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ABSTRACT: Liver iron deposits are frequent in viral C cirrhotic patients but their role is not well defined.
To investigate the effect of liver iron excess on the prevalence of hepatocellular carcinoma (HCC) in patients with viral C cirrhosis.
Hepatic iron was evaluated retrospectively using a semiquantitative method in liver biopsies of 104 viral C cirrhotic patients, 48 with HCC and 56 controls (HCC free). Corrected total iron score (0-60) was defined by the sum of three scores: hepatocytic iron score (0-36), sinusoidal iron score (0-12), and portal iron score (0-12), multiplied by 3/3, 2/3, or 1/3 according to the heterogeneous iron localisation in the nodules.
After adjustment for known risk factors for HCC, regression analysis showed that iron deposits (corrected total iron score >0) were more frequent in HCC patients than in controls (odds ratio 4.94; 95% confidence interval 1.59-15. 32; p=0.0056). The median of corrected total iron score was significantly higher in HCC patients than in controls (odds ratio 1. 092; 95% confidence interval 1.01-1.13; p=0.021). This liver iron overload was sinusoidal (odds ratio 5.2; 95% confidence interval 1. 82-15.11; p=0.0022).
Liver iron deposition was more frequent and more important in viral C cirrhotic patients with HCC than in HCC free controls. Liver iron overload seems to contribute to the development of HCC in patients with viral C cirrhosis.
Gut 05/2000; 46(5):711-4. · 10.11 Impact Factor
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ABSTRACT: Antiphospholipid antibodies (aPL) have been detected in various liver diseases, particularly cirrhosis. The role of alcoholic consumption per se has been suggested. The aim of our study was to assess the prevalence of aPL in patients with alcoholic liver disease at various states and to correlate the presence of aPL with both liver injury and alcoholic consumption. Three groups were prospectively included. Group A: 74 controls (age- and sex-matched); group B: 46 patients with alcoholic steatosis; group C: 28 patients with alcoholic cirrhosis. For each patient, lupus anticoagulant, anticardiolipin antibodies and anti-beta2-glycoprotein I antibodies were tested. The prevalence of aPL (presence of at least one positive test) was 5% in group A, 20% in group B and 50% in group C (P < 0.04). No correlation appeared between aPL and Child Pugh score in group C. No correlation was found between the presence of aPL and alcohol intake in patients with either steatosis or cirrhosis. Our study confirms that aPL positivity is more frequently encountered in patients with alcoholic liver disease than in controls. Their prevalence increases with the degree of histological damage but not with the level of alcoholic intake.
Lupus 02/2000; 9(6):451-5. · 2.34 Impact Factor
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ABSTRACT: Increased plasma and CSF concentrations of substances which bind to brain benzodiazepine receptors have previously been reported in cirrhotic patients with hepatic encephalopathy (HE). However, their relationship to previous intake of pharmaceutical benzodiazepines has not been clearly established. In the present study, plasma levels of benzodiazepine receptor ligands (BZRLs) were measured using a sensitive radioreceptor assay in 12 control subjects with no evidence of hepatic, neurological or psychiatric illness, 11 cirrhotic patients without HE, 24 cirrhotic patients with moderate (grade I-II) HE and in 45 cirrhotic patients with severe (grade II-IV) HE. In addition, CSF concentrations of BZRLs were measured in 8 cirrhotic patients with HE and an equal number of age-matched controls. Recent intake (within 10 days) of pharmaceutical benzodiazepines was assessed by detailed review of medical files, and interviews with the patient, at least one family member as well as the pharmacist. Significantly increased plasma concentrations of BZRLs were observed in cirrhotic patients with severe encephalopathy (p < 0.02) compared to controls and to cirrhotic patients without (or with mild) neurological impairment. Increased plasma BZRLs could be accounted for by prior exposure to benzodiazepine medication in all cases. CSF concentrations of BZRLs in cirrhotic patients were not significantly different from control values. These findings do not support a role for "endogenous" benzodiazepines in the pathogenesis of HE in chronic liver disease but suggest that pharmaceutic benzodiazepines administered to cirrhotic patients as sedatives or as part of endoscopic work-up could have contributed to the neurological impairment in some patients.
Metabolic Brain Disease 09/1998; 13(3):201-10. · 2.20 Impact Factor
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ABSTRACT: Although the efficacy of 5-fluorouracil (5-FU) modulated by leucovorin is well established for advanced colorectal cancer, the question of the most effective regimen and optimal dose of leucovorin remains unanswered. This prospective randomized trial compares low-dose (group 1) and high-dose (group 2) leucovorin, combined with the same dose of 5-FU to determine whether high-dose leucovorin was more beneficial than low-dose on overall survival. Inclusion criteria were: unresectable metastatic colorectal carcinoma, with or without evaluable tumor response; a performance status of less than grade 3 (World Health Organization classification); and no previous chemotherapy for metastases. Forty-two patients were randomized in group 1 (leucovorin, 20 mg/m2/day, days 1 through 5) and 41 patients in group 2 (leucovorin, 200 mg/m2/day, days 1-5). All the patients in the two groups received a 1-hour infusion of 400 mg/m2/day 5-FU every 4 weeks. The two groups were matched with no statistically significant differences in gender ratio, site of primary tumor, performance status, and tumor extent. Toxicity in the two regimens was low and not significantly different between the two groups. Overall median survival was 346 days in group 1 and 323 days in group 2 and was not significantly different between the two groups. At 1 year, the test of equivalence was significant (p < 0.01), demonstrating an absence of more than 20% benefit in 1-year survival for the high-dose regimen. The use of high-dose leucovorin combined with 5-FU in the 5-day regimen does not significantly improve overall survival for patients who have metastatic colorectal cancer.
American Journal of Clinical Oncology 07/1998; 21(3):233-6. · 2.01 Impact Factor
