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C Piat

Publications and source records attributed to C Piat.

15 recordsLinked to original sources
PubMed1997

Inhibition of biliary bicarbonate secretion in ethinyl estradiol-induced cholestasis is not associated with impaired activity of the Cl-/HCO-3 exchanger in the rat.

BACKGROUND/AIMS: Bicarbonate is a major component of bile salt independent bile flow, which is impaired in ethinyl estradiol (EE)-cholestasis. To examine this subject in EE-cholestasis, we studied: 1) basal and glucagon-stimulated biliary bicarbonate secretion both in vivo and in the isolated perfused rat liver (IPRL); 2) H+/HCO-3 transport processes in isolated rat hepatocyte couplets. METHODS: Rats received EE (5 mg.kg b.w.-1) for 5 days. Intracellular pH (pHi) was measured (BCECF-AM) using a single-cell microfluorimetric setup. RESULTS: Bile flow was markedly (p < 0.01) decreased in EE-treated rats. Bicarbonate concentration in bile was decreased (p < 0.01) and bicarbonate secretion was 2.5-fold lower in EE-treated animals than in controls, both in bile-fistula rats [19.5 +/- 5.1 (n = 23) vs 54.2 +/- 5.7 (n = 20) nmol.min-1g liver-1; p < 0.01] and in the IPRL [11 +/- 2 (n = 8) vs 24 +/- 3 (n = 8) nmol.min-1.g liver-1; p < 0.01]. In control IPRL, a bile/perfusate gradient for bicarbonate is maintained, while it is lost in EE-treated IPRL because of the lower bicarbonate concentration in bile. Glucagon stimulated bile flow and bicarbonate secretion to a similar extent in EE-treated and control IPRL (+25% vs +23%). Resting pHi of EE-treated hepatocyte couplets was higher in comparison with controls in KRB [7.25 +/- 0.07 (n = 35) vs 7.20 +/- 0.05 (n = 33); p < 0.02] but similar in Hepes [7.08 +/- 0.07 (n = 24) vs 7.05 +/- 0.06 (n = 26)]. Basal activity of the Cl-/HCO-3 exchanger was similar in EE-treated and control hepatocyte couplets [H+ flux = 2.87 +/- 1.12 (n = 18) vs 3.01 +/- 1.23 mM/min (n = 15)] and was stimulated to a similar extent by glucagon. Na+/HCO3-symport activity was increased in EE-treated hepatocyte couplets (p < 0.05) while the Na+/H+ exchanger was unchanged. CONCLUSIONS: Bicarbonate biliary secretion is markedly impaired during EE-cholestasis in association with a marked decrease of bile salt independent bile flow. However, the Cl-/HCO-3 exchanger and its hormonal regulation are normal, indicating that the lower bicarbonate excretion in EE-cholestasis is not due to a compromised activity of this anion exchanger. Since the bile/perfusate gradient for bicarbonate is dissipated in EE-treated IPRL, the impaired bicarbonate excretion could be caused by a reflux of biliary bicarbonate via leaky tight junctions.

Animals↗
PubMed1997

Effects of isosorbide-5-mononitrate compared with propranolol on first bleeding and long-term survival in cirrhosis.

BACKGROUND & AIMS: Isosorbide-5-mononitrate (Is-5-Mn) exerts beneficial hemodynamic effects in portal hypertension, yet the long-term clinical value is uncertain. The aim of this study was to determine the long-term effects of Is-5-Mn vs. propranolol (Pro) on first bleeding, complications, and death in cirrhosis. METHODS: One hundred eighteen patients included in a previously published randomized trial comparing Is-5-Mn (20 mg three times daily) with Pro were followed up for up to 7 years (range, 2-91 months). Fifty-seven patients received Is-5-Mn and 61 received Pro. RESULTS: Thirty episodes of first upper bleeding occurred; 16 were in the Is-5-Mn group. Actuarial probability of bleeding did not differ between the two groups. Endoscopic variceal red signs were the only independent predictors of early bleeding. Of the 52 patients who died, 28 were in the Is-5-Mn group. The likelihood of death was greater among patients assigned to Is-5-Mn than to Pro, but only in patients older than 50 years (72% vs. 48% at 6 years; P = 0.006). Child-Pugh score, bleeding, age, and assignment to Is-5-Mn were independent predictors of death. The likelihood of death without bleeding was also higher (P = 0.05) in the Is-5-Mn group. CONCLUSIONS: Is-5-Mn is as effective as Pro in preventing early bleeding but is associated with higher long-term mortality.

