Search PubMed⌕ Search

Biomedical subjects

D Guyader

Publications and source records attributed to D Guyader.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Epidemiology of hepatitis C virus infection in 1,304 HCV positive patients: variations according to the origin of transmission and year of diagnosis].

UNLABELLED: The evolution of epidemiological data on hepatitis C virus infection is poorly documented and thus the impact of screening is difficult to evaluate. AIM: To study epidemiological variations based on the origin of transmission and the year of diagnosis of hepatitis C virus infection. METHODS: The files of all 1304 patients seen in the hepatology unit of the Rennes University Hospital were analyzed (retrospectively before and prospectively after October 1995) in relation to epidemiological features. RESULTS: Despite widespread screening which is the source of 60% of the diagnoses, the total number of new cases of hepatitis C infection per year has not increased. Compared to patients diagnosed in the first years following the discovery of the virus, patients recently identified were younger (42 +/- 14 years) and frequently drug addicts (40%). Aminotransaminases were normal in 20% of cases. The frequency of cirrhosis has declined (17%). There has been a decrease in the proportion of patients who undergo liver biopsy (50%) and treatment with interferon (one third of patients). CONCLUSIONS: The impact of screening on the number of newly treated patients seems to be lower than previously predicted.

Adult↗
PubMed1997

Prospective randomized trial of chemoembolization versus intra-arterial injection of 131I-labeled-iodized oil in the treatment of hepatocellular carcinoma.

Intra-arterial injection of radioactive Lipiodol has shown promising results in patients with hepatocellular carcinoma (HCC) and portal obstruction. The aim of this prospective, randomized trial was to compare the efficacy and tolerance of 131I-labeled Lipiodol and chemoembolization for the treatment of patients with HCC. From September 1990 to September 1993, 142 patients (135 men, 7 women; age: 65 +/- 6.6 years) were randomly assigned to treatment groups and given either intra-arterial injections of 131I-labeled Lipiodol (60 mCi; 2.2 GBq) (n = 73) or chemoembolization (70 mg cisplatin) (n = 69). Subsequent injections were given at 2, 5, 8, 12, and 18 months. Tumor response was assessed on the basis of tumor size and serum alpha-fetoprotein levels. Patient tolerance was assessed clinically and angiographically. Survival rate was the main end-point. A total of 129 patients (65 in the 131I-labeled Lipiodol group and 64 in the chemoembolization group) were available for analysis; 13 were excluded, mainly because of portal vein thrombosis. The two groups were comparable. Actuarial survival curves were not significantly different between the two groups. Overall survival rates at 6 months, 1, 2, 3, and 4 years were 69%, 38%, 22%, 14%, and 10%, and 66%, 42%, 22%, 3%, and 0% in the 131I-labeled Lipiodol and chemoembolization groups, respectively. Reduction in tumor size was similar for the two groups, with complete response in 1 and 0 patients and partial response in 15 and 16 patients in the 131I-labeled Lipiodol and chemoembolization groups, respectively. Tolerance was significantly better in the 131I-labeled Lipiodol group both clinically (3 severe side effects vs. 29 in the chemoembolization group; P < .001) and angiographically (1 arterial thrombosis vs. 10 in the chemoembolization group; P < .01). In terms of patient survival and tumor response, radioactive 131I-labeled Lipiodol and chemoembolization were equally effective in the treatment of HCC, but tolerance to 131I-labeled Lipiodol was significantly better.

Aged↗
PubMed1997

Novel orally active iron chelators (3-hydroxypyridin-4-ones) enhance the biliary excretion of plasma non-transferrin-bound iron in rats.

BACKGROUND/AIMS: It is well documented that levels of plasma non-transferrin-bound iron (NTBI), a particularly toxic form of iron, are increased in iron overload disorders. In light of the pathogenetic importance of NTBI in chronic iron overload, we have studied the ability of new orally active iron chelators to promote the biliary excretion of iron originating as plasma 55Fe-NTBI. METHODS: Biliary iron kinetics of plasma 55Fe-labeled NTBI and cumulative recoveries of 55Fe in bile were determined in normal and carbonyl iron-loaded rats receiving a single intragastric dose of iron chelator. These chelators were the novel hydroxypyridin-4-one compounds CP102, CP41, and their respective pro-drugs CP117 and CP165. RESULTS: The cumulative recovery of 55Fe in bile of normal rats was increased by 5.2-, 7.9-, 11.5-, and 9.2-fold with CP102, CP117, CP41 and CP165, respectively. In iron overloaded rats, these compounds increased the cumulative recovery by 28.6-, 48.6-, 72.6-, and 32-fold, respectively. All the chelators had a choleretic effect, were metabolized by the liver as demonstrated by HPLC study of bile, and were not cytotoxic since normal plasma transaminase levels were maintained at the end of the experiments. CONCLUSIONS: These chelators have potential interest for the treatment of iron overload conditions and may offer advantages over simple N-alkyl-hydroxypyridinones such as deferiprone (CP20, L1).

Animals↗
PubMed1995

Interferon and ursodeoxycholic acid combined therapy in the treatment of chronic viral C hepatitis: results from a controlled randomized trial in 80 patients.

