- Email: [email protected]
King's college hospital experience of OLT for HCC
92
Posters
1 P/CO4/02i 1 KING'S COLLEGE HOSPITAL EXPERIENCE OF OLT FOR HCC ,I. McCall. M. Rela. M. Kallife. P. Muiesan. P Gibbs. J Karani. B Portmann. J O’Gradv. N Heaton. Liver Transplant Surgical Service and Institute of Liver Studies, King’s College Hospital, London, United Kingdom Ninety two patients with HCC underwent OLT at King’s College Hospital between January 1989 and October 1997. There were 76 males and 16 females with median (range) age of 55 (15-69) years. HCC was diagnosed pre-operatively in 70 and was an incidental finding in 22. Patients evaluated for OLT underwent routine liver ultrasound and alpha fetoprotein level, and additional tests were only done to investigate abnormal findings. Viral hepatitis was the commonest cause of underlying cirrhosis in patients with HCC, followed by alcohol. The pTNM stage was stage 1 in 19, stage 2 in 23, stage 3 in 25, and stage 4a in 22 (unclassified in 2). The median tumour size was 2.7cm, range 0.69, and the median tumour number was 2, range l->3. Pre-operative chemoembolisation and post-operative chemotherapy were used selectively throughout the series. Patients were followed up until death, or to October 1997 (median follow up 36 months). 70 patients are alive, 3 of whom have recurrent tumour. 22 patients have died of the following causes; peri-operative mortality 8, recurrent viral disease 6, tumour recurrence 5, and late sepsis 2. Of the 8 patients with tumour recurrence, 4 had stage 4a disease and 3 had tumours over 5 cm or more than 3 lesions. Only one patient with an incidentally diagnosed tumour has developed recurrence. This study confirms that HCC with small volume disease, whether diagnosed before or after surgery, does not have a major detrimental effect on long term outcome in patients with cirrhosis undergoing OLT. Ultrasound and alpha fetoprotein levels missed some patients with HCC, however only 1 patient with clinically important disease escaped detection pre-operatively.
GRANULOCYTECOLONY STIMULATING FACTOR ADMINISTRATION ACCELERATES HEPATOCYTE PROLIFERATION IN CARBON TETRACHLORIDE INDUCED RAT LIVER INJURY S.Theocharis.
A.Mareeli.
G.Kouraklis. M.Mvkoniatis*.
Depts of Histology-Embryology University of Athens, Greece.
CKittas.
and *Experimental Pharmacology,
Carbon tetrachloride (Ccl,) administration in rats, induces centrilobular hepatocellular necrosis, followed by regeneration.We have recently shown that the administration of Granulocyte-Colony Stimu-
lating Factor (G-CSF) enhances and accelerates hepatocyte proliferation after partial hepatectomy (Clin Sci, 92:315, 1997).The aim of the present study was to examine the effect of G-CSF administration on hepatocyte regeneration due to Ccl, induced liver injury.The intraperitoneal (ip) administration of 1 mL CC&/Kg of body weight (bw) in male Wistar rats, was followed by ip administration either of saline (Group A) or G-CSF (Granulokine, Roche, Switzerland) 1500 pg/Kg of bw (Group B), 2 h later.The animals were sacrificed at 0,12,24, 36,48,60 and 72 h post-CC& administrationThe rate of tritiated thymidine incorporation into hepatic DNA, the enzymatic activity of liver thymidine kinase, the assessment of mitotic and proliferating cell nuclear antigen (PCNA) labeling index in hepatocytes, were used to estimate liver regeneration.The hepatocyte regeneration after CCI, induced injury, presented peak at 48 h post-CC& treatment (Group A). When G-CSF was administered in Ccl,-treated rats (Group B), the peak of hepatic regeneration was enhanced and transposed at the time point of 36 h (p
TISSUE CHARACTERIZATION OF SMALL HEPATIC TUMORS. QUANTITATIVE DOPPLER SPECTRAL ANALYSIS VS. POWER DOPPLER FLOW IMAGING.
M. ValPlmlP11. Gastroenterologia.
Dipartimento di Medicina Universita di Bologna. Bologna, Italy.
Interna
e
at CD and in 38/41 cases (92.7%) at PD (p=O.Ol). Presence and distribution of both CD and PD signals did not differ in beni n and mali nant lesions. Quantitative spectral analysis showed the fo fiowmg resu sts: tn w ~~(91 ANQYB lEe2t655_1587f714 1768f707 722f467 p=NS Hz 53*14 D=0.m 88f21 154zt43 15&46 86M0 p =O.QQtj PI 6W32 p O.op2 A cut-off of 60 (RI) and 100 (PI) allow to identify malignant lezons with an accuracy of 94.9%, while ACT (cut-off 115 ms) dtfferentiates HCC from MET with an accuracy of 84.6%. conclusions: PD is more sensitive than CD in identifying vascular signals in small liver tumors. Neither color and power-Doppler features nor peak Doppler frequency can be utilized to differentiate benign from malignant lesions. Quantitative spectral analysis criteria such as im edance indices (RI and PI) and ACT were found to be accurate in di&rentiating benign from malignant lesions and in identifying HCC.