Adrenergic beta-Antagonists↗
PubMed1997

[Epidemiology of Microsporum langeronii tinea capitis in the Paris suburban area. Results of 2 school and familial surveys].

INTRODUCTION: One epidemiologic survey was carried out in two children communities, following detection of several cases of Microsporum langeronii tinea capitis. PATIENTS AND METHODS: In one case, 3 year-old children from a day-nursery were contaminated by a child originating from France, who had been previously infected by contact with a friend originating from Ivory Coast. In the second case, lesions were diagnosed in a nursery-school in African children born in France. These were treated before epidemic progression into the school. RESULTS: Our study confirms data from the literature concerning the risk of contamination by Microsporum langeronii, with a familial contamination being more frequent than scholar one. DISCUSSION: The interest of our study was the rapid starting of the epidemiologic survey after first case diagnosis (one to two months) and the treatment of all the patients without scholar eviction. Treatment of all affected patients as well as "asymptomatic carriers" leaded to the arrest to the epidemy. No case of relapse was noted during the following year.

Adolescent↗
PubMed1995

Effect of S-adenosyl-L-methionine on ethanol cholestasis and hepatotoxicity in isolated perfused rat liver.

We investigated whether S-adenosyl-L-methionine (SAMe) influences the inhibitory effect of ethanol on bile secretion and ethanol hepatotoxicity in the isolated perfused rat liver. SAMe (25 mg/kg intramuscularly three times a day) was administered for three days consecutively. Liver was then isolated and perfused with taurocholate to stabilize bile secretion and exposed to 1% ethanol for 70 min. The effect of ethanol on bile flow, bile salt biliary secretion, oxygen liver consumption, AST and LDH release in the perfusate, and hepatic concentration of glutathione, malondialdehyde, and diene conjugates was compared between SAMe-treated livers (N = 11) and paired controls (N = 11). Control experiments without ethanol were also performed (N = 6). Exposure to 1% ethanol induced a significantly (P < 0.03) higher inhibition of bile flow (-35% vs 17%) and bile salt secretion (-28% vs 16%) in untreated compared with SAMe-treated livers. During 1% ethanol exposure, the release of LDH and AST in the perfusate was significantly lower (P < 0.02) in SAMe-treated livers. Oxygen liver consumption was markedly inhibited by 1% ethanol administration (P < 0.02 vs controls without ethanol), an effect almost totally prevented by SAMe treatment (P < 0.02 vs ethanol controls). The hepatic concentration of total glutathione was significantly (P < 0.02) decreased by 1% ethanol exposure, but this effect was less pronounced in SAMe-treated than in untreated controls (P < 0.02). The hepatic levels of malondialdehyde and diene conjugates were not significantly changed by ethanol exposure in either SAMe-treated or control livers in comparison to ethanol-free controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effect of glucagon on intracellular pH regulation in isolated rat hepatocyte couplets.

