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Hepatitis B-virus (HBV) markers in serum and liver tissue of HBsAg carriers after liver transplantation and treatment with anti-HBs-hyperimmune globulin
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“EPATlTlS B-“‘RUS (HEW) HARKERS IN SERUM AN0 LIVER TISSUE OF HasAg CARRIERS AFTER LlYER TRANSPLANTATION AND TREATMENT WITH ANTI-HGs-HVPERlW4JNE GLOBULIN U.Hopf, B.NOller. R.Steffen*. N.O. Gechstein*. G.Gl"mhardt*. P.Ne"ha"s*. O.P"hn Dept. of Int. Medicine. and OeQt. of Surgery+ Univ.-Klinikum Rudolf Yiwh~w. Standort Chariottenbur". Freie UniversitBt Berlin (FRGI
Liver transplantation in patient; wth positive tBsAg st*f"s is a matter of controversy, since reWection of the transplanted organ with HGV and septic complications of surgery have been observed in a relatively large nun&r of casts. There are few documented follow up studies of WY markers including HGY replication and delta virus SuQePinfection in patients undergoing liver transplantation. The QWPe"t study investigated these questions. PATIENTS: IS patients underwent liver transplanatation in ow institution between September 1988 and April ,989. All QStbZ"tS survived. 7 Of the 15 patients were NGsAg PositlYe QPe"iO"S to surgery. Two cases were HL%Ag and NW-ONA positive. while 5 were HGeAg and HBY-DNA negative. HGV superinfection was found in two patients with negative findings for HGeAg. All 7 patients with positive HGsAg status received anti-HGS hyperimwne globulin administered according to the plan developed by the Wdlzinische HOchscb"Le Hannover: 10.000 U of Hepatect (Biotest. FRG) 1.~. d"ring the anhepatic pIme and 1,000 U i.v. daily during the first postoperative week. RESULTS: Elimlnatlon of H&As was observed in 5 of 7 QatientS who hwe r.?ma,ned"BrAg negatimng the fOl,Ow "Q QWLDd t0 date. C,,S Of tnese 5 Qatie"tS demonstrated HGV replication preoperatiuely, and 1 patient had evidence of superinfection with HDV. Synthesis of HGV or HDV markers has not been documented in a siwjle case during PosttransLllantatlon follow "Q. None of the seven patients developed sepsis. CONCLLWONS: The treatment regiwen followed in this study represents a Qosribility for permanent elimination of HGsAg after liver transplantation in patients wrth preoperative replication of HGV or s"perl"fect‘on with HO". Our Qrellminary data do n,t wggest an ""avoidably high pate of postoperative septic fomQlic~tions in HGsAg carriers.
J3
ESCHERlCHlA COLI ROUGH(R) MUTANTS lN THE GUT AN0 LIPID A LN THE LIVER FROM PATlENTS WITH PRlNARV BILIARV CIRRHOSIS (PGC). ".Hopf, G.Mbller, R.Ster"erowicz, A.Rodloff. H.Lobeck, M.F,'e"de"ber9*. C.Gala"os*. Dept. of Int. Med>c,ne, U",v.-Kl,n,k"m Rudolf VIrchov and lnst,t"t fur Mikrobiologle, Frele Universit;it Berlin and Max-Planck-lnstitutr. Freiburg. FRG.
PGC-speclflc antuutochondrial antibodIes (AMA) recognize cell menware proteins of ent.eroSacterlaceae and al'e Induceable in rabbits with Rb and Rc mUtaRtS of Sam?lla minnesota (Lancet ll,1166,1988). The followng studies are concerned with deRa"stration of enterobacterlal R-mutants 1" the stool of patients with chronic inflammatory liver diseases and the intrahepatic presence of lipid A, which rePresents a conr0n antigenic Component of the cell wall in gram-neqa*ive bacteria. AMA-positive atients with PBC in stages l-IV (~21) a,d QatW"tS with ChrO",‘ WQatltiS type B (n=lS) and +G type (n-15) were investigated and COinpared w,th healthy controls (n=ZO). Methods: Stool specimens were suspended I" steP,le phosphate buffered 511t solution (pH ?.5)spread on SeleCtlYe agar media. R colonzes were counted and conflrned by agglutlnatinn with S% saline solution. LLYW tlss"e w$s investigated w:th monoclanal antibodles against liptd A by peroxidase-antipergxidase-technique. Results: All stool samples from PGC patents contaIned E. co11 R mutants constituting I?&5Om total amount of E.coll. hong the healthy controls R m"tants were detectable in only one stool sample. In the groups YLth chronic viral hepatitis R rrmtants were found in a q"arteP of cases. Deposits of lipid A were observed rn the cytoplasm of hepatocytes in 11 patients with PBC. while liver tlss"e from patwnts with chronic viral hepatitis did not contain bePatoce1lul.w llpid A. Conclusions: The data SuPport ollr hypothesis that intestinal E. toll R mutants we involved I" the etiology of PGC and that antigens released from the e"tWObXtWial cell wall could play ? QathOge"etiC role. The blO,ogiCal acti"itieS Of lipid A explain characteristic inununopathologlcalphenomena in PGC.
