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T Coste

Publications and source records attributed to T Coste.

At least 19 recordsLinked to original sources
PubMed2006

Decentralising tuberculosis case management in two districts of Burkina Faso.

SETTING: In West Africa, national tuberculosis programmes (NTPs) face many problems due to the low performance of health care delivery systems and patients' social and cultural environment. OBJECTIVE: To improve the case management of TB in Burkina Faso. DESIGN: Using the operational research process as a tool, TB case management was decentralised from the district hospital to eight primary health care centres in 2003. RESULTS: Twelve months after decentralisation, the quality of case detection remained satisfactory. The delay between the identification of TB suspects with chronic cough and the confirmation of TB was reduced from 13 to 6 days. The detection rate of TB suspects during the study (30%) was twice as high as for 2001 and 2002 (15%). However, the detection rate for smear-positive TB cases decreased from 32.3% in 2001 and 2002 to 6.5% during the year of the study. CONCLUSION: Sufficient time and commitment are essential to obtain a case management system that is decentralised and effective. Efforts therefore need to continue to obtain more information and better results.

Burkina Faso↗
PubMed2002

Genetic and environmental regulation of Na/K adenosine triphosphatase activity in diabetic patients.

Even if the pathogenesis of diabetic neuropathy is incompletely understood, an impaired Na/K adenosine triphosphatase (ATPase) activity has been involved in this pathogenesis. We previously showed that a restriction fragment length polymorphism (RFLP) of the ATP1-A1 gene encoding for the Na/K ATPase's alpha 1 isoform is associated with a low Na/K ATPase activity in the red blood cells (RBCs) of type 1 diabetic patients. We thus suggested that the presence of the variant of the ATP1A1 gene is a predisposing factor for diabetic neuropathy, with a 6.5% relative risk. Furthermore, there is experimental evidence showing that lack of C-peptide impairs Na/K ATPase activity, and that this activity is positively correlated with C-peptide level. The aim of this study was to evaluate the respective influence of genetic (ATP1-A1 polymorphism) and environmental (lack of C-peptide) factors on RBC's Na/K ATPase activity. Healthy and diabetic European and North African subjects were studied. North Africans were studied because there is a high prevalence and severity of neuropathy in this diabetic population, and ethnic differences in RBC's Na/K ATPase activity are described. In Europeans, Na/K ATPase activity was significantly lower in type 1 (285 +/- 8 nmol Pi/mg protein/h) than in type 2 diabetic patients (335 +/- 13 nmol Pi/mg protein/h) or healthy subjects (395 +/- 9 nmol Pi/mg protein/h). Among type 2 diabetic patients, there was a significant correlation between RBC's Na/K ATPase activity and fasting plasma C-peptide level (r = 0.32, P <.05). In North Africans, we confirm the ethnic RBC's Na/K ATPase activity decrease in healthy subjects (296 +/- 26 v 395 +/- 9 nmol Pi/mg protein/h, r < 0.05), as well as in type 1 diabetic patients (246 +/- 20 v 285 +/- 8 nmol Pi/mg protein/h; P <.05). However, there is no relationship between the ATP1A1 gene polymorphism and Na/K ATPase activity. ATP1A1 gene polymorphism could not explain the ethnic difference. We previously showed that Na/K ATPase activity is higher in type 1 diabetic patients without the restriction site on ATP1A1 than in those heterozygous for the restriction site. This fact was not observed in healthy subjects. In type 2 diabetic patients, association between ATP1A1 gene polymorphism and decreased enzyme activity was found only in patients with a low C-peptide level. Therefore, the ATP1-A1 gene polymorphism influences Na/K ATPase activity only in case of complete or partial C-peptide deficiency, as observed in type 1 and some type 2 diabetic patients, without any correlation with hemoglobin A1c (HbA1c). Correlation observed between C-peptide levels and RBC's Na/K ATPase suggests that the deleterious effect of C peptide deficiency on Na/K ATPase activity is worse in the presence of the restriction site. This may explain the high relative risk of developing the neuropathy observed in type 1 diabetic patients bearing the variant allele.

Adult↗
PubMed2001

APACC, a French prospective study on aspirin efficacy in reducing colorectal adenoma recurrence: design and baseline findings.

