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Biomedical subjects

W Yeo

Publications and source records attributed to W Yeo.

At least 37 records · Page 2Linked to original sources
PubMed2001

Gross elevation of TT virus genome load in the peripheral blood mononuclear cells of cancer patients.

TT virus (TTV) is a recently described circular DNA virus of about 3.8 kb, which is related to the circoviridae viruses. It is commonly detected in healthy subjects and no association with any specific disease has been established. TTV was initially thought to be hepatotropic, but subsequent reports have shown that it is detectable in other tissues, including kidney, prostate, mammary gland, brain, bone marrow, and peripheral blood mononuclear cells. Plasma samples from cancer patients and healthy subjects were tested for the presence or absence of TTV by heminested polymerase chain reaction (PCR). We also developed a quantitative competitive PCR (QC-PCR) assay for TTV that permits accurate measurement of TTV DNA load. Using this assay, the TTV genome load in peripheral blood mononuclear cells (PBMCs) of healthy control subjects (n = 50) and patients with various types of cancer (n = 148), including breast cancer, non-Hodgkin's lymphoma, colon cancer, hepatocellular carcinoma, nasopharyngeal carcinoma, and other cancers, was measured. TTV DNA was detected in 69 of 100 plasma samples (69%) of cancer patients tested and in 39 of 100 plasma samples (39%) randomly selected from 1000 plasma samples of blood donors (p < 0.05). TTV DNA was detectable in the PBMCs of 99% of the cancer patients and 86% of the controls. However, the median virus load was more than 100-fold higher in the cancer patients (3599 copies/100,000 cells) than among the controls (30 copies/100,000 cells; p < 0.0001). There was no significant difference in TTV load among the different cancer types. Using a cutoff value of >250 copies per 100,000 PBMCs, 93.2% of cancer patients were "positive" compared to only 4% of healthy control subjects. Almost all the cancer patients have TTV infection and their TTV genome load in PBMCs is significantly higher than that in control subjects. It remains to be elucidated whether such findings are specific to cancer patients or occur in all seriously ill subjects.

Adult↗
PubMed2001

Cross-cultural validation of the McGill Quality of Life questionnaire in Hong Kong Chinese.

The main focus of palliative care services is to improve patients' quality of life (QOL). The potential value of assessment of QOL in palliative care is being increasingly recognized. The McGill Quality of Life questionnaire (MQOL) is designed specifically for palliative care patients, but its cross-cultural validity needs to be determined before it can be applied in populations of different cultures and ethnic groups. The cross-cultural validity of MQOL was investigated using a translated and modified version in Chinese--the MQOL-HK--in 462 palliative care patients in Hong Kong. Results show that the MQOL-HK is acceptable, valid and reliable. There is good acceptability, construct validity, convergent and divergent validity, test-retest and inter-rater reliability. Our study confirms that QOL does have cross-culturally robust constructs. Principal components analysis shows that the domains of physical, psychological, existential and support are all relevant and applicable in Chinese culture. Multiple regression analysis reveals that existential domain is the most important domain in predicting overall QOL. 'Face', eating and sex are additional facets of QOL that also need to be considered. The worst physical symptom on admission is the item of QOL with the lowest score, which need more care and attention by palliative care workers. A cross-culturally validated QOL instrument cannot just help ensure an accurate evaluation of profile, determinants, and changes of QOL, but is also a valuable asset for future comparison and evaluation of palliative care services and interventions across the world.

Adolescent↗
PubMed2001

The cost of palliative care for hepatocellular carcinoma in Hong Kong.

BACKGROUND: Hepatocellular carcinoma (HCC) is endemic in parts of Asia and Africa and most patients are not suitable for treatment with a curative approach. Little is known about the cost of palliative care for HCC. OBJECTIVE: To determine: (i) patient-specific costs of palliative care of HCC; and (ii) individual factors that drive patient-specific costs and to develop a model of cost per case under alternative circumstances. METHODS: 204 patients with inoperable HCC were prospectively tracked from first hospitalisation until death for health service utilisation. A societal perspective of cost was taken, including costs of formal and informal services incurred by payers, caregivers and patients. Observational data from a large Hong Kong cancer care programme were used. A regression analysis was performed using formal costs only, with the cost per observed day as the dependent variable. RESULTS: The median survival was 95 days and the mean observation period was 153 days. The mean value per person for formal healthcare cost was 30 983 Hong Kong dollars [$HK] ($US3872, 1998 values). The distribution of cost values were positively skewed. The regression analysis showed that age, days of observation and survival were negatively related to cost per observed day, and the Child-Pugh grading of severity of liver cirrhosis was positively related to cost per observed day. A sensitivity analysis based on the regression equation indicated that nonsurvivorship doubles the cost per case, increased severity as measured by the Child-Pugh Index adds about 50% to the cost, and chemotherapy increases cost 2-fold. CONCLUSIONS: The relatively modest average cost per patient with HCC in Hong Kong reflects the short median survival and subsequently the limited use of inpatient care and chemotherapy.