s42
“EPATlTlS B-“‘RUS (HEW) HARKERS IN SERUM AN0 LIVER TISSUE OF HasAg CARRIERS AFTER LlYER TRANSPLANTATION AND TREATMENT WITH ANTI-HGs-HVPERlW4JNE GLOBULIN U.Hopf, B.NOller. R.Steffen*. N.O. Gechstein*. G.Gl"mhardt*. P.Ne"ha"s*. O.P"hn Dept. of Int. Medicine. and OeQt. of Surgery+ Univ.-Klinikum Rudolf Yiwh~w. Standort Chariottenbur". Freie UniversitBt Berlin (FRGI
Liver transplantation in patient; wth positive tBsAg st*f"s is a matter of controversy, since reWection of the transplanted organ with HGV and septic complications of surgery have been observed in a relatively large nun&r of casts. There are few documented follow up studies of WY markers including HGY replication and delta virus SuQePinfection in patients undergoing liver transplantation. The QWPe"t study investigated these questions. PATIENTS: IS patients underwent liver transplanatation in ow institution between September 1988 and April ,989. All QStbZ"tS survived. 7 Of the 15 patients were NGsAg PositlYe QPe"iO"S to surgery. Two cases were HL%Ag and NW-ONA positive. while 5 were HGeAg and HBY-DNA negative. HGV superinfection was found in two patients with negative findings for HGeAg. All 7 patients with positive HGsAg status received anti-HGS hyperimwne globulin administered according to the plan developed by the Wdlzinische HOchscb"Le Hannover: 10.000 U of Hepatect (Biotest. FRG) 1.~. d"ring the anhepatic pIme and 1,000 U i.v. daily during the first postoperative week. RESULTS: Elimlnatlon of H&As was observed in 5 of 7 QatientS who hwe r.?ma,ned"BrAg negatimng the fOl,Ow "Q QWLDd t0 date. C,,S Of tnese 5 Qatie"tS demonstrated HGV replication preoperatiuely, and 1 patient had evidence of superinfection with HDV. Synthesis of HGV or HDV markers has not been documented in a siwjle case during PosttransLllantatlon follow "Q. None of the seven patients developed sepsis. CONCLLWONS: The treatment regiwen followed in this study represents a Qosribility for permanent elimination of HGsAg after liver transplantation in patients wrth preoperative replication of HGV or s"perl"fect‘on with HO". Our Qrellminary data do n,t wggest an ""avoidably high pate of postoperative septic fomQlic~tions in HGsAg carriers.
J3
ESCHERlCHlA COLI ROUGH(R) MUTANTS lN THE GUT AN0 LIPID A LN THE LIVER FROM PATlENTS WITH PRlNARV BILIARV CIRRHOSIS (PGC). ".Hopf, G.Mbller, R.Ster"erowicz, A.Rodloff. H.Lobeck, M.F,'e"de"ber9*. C.Gala"os*. Dept. of Int. Med>c,ne, U",v.-Kl,n,k"m Rudolf VIrchov and lnst,t"t fur Mikrobiologle, Frele Universit;it Berlin and Max-Planck-lnstitutr. Freiburg. FRG.
PGC-speclflc antuutochondrial antibodIes (AMA) recognize cell menware proteins of ent.eroSacterlaceae and al'e Induceable in rabbits with Rb and Rc mUtaRtS of Sam?lla minnesota (Lancet ll,1166,1988). The followng studies are concerned with deRa"stration of enterobacterlal R-mutants 1" the stool of patients with chronic inflammatory liver diseases and the intrahepatic presence of lipid A, which rePresents a conr0n antigenic Component of the cell wall in gram-neqa*ive bacteria. AMA-positive atients with PBC in stages l-IV (~21) a,d QatW"tS with ChrO",‘ WQatltiS type B (n=lS) and +G type (n-15) were investigated and COinpared w,th healthy controls (n=ZO). Methods: Stool specimens were suspended I" steP,le phosphate buffered 511t solution (pH ?.5)spread on SeleCtlYe agar media. R colonzes were counted and conflrned by agglutlnatinn with S% saline solution. LLYW tlss"e w$s investigated w:th monoclanal antibodles against liptd A by peroxidase-antipergxidase-technique. Results: All stool samples from PGC patents contaIned E. co11 R mutants constituting I?&5Om total amount of E.coll. hong the healthy controls R m"tants were detectable in only one stool sample. In the groups YLth chronic viral hepatitis R rrmtants were found in a q"arteP of cases. Deposits of lipid A were observed rn the cytoplasm of hepatocytes in 11 patients with PBC. while liver tlss"e from patwnts with chronic viral hepatitis did not contain bePatoce1lul.w llpid A. Conclusions: The data SuPport ollr hypothesis that intestinal E. toll R mutants we involved I" the etiology of PGC and that antigens released from the e"tWObXtWial cell wall could play ? QathOge"etiC role. The blO,ogiCal acti"itieS Of lipid A explain characteristic inununopathologlcalphenomena in PGC.
s42