UNLABELLED: Colorectal cancer is the second most frequent cause of death from cancer in western countries. Many lines of evidence suggest that non-steroidal anti-inflammatory drugs (NSAIDs) may offer chemoprevention against colorectal cancer. A multicentre, double-blind, randomized, controlled trial is underway to determine the efficacy of regular aspirin intake (160 or 300 mg/day) in reducing colorectal adenoma recurrence. We now report the baseline characteristics of subjects enrolled into the trial. RESULTS: A total of 618 polyps were excised from 274 patients at the baseline colonoscopy. Men had on average (+/-SD) 2.5 +/- 1.8 polyps per subject and women had 1.7 +/- 1.2. Ninety-one (33.7%) had three or more adenomas and 183 (67.8%) had more than one adenoma measuring 10 mm or more in diameter. The mean (+/-SD) age of the subjects was 57.7 (+/- 9.4) years. Sixty-seven (24.9%) reported that they had previously had adenoma(s), 95 (35.2%) reported a family history of colorectal cancer and 41 (15.2%) a family history of colorectal adenomas. PERSPECTIVE: All subjects will undergo a one-year clearance colonoscopy by February 2001. Clinical, molecular biological and dietary data will enable us to investigate other factors influencing the recurrence of adenomas in this group of high-risk subjects.

Adenoma↗
PubMed2001

Na,K-atpase alterations in diabetic rats: relationship with lipid metabolism and nerve physiological parameters.

Type 1 diabetes induces several metabolic and biochemical disturbances which result in the alteration ofNa,K-ATPase, an enzyme implicated in the physiopathology of neuropathy Several fatty acid supplementations lessen this alteration. The aims of this study were to determine the possible relationships between Na,K-ATPase activity in nerves and red blood cells (RBCs) and, on one hand, the fatty acid alterations induced by diabetes in these tissues and plasma and on the other, on nerve physiological parameters. Two groups of rats, control and diabetic (n = 15), were sacrified 8 weeks after induction of diabetes with streptozotocin. Nerve conduction velocity (NCV), nerve blood flow (NBF), Na,K-ATPase activity and membrane fatty acid composition of sciatic nerves, red blood cells (RBCs) and plasma were measured. NCV, NBF and Na,K-ATPase activity in RBCs and in sciatic nerves were significantly decreased in diabetic rats. We revealed a positive correlation between Na,K-ATPase activity in sciatic nerves and both NBF and NCV and between Na,K-ATPase activity in RBCs and NBF and the same activity in sciatic nerve. Diabetes induced major changes in plasma fatty acids and RBC membranes and less important changes in sciatic nerve membranes. Na,K-ATPase activity correlated negatively with C20: 4 (n-6) and C22: 4 (n-6) levels in nerves and with C18: 2 (n-6) levels in RBCs. During diabetes, changes in the membrane fatty acid composition suggest the existence of a tissue-specific regulation, and the decrease in Na,K-ATPase activity correlates with the alteration in the level of specific fatty acids in RBCs and sciatic nerves. Modifications in the lipidic environment of Na,K-ATPase would be involved in the alteration of its activity. Na,K-ATPase activity seems to be implicated in the decrease of both NCV and NBF during diabetes.

Animals↗
PubMed2000

The effects ex vivo and in vitro of insulin and C-peptide on Na/K adenosine triphosphatase activity in red blood cell membranes of type 1 diabetic patients.

