Critical care medicine · 1997
Decreased plasma gelsolin concentrations in acute liver failure, myocardial infarction, septic shock, and myonecrosis.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Suhler E, Lin W, Yin H L, Lee W M
Аннотация
OBJECTIVE: To quantitate gelsolin concentrations in serum of patients with a variety of conditions involving actin release into the circulation.
DESIGN: Prospective evaluation of sera on consecutive patients.
SETTING: Metropolitan county hospital.
PATIENTS: Ninety hospital patients with a variety of well-characterized diseases.
INTERVENTIONS: None.
MEASUREMENTS AND MAIN RESULTS: Sera were studied from patients with acute liver failure (n = 18), chronic hepatitis (n = 17), cirrhosis of varying etiology (n = 17), pancreatitis (n = 10), acute myocardial infarction (n = 10), myonecrosis due either to polymyositis or crush injuries (n = 12), and septic shock (n = 6); results were compared with sera from healthy individuals (n = 25). Gelsolin was quantified by Western blotting with monoclonal anti-gelsolin and laser densitometry. Significant reductions in mean gelsolin concentrations compared with healthy controls were observed in patients with acute liver failure (47%), myocardial infarction (69%), sepsis (51%), and myonecrosis (66%). An inverse correlation was observed between gelsolin concentration and severity of illness, as indicated by the magnitude of serum enzyme concentrations.
CONCLUSIONS: Gelsolin depletion occurs in a variety of tissue injury syndromes. Depletion of actin-scavenger capacity in the presence of continued actin release may affect outcome in situations of severe organ damage.
DESIGN: Prospective evaluation of sera on consecutive patients.
SETTING: Metropolitan county hospital.
PATIENTS: Ninety hospital patients with a variety of well-characterized diseases.
INTERVENTIONS: None.
MEASUREMENTS AND MAIN RESULTS: Sera were studied from patients with acute liver failure (n = 18), chronic hepatitis (n = 17), cirrhosis of varying etiology (n = 17), pancreatitis (n = 10), acute myocardial infarction (n = 10), myonecrosis due either to polymyositis or crush injuries (n = 12), and septic shock (n = 6); results were compared with sera from healthy individuals (n = 25). Gelsolin was quantified by Western blotting with monoclonal anti-gelsolin and laser densitometry. Significant reductions in mean gelsolin concentrations compared with healthy controls were observed in patients with acute liver failure (47%), myocardial infarction (69%), sepsis (51%), and myonecrosis (66%). An inverse correlation was observed between gelsolin concentration and severity of illness, as indicated by the magnitude of serum enzyme concentrations.
CONCLUSIONS: Gelsolin depletion occurs in a variety of tissue injury syndromes. Depletion of actin-scavenger capacity in the presence of continued actin release may affect outcome in situations of severe organ damage.