HISTOLOGICAL VARIABLES PREDICTIVE OF HEPATOCELLULAR CARCINOMA (HCC) IN PATIENTS . . ~ WITH GENETIC HEMOCHROoMATOSIS (GI-I) . * MU. * AMDN,Fv. . . . ere’. M Del Vmo. V M&m. G Fw 1st Med Int Fisiopat Med, Osp Maggiore IRCCS, *Ist Scieni Biomed Osp S.Paolo, Univ Milano, ‘Div Med I Osp Fatebenefratelli, Milano, “Dip Pat01 Sperimentale, Univ Bologna, Italia. Liver cell dysplasia (LLCD) and high hepatocytes proliferative activity evaluated by argyrophilic nucleolar organizer regions (AgNOR) have been recently identified as major risk factors for HCC in pts with GH-unrelated cirrhosis. To assess whether also in pts with GH LLCD and AgNOR can predict HCC occurrence, we studied 74 pts (52 with and 22 without cirrhosis). LLCD was assessed in routinely stained and AgNOR in silver stained sections; high proliferative index (AgNOR-PI) defined by a % of hepatocyte positive >2.5. LLCD and AgNOR-PI >2.5 were present in 14 (27%) and 9 (17%) pts with cirrhosis but in none without cirrhosis. HBV, HCV infection and/or alcohol abuse were present in lo/14 pts with LLCD and 8/!J pts with AgNORPI ~2.5, being HBV the most frequent: 55% in LLCD and 44% in AgNOR-PI >2.5 @=0.02 vs other risk factors). During follow up (range 6-273 months) 14 pts developed HCC, all cirrhotics. Of the 14 pts with LLCD and of the 9 with AgNOR-PI >2.5,6 (43%) and 5 (55%) developed HCC. Mean follow up from diagnosis of GH to HCC was 46.0~36 months in pts with and 109.3~47 months in pts without dysplasia and/or AgNOR-PI >2.5 @=O.Ol). In conclusion, also in pts with cirrhosis due to GH, LLCD and AgNOR-PI >2.5 can predict HCC occurrence, mainly when HBV infection coexists. HCC develops in a significantly shorter interval of time in pts with LLCD and AgNOR-PI >2.5 than in those without these variables.
Posters
1 P/CO4/02i 1 KING'S COLLEGE HOSPITAL EXPERIENCE OF OLT FOR HCC ,I. McCall. M. Rela. M. Kallife. P. Muiesan. P Gibbs. J Karani. B Portmann. J O’Gradv. N Heaton. Liver Transplant Surgical Service and Institute of Liver Studies, King’s College Hospital, London, United Kingdom Ninety two patients with HCC underwent OLT at King’s College Hospital between January 1989 and October 1997. There were 76 males and 16 females with median (range) age of 55 (15-69) years. HCC was diagnosed pre-operatively in 70 and was an incidental finding in 22. Patients evaluated for OLT underwent routine liver ultrasound and alpha fetoprotein level, and additional tests were only done to investigate abnormal findings. Viral hepatitis was the commonest cause of underlying cirrhosis in patients with HCC, followed by alcohol. The pTNM stage was stage 1 in 19, stage 2 in 23, stage 3 in 25, and stage 4a in 22 (unclassified in 2). The median tumour size was 2.7cm, range 0.69, and the median tumour number was 2, range l->3. Pre-operative chemoembolisation and post-operative chemotherapy were used selectively throughout the series. Patients were followed up until death, or to October 1997 (median follow up 36 months). 70 patients are alive, 3 of whom have recurrent tumour. 22 patients have died of the following causes; peri-operative mortality 8, recurrent viral disease 6, tumour recurrence 5, and late sepsis 2. Of the 8 patients with tumour recurrence, 4 had stage 4a disease and 3 had tumours over 5 cm or more than 3 lesions. Only one patient with an incidentally diagnosed tumour has developed recurrence. This study confirms that HCC with small volume disease, whether diagnosed before or after surgery, does not have a major detrimental effect on long term outcome in patients with cirrhosis undergoing OLT. Ultrasound and alpha fetoprotein levels missed some patients with HCC, however only 1 patient with clinically important disease escaped detection pre-operatively.
GRANULOCYTECOLONY STIMULATING FACTOR ADMINISTRATION ACCELERATES HEPATOCYTE PROLIFERATION IN CARBON TETRACHLORIDE INDUCED RAT LIVER INJURY S.Theocharis.
A.Mareeli.
G.Kouraklis. M.Mvkoniatis*.
Depts of Histology-Embryology University of Athens, Greece.