The decrease in Na/K adenosine triphosphatase (ATPase) activity observed in several tissues of type 1 diabetic patients is thought to play a role in the development of long-term complications. Infusion of insulin may restore this enzyme activity in red blood cells (RBCs), and recent arguments have been developed for a similar role of C-peptide. The aims of this study were to determine whether insulin acts directly on the RBC enzyme and to evaluate the effect of C-peptide on Na/K ATPase activity. Thirty-nine C-peptide-negative type 1 diabetic patients were studied (blood glucose, 11.2 +/- 1.49 mmol/L; hemoglobin A1c [HbA1c], 8.9% +/- 0.1%, mean +/- SEM). Blood samples were obtained in the morning, before breakfast and insulin injection. Intact and living RBCs were resuspended in their own plasma and incubated with or without insulin (50 microU/mL) or C-peptide (6 nmol/L). Ex vivo by microcalorimetry, the heat produced after 1 hour by the enzyme-induced hydrolysis of adenosine triphosphate (ATP), was measured in a thermostated microcalorimeter at 37 degrees C. The results showed that Na/K ATPase activity was significantly increased by insulin (12.4 +/- 0.5 v 15.4 +/- 0.9 mW/L RBCs, P < .05, n = 23) but not by C-peptide (11.9 +/- 0.7 v 12.9 +/- 0.9 mW/L RBCs, NS, P = .26, n = 12). In another experiment, RBC suspensions were incubated at 37 degrees C in a water bath with or without insulin (50 microU/mL) or C-peptide (6 nmol/L) for 10 minutes. RBC membranes were isolated and Na/K ATPase activity was assessed by measuring inorganic phosphate release at saturating concentrations of all substrates. The results showed that insulin and C-peptide significantly increased RBC Na/K ATPase activity (342 +/- 25, P < .005 and 363 +/- 30, P < .005, respectively v255 +/- 22 nmol Pi x mg protein(-1) x h(-1), n = 14). We conclude that insulin and C-peptide act directly on RBC Na/K ATPase, thus restoring this activity in type 1 diabetic patients. The stimulatory effect of C-peptide observed in vitro on RBC Na/K ATPase activity confirms that C-peptide plays a physiological role.

Adult↗
PubMed2000

[Hepatitis C virus contamination of endoscopes and biopsy forceps].

BACKGROUND: Procedures such as digestive endoscopy may explain some unclear contaminations by HCV. AIMS: The aims of this study were to detect HCV genome on endoscopes and biopsy-forceps used in patients with known chronic HCV infection and to determine its presence in their gastric juice and saliva. METHODS: A gastroscopy with antral biopsies was performed in 48 patients with non-treated replicative chronic hepatitis C. Samples were obtained after pushing 10 mL of sterile water through the biopsy-suction channel and after immersing the brush used to clean this channel. The biopsy-forceps were also immersed and their tips brushed in 10 mL of sterile water. This sampling technique was repeated three times: immediately after the endoscopic procedure (T0), after washing with a detergent (T1) and after immersion for 20 minutes in a 2% glutaraldehyde solution (T2). The HCV genome was detected by polymerase chain reaction (PCR, Amplicor - Roche Diagnostics Systems). For the last 15 patients, samples of gastric juice and saliva were obtained before antral biopsies and used to detect HCV genome. RESULTS: HCV genome was detected in the biopsy-suction channel in 13 cases (27%) at T0 and in one case (2%) at T1. It was undetectable after completion of the disinfection procedure (T2). Three biopsy-forceps (6%) were PCR positive immediately after the endoscopy but none at T1 and T2. HCV genome was found in the gastric juice in three cases. In all of them, it was also found at T0 in the biopsy-suction channel but not on the biopsy-forceps. When saliva contained HCV genome (4 cases), it was present in the biopsy-suction channel in only one case. In this case, the gastric juice was also PCR positive. CONCLUSIONS: HCV genome is detected in 27% of cases in the biopsy-suction channel after an endoscopic procedure performed on patients with chronic HCV infection. The biopsy-forceps are PCR positive in 6% of cases. The infected gastric juice may play a role in the contamination of the endoscopes. The complete disinfection procedure seems effective to eliminate HCV.

Biopsy↗
PubMed1999

Role of transforming growth factor beta type II receptor in hepatic fibrosis: studies of human chronic hepatitis C and experimental fibrosis in rats.

Transforming growth factor beta (TGF-beta) is an antiproliferative and profibrogenic cytokine that signals through a receptor consisting of type I and type II (TbetaRII) components. We have examined changes in the expression of TbetaRII during liver injury, correlating this with the antiproliferative and profibrogenic effects of TGF-beta1. The experimental material consisted of biopsy samples of liver from patients with chronic hepatitis C and rats in which liver injury was induced by ligation of the common bile duct. Stellate cells were isolated from normal or injured rat liver and studied as fresh isolates. In the biopsy samples from patients, mRNAs for TGF-beta1 and TbetaRII were measured using competitive reverse polymerase chain reaction (PCR). TGF-beta1 mRNA was significantly increased in chronic hepatitis C relative to healthy controls (P =.03), while TbetaRII mRNA was significantly decreased (P =.001). In the rat model, 5 days after bile duct ligation during increased TGF-beta expression, mRNA for TbetaRII in stellate cells was 40% of that in stellate cells from control livers. This coincided with increased expression of collagen I mRNA and proliferation of stellate cells. The reciprocal relationship between expression of TGF-beta and the type II receptor suggest ligand-mediated receptor down-regulation. The decreased level of TbetaRII appears to be permissive for proliferation while supporting ongoing fibrogenesis. We conclude that modulation of this receptor may be critical to the progression of wound repair in liver.

