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  • 1995-1999  (2)
  • Key words Atherosclerosis – extracellular matrix – HMG-CoA reductase inhibitors – smooth muscle – thrombospondin  (1)
  • Key words: Laparoscopic cholecystectomy  (1)
Material
Years
  • 1995-1999  (2)
Year
Keywords
  • 1
    ISSN: 1433-0385
    Keywords: Key words: Laparoscopic cholecystectomy ; Long-term outcome ; Postcholecystectomy syndrome ; Gallstones. ; Schlüsselwörter: Laparoskopische Cholecystektomie ; Langzeitresultate ; Postcholecystektomiesyndrom ; Gallensteine.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Fragestellung: Wir untersuchten Art und Häufigkeit der Beschwerden nach laparoskopischer Cholecystektomie sowie Einfluß des präoperativen Beschwerdebildes und des perioperativen Verlaufes auf das Langzeitergebnis. Material und Methode: Zwischen September 1994 und August 1995 haben wir prospektiv und standardisiert 268 Patienten erfaßt und laparoskopisch cholecystektomiert. Nach durchschnittlich 16 Monaten (12–25 Monate) wurden 253 Patienten (94 %) telephonisch und bei Bedarf klinisch nachkontrolliert. Ergebnisse: Bei der Nachkontrolle waren die Beschwerden eingeteilt nach Visick-Score: Grad I (symptomfrei): 164 Patienten (65 %); Grad II: 72 (28 %); Grad III: 12 (5 %) und Grad IV: 5 (2 %). Aufgrund der Befragung und Abklärungen bei 15 % der Patienten konnten wir folgende Ursachen für das „Postcholecystektomiesyndrom“ definieren: Residualsteine 1 %, subhepatische Kollektionen 0,8 %, Narbenhernie 0,4 %. Narbenschmerzen 2,4 %, peptische Krankheiten 4 %, funktionelle Beschwerden 26 %. Patienten mit typischen oder atypischen Beschwerden präoperativ unterschieden sich nicht in der Art und Häufigkeit der Beschwerden ein Jahr nach laparoskopischer Cholecystektomie. Anzahl und Lokalisation der vorausgegangenen Laparotomien oder der intraoperative Galleverlust hatten ebenfalls keinen Einfluß auf die Art oder Schwere der Postcholecystektomiebeschwerden. Schlußfolgerungen: 93 % der Patienten ein Jahr nach laparoskopischer Cholecystektomie haben keine oder unerhebliche Beschwerden. Weder Art der Beschwerden präoperativ, Anzahl vorausgegangener Laparotomien noch der intraoperative Galleverlust haben Einfluß auf das Langzeitresultat.
    Notes: Summary. Aims: We studied the nature and frequency of symptoms 1 year after laparoscopic cholecystectomy in order to define pre- and perioperative factors that influence the long-term outcome. Method: Between September 1994 and August 1995 we prospectively evaluated 268 patients undergoing laparoscopic cholecystectomy using a standard questionnaire. After an average of 16 months (12–25 months) the patients were asked about their symptoms using a similar questionnaire by telephone or were followed up clinically if necessary. Results: In the long-term follow-up the severity of the symptoms according to the Visick score were: Visick I (no symptoms): 164 patients (65 %); Visick II: 72 (28 %); Visick III: 12 (5 %); Visick IV: 5 (2 %). The aetiologies of the postcholecystectomy syndrome were: residual stones 1 %, subhepatic liquid formation 0.8 %, incisional hernia 0.4 %, peptic diseases 4 %, wound pain 2.4 %, functional disorders 26 %. Patients with typical or atypical symptoms preoperatively showed no difference in the outcome 1 year after laparoscopic cholecystectomy. Neither did the number and location of laparotomies prior to cholecystectomy or the gallbladder perforation or loss of stones intraoperatively influence the severity of the postcholecystectomy symptoms. Conclusions: One year after laparoscopic cholecystectomy 93 % of the patients have no or only minor abdominal symptoms. Neither the number and location of the laparotomies prior to cholecystectomy nor the loss of gallstones intraoperatively have an impact on the long-term result.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: Key words Atherosclerosis – extracellular matrix – HMG-CoA reductase inhibitors – smooth muscle – thrombospondin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical studies have shown that treatment with 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors can stabilize atherosclerotic plaques and slow their progression. One determinant of plaque stability and size is the composition of the vascular extracellular matrix. The aim of this study was to evaluate the effects of different HMG-CoA reductase inhibitors on the expression of major components of the vascular extracellular matrix in smooth muscle cells. Cultured human vascular smooth muscle cells were incubated for 24–72 h with the HMG-CoA reductase inhibitors lovastatin (1–50 μmol/L), simvastatin (0.05–20 μmol/L), and pravastatin ( 1–100 μmol/L). RNA expression of the extracellular matrix proteins thrombospondin-1, fibronectin, collagen type I, and biglycan as well as expression of the cytokine TGF-β1 was determined by Northern blotting. Extracellular matrix protein secretion was visualized by immunofluorescence. In addition, cell proliferation and viability were measured using BrDU-ELISAs, MTT-tests, and direct cell counting. Expression of thrombospondin-1 was significantly decreased after 24 h incubations with lovastatin in concentrations as low as 1 μmol/L. Coincubation with the cholesterol precursor mevalonate completely reversed this effect. The downregulation of thrombospondin-1 expression occured in the same concentration range that also inhibited cell proliferation. In contrast, lovatatin did not affect expression of fibronectin, whereas collagen type I and biglycan expression decreased only after long incubations with high, toxic lovastatin concentrations. Simvastatin, but not the very hydrophilic compound pravastatin, had a similar effect on extracellular matrix expression as lovastatin. In summary, lovastatin and simvastatin predominantly decrease the expression of the glycoprotein thrombospondin-1, which is functionally associated with smooth muscle cell migration and proliferation. In contrast, expression of plaque-stabilizing extracellular proteins such as collagen type I and biglycan are much less affected.
    Type of Medium: Electronic Resource
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