CKittas.
and *Experimental Pharmacology,
Carbon tetrachloride (Ccl,) administration in rats, induces centrilobular hepatocellular necrosis, followed by regeneration.We have recently shown that the administration of Granulocyte-Colony Stimu-
lating Factor (G-CSF) enhances and accelerates hepatocyte proliferation after partial hepatectomy (Clin Sci, 92:315, 1997).The aim of the present study was to examine the effect of G-CSF administration on hepatocyte regeneration due to Ccl, induced liver injury.The intraperitoneal (ip) administration of 1 mL CC&/Kg of body weight (bw) in male Wistar rats, was followed by ip administration either of saline (Group A) or G-CSF (Granulokine, Roche, Switzerland) 1500 pg/Kg of bw (Group B), 2 h later.The animals were sacrificed at 0,12,24, 36,48,60 and 72 h post-CC& administrationThe rate of tritiated thymidine incorporation into hepatic DNA, the enzymatic activity of liver thymidine kinase, the assessment of mitotic and proliferating cell nuclear antigen (PCNA) labeling index in hepatocytes, were used to estimate liver regeneration.The hepatocyte regeneration after CCI, induced injury, presented peak at 48 h post-CC& treatment (Group A). When G-CSF was administered in Ccl,-treated rats (Group B), the peak of hepatic regeneration was enhanced and transposed at the time point of 36 h (p
TISSUE CHARACTERIZATION OF SMALL HEPATIC TUMORS. QUANTITATIVE DOPPLER SPECTRAL ANALYSIS VS. POWER DOPPLER FLOW IMAGING.
M. ValPlmlP11. Gastroenterologia.
Dipartimento di Medicina Universita di Bologna. Bologna, Italy.
Interna
e
at CD and in 38/41 cases (92.7%) at PD (p=O.Ol). Presence and distribution of both CD and PD signals did not differ in beni n and mali nant lesions. Quantitative spectral analysis showed the fo fiowmg resu sts: tn w ~~(91 ANQYB lEe2t655_1587f714 1768f707 722f467 p=NS Hz 53*14 D=0.m 88f21 154zt43 15&46 86M0 p =O.QQtj PI 6W32 p O.op2 A cut-off of 60 (RI) and 100 (PI) allow to identify malignant lezons with an accuracy of 94.9%, while ACT (cut-off 115 ms) dtfferentiates HCC from MET with an accuracy of 84.6%. conclusions: PD is more sensitive than CD in identifying vascular signals in small liver tumors. Neither color and power-Doppler features nor peak Doppler frequency can be utilized to differentiate benign from malignant lesions. Quantitative spectral analysis criteria such as im edance indices (RI and PI) and ACT were found to be accurate in di&rentiating benign from malignant lesions and in identifying HCC.
HISTOLOGICAL VARIABLES PREDICTIVE OF HEPATOCELLULAR CARCINOMA (HCC) IN PATIENTS . . ~ WITH GENETIC HEMOCHROoMATOSIS (GI-I) . * MU. * AMDN,Fv. . . . ere’. M Del Vmo. V M&m. G Fw 1st Med Int Fisiopat Med, Osp Maggiore IRCCS, *Ist Scieni Biomed Osp S.Paolo, Univ Milano, ‘Div Med I Osp Fatebenefratelli, Milano, “Dip Pat01 Sperimentale, Univ Bologna, Italia. Liver cell dysplasia (LLCD) and high hepatocytes proliferative activity evaluated by argyrophilic nucleolar organizer regions (AgNOR) have been recently identified as major risk factors for HCC in pts with GH-unrelated cirrhosis. To assess whether also in pts with GH LLCD and AgNOR can predict HCC occurrence, we studied 74 pts (52 with and 22 without cirrhosis). LLCD was assessed in routinely stained and AgNOR in silver stained sections; high proliferative index (AgNOR-PI) defined by a % of hepatocyte positive >2.5. LLCD and AgNOR-PI >2.5 were present in 14 (27%) and 9 (17%) pts with cirrhosis but in none without cirrhosis. HBV, HCV infection and/or alcohol abuse were present in lo/14 pts with LLCD and 8/!J pts with AgNORPI ~2.5, being HBV the most frequent: 55% in LLCD and 44% in AgNOR-PI >2.5 @=0.02 vs other risk factors). During follow up (range 6-273 months) 14 pts developed HCC, all cirrhotics. Of the 14 pts with LLCD and of the 9 with AgNOR-PI >2.5,6 (43%) and 5 (55%) developed HCC. Mean follow up from diagnosis of GH to HCC was 46.0~36 months in pts with and 109.3~47 months in pts without dysplasia and/or AgNOR-PI >2.5 @=O.Ol). In conclusion, also in pts with cirrhosis due to GH, LLCD and AgNOR-PI >2.5 can predict HCC occurrence, mainly when HBV infection coexists. HCC develops in a significantly shorter interval of time in pts with LLCD and AgNOR-PI >2.5 than in those without these variables.