Adult↗
PubMed1999

Beneficial effects of gamma linolenic acid supplementation on nerve conduction velocity, Na+, K+ ATPase activity, and membrane fatty acid composition in sciatic nerve of diabetic rats.

Metabolic and vascular abnormalities are implicated in the pathogenesis of diabetic neuropathy. Two principal metabolic defects are altered lipid metabolism resulting from the impairment of delta-6-desaturase, which converts linoleic acid (LA) into gamma linolenic acid (GLA), and reduced nerve Na+, K+ ATPase activity. This reduction may be caused by a lack of incorporation of (n-6) fatty acids in membrane phospholipids. Because this ubiquitous enzyme maintains the membrane electrical potential and allows repolarization, disturbances in its activity can alter the process of nerve conduction velocity (NCV). We studied the effects of supplementation with GLA (260 mg per day) on NCV, fatty acid phospholipid composition, and Na+, K+ ATPase activity in streptozotocin-diabetic rats. Six groups of 10 rats were studied. Two groups served as controls supplemented with GLA or sunflower oil (GLA free). Two groups with different durations of diabetes were studied: 6 weeks with no supplementation and 12 weeks supplemented with sunflower oil. To test the ability of GLA to prevent or reverse the effects of diabetes, two groups of diabetic rats were supplemented with GLA, one group for 12 weeks and one group for 6 weeks, starting 6 weeks after diabetes induction. Diabetes resulted in a 25% decrease in NCV (P < 0.0001), a 45% decrease in Na+, K+ ATPase activity (P < 0.0001), and an abnormal phospholipid fatty acid composition. GLA restored NCV both in the prevention and reversal studies and partially restored Na+, K+ ATPase activity in the preventive treatment group (P < 0.0001). These effects were accompanied by a modification of phospholipid fatty acid composition in nerve membranes. Overall, the results suggest that membrane fatty acid composition plays a direct role in NCV and confirm the beneficial effect of GLA supplementation in diabetic neuropathy.

Journal Article↗
PubMed1999

Fish oil supplementation prevents diabetes-induced nerve conduction velocity and neuroanatomical changes in rats.

Diabetic neuropathy has been associated with a decrease in nerve conduction velocity, Na,K-ATPase activity and characteristic histological damage of the sciatic nerve. The aim of this study was to evaluate the potential effect of a dietary supplementation with fish oil [(n-3) fatty acids] on the sciatic nerve of diabetic rats. Diabetes was induced by intravenous streptozotocin injection. Diabetic animals (n = 20) were fed a nonpurified diet supplemented with either olive oil (DO) or fish oil (DM), and control animals (n = 10) were fed a nonpurified diet supplemented with olive oil at a daily dose of 0.5 g/kg by gavage for 8 wk. Nerves were characterized by their conduction velocity, morphometric analysis and membrane Na, K-ATPase activity. Nerve conduction velocity, as well as Na,K-ATPase activity, was improved by fish oil treatment. A correlation was found between these two variables (R = 0.999, P < 0.05). Moreover, a preventive effect of fish oil was observed on nerve histological damage [endoneurial edema, axonal degeneration (by 10-15%) with demyelination]. Moreover, the normal bimodal distribution of the internal diameter of myelinated fibers was absent in the DO group and was restored in the DM group. These data suggest that fish oil therapy may be effective in the prevention of diabetic neuropathy.

Animals↗
PubMed1999

Relationship between neuropathy, hypertension and red blood cell Na/K ATPase in patients with insulin-dependent diabetes mellitus.