Aged↗
PubMed2001

Quantitative correlation of cytokeratin 19 mRNA level in peripheral blood with disease stage and metastasis in breast cancer patients: potential prognostic implications.

Mortality among patients with breast cancer (BC) is mainly caused by metastasis. We determined the circulating tumor burden in BC patients by semiquantitative reverse transcription-polymerase chain reaction using carcinoembryonic antigen (CEA) and cytokeratin 19 (CK19) mRNAs as molecular markers. We distinguished the mRNA levels in circulation between BC patients and healthy controls with reference to a BC-derived cell line, SK-BR-3. We prospectively analyzed peripheral blood samples from 33 BC patients and 26 healthy controls. We found CEA mRNA in 97% of patients and 92% of normal controls, and CK19 mRNA in 72% of patients and 19% of controls. CEA and CK19 mRNAs in normal peripheral blood were most likely derived from illegitimate transcription. In 10 patients, of whom 9 (90%) developed systemic metastases, the upper limit of CK19 mRNA of normal controls was exceeded. As compared with normal controls, significantly elevated CK19 mRNA levels in the patients appeared to originate from circulating malignant BC cells (P<0.0001). It was clinically significant that the mean CK19 mRNA level increased with advancing disease stage. Of prognostic value, we report for the first time that BC patients with CK19 mRNA elevation had notably shorter (approximately 3-year reduction) overall survival than patients with normal CK19 mRNA levels (P=0.045). Quantification of CK19 mRNA may prove useful for cancer staging, disease monitoring and prognostic assessment among BC patients.

Adult↗
PubMed2001

Caspase-mediated cleavage of TRAF3 in FasL-stimulated Jurkat-T cells.

The tumor necrosis factor receptor (TNFR)-associated factor (TRAF) proteins play a central role in the early steps of signal transduction by TNFR superfamily proteins, which induce various cellular responses, including apoptosis. Influences of TRAF proteins on the regulation of cell death and physical interactions between TRAFs and caspases have been reported. In this study, we demonstrate that TRAF3 is proteolyzed during cell death in a caspase-dependent manner. TRAF3 was found to be cleaved by incubation with caspase3 in vitro and by Fas- or CD3-triggering in Jurkat-T cells. The Fas- or CD3-induced cleavage of TRAF3 was blocked by caspase inhibitors and by introduction of alanine substitutions for D347 and D367 residues. Furthermore, the amino-terminal fragment of TRAF3 showed a different intracellular localization from the full-length TRAF3 with preferential distribution to particulate fractions and the nucleus. These findings suggest that TRAF3 may be regulated by caspases during apoptosis of T cells.

Amino Acid Chloromethyl Ketones↗
PubMed2001

Hepatitis B virus reactivation during cytotoxic chemotherapy-enhanced viral replication precedes overt hepatitis.

The diagnosis of HBV reactivation during cytotoxic chemotherapy is based on an abrupt rise in levels of serum HBV DNA in conjunction with a hepatitic picture and in the absence of other causes of hepatitis. However, several cases of "hepatitis" have been noted during chemotherapy in HBsAg-positive patients, for which no cause could be found and in which HBV DNA levels were negative. One possible explanation is that HBV reactivation may, indeed, have been the cause but that HBV DNA levels became negative by the time ALT levels peaked and the clinical diagnosis of hepatitis was made. During the course of a longitudinal study of HBsAg-seropositive cancer patients who were monitored during standard chemotherapy, the opportunity was available to test this hypothesis.

Adult↗
PubMed2000

A phase II study of gemcitabine plus oral etoposide in the treatment of patients with advanced nonsmall cell lung carcinoma.

