Intervention study to improve smoking cessation during hospitalization.

OBJECTIVES: In France, hospitals have been smoke free since February 2007. A period of hospitalization may be a good time to enhance a smoker's motivation to quit. This study aimed to assess whether training medical staff in smoking cessation management might improve the rate of smoking cessation during hospitalization. STUDY DESIGN: Non-randomized intervention study. METHODS: Staff of the participating care units either received (intervention group) or did not receive (control group) training in smoking cessation management. The dependent variable was the proportion of inpatients that continued to smoke before (Period 1) and after (Period 2) the training session. RESULTS: In total, 358 patients were included. In Period 1, 55.6% and 50% of the smokers from the intervention and control groups stopped smoking, respectively; the corresponding rates in Period 2 were 64.3% and 48.1%. In Period 2, 36.4% and 31.8% of the smokers from the intervention and control groups claimed that they had received motivational counselling. In the intervention group, the request rate for nicotine replacement therapy (NRT) was higher (41.7%) compared with the control group (11.1%). In both groups, patients asked for NRT more often (P < 0.001) when they had received motivational counselling. CONCLUSIONS: This study was not able to demonstrate that training medical staff in smoking cessation management has a significant impact on smoking cessation in hospitalized smokers. The delivery of medium-intensity support to all smokers appears to be out of reach of physician/nurse teams. New strategies are needed, including a team specifically dedicated to the problems of addiction.

Contraction of human colonic circular smooth muscle cells is inhibited by the calcium channel blocker pinaverium bromide.

UNLABELLED: The effects of L-type calcium channel blockers (CCBs) selective for the gastrointestinal tract (pinaverium) or non-selective (nicardipine and diltiazem), were investigated on CCK-, CCh- or KCl-induced contraction of smooth muscle cells (SMC) isolated from the circular muscle layer of normal or of inflamed human colons. In the normal tissue colon, whatever the contractile agent used, CCK-8 (1nM), CCh (1nM) or KCl (20mM), a micromolar concentration of pinaverium significantly inhibited contraction (88.36%, 93.10%, 93.92% inhibition respectively); this effect was concentration-dependent for CCh (IC50 = 0.73 +/- 0.08nM) and for CCK (IC50 = 0.92 +/- 0.12nM). In parallel, both nicardipine and diltiazem inhibit significantly contraction of isolated SMC. In inflamed colons, pinaverium (1 microM) display a significant higher efficacy than diltiazem or nicardipine to reduce cell contraction induced by CCK-8 or by KCl. In addition, RT-PCR experiments were performed to evidence tissue specificity of the L-type calcium channel. They revealed the expression of the messenger of the a-1 subunit L-type calcium channel (binding site of such CCBs), consistent with the expression of the rbC-2 splice variant of the alpha1-C gene. IN CONCLUSION: (i) the inhibition by calcium channel blockers of agonist-induced contractile activity suggest a modulation of SMC contraction upon extracellular calcium via 'L-type' voltage-dependent calcium channel; (ii) this study provides a rationale for the clinical use of pinaverium in colonic motor disoders affecting the contractility of SMC, since it appeared to decrease the contraction even in pathological situation; and (iii) RT-PCR experiments confirms the presence in human colon SMC of the alpha-1 subunit mRNA of calcium channel.

Impaired fibrinolytic capacity in patients with inflammatory bowel disease.

The venous occlusion test was applied to 17 patients with inflammatory bowel disease (IBD; 7 cases of Crohn's disease, 10 cases of ulcerative colitis). Results were compared to those obtained in 20 healthy matched control subjects. Patients with IBD had significantly decreased t-PA Ag release (p less than 0.001) and had no significant vWF Ag release. Residual PAI activity was evidenced after venous stasis in the IBD group but not in the control group. Hypofibrinolysis was more important in patients with an evolutive IBD than in patients with IBD in remission. Impaired systemic fibrinolytic capacity might contribute to an increased risk for thromboembolic complications and to the pathogenesis of inflammatory bowel disease.

Calcitonin gene-related peptide-induced relaxation of isolated human colonic smooth muscle cells through different intracellular pathways.

Calcitonin gene-related peptide (CGRP) plays a significant role in the non-adrenergic non-cholinergic (NANC) regulation of intestinal tract motility. In this work, the contractile properties of enzymatically isolated circular smooth muscle cells (SMC) from human colon in response to CGRP were evaluated. Relaxation by CGRP (1 microM) was determined in cells maximally contracted by carbachol (CCh, 1 nM). