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Liver transplantation for metabolic disorders in children
Comparisonof nepatomalCarcinogenesiswith Normal Adult and Foetal Hepatocytesin Rats C.G.Schu1r.e , U.N.Riede", K.Joh*‘* Departmentsof Surgery and Pathology**,Univ. of Freiburg, Sundgauallee 45, D-7800 Freiburg,West Germany; Nishi ShinbashiUniversityof Tokyo**', Japan. A quantitativeultrastructuralanalysis wes made of chemically-induced Morris hepatomas in ratS to compare the carcinogenesisof hepatomas with both normal and foetal liver tissue. 20 animals each of 4 differentgradings of Morris hepatomaswere compared with the seme number of normal adult and foetal rats. Our findings showed that although each type of hepatoma has a characteristiccytoarchitecture,all hepatomasshow a varying degree of differentiation dependingon their growth rate. Whereas the rough endoplasmicreticulum in hepatoma cells hardly changed in comparisonto the control hepatocytes, the smcoth endoplasmicreticulumand percxisome values drop considerablyin all hepatoma cells examined (p ( 0.01). Runour-specificmorphometric changes "c:ur in the mitochondria:In comparisonto adult liver cells, the chondriomaof turnourcells comprise a larger number of smaller mitocnondria, the amount of christaemembrane per cell decreasing with increasingcell differentiation(p < 0.01). A similaritywas observedbetweenthe cytoplasmof hepatomacells and foetal hepatocytes.However, the surface of mitochondrialcristae per unit volume of the mitochondriaand the mitochondrialunit volume in malignant cells differ from those in foetal Cells.
LIVER TRANSPLANTATION DISORDERS IN CHILDREN.
FOR
A.Si~ilruya.H.Si~ibata.A.Tal;e~~cl~: IJep:.oiint medicinc.Kiras;lt" Cniv. Kansgawa..I.lpan.
ALDH was reported and as corrrsn"lldin# t" ALDll3.To make clear the incidcnre *IlId
sprcific ALIJH isoz)mrx et PH3.G which wnu HO, deter:tahJnin non.tumor liver*: ISSW from same patients by isoelectriclorusinp grl electrophoresii.Tba mobility of this terrorspwlfic inozyme was rrseoble :o that of the stom:~cbend the lung tissues whirL were reported to vontain ALDH:l.This isozyae
hand YIRS nezativn for immunostoin:na(0 anti-ALDHl snil anti-ALDH2. Tolai ',\LUH activity of the tum"r(4.3i4.0u!n)wias Iowr than that of non-tumor tissues(3.0=3.0). There wae no diffrrwxe au tot41 ILDH 28tisity !ka%vwl KC tis.,,,* with and vitbout tumor associated ALDH. These results
'TPZ4Ti4ZNTWITHOtUU.NORFLOXACIN INTFE PXVENTION OF INFECTIONSIN CIRRHOTICSMUST BE COlQIM_0US
METABOLIC
E Sokal. J de Ville de Govet. F Van University of Hoof. J B otte. Hospital, 1200 LUC Louvain, St Brussels.
G. Soriano,A. Tcmis,C. Guamer, C. Fem&ndez:, M. Teixid6.R. Mirelis',G. Prats*and F. Vilardell Dept. of Gastroenterology and Microbiology*, iiospital SantaCreui Sant Pau. Barcelona.Spain. Selectiveintestinaldecontamination (SID)with norfloxacin(NFX) is useful to preventinfections in cirmotic patients(CP) at high risk. The aim of the presentstudywas to determinethe durationof SID achievedwith oral NlX in CP and, therefore, whethertreatmentwith NFX shouldbe intermittent or must be continua's. PATImS AWL .NETHODS. FourteenCP receivedoral NFX (10 patients400 q/day and 4. 4CO mg bid) during7 days.Bacterialcountswere performedin fecal samples collectedbefore and after treatment,and then everyweek until total recoveryof fecal flora to the initialvalue. RESULTS.In 13 of the 14 CP enterobacteria could not be isolatedat the end of the treatment(mean beforetreatment2.0~108cfh/g,after treatment
of 180 paediatric liver transplant recipients, 19 (10.5%) had transplant for a metabolic disorder. Four had a1-antitrypsin deficiency (mean age 9.1 Y), 5 Wilson's disease (mean age 11.2 y), 3 tyrosinemia (Em, ly & 4y), 1 type IV glycogenosis (1 y). Five four had no liver insufficiency: Crigler-Najjar syndromes (2.2, 3., 3.5 h 7.5 Y), 1 type I glycogf3-tosls (7 (lOY* primary hyperoxalurla y),l +$ver-kidney transpla;;:;;;:). Type died glycogenosls subsequently from related cardiac failure. Three patients died from cause.9 non related to their original diseases.1 year actuarial surv+val is 79.6%. Patients with tiyfroslnemla.kept succlnylmild elevation acetonuria. Primary oxaluria patient keeps high oxalurla 4 months after a-l-antitrypsin transplantation. associated proteinuria disappeared in 1 patient. transplantation Liver corrects metabolic disorders of
liver origin. Potential pathogenicity remains in other tissues for pluriorgan metabolic defects.