BACKGROUND: The authors have designed a non-cisplatin-based chemotherapy regimen for the treatment of patients with advanced nonsmall cell lung carcinoma (NSCLC). This regimen capitalizes on the mild toxicity of gemcitabine, a novel nucleoside analog. METHODS: A total of 46 chemotherapy-naive patients with histologically confirmed Stage IIIB or IV NSCLC were enrolled. Eligible patients were treated with gemcitabine 1000 mg/m(2) on Days 1, 8, and 15, plus oral etoposide 50 mg daily for 14 days, which was increased to 21 days if there was no World Health Organization (WHO) Grade 3 or 4 toxicity in the 1st 2 cycles (each cycle was 28 days long). All patients were included for analysis of response and survival according to an intention-to-treat principle. RESULTS: The overall response rate was 43.5% (95% confidence interval [CI], 30. 7-60.2%). There was 1 complete response (2.2%) and 19 partial responses (41.3%). The median survival was 48.0 weeks (95% CI, 38. 1-75.9 weeks) and the 1-year survival rate was 45% (95% CI, 29-62%). The median time to progression for all patients was 39.2 weeks (95% CI, 35.7-49.7 weeks). World Health Organization (WHO) Grade 3 and 4 anemia, neutropenia, and thrombocytopenia was reported in 29%, 32%, and 18% of patients, respectively. Two patients had reactivation of hepatitis B viral infection that resulted in WHO Grade 4 hepatic dysfunction. Other nonhematologic toxicities were uncommon. CONCLUSIONS: This non-cisplatin-based regimen of gemcitabine and oral etoposide achieved a high response and survival rate. Toxicity appeared to be less severe than that associated with existing cisplatin-based regimens. A randomized study of this regimen versus a cisplatin-based regimen is indicated.

Adult↗
PubMed2000

Frequency of hepatitis B virus reactivation in cancer patients undergoing cytotoxic chemotherapy: a prospective study of 626 patients with identification of risk factors.

Hepatitis B virus (HBV) reactivation is a well-described complication in cancer patients who receive cytotoxic chemotherapy and may result in varying degrees of liver damage. As chemotherapy is used increasingly in cancer patients, HBV reactivation during cytotoxic treatment may become a more common problem. In lymphoma patients, the incidence of chronic HBV infection has been reported to be 26%, of whom 47% developed HBV reactivation during chemotherapy. However, corresponding data for patients with other malignancies undergoing cytotoxic chemotherapy are not known. In this prospective study, hepatitis B surface antigen (HBsAg) was determined in 626 consecutive cancer patients who received cytotoxic chemotherapy over a 12-month period. Seventy-eight patients (12%) were found to be HBsAg positive. Thirty-four (44%) developed raised alanine transaminase during their course of chemotherapy. In these 34 patients, hepatitis was attributed to HBV reactivation in 15 patients (44%), chronic active HBV infection in 1 patient (3%), hepatitis C infection in 1 patient (3%), malignant hepatic infiltration in 2 patients (6%), and the use of hepatotoxic chemotherapeutic agents in 11 patients (32%). The causes of hepatitis were unknown in 4 patients (12%). HBV reactivation was more likely to develop in patients who were male, younger age, HBeAg seropositive, and those with lymphoma. Presence of malignant hepatic infiltration, baseline pre-treatment alanine transaminase, total bilirubin, and HBV DNA levels did not correlate with the development of HBV reactivation. Of the 15 patients who developed HBV reactivation, antiviral therapy with lamivudine was available and used in 9. There was no HBV-related mortality during chemotherapy. It is concluded that in patients with chronic HBV infection under chemotherapy, HBV reactivation occurs in nearly 20% of them and accounts for 44% of hepatitis cases. The risk factors identified include male sex, younger age, HBeAg seropositive, and the diagnosis of lymphoma. In HBV endemic areas, patients with risk factors for HBV reactivation should be identified prior to receiving cytotoxic treatment and monitored closely. The potential benefit of lamivudine requires further confirmation.

Adult↗
PubMed2000

Hemorrhagic pyelitis, ureteritis, and cystitis secondary to cyclophosphamide: case report and review of the literature.