Hypertension has been proposed as an independent risk factor for diabetic neuropathy. In insulin-dependent diabetic (IDDM) patients suffering from neuropathy, red blood cell (RBC) Na/K ATPase is decreased. Such a decrease might be involved in the physiopathology of hypertension and therefore be the link between hypertension and neuropathy. To confirm this hypothesis, we studied 104 IDDM patients with a long duration of disease by looking at the association between neuropathy and hypertension and by comparing RBC Na/K ATPase activity in subgroups. The independent risk factors associated with neuropathy were hypertension, triglyceride level, diabetes duration and low RBC Na/K ATPase activity. Contrary to our expectations, Na/K ATPase was not decreased in hypertensive patients (294 +/- 16 nmol Pi/mg prot/h vs 303 +/- 9), but those treated with angiotensin converting enzyme (ACE) inhibitor had higher RBC Na/K ATPase activity than those treated with calcium blockers (355 +/- 15 nmol Pi/mg prot/h vs 216 +/- 10). These results confirm the association between neuropathy and hypertension, on the one hand, and neuropathy and decreased Na/K ATPase, on the other, and show that hypertension in IDDM patients was not associated with decreased RBC Na/K ATPase. Moreover, ACE inhibitor treatment in IDDM patients, whether hypertensive or not, was associated with higher levels of RBC Na/K ATPase, which could account for its beneficial effect on diabetic neuropathy.

Adolescent↗
PubMed1998

Hepatitis C virus genotypes implicated in mixed cryoglobulinemia.

Recent reports suggest that hepatitis C virus (HCV) might be a causative agent of mixed cryoglobulinemia. To determine whether the HCV genotype is a factor implicated in the onset of cryoglobulinemia, genotyping by direct sequencing of polymerase chain reaction products of the 5' non coding region was carried out among 45 HCV-infected patients. Genotypes 1 and 2 were found more prevalent in symptomatic cryoglobulinemia patients. Due to the presence of genotypes 4 and 5 found in this panel of French patients (9.3%), HCV genotyping based on sequence determination is recommended.

Case-Control Studies↗
PubMed1998

Erythrocyte Na/K ATPase activity and diabetes: relationship with C-peptide level.

Erythrocyte Na/K ATPase activity is decreased in Type I diabetic patients; for Type II diabetic patients, literature data are controversial. Therefore, we have compared this enzymatic activity in 81 patients with Type I diabetes mellitus, 87 with Type II diabetes mellitus and 75 control subjects. Mean erythrocyte Na/K ATPase activity was lower in the Type I diabetic patients (285 +/- 8 nmol Pi x mg protein(-1) x h(-1)) than in the control subjects (395 +/- 9 nmol Pi x mg protein(-1) x h(-1)) whereas that of the Type II diabetic patients did not differ from that of control subjects. Sex, age, body mass index, and HbA1c levels did not influence erythrocyte Na/K ATPase activity. The 25 Type II diabetic patients treated with insulin, however, had lower Na/K ATPase activity than the 62 on oral treatment (264 +/- 18 vs 364 +/- 16 nmol Pi x mg protein(-1) x h(-1), p < 0.001) but similar to that of Type I diabetic patients. Among the Type II diabetic patients, stepwise regression analysis showed that fasting C-peptide level was the only factor independently correlated with Na/K ATPase activity; it explained 23% of its variance. In fact, in the insulin-treated patients, those with almost total endogenous insulin deficiency (C-peptide < 0.2 nmol x l(-1)) had the lower Na/K ATPase activity (181 +/- 21 vs 334 +/- 17 nmol Pi x mg protein(-1) x h(-1), p < 0.0001). The biological effects of treatment with C-peptide have recently led to the suggestion that this peptide could have a physiological role through the same signalling pathway as insulin, involving G-protein and calcium phosphatase and thus restoring Na/K ATPase activity. The relationship we describe between endogenous C-peptide and this activity is a strong argument for this physiological role.

Adult↗
PubMed1998

Alterations of Na,K-ATPase isoenzymes in the rat diabetic neuropathy: protective effect of dietary supplementation with n-3 fatty acids.