To elucidate mechanisms of glucagon-induced bicarbonate-rich choleresis, we investigated the effect of glucagon on ion transport processes involved in the regulation of intracellular pH (pHi) in isolated rat hepatocyte couplets. It was found that glucagon (200 nM), without influencing resting pHi, significantly stimulates the Cl-/HCO3- exchange activity. The effect of glucagon was associated with a sevenfold increase in cAMP levels in rat hepatocytes. The activity of the Cl-/HCO3- exchanger was also stimulated by DBcAMP + forskolin. The effect of glucagon on the Cl-/HCO3- exchange was individually blocked by two specific and selective inhibitors of protein kinase A, Rp-cAMPs (10 microM) and H-89 (30 microM), the latter having no influence on the glucagon-induced cAMP accumulation in isolated rat hepatocytes. The Cl- channel blocker, NPPB (10 microM), showed no effect on either the basal or the glucagon-stimulated Cl-/HCO3 exchange. In contrast, the protein kinase C agonist, PMA (10 microM), completely blocked the glucagon stimulation of the Cl-/HCO3- exchange; however, this effect was achieved through a significant inhibition of the glucagon-stimulated cAMP accumulation in rat hepatocytes. Colchicine pretreatment inhibited the basal as well as the glucagon-stimulated Cl-/HCO3- exchange activity. The Na+/H+ exchanger was unaffected by glucagon either at basal pHi or at acid pHi values. In contrast, glucagon, at basal pHi, stimulated the Na(+)-HCO3- symport. The main findings of this study indicate that glucagon, through the cAMP-dependent protein kinase A pathway, stimulates the activity of the Cl-/HCO3- exchanger in isolated rat hepatocyte couplets, a mechanism which could account for the in vivo induced bicarbonate-rich choleresis.

Animals↗
PubMed1995

[Degenerative vertebral dislocation].

Degenerative vertebral dislocations (laterolisthesis) are responsible for progressive transverse intervertebral shift. These changes appear like a translation of the lateral edge of a vertebra compared to that of the underlying vertebra and are easily diagnosed. Vertebral dislocations can be secondary to active lumbar scoliosis or unilateral or asymmetrical degenerative spondylolisthesis. In every case, the appearance of laterolisthesis is reflected by the onset or aggravation of scoliosis which may become self-perpetuating. This lesion is secondary to osteoarthritic disruption of the integrity of the intervertebral disk and ligaments. Open and closed patterns have been described depending on the side of the associated disk opening. The onset of a rotatory dislocation reflects the progressive evolution of the deformity, which may require medical treatment, or surgical reduction and fixation by vertebral arthrodesis.

Humans↗
PubMed1993

Isosorbide-5-mononitrate versus propranolol in the prevention of first bleeding in cirrhosis.

BACKGROUND: Hemodynamic studies have shown the efficacy of nitrates in reducing portal pressure in cirrhosis. We therefore studied the efficacy of isosorbide-5-mononitrate vs. propranolol in the prevention of first bleeding within a prospective controlled trial. METHODS: One hundred eighteen cirrhotics with esophageal varices were blindly randomized to receive 20 mg of isosorbide-5-mononitrate three times a day (n = 57) or propranolol (n = 61) up to the maximum tolerated dose. Both groups also received ranitidine (150 mg/day). RESULTS: The median follow-up was 29 months. Twenty-six patients dropped out (13 in the isosorbide group) because of poor compliance or complications unrelated to treatment. Eighteen patients died (9 in the isosorbide-treated group), 6 due to bleeding. The 1- and 2-year actuarial percentages of patients free of bleeding was 90.8% and 82.2% in the isosorbide-5-mononitrate--and 93.9% and 85.8% in the propranolol-treated groups, respectively (P = NS). These values are higher than those expected from the North Italian Endoscopic Club predicting scores. There were few major side effects in either group. The 2-year survival rate did not differ between the two groups (82.2% vs. 85.4%). CONCLUSIONS: Isosorbide-5-mononitrate administered orally is a safe and effective alternative to propranolol in the prophylaxis of bleeding in cirrhosis.

Aged↗
PubMed1993

[Vitamin-resistant hypophosphatemic rickets and spinal cord compression. Apropos of 2 cases].