OBJECTIVE: Hemorrhagic cystitis is a well-known complication of cyclophosphamide therapy but extensive involvement of the entire urinary tract is far less common. We report here a patient who developed severe hemorrhagic pyelitis, ureteritis, and cystitis after one cycle of cyclophosphamide-containing combination chemotherapy. METHOD: A patient with synchronous carcinoma of the ovary and the uterus developed severe hemorrhagic pyelitis, ureteritis, and cystitis leading to bilateral hydronephroses and acute renal failure after one cycle of combination chemotherapy containing cyclophosphamide. The blood clots in the upper urinary tract were aspirated endoscopically and bilateral internal ureteric stents were inserted. RESULT: She underwent a prolonged diuretic phase with several episodes of hypokalemia, hypomagnesemia, and hypocalcemia and required intensive fluid and electrolytes replacement. Subsequently, she recovered fully with the ureteric stents removed 26 days later. CONCLUSION: In contrast to previous reports, where 2.8 g of cyclophosphamide was estimated to be the minimum cumulative dose required to cause hemorrhagic cystitis, this case illustrates that severe hemorrhagic complication can occur even after a low dose of cyclophosphamide (600 mg/m(2), total dose of 846 mg). Prompt diagnosis and intervention may be life-saving.

Antineoplastic Agents, Alkylating↗
PubMed2000

TT virus: a study of molecular epidemiology and transmission of genotypes 1, 2 and 3.

BACKGROUND: TT virus (TTV) is a recently discovered virus, which is not related to any other known virus infecting humans. OBJECTIVES: To investigate: (i) the world-wide distribution of the three major TTV genotypes; and (ii) the possible routes of viral transmission. STUDY DESIGN: (i) The phylogenetic distribution of 494 TTV isolates originating from 31 countries was analysed, using partial ORF1 sequences. (ii) Faeces samples (n=22) and saliva samples (n=72) from French individuals were tested for the presence of TTV DNA. (iii) Viral titres in paired serum and saliva samples were compared. RESULTS: (i) Genotypes 1, 2 and 3 were distributed world-wide, with a high proportion of type 1 in Asia (71%) and no type 3 identified in Africa to date. In the USA, 77% of isolates were grouped in four clusters only (genetic distances <10%). This was also the case of 76% of French isolates, 76% of Japanese isolates, and 89% of Hong Kong isolates. (ii) TTV DNA was detected in 18% of faeces samples and 68% of saliva samples tested. (iii) Viral titre in saliva samples was 100-1000 times higher than that of the corresponding serum. CONCLUSIONS: (i) The observed epidemiological distribution of TTV isolates is compatible with an ancient dissemination of viral ancestors belonging to the different genotypes and a slow genetic evolution in sedentary populations. (ii) Besides the possible transmission of TTV by the parental and oral-faecal routes, the high titre of TTV DNA observed in saliva raises the hypothesis of the viral transmission by saliva droplets. This route of transmission could explain the high degree of exposure to viral infection observed in the general population.

Blood Donors↗
PubMed2000

Frequent integration of precore/core mutants of hepatitis B virus in human hepatocellular carcinoma tissues.

The development of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) frequently follows persistent HBV infection and may arise in individuals who are hepatitis B e antigen (HBeAg) negative, indicating the possible presence of precore/core mutants. It is unclear whether precore/core mutants are associated with tumour development or are selected for after chromosomal integration of the wild-type viral DNA. We studied the status and sequence variation of the precore/core region of HBV in 56 patients with HBV-associated HCC and in various corresponding non-tumour tissues by Southern blot analysis, polymerase chain reaction and direct sequencing. Southern blot showed that integrated HBV DNA existed in 43 of 56 HCC tissues. Sequence analysis revealed mutations in 65% of the HCC (26/40) and 45% (14/31) of the corresponding non-tumour tissues. The mutation at nucleotide (nt) 1896, known to prevent HBeAg synthesis, was detected in 40% (16/40) of the tumours and in 35.4% (11/31) of the non-tumour tissues. Other mutations were found at nt 1899 (eight of 40 in HCC; three of 31 in non-tumour tissues), nt 1898 (seven of 40 in HCC; two of 31 in non-tumour tissues), nt 1912 (seven of 40 in HCC; none of 31 in non-tumour tissues) and nt 1886 (three of 40 in HCC; none of 31 in non-tumour tissues). To determine whether this finding merely reflected the prevalence of such mutants in this geographical region, HBV DNA from the sera of patients (also in this region) with acute and chronic hepatitis were sequenced. The nt 1896 mutant was found in 5.6% (one of 18) of patients with acute hepatitis B and in 22.8% (nine of 35) of patients with chronic hepatitis B. However, the nt 1898 mutation was not found in any of these sera. The precore/core mutant was observed with increasing frequency from acute hepatitis to chronic hepatitis, non-tumour and HCC, and this difference in frequency was significant between HCC and acute hepatitis B groups (P < 0.01), suggesting that the precore/core mutant or hepatocytes harbouring this mutant may be under immune selection and that such mutations may facilitate integration and subsequent tumour development.

