Hepato-gastroenterology · 2002
Infectious factors in acute acalculous cholecystitis.
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Teixeira João Paulo Araújo, Malheiro Luís, Pontinha Nuno, Friões Fernando, da Fonseca Freitas, Saleiro Vaz, Saraiva A Carlos
Аннотация
BACKGROUND/AIMS: The infection is shown as a secondary phenomenon in lithiasic acute cholecystitis. However, its importance in acute gallbladder inflammation without lithiasis has not been sufficiently clarified. In this context, we tried to investigate this issue by resorting to animal research. Similarly we studied the repercussions of Diclofenac (NSAID) in bacteriological features of the bile in the operated animals.
METHODOLOGY: We provoked acute cholecystitis in pigs by the ligature of biliary pedicle associated to the gallbladder introduction of "Lysophosphatidylcoline". Two series of animals were used: P1 (pigs not treated with Diclofenac) with 17 pigs and P2 (pigs treated with Diclofenac) with 23. In the latter group we associated the administration of Diclofenac given before the production of acute cholecystitis and administered for 4 days. The microbiology of the bile was studied in 34 pigs. The following parameters were valorized: histological gallbladder lesions and microorganisms in bacteriological examination of the bile.
RESULTS: Severe lesions of acute cholecystitis were registered in 82.3% of the animals. Positive bile cultures were registered in 64.1% of group P1 and 65.5% in the group P2. The simultaneous administration of Diclofenac in the P2 group did not cause a regression of gallbladder lesions or in microbial agents in the bile in relation to the first group (P = 0.649, and P = 0.781, respectively).
CONCLUSIONS: Our investigations allow us to conclude by valorization the infection factor in acute acalculous cholecystitis. On the other hand, the absence of repercussion of Diclofenac in acute acalculous cholecystitis was demonstrated not only in histological gallbladder lesions, but also in bile infection.
METHODOLOGY: We provoked acute cholecystitis in pigs by the ligature of biliary pedicle associated to the gallbladder introduction of "Lysophosphatidylcoline". Two series of animals were used: P1 (pigs not treated with Diclofenac) with 17 pigs and P2 (pigs treated with Diclofenac) with 23. In the latter group we associated the administration of Diclofenac given before the production of acute cholecystitis and administered for 4 days. The microbiology of the bile was studied in 34 pigs. The following parameters were valorized: histological gallbladder lesions and microorganisms in bacteriological examination of the bile.
RESULTS: Severe lesions of acute cholecystitis were registered in 82.3% of the animals. Positive bile cultures were registered in 64.1% of group P1 and 65.5% in the group P2. The simultaneous administration of Diclofenac in the P2 group did not cause a regression of gallbladder lesions or in microbial agents in the bile in relation to the first group (P = 0.649, and P = 0.781, respectively).
CONCLUSIONS: Our investigations allow us to conclude by valorization the infection factor in acute acalculous cholecystitis. On the other hand, the absence of repercussion of Diclofenac in acute acalculous cholecystitis was demonstrated not only in histological gallbladder lesions, but also in bile infection.