Adults with X-linked vitamin-resistant hypophosphatemic rickets can develop spinal cord compression as a result of spinal canal stenosis due to involvement of the spine with the increased periosteal and ligamentary calcification which is typical of the disease. Two cases are reported. In both patients, spinal cord compression manifested as rapidly progressive spastic paraplegia due to compression at T9 and T5, respectively. Decompressive laminectomy ensured full recovery in one case but was ineffective in the other. In both cases, paraplegia developed approximately one year after initiation of therapy combining a metabolite of vitamin D and phosphorus in high doses. Current imaging techniques (CT scan, magnetic resonance imaging) provide highly accurate information on the anatomic mechanism of the stenosis, its often multiple locations, and its course. Three factors are involved in the stenosis, in variable degrees: thickening of the laminae, hypertrophy of the facet joints, thickening and calcification of the yellow ligament. Magnetic resonance imaging is the investigation of choice in these patients. A deleterious effect vitamin D-phosphorus treatment cannot be outruled. The appropriateness of initiating this treatment should be prudently discussed and treated patients should be closely monitored.

Follow-Up Studies↗
PubMed1992

The effect of lactulose and lactitol administration on fecal fat excretion in patients with liver cirrhosis.

Mild to moderate fat malabsorption is frequently present in patients with liver cirrhosis. We investigated the influence of lactulose or lactitol treatment on fecal fat excretion in 18 patients with liver cirrhosis. All patients were Child Pugh class A or B and had not taken any therapy that could have affected intestinal absorption in the previous months. The dose of lactulose or lactitol was individually adjusted to maintain two semiliquid bowel movements per day. Steatorrhea was determined before and after a minimum of 7 days, when the cathartic effect was stabilized. Treatment with nonabsorbable disaccharides induced mild to moderate steatorrhea in 50% of patients. No differences were observed between the effects of lactulose and lactitol, but fecal fat excretion exceeded 10 g/day in two patients taking lactulose. These findings indicate that treatment with nonabsorbable disaccharides may increase fecal fat excretion in patients with liver cirrhosis. This factor should be taken into consideration when a cirrhotic patient has to take these drugs for a long time.

Adult↗
PubMedDate not supplied

Ultrastructural features of danazol-induced cholestasis: a case study.

A case study of a severe cholestatic syndrome induced by danazol, with ultrastructural description of liver morphology, is reported. Cholestasis appeared after 3 months treatment with danazol (300 mg/daily) and completely resolved 2 months after withdrawal. In spite of the severe increase in serum bilirubin and total serum bile salts, transaminases were only slightly elevated and GGT and alkaline phosphatases were almost normal. Light microscopy shows a pattern of predominantly centrolobular cholestasis without necrosis, with minimal inflammatory infiltrate and with no sign of bile ductule involvement. At the ultrastructural level very dilated bile canaliculus predominate with stunted or loss of microvilli and dense bile material in the lumen. Nonspecific alterations were seen in hepatocyte intracellular organelles. It is suggested that danazol may cause a rare but severe hepatocanalicular cholestasis, differing from the "bland" cholestasis frequently described during therapy with other anabolic steroids.

Bilirubin↗
PubMedDate not supplied

Zinc and other trace elements in liver cirrhosis.

Alterations in trace element concentrations may be observed in patients with chronic liver disease. Notably, selenium and zinc levels are reduced both in serum and in liver tissue of cirrhotic patients. Low selenium levels have been involved in the pathogenesis of liver damage as this element is important in controlling the levels of toxic oxygen radicals in the cells. Zinc deficiency has been involved in the pathogenesis of a number of clinical findings in chronic liver disease. These include the possible role of zinc deficiency in the pathogenesis of hepatic encephalopathy, by inducing alterations in urea metabolism. In CC14 cirrhotic rats oral zinc supplementation reduces ammonia levels and increases OCT activity in the liver. Oral zinc supplementation has been also proposed in the treatment of cirrhotic patients with chronic hepatic encephalopathy, the results however are not yet conclusive.

Humans↗