Adult↗
PubMed2000

Sequence variations of precore/core and precore promoter regions of hepatitis B virus in patients with or without viral reactivation during cytotoxic chemotherapy.

Reactivation of the hepatitis B virus (HBV) is a well-described complication among cancer patients undergoing cytotoxic chemotherapy. Mutations in the preC/C and the preC promoter regions of HBV have been reported in some patients who developed this condition. A G-to-A mutation at nt 1896 in the preC/C region (HBeAg negative/ anti-HBe positive) has been associated with more severe liver disease than that caused by wild type virus. In addition, it has been suggested that patients with these mutations may be more likely to reactivate than those with the wild type virus. Whether or not such mutations were present before the commencement of or developed during the course of cytotoxic chemotherapy is not known. In this study, 28 cancer patients (consisting of 14 consecutive patients who developed HBV reactivation and another 14 who had no reactivation during cytotoxic chemotherapy) are reported. The objectives were firstly, to determine the prechemotherapy HBeAg status and nucleotide sequences of the preC/C and preC promoter regions of HBV in order to determine if these parameters affected the rate of reactivation, and secondly, for those who developed reactivation, to determine whether the mutations were present before chemotherapy or developed during, possibly as a result of, cytotoxic chemotherapy. HBV DNA was amplified by PCR and nucleotide sequencing performed on samples taken prior to chemotherapy and at the time of reactivation. Results revealed that 16 of the 28 patients were HBeAg negative/anti-HBe positive. Of these 16, four (57%) of the seven patients who had nt 1896 mutation, but only one (17%) of the six who had the wild type HBV genome, developed reactivation. Three had no detectable HBV DNA. In the majority of cases, the type of virus, i.e. wild/mutant at preC/C, that was detected during the reactivation was identical to that detected in the pretreatment samples. With respect to the preC promoter region, the two commonest mutations detected were at nt 1762 (A to T) and nt 1764 (G to A). When this region was translated into amino acid sequences, stop codons leading to truncated X protein at carboxyl terminus were found in four patients, three of whom developed HBV reactivation. We conclude that chronic HBV carriers who are HBeAg negative/anti-HBe positive with nt 1896 mutation (G to A) may be more likely to develop HBV reactivation during cytotoxic chemotherapy than those with the wild type virus. Cytotoxic chemotherapy does not appear to select out mutant HBV, or to be consistently mutagenic in patients who develop HBV reactivation. The occurrence of stop codons in the amino acid sequences of the X protein in three patients who developed HBV reactivation, including one who was detected only at the time of reactivation, is of particular interest, as such mutant viruses remain replication competent.

Adult↗
PubMed2000

Longitudinal colour doppler study of superficial lymph nodes in non-Hodgkin's lymphoma patients on chemotherapy.

AIMS/METHODS: A longitudinal study of 22 malignant lymph nodes by colour Doppler (CD) and/or colour power (CP) ultrasonography was undertaken in 12 non-Hodgkin's lymphoma patients to delineate changes in vascularity, and correlate this response with clinical outcome. RESULTS: Reduced vascularity in response to chemotherapy was shown to be a positive prognostic sign. CONCLUSIONS: More persistent nodal vascularity may signify a less favourable prognosis.

Adult↗
PubMed2000

Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: precore/core mutations may play an important role.

