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Endoscopic variceal ligation for bleeding oesophageal varices
101
INFLUENCEOF DIETARY ZINC ON HEPATIC COLLAGEN AND PROLYL-HYDROXYLASE ACTiVITY IN ALCOHOLIC RATS. & Gin&net. A. Pa&s. ?1,CabaIlerIa. 5. Al& R. -s Liver Unit. HospsamniFi Deulofeu8 J. --universitv of Barcelona. Barcelona, Provincial. Spain. The effect of dietary zinc on hepatic collagen prolylhydroxylase activity (PH-ase) in and alcoholicrats has been investigatedin 4 groups of male Wistar rats fed for 12 weeks with liquid ethanol diet with different zinc concentrations (standard diet: 7.6 mg/l: zinc deficient: 3.4 mgt'l: and zinc supplemented: 76 mg/l and 300 mgfl) and in
a control group of rats receivingstandard liquid diet (7.6 rig/lzinc) without ethanol. There vrere no significant differences in hepatic collagen concentrationand PH-ase activity between alcoholic and normal rats receiving 7.5 mg/l of Zn (collagen: 77*5 and 73i6 gfmg prot: PH-
(range 207) banus w-Ii-2 ap?Jiad ir. Xc with a r.otaJ of 261 banes
in a f%rtXf
first
sessicn
53 sessions.
ase: 37 f 26 and 36 f 22 cpm/mg prot). Rats fed wit’\ deficient zinc diet showed an increased PH-ase activity (75 * 10 cpm/mg prot. ~~0.05) although no changes in hepatic collagen (77*10 g/mg prot) were observed in comparison with rats fed with standard
alcoholicdiet. By contrast. hepatic collagenwas significantlylower in rats zinc supplemented(66 * 4 and 53 f 3 g/mg prot. pt0.05 and pcO.01). and hepatic pH-ase activitywas particularlylower in rats receiving 300 mg/l of zinc (18 f 20 cpmlmg prot). These results indicate that dietary zinc influenceshepatic fibrogenesisin alcoholic rats. (Supportedby CAYCIT grant PA85-0078)
(11 G 'ISteiqar:
103 2REVENTS NORFLOXACIN SPONTANEOUS BACTERIAL PERITOWITIS(SSP) IN CIRRHOSIS. FINAL RESULTS nF A MULTICENTE?DOUBLE-BLINDPLACEBO CONTROLELI STUDY. P Giner. A Rimola. R Planas y Varqas. M For&. MT Miranda.-LRodri9?.-A-1. F Marco. i Almela, J &c&. JM Salmeron M Esteve A Gin& JM Mars&s; -~_&_~R Esteban. E Lissen. MT Jimenez. 2 Berenauer, V Arroyo. 2 Rod&. Liver Unit. Hospital Clinic, Barcelona.Spain. To
investigate
were
similar
whether
selective
104 NITRIC OXIDE PRODUCTIONBY MONOCVTES IN ALCOHOLIC LIVER DISEASE: A MEDIATOR OF LOCALISED AND SYSTEMIC EFFECTS R. Goldin and N. Hunt Departmentof Histopathology,St Mary's Hospital Medical School, London, UK Increasingattention is being paid to the role of cells of the mononuclearphagocyte family in the pathogenesisof aIcohoJic liver disease. They are known-to produce a number of inflammatory mediators includingIL-I. IL-6 and TNF. A recently described-mediatorproduced by these cells is nitric oxide (NO). first characterisedas endothelialderived relaxing factor. We have studied ND productionby circulatingmonocytes in 14 controls and 23 patients with alcoholic liver disease. NO productionwas measured indirectlyby assessing nitrite formation. Normal monocytes were found to produce small amounts of NO and this could be increasedover 6 fold by endotoxin. This effect was abrogated by the addition of an inhibitorof NO synthesis,L-n-monomethyl-arginine (L-NMMA). In contrast the monocytes from alcoholicsproduced high basal levels of NO and this could not be significantlyincreasedby the addition of endotoxin. NO formationwas also blocked by the addition of LNMNA. NO may act locally, e.g. it is known to be cytotoxic.or systemicallyby producing vasodilatation.
intestinal
decontamination (SID) prevents SEP recurrence. 80 cirrhoticswho had recoveredfrom an episode of SBP were included in a double-blind trial aimed at comparing norfloxacin (400 mgfday orally:- 40 patients) YS placebo (40 patients). Both groups regarding
clinical
and
laboratory
data
at inclusionand microbiologicalcharacteristicsof the index SBP. The mean follow-upperiod in the whole series was 6.421 months (range l-19). Long-
term
norfloxacin administration significantly reduced the probabilityof S8P recurrence during follow-up (SBP recurrence probability rate at 1 year: 209. in the ncrfloxacin group vs 682 in the placebo group: p=D.O06). This effect was due to a marked reduction in the probability of developing SBP caused by aerobic gramnegative bacteria
(norfloxacin: 3% vs placebo: 602; p=O.OOl).Only one patient developed side effects related to norfloxacin (oral and esophagealcandidiasiswhich resolved vlith oral nystatin). These results indicate that long-term SID with norfloxacin is effective
in preventing
SBP recurrence
gramnegativebacteria in cirrhosis.
