title: Systemic prostacyclin in cirrhotic patients. Relationship with portal hypertension and changes after intestinal decontamination.
abstract: The total body production of prostacyclin was shown to be increased in cirrhotic patients, suggesting that its synthesis by blood vessels of the systemic circulation is enhanced. However, the mechanism by which the synthesis of systemic prostacyclin is stimulated is not known. The present study investigated the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha, an index of total body prostacyclin synthesis, first, in cirrhotics with portal hypertension (n = 19) as compared with cirrhotics with reduced portal pressure after portacaval shunt surgery (n = 18) and with control noncirrhotic subjects (n = 11), and; second, in cirrhotics before and after intestinal decontamination by oral nonabsorbable antibiotics (n = 9 antibiotic treated patients, n = 10 control nontreated cirrhotics). Control noncirrhotic subjects showed lower urinary excretion of 2,3-dinor-6-keto-PGF1 alpha than both groups of cirrhotics (P less than 0.001). Interestingly, urinary excretion of 2,3-dinor-6-keto-PGF1 alpha was significantly higher in cirrhotics with portacaval shunt than in those with portal hypertension (P less than 0.01). The urinary excretion of 2,3-dinor-6-keto-PGF1 alpha decreased significantly after intestinal decontamination in the antibiotic-treated group (580.1 +/- 232.4 vs. 431.2 +/- 219.2 pg/mg creatinine; P less than 0.05) but not in nontreated patients (543.9 +/- 214.4 vs. 581.2 +/- 281.4 pg/mg creatinine; P = NS). These data suggest that the increased urinary excretion of 2,3-dinor-6-keto-PGF1 alpha observed in cirrhotics is not directly related to portal hypertension itself but to portal blood factors that bypass the liver. Some such factors may be of intestinal bacterial origin.
authors.affiliation: Sección de Hepatología de la Escuela de Patología Digestiva, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Guarner
authors.forename: G
authors.initials: G
authors.lastname: Soriano
authors.forename: J
authors.initials: J
authors.lastname: Such
authors.forename: M
authors.initials: M
authors.lastname: Teixidó
authors.forename: I
authors.initials: I
authors.lastname: Ramis
authors.forename: O
authors.initials: O
authors.lastname: Bulbena
authors.forename: J
authors.initials: J
authors.lastname: Roselló
authors.forename: F
authors.initials: F
authors.lastname: Guarner
authors.forename: E
authors.initials: E
authors.lastname: Gelpi
authors.forename: J
authors.initials: J
authors.lastname: Balanzó
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000652:urine; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001419:Bacteria / Q000187:drug effects; D011464:Epoprostenol / Q000378:metabolism*; D006801:Humans; D006975:Hypertension, Portal / Q000150:complications / Q000378:metabolism* / Q000601:surgery; D007422:Intestines / Q000187:drug effects* / Q000382:microbiology; D008103:Liver Cirrhosis / Q000150:complications / Q000378:metabolism*; D011167:Portacaval Shunt, Surgical
chemical_list: D000900:Anti-Bacterial Agents; D015121:6-Ketoprostaglandin F1 alpha; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; D011464:Epoprostenol