Reactivation of the hepatitis B virus (HBV) is a rare, but well described complication of cytotoxic chemotherapy that may result in hepatic failure. Patients who are chronic carriers of the HBV and who have a G to A mutation at nucleotide 1896 in the precore region may develop more severe liver disease, possibly because of rapid selection and enhanced replication ability of the mutant strain. Such mutant viruses have been implicated occasionally in chemotherapy induced reactivation of hepatitis B virus. In this report, 5 patients with solid tumours were identified to have developed severe hepatitis B virus related liver disease during treatment with cytotoxic agents (with dexamethasone as anti-emetic). All had clinical and serological evidence of reactivation of the HBV. Three patients developed icteric hepatitis; 2 fully recovered, and 1 had died from progressive metastatic disease while recovering from the reactivation. The other two died from progressive liver failure. Direct sequencing of the polymerase chain reaction (PCR) products of the precore (preC) and precore promoter region of the HBV-DNA was carried out on the patients' serum samples taken during the episode of reactivation. In each case, similar mutations (G to A) in nucleotide 1896 of the preC region were found, together with additional mutations in the preC promoter. The present findings suggest that reactivation involving a mutant hepatitis B virus may lead to liver failure, which is possibly more severe than that caused by wild type HBV, and can be triggered by cytotoxic chemotherapy, or the administration of corticosteroids. In Eastern Asia the HBV carriage rate in adults is high. HBV reactivation and severe liver disease during cytotoxic treatment may become a serious and common problem in this region as cytotoxic chemotherapy is more widely used. Patients should be screened routinely for HBsAg in endemic areas of chronic hepatitis B virus infection prior to receiving cytotoxic treatment. The possibility of HBV reactivation should be considered in patients developing liver dysfunction. Patients who are HBeAg negative/Anti-HBe positive, and are suspected to be having an HBV reactivation, should have HBV-DNA levels measured for confirmation as they may carry a mutant HBV.

Adult↗
PubMed2000

Frequent p15 promoter methylation in tumor and peripheral blood from hepatocellular carcinoma patients.

We prospectively analyzed p15 methylation patterns in 25 surgically resected tumors and 130 plasma, serum, and buffy coat samples from hepatocellular carcinoma (HCC) patients, controls with chronic hepatitis/cirrhosis, and healthy subjects. Using methylation-specific PCR, we demonstrated for the first time p15 promoter methylation in 64% of tumors and 25% (4 of 16) of patients' plasma and serum samples. Concurrent p15 and p16 methylation was shown in 48% of tumors, and p15/p16 methylation was detected in the plasma/serum of 92% (11 of 12) of patients. Of note, 75% of 12 patients with concurrent tumor methylation developed clinical metastasis/recurrence (P = 0.027). In buffy coat samples, p15 methylation was detected in all eight patients with tumor p15 methylation, suggesting the presence of circulating tumor cells. None of the control samples were methylation positive. Our data underscore the important role(s) of p15 and p16 methylation in hepatocarcinogenesis and tumor progression. Among 92% (23 of 25) of patients with tumor p15/p16 methylation, circulating tumor DNA and HCC cells were detected in the peripheral blood of 87% (20 of 23) of patients. The combination of these epigenetic markers may prove valuable for noninvasive HCC diagnosis and disease monitoring.

Blotting, Southern↗
PubMed1999

Adjuvant intra-arterial iodine-131-labelled lipiodol for resectable hepatocellular carcinoma: a prospective randomised trial.

BACKGROUND: Resection of hepatocellular carcinoma is potentially curative, but local recurrence is common. In this prospective randomised trial, we aimed to find out if one dose of postoperative adjuvant intra-arterial iodine-131-labelled lipiodol could reduce the rate of local recurrence and increase disease-free and overall survival. METHODS: Patients who underwent curative resection for hepatocellular carcinoma and recovered within 6 weeks were randomly assigned one 1850 MBq dose of 131I-lipiodol or no further treatment (controls). We compared rates of recurrence and disease-free and overall survival (the primary endpoints) between the two groups by intention to treat. We planned an interim analysis when 30 patients (both groups together) had been followed up for a median of 2 years, with the intention of stopping early if the between-group difference in disease-free survival was significant (p=0.029). FINDINGS: Between April, 1992, and August, 1997, we recruited 43 patients: 21 received intra-arterial 131I-lipiodol and 22 received no adjuvant treatment. During a median follow-up of 34.6 (range 14.1-69.7) months, there were six (28.5%) recurrences among the 21 patients in the adjuvant treatment, compared with 13 (59%) in the controls (p=0.04). Median disease-free survival in the treatment and control groups was 57.2 (0.4-69.7) and 13.6 (2.1-68.3) months, respectively (p=0.037). 3-year overall survival in the treatment and control groups was 86.4% and 46.3%, respectively (p=0.039). The interim analysis showed a significant increase in disease-free survival in the treatment group compared with the controls (p=0.01), so we closed the trial early. 131I-lipiodol had no significant toxic effects. INTERPRETATION: In patients with hepatocellular carcinoma, one 1850 MBq dose of intra-arterial 131I-lipiodol given after curative resection significantly decreases the rate of recurrence and increases disease-free and overall survival.

Adolescent↗