Diabetic neuropathy is a degenerative complication of diabetes accompanied by an alteration of nerve conduction velocity (NCV) and Na,K-ATPase activity. The present study in rats was designed first to measure diabetes-induced abnormalities in Na,K-ATPase activity, isoenzyme expression, fatty acid content in sciatic nerve membranes, and NCV and second to assess the preventive ability of a fish oil-rich diet (rich in n-3 fatty acids) on these abnormalities. Diabetes was induced by intravenous streptozotocin injection. Diabetic animals (D) and nondiabetic control animals (C) were fed the standard rat chow either without supplementation or supplemented with either fish oil (DM, CM) or olive oil (DO, CO) at a daily dose of 0.5 g/kg by gavage during 8 weeks. Analysis of the fatty acid composition of purified sciatic nerve membranes from diabetic animals showed a decreased incorporation of C16:1(n-7) fatty acids and arachidonic acids. Fish oil supplementation changed the fatty acid content of sciatic nerve membranes, decreasing C18:2(n-6) fatty acids and preventing the decreases of arachidonic acids and C18:1(n-9) fatty acids. Protein expression of Na,K-ATPase alpha subunits, Na,K-ATPase activity, and ouabain affinity were assayed in purified sciatic nerve membranes from CO, DO, and DM. Na,K-ATPase activity was significantly lower in sciatic nerve membranes of diabetic rats and significantly restored in diabetic animals that received fish oil supplementation. Diabetes induced a specific decrease of alpha1- and alpha3-isoform activity and protein expression in sciatic nerve membranes. Fish oil supplementation restored partial activity and expression to varying degrees depending on the isoenzyme. These effects were associated with a significant beneficial effect on NCV. This study indicates that fish oil has beneficial effects on diabetes-induced alterations in sciatic nerve Na,K-ATPase activity and function.

Animals↗
PubMed1998

[Effectiveness and safety of lansoprazole in the treatment of Zollinger-Ellison syndrome. First six months of treatment].

OBJECTIVES: The aim of this prospective study was to confirm the efficacy and safety of lansoprazole in patients with Zollinger-Ellison syndrome (ZES). METHODS: Fourteen patients (5 W, 9 M) with ZES, age (mean +/- SD) 55.5 +/- 12.8 years, were included in the study. STUDY DESIGN: initially and at 1, 3 and 6 months thereafter the following items were assessed: clinical signs, fasting serum gastrin (FSG), basal acid output (BAO) before next dose of lansoprazole. BAO < 10 mmol H+/h was considered as efficient. Initially and at 6 months, laboratory tests (hematology, liver, renal and hormonal), endoscopy and histological enterochromaffin-like cell and gastrin cell density assessments were performed. Lansoprazole initial dose was adjusted according to clinical symptoms and secretory studies. RESULTS: At 6 months, lansoprazole doses of 60, 90, 120 and 180 mg/d maintained BAO < 10 mmol H+/h in 9, 2, 1 and 1 patient, respectively. No significant changes in FSG, endocrine cells densities and biological parameters were noted during treatment. Neither adverse events nor carcinoid tumors were observed. We conclude that lansoprazole is efficient and well tolerated in patients with ZES.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Circulating albumin messenger RNA in hepatocellular carcinoma: results of a multicenter prospective study.

The presence of circulating tumor cells might be an indicator of hematogenous spread of tumor cells leading to extrahepatic metastasis. Messenger RNA (mRNA) expression of human albumin, as a liver specific cell marker, has been proposed for this purpose in hepatocellular carcinoma. We conducted a multicenter prospective study in 101 patients with biopsy-proven hepatocellular carcinoma followed-up every 3 months for 1 year or until death. At entry into the study, albumin mRNA was detected in the blood by reverse transcription-polymerase chain reaction (RT-PCR). At entry into the study, 45% of the patients had a positive albumin mRNA test, 53% a single tumor, 16% a portal or venous hepatic thrombosis, and 16% had proven metastasis. After 1 year, there was no significant difference in survival of patients with positive or negative albumin mRNA at entry (P = .16, log-rank test). When patients with metastasis at entry were excluded, again survival did not differ between the two groups (P = .20). Independent prognostic factors of survival were radical therapeutic procedures, metastasis, number of tumors, Child-Pugh score, and thrombosis, but not the albumin mRNA test. Taking the presence of metastasis as a reference, the specificity of the test was 56%, its sensitivity 50%, and its negative predictive value 85%. The present study shows that circulating albumin mRNA detected by means of RT-PCR fails to provide significant information in the diagnosis and prognosis of hepatocellular carcinoma. Further studies are needed to determine whether the use of specific tumor markers could have clinical relevance in this setting.

Adult↗