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  • Amanita phalloides  (1)
  • Bone marrow myeloid cell kinetics  (1)
  • Fulminante Lebernekrose  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Fulminante Lebernekrose ; Hirnödem ; Mannitol ; Kohlehämoperfusion ; Leberzellregeneration ; Fulminant liver necrosis ; Brain edema ; Mannitol ; Charcoal hemoperfusion ; Liver cell regeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The clinical course of a 26 year old female patient with acute liver necrosis and coma due to hepatitis B is reported. The disturbances of conciousness had improved. The patient survived 41 days after the beginning of the coma and developped livercell regeneration and an acute post-hepatitic liver cirrhosis. As a grave complication a septicemia with aspergillus was observed. The patient died because of gastro-intestinal hemorrhage. At autopsy there were no signs of brain edema. The treatment consisted in: daily infusions with coenzyme A, nicotinamid-adenin-dinucleotide, alpha lipoic acid and cocarboxylase to improve the metabolic disorders and the clinical picture; mannitol intravenously to prevent and to treat cerebral edema; 33 charcoal-hemoperfusions to remove toxic substances of acute liver failure. Treatment of the aspergillus infection with 5-fluorocytosine and amphotericine B and infusion of concentrated ascites led to a decompensation of liver functions. From this observation the following conclusions can be drawn: after an acute viral hepatic necrosis, new synthetic functions and improvements of the disturbed intermediary metabolism in regenerated liver-cells can eventually be seen only after twenty-four to thirty days. With systematically applicated mannitol infusions it is possible to treat cerebral edema effectively.
    Notes: Zusammenfassung Es wird der Verlauf einer durch Hepatitis B bedingten, akuten Lebernekrose mit Coma bei einer 26jährigen Patientin beschrieben. Die Bewußtseinsstörung besserte sich. Die Patientin überlebte 41 Tage und entwickelte Leberzellregenerate und eine akute posthepatitische Leberzirrhose. Im Verlauf trat als schwere Komplikation eine Pilzsepsis auf. Die Patientin starb an einer Magendarmblutung. Bei der Autopsie fand sich kein Hirnödem. Die Behandlung beständ in täglichen Infusionen von Coenzym A, Nikotinamid-adenin-dinukleotid, alpha-Liponsäure und Cocarboxylase zur Besserung von metabolischen Störungen und klinischem Bild; Mannitol intravenös, zur Verhinderung und Behandlung des Hirnödems; 33 Kohlehämoperfusionen, zur Entfernung toxischer Substanzen. Behandlung der Aspergillus-Infektion mit 5-Fluorocytosin und Amphotericin B und Infusion des konzentrierten Ascites führten zu einer Dekompensation der Leberfunktionen. Aus dieser Beobachtung können folgende Schlüsse gezogen werden: Nach einer akuten viralen Lebernekrose kann es erst nach 24–30 Tagen zur Wiederaufnahme synthetischer Funktionen und zur Besserung des gestörten Intermediärstoffwechsels in regenerierten Leberzellen kommen. Mit systematischer Mannitol-Therapie ist es möglich, das Hirnödem wirksam zu bekämpfen.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 40 (1984), S. 1268-1270 
    ISSN: 1420-9071
    Keywords: Mushroom poisoning ; Amanita phalloides ; ethanol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Survival of mice after lethal doses of a lyophilizate fromAmanita phalloides (‘death cap’) was markedly increased by single doses of ethanol applied 30 min before or 5 min after the mushroom. Hepatic histopathological damage (confluent necrosis) was largley prevented. Acute, but not chronic, consumption of ethanol may thus influence favorably the outcome of death cap poisoning and should be taken into consideration in the evaluation of therapeutic measures.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0584
    Keywords: Lung cancer ; Granulocyte-macrophage colony-stimulating factor ; Chemotherapy ; Bone marrow myeloid cell kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Information on the kinetics of bone marrow (BM) myeloid precursors (BMMP) is required for integrating cancer chemotherapy with granulocyte-macrophage colony-stimulating factor (rhGM-CSF), with the aim of reducing neutropenia. Using bivariate flow-cytometric analysis of the in vivo incorporation of bromodeoxyuridine (BUDR) vs DNA content we have studied the kinetics of BMMP in 21 patients with SCLC during the first of six chemotherapy courses (etoposide, epirubicin, andcis-platinum, days 1–3, every 21 days), given alone (eight patients) or followed by rhGM-CSF (10μg/kg/day s.c, days 4–14) as BM rescue (eight patients) or both preceded (days -17 to -7, as BM priming) and followed by rhGM-CSF (five patients). At 11–14 days after the start of these therapies there was an increase in the baseline proliferative activity of proliferating BMMP and a shortening in the time needed by the metamyelocyte to mature and to leave the marrow. Both effects were greater and were maintained to a significantly greater degree a week later in patients who received chemotherapy plus rhGM-CSF rescue than in those who received chemotherapy alone or rhGM-CSF priming alone. At day 11–14 the pretreatment median cell production rate of pBMMP was increased by 340%, 150%, and 183% and the maturation time was reduced by 80%, 45%, and 57%, respectively, in the three groups. A week later, the corresponding figures were 206%, 111%, and 157% and 50%, 18%, and 45%. Hence, an identical rhGM-CSF schedule is more effective in increasing the neutrophil production by BMMP when given following chemotherapy as BM rescue than before it as BM priming. In both the rescue and the priming schedule, the increase in proliferative activity of BMMP just at the end of rhGM-CSF stimulation was linked to both an increase in the labeling index and a reduction in duration of S-phase (TS), while a week later it was linked solely to reduction in TS. This could actually reduce one of the two kinetic targets of subsequently administered cytostatics, i.e., a high LI and a long time spent in S phase. From this study, accurate kinetic data can be obtained with the in vivo BUDR technique that are useful in scheduling rhGM-CSF.
    Type of Medium: Electronic Resource
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