Straight hair associated with interferon-alfa plus ribavirin in hepatitis C infection.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C Chapoutot.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Liver iron deposits are frequent in viral C cirrhotic patients but their role is not well defined. AIMS: To investigate the effect of liver iron excess on the prevalence of hepatocellular carcinoma (HCC) in patients with viral C cirrhosis. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.
BACKGROUND/AIMS: Bacterial infections, specially Staphylococcus aureus (S. aureus) septicemia, remain a leading cause of death following liver transplantation. It has been demonstrated that nasal carriage of S. aureus is associated with invasive infections in patients undergoing hemodialysis and could be decreased by use of antibiotic nasal ointment. However, in cirrhotic patients, the frequency of nasal carriage is unknown. The aims of this study were to determine the prevalence of S. aureus nasal carriage in cirrhotic patients and to assess nosocomial contamination. METHODS: One hundred and four patients were included in a prospective study, 52 cirrhotic and 52 control (hospitalized patients without cirrhosis or disease which might increase the rate of nasal carriage of S. aureus). On admission and after a few days of hospitalization, nasal specimens from each anterior naris were obtained for culture. S. aureus was identified by the gram strain, positive catalase and coagulase reactions; antibiotic susceptibility was determined using a disk-diffusion test. RESULTS: Both groups were similar with regard to age and sex. The prevalence of nasal colonization on hospital admission was 56% in cirrhotic patients and 13% in control patients (p = 0.001). After an average of 4 days, 42% of cirrhotics and 8% of control patients were colonized (p = 0.001), without any nosocomial contamination. Three strains out of 29 were oxacillin-resistant in cirrhotic patients, and none in controls (p>0.05). There was no statistical difference in carriage rate according to sex, age, cause of cirrhosis and Child-Pugh score. Previous hospitalization (OR, 6.3; 95% CI, 2.3 to 19.9; p = 0.0006) and cirrhosis (OR, 4.4; 95% CI, 1.5 to 13.4; p = 0.0048) were independent predictors of colonization. CONCLUSION: Cirrhotic patients had a higher S. aureus nasal carriage rate than control subjects. Previous hospitalization and cirrhosis diagnosis were correlated to nasal colonization. Further studies are necessary to determine if nasal decontamination could reduce S. aureus infections after liver transplantation.
OBJECTIVES: To study the frequency of tumor seeding after percutaneous biopsy of hepatocellular carcinoma and to evaluate the impact on long-term survival. METHODS: Records of 150 patients with cirrhosis who underwent ultrasound-guided aspiration biopsy for hepatocellular carcinoma between 1989 and 1996 were reviewed in June 1998. Liver transplantation was performed in 7 patients. One to three needle passes were performed with 18 to 20 gauge needles. Follow-up included regular clinical examinations and ultrasonography or computerized tomography. RESULTS: Four cases (2.66%) of subcutaneous metastasis were noted at the needle insertion site; none in transplanted patients. All patients had viral cirrhosis, Okuda class I. Nodules were detected 4, 12, 22 and 24 months after biopsy. The second patient is alive 24 months after tumor seeding. For other patients, survival time was 4, 24 and 60 months respectively, without local tumor extension after surgical resection or radiotherapy. During a mean 11.8 months of follow-up, 127 patients died without tumor seeding. Eleven patients are still being followed and have no signs of needle tract implantation of hepatocellular carcinoma (mean follow-up 34.7 months). CONCLUSION: The prevalence of tumoral seeding after percutaneous biopsy of hepatocellular carcinoma was 2.66%, which is higher than in previous studies. After liver transplantation, no evidence of needle tract seeding was identified. Survival did not seem to be influenced by local evolution.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The incidence of listeriosis is increased in immunosuppressed patients. We report a case of spontaneous bacterial peritonitis with bacteraemia caused by Listeria monocytogenes in a 47-year old woman with liver transplantation. Complete recovery was achieved after amoxicillin and amikacin therapy. High doses of corticosteroids and OKT3 monoclonal therapy may have favoured the occurrence of infection. In liver transplant recipients, regular stool screening could be proposed, and trimethoprim-sulfamethoxazole antibioprophylaxy could be used when Listeria monocytogenes is isolated in stool culture or immunosuppressive therapy is increased.
Explore the source record for details and available documents.
Secondary sclerosing cholangitis leads to slow and often irreversible destruction of the walls of both intra- and extrahepatic bile ducts. As for primary sclerosing cholangitis, clinical signs and laboratory findings reveal cholestasis. The diagnosis is confirmed by retrograde endoscopic cholangiography which shows narrowed bile ducts and rarefied ramifications of the intra-hepatic ductal system. Several causes have been identified including infectious causes with or without a relationship to bile duct obstruction and human immunodeficiency virus infection as well as ischaemic related causes after chemotherapy, arterial embolization or liver transplantation. Other causes include chemical aggression after treatment for hydatic cysts and post-surgical complications due to a damaged bile tract. Treatment is difficult and often dependent on the cause.