s112
LIVER TRANSPLANTATION DISORDERS IN CHILDREN.
FOR
A.Si~ilruya.H.Si~ibata.A.Tal;e~~cl~: IJep:.oiint medicinc.Kiras;lt" Cniv. Kansgawa..I.lpan.
ALDH was reported and as corrrsn"lldin# t" ALDll3.To make clear the incidcnre *IlId
sprcific ALIJH isoz)mrx et PH3.G which wnu HO, deter:tahJnin non.tumor liver*: ISSW from same patients by isoelectriclorusinp grl electrophoresii.Tba mobility of this terrorspwlfic inozyme was rrseoble :o that of the stom:~cbend the lung tissues whirL were reported to vontain ALDH:l.This isozyae
hand YIRS nezativn for immunostoin:na(0 anti-ALDHl snil anti-ALDH2. Tolai ',\LUH activity of the tum"r(4.3i4.0u!n)wias Iowr than that of non-tumor tissues(3.0=3.0). There wae no diffrrwxe au tot41 ILDH 28tisity !ka%vwl KC tis.,,,* with and vitbout tumor associated ALDH. These results
'TPZ4Ti4ZNTWITHOtUU.NORFLOXACIN INTFE PXVENTION OF INFECTIONSIN CIRRHOTICSMUST BE COlQIM_0US
METABOLIC
E Sokal. J de Ville de Govet. F Van University of Hoof. J B otte. Hospital, 1200 LUC Louvain, St Brussels.
G. Soriano,A. Tcmis,C. Guamer, C. Fem&ndez:, M. Teixid6.R. Mirelis',G. Prats*and F. Vilardell Dept. of Gastroenterology and Microbiology*, iiospital SantaCreui Sant Pau. Barcelona.Spain. Selectiveintestinaldecontamination (SID)with norfloxacin(NFX) is useful to preventinfections in cirmotic patients(CP) at high risk. The aim of the presentstudywas to determinethe durationof SID achievedwith oral NlX in CP and, therefore, whethertreatmentwith NFX shouldbe intermittent or must be continua's. PATImS AWL .NETHODS. FourteenCP receivedoral NFX (10 patients400 q/day and 4. 4CO mg bid) during7 days.Bacterialcountswere performedin fecal samples collectedbefore and after treatment,and then everyweek until total recoveryof fecal flora to the initialvalue. RESULTS.In 13 of the 14 CP enterobacteria could not be isolatedat the end of the treatment(mean beforetreatment2.0~108cfh/g,after treatment
of 180 paediatric liver transplant recipients, 19 (10.5%) had transplant for a metabolic disorder. Four had a1-antitrypsin deficiency (mean age 9.1 Y), 5 Wilson's disease (mean age 11.2 y), 3 tyrosinemia (Em, ly & 4y), 1 type IV glycogenosis (1 y). Five four had no liver insufficiency: Crigler-Najjar syndromes (2.2, 3., 3.5 h 7.5 Y), 1 type I glycogf3-tosls (7 (lOY* primary hyperoxalurla y),l +$ver-kidney transpla;;:;;;:). Type died glycogenosls subsequently from related cardiac failure. Three patients died from cause.9 non related to their original diseases.1 year actuarial surv+val is 79.6%. Patients with tiyfroslnemla.kept succlnylmild elevation acetonuria. Primary oxaluria patient keeps high oxalurla 4 months after a-l-antitrypsin transplantation. associated proteinuria disappeared in 1 patient. transplantation Liver corrects metabolic disorders of
liver origin. Potential pathogenicity remains in other tissues for pluriorgan metabolic defects.
s112