Because 70% to 75% of patients with chronic hepatitis C either do not respond to or relapse after interferon (IFN) therapy, and because ursodeoxycholic acid (UDCA) has been shown to reduce aminotransferase levels in patients with chronic hepatitis, we undertook a prospective controlled randomized trial of IFN (group I) versus IFN plus UDCA (group II) in 80 patients with chronic hepatitis C. IFN was administered in both groups for 6 months (3 to 5 million units [MU] three times a week), and in group II UDCA (10 mg/kg/d) was administered with IFN and then alone for 3 additional months. Response to therapy was defined as the normalization of alanine transaminase (ALT) levels. The results showed that 6 months after cessation of IFN, 59% of responders had relapsed in group I but only 27% had relapsed in group II (P = .03). There was no difference between the two groups for the initial (month 6) and the late (months 15 and 18) response rates to IFN. There was no virological effect or significant histological improvement attributable to the addition of UDCA to IFN treatment. In conclusion, the results of this study show that the addition of UDCA to IFN therapy significantly prolongs the period for which serum ALT remain, within the normal range after discontinuation of IFN. Further studies would be required to determine whether UDCA has any potential for long-term amelioration of the histological severity of liver disease caused by hepatitis C virus (HCV) infection, and, therefore, whether it could be advocated as an adjunct to antiviral therapy.

Adult↗
PubMed1994

Serum increase and liver overexpression of carbohydrate 19.9 antigen in patients with genetic haemochromatosis.

CA 19.9 antigen is mainly secreted by biliary and pancreatic duct cells. Its metabolism could be modified in genetic haemochromatosis by iron accumulation within these cells. Therefore, CA 19.9 was assayed in the serum samples of 84 patients with genetic haemochromatosis before and after iron depletion and immunolocalised in the liver of 24 untreated genetic haemochromatosis cases. The study showed that serum CA 19.9 (N < 37 IU/l) was increased (SD) before treatment (41.2 (34)) when compared with after the venesection period (16 (12)), and correlated, before treatment, with the amount of iron excess, transaminases, fibrosis, and biliary iron deposits. Hepatic CA 19.9 was located within the cytoplasm of bile duct and cholangiolar cells. In conclusion, this study shows that a mild, reversible, and non-specific increase in serum CA 19.9 is common in genetic haemochromatosis patients and shows that this increase is related to iron excess, directly or through associated liver damage. The unexplained finding of a mild increase in serum CA 19.9 should lead, in a patient with no diagnosis, to the search for liver iron overload, and, in a patient with untreated genetic haemochromatosis, not to further diagnostic procedures unless this finding persists after completion of the venesection treatment.

Alkaline Phosphatase↗
PubMed1994

Hemochromatosis: diagnosis and quantification of liver iron with gradient-echo MR imaging.

PURPOSE: To assess the role of magnetic resonance (MR) imaging in detection and quantification of liver iron overload. MATERIALS AND METHODS: MR imaging at 0.5 T was prospectively performed on 77 patients (67 with liver iron overload and 10 without) who underwent a liver biopsy with biochemical determination of the liver iron concentration (LIC) (normal, < 36 mumol per gram of liver tissue [dry weight]). Ratios of signal intensities and liver T2 relaxation time were calculated from images obtained with spin-echo and breath-hold gradient-echo (GRE) sequences. RESULTS: Liver-to-tissue signal intensity ratios were better correlated with LIC than T2 relaxation time. Long-echo-time GRE sequences were the most sensitive for detection of slight overload. Thus, high sensitivity (94%) and specificity (90%) were obtained with a liver-to-fat ratio threshold of 1. The quantification of iron with MR imaging was accurate when the LIC was 80-300 mumol/g. For heavy overload, above 300 mumol/g, quantification was impossible owing to complete signal loss. Pancreatic and splenic signal intensity were unchanged in most cases. CONCLUSION: This method, which can be improved by using more sensitive sequences with a high-field-strength system, should be competitive with biopsy for the diagnosis of substantial liver iron overload.

Female↗
PubMed1994

Biliary excretion of plasma non-transferrin-bound iron in rats: pathogenetic importance in iron-overload disorders.

Plasma non-transferrin-bound iron (NTB-iron) is a potentially toxic form of iron, which is efficiently taken up by the normal, as well as the chronically iron-overloaded liver. In fact, NTB-iron may represent the major source of iron gaining access to hepatocytes in the iron-loaded state. We postulated that efficient biliary excretion of this form of iron could protect against iron-related hepatocellular injury. To characterize the biliary excretion of NTB-iron in intact normal and iron-loaded rats, the plasma disappearance and biliary excretion kinetics of plasma 55Fe-labeled NTB-iron were determined. In normal rats, prompt biliary excretion of plasma NTB-iron was evident, with peak radioactivity approximately 10 min after 55Fe injection (4.1% mean recovery at 3 h). In contrast, biliary iron excretion in iron-loaded rats was minimal (0.1%). In normal rats, a marked increase in biliary excretion of plasma NTB-iron was observed after intravenous desferrioxamine (mean recovery 20.9%) and the new oral iron chelator 1,2-dimethyl-3-hydroxypyrid-4-one administered intravenously (mean recovery 16.1%) or orally (11.4%). In iron-loaded rats, the cumulative recoveries of 55Fe in bile achieved by chelators were lower than in controls (7.6, 3.9, and 3.7%, respectively). Collectively, these findings demonstrate that 1) the normal liver rapidly excretes significant amounts of plasma NTB-iron in bile; 2) the iron-loaded liver exhibits a marked decrease in the capacity to excrete plasma NTB-iron into bile; and 3) chelating agents greatly enhance the biliary excretion of plasma NTB-iron, although the response in terms of cumulative recoveries is less pronounced in the iron-loaded state.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