ; Fever ; Phospholipase A2 ; C-reactive protein ; Elastase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is increasing evidence that the hypercortisolemia in inflammatory diseases suppresses the elaboration of proinflammatory cytokines, thus protecting the host from its own defence reactions. In severe sepsis and septic shock cortisol levels are usually elevated, but some patients may have relative adrenal insufficiency. This may contribute to the overwhelming systemic inflammatory response syndrome. We evaluated the impact of low-dose hydrocortisone infusion (10 mg/h) on the course of the systemic inflammatory response syndrome. This dose corresponds to a maximum secretory rate of cortisol achieved in corticotropin-stimulated healthy humans. In a prospective observational study 57 surgical patients with severe sepsis or septic shock were studied, of which in addition to the conventional treatment 12 patients were infused with low-dose hydrocortisone, and 45 were treated without any corticosteroid. In the longitudinal analysis the systemic inflammatory response — as judged by body temperature, cardiovascular response, and kinetics of inflammatory mediators such as phospholipase A2, C-reactive protein, and neutrophil elastase — started to differ in favor of the hydrocortisone-treated patients after 2 days of treatment (P 〈 0.05, Mann-Whitney U test). The difference disappeared after withdrawal of exogenous cortisol. Shock reversal was achieved in all patients treated with low-dose hydrocortisone. The data provide evidence that low-dose hydrocortisone infusion attenuates the systemic inflammatory response in human septic shock. From an immunological point of view a relative cortisol deficiency may contribute to the amplified immune response in systemic inflammatory diseases. A randomized clinical trial must clarify the impact of low-dose hydrocortisone infusion on the clinical course and outcome of septic shock patients.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 67 (1989), S. 144-148 
    ISSN: 1432-1440
    Keywords: Phospholipase A1 ; Phospholipase A2 ; Inflammation ; Pancreas ; Phagocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The development of a photometric procedure to measure phospholipase A activity has extended previous observations that this enzyme activity increases in several pathological states including pancreatic and inflammatory diseases. Serum phospholipase A in pancreatitis was characterized as a mixture of the pancreatic enzyme and a different phospholipase with a pH optimum at 8.0. The latter enzyme was also observed in nonpancreatic diseases like septicemia and acute lung failure which are characterized by an increase in tissue phagocyte activity. The possible pathogenic role of phospholipase(s) A, their intracellular regulation and the proposed mechanisms of release into the blood stream are discussed with respect to the present pathobiochemical knowledge. This includes the mechanism of activation of phagocytosis and the possible role of lipocortins known to be stimulated by glucocorticoid treatment.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Monatsschrift Kinderheilkunde 145 (1997), S. 652-655 
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Glutarazidurie Typ I ; Glutaryl-CoA-Dehydrogenase ; Diagnostik ; Key words Glutaric aciduria type I ; Glutaryl-CoA-dehydrogenase ; Diagnosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary We present an algorithm for the rational diagnosis of glutaric aciduria type I (GA1). Normal urinary organic acids in patients with non-specific clinical features and normal results of brain imaging render the diagnosis highly unlikely, and no further investigations are required. In other patients, the diagnostic strategy depends on the individual clinical, neuroradiological and biochemical findings. GCDH enzyme analysis should be reserved for patients in whom GA1 is very likely.
    Notes: Zusammenfassung Dargestellt wird ein Algorithmus, mit dessen Hilfe eine Glutarazidurie Typ I (GA1) mit rationalem Aufwand zuverlässig diagnostiziert werden kann. Wichtigste Untersuchung ist die genaue Analyse der organischen Säuren im Urin. Ergibt diese ein unauffälliges Ergebnis, sind bei Patienten mit unspezifischer Klinik und untypischen Befunden in der zerebralen Bildgebung keine weiteren Untersuchungen notwendig. Ansonsten richtet sich das diagnostische Vorgehen nach den klinischen, neuroradiologischen und biochemischen Befunden. Die enzymatische Analytik sollte nur bei dringendem Verdacht auf GA1 durchgeführt werden.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Glutarazidurie Typ I ; Makrozephalie ; Subdurale Hygrome bzw. Hämatome ; Kindesmißhandlung ; Therapie der Glutarazidurie Typ I ; Key words Glutaric aciduria type I ; Macrocephaly ; Subdural hygromas and hematomas ; Battered child syndrome ; Treatment of glutaric aciduria type I
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Glutaric aciduria type I is a disease caused by deficiency of the enzyme Glutaryl CoA-Dehydogenase with an increased urinary excretion of glutaric and 3-hydroxy-glutaric acid. We report on two patients in whom glutaric aciduria type I was misdiagnosed as battered child syndrome because of subdural hygromas which are a peculiar feature of the underlying metabolic disease. The characteristic neuroradiologic manifestations of glutaric aciduria type I are illustrated. We also report on two patients who were diagnosed because of macrocephaly in the newborn period lacking neurological symptoms. They were treated at the presymptomatic stage of the disease and developed almost normally up to the age of now five and six years.
    Notes: Zusammenfassung Die Glutarazidurie Typ I wird durch einen Defekt des Enzyms Glutaryl-CoA-Dehydrogenase verursacht und durch die vermehrte Ausscheidung von Glutarsäure und 3-Hydroxy-Glutarsäure im Urin diagnostiziert. Wir berichten hier vom tragischen Fall der Fehldiagnose 2er Patienten mit Glutarazidurie Typ I als Kindesmißhandlung aufgrund einer Fehldeutung der für die zugrundeliegende Stoffwechselerkrankung pathognomonischen subduralen Hygrome und Hämatome. Die für die Erkrankung charakteristischen neuroradiologischen Veränderungen werden dargestellt. Den Krankengeschichten der betroffenen Patienten wird der Verlauf 2er dank früher Diagnosestellung bei isolierter Makrozephalie erfolgreich behandelter Patienten mit Glutarazidurie Typ I gegenübergestellt.
    Type of Medium: Electronic Resource
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