caused
1390 km.J.Sbrg.lS?.'-25
by
S26
INFLUENCEOF DIETARY ZINC ON HEPATIC COLLAGEN AND PROLYL-HYDROXYLASE ACTiVITY IN ALCOHOLIC RATS. & Gin&net. A. Pa&s. ?1,CabaIlerIa. 5. Al& R. -s Liver Unit. HospsamniFi Deulofeu8 J. --universitv of Barcelona. Barcelona, Provincial. Spain. The effect of dietary zinc on hepatic collagen prolylhydroxylase activity (PH-ase) in and alcoholicrats has been investigatedin 4 groups of male Wistar rats fed for 12 weeks with liquid ethanol diet with different zinc concentrations (standard diet: 7.6 mg/l: zinc deficient: 3.4 mgt'l: and zinc supplemented: 76 mg/l and 300 mgfl) and in
a control group of rats receivingstandard liquid diet (7.6 rig/lzinc) without ethanol. There vrere no significant differences in hepatic collagen concentrationand PH-ase activity between alcoholic and normal rats receiving 7.5 mg/l of Zn (collagen: 77*5 and 73i6 gfmg prot: PH-
(range 207) banus w-Ii-2 ap?Jiad ir. Xc with a r.otaJ of 261 banes
in a f%rtXf
first
sessicn
53 sessions.
ase: 37 f 26 and 36 f 22 cpm/mg prot). Rats fed wit’\ deficient zinc diet showed an increased PH-ase activity (75 * 10 cpm/mg prot. ~~0.05) although no changes in hepatic collagen (77*10 g/mg prot) were observed in comparison with rats fed with standard
alcoholicdiet. By contrast. hepatic collagenwas significantlylower in rats zinc supplemented(66 * 4 and 53 f 3 g/mg prot. pt0.05 and pcO.01). and hepatic pH-ase activitywas particularlylower in rats receiving 300 mg/l of zinc (18 f 20 cpmlmg prot). These results indicate that dietary zinc influenceshepatic fibrogenesisin alcoholic rats. (Supportedby CAYCIT grant PA85-0078)
(11 G 'ISteiqar:
103 2REVENTS NORFLOXACIN SPONTANEOUS BACTERIAL PERITOWITIS(SSP) IN CIRRHOSIS. FINAL RESULTS nF A MULTICENTE?DOUBLE-BLINDPLACEBO CONTROLELI STUDY. P Giner. A Rimola. R Planas y Varqas. M For&. MT Miranda.-LRodri9?.-A-1. F Marco. i Almela, J &c&. JM Salmeron M Esteve A Gin& JM Mars&s; -~_&_~R Esteban. E Lissen. MT Jimenez. 2 Berenauer, V Arroyo. 2 Rod&. Liver Unit. Hospital Clinic, Barcelona.Spain. To
investigate
were
similar
whether
selective
104 NITRIC OXIDE PRODUCTIONBY MONOCVTES IN ALCOHOLIC LIVER DISEASE: A MEDIATOR OF LOCALISED AND SYSTEMIC EFFECTS R. Goldin and N. Hunt Departmentof Histopathology,St Mary's Hospital Medical School, London, UK Increasingattention is being paid to the role of cells of the mononuclearphagocyte family in the pathogenesisof aIcohoJic liver disease. They are known-to produce a number of inflammatory mediators includingIL-I. IL-6 and TNF. A recently described-mediatorproduced by these cells is nitric oxide (NO). first characterisedas endothelialderived relaxing factor. We have studied ND productionby circulatingmonocytes in 14 controls and 23 patients with alcoholic liver disease. NO productionwas measured indirectlyby assessing nitrite formation. Normal monocytes were found to produce small amounts of NO and this could be increasedover 6 fold by endotoxin. This effect was abrogated by the addition of an inhibitorof NO synthesis,L-n-monomethyl-arginine (L-NMMA). In contrast the monocytes from alcoholicsproduced high basal levels of NO and this could not be significantlyincreasedby the addition of endotoxin. NO formationwas also blocked by the addition of LNMNA. NO may act locally, e.g. it is known to be cytotoxic.or systemicallyby producing vasodilatation.
intestinal
decontamination (SID) prevents SEP recurrence. 80 cirrhoticswho had recoveredfrom an episode of SBP were included in a double-blind trial aimed at comparing norfloxacin (400 mgfday orally:- 40 patients) YS placebo (40 patients). Both groups regarding
clinical
and
laboratory
data
at inclusionand microbiologicalcharacteristicsof the index SBP. The mean follow-upperiod in the whole series was 6.421 months (range l-19). Long-
term
norfloxacin administration significantly reduced the probabilityof S8P recurrence during follow-up (SBP recurrence probability rate at 1 year: 209. in the ncrfloxacin group vs 682 in the placebo group: p=D.O06). This effect was due to a marked reduction in the probability of developing SBP caused by aerobic gramnegative bacteria
(norfloxacin: 3% vs placebo: 602; p=O.OOl).Only one patient developed side effects related to norfloxacin (oral and esophagealcandidiasiswhich resolved vlith oral nystatin). These results indicate that long-term SID with norfloxacin is effective
in preventing
SBP recurrence
gramnegativebacteria in cirrhosis.
caused
1390 km.J.Sbrg.lS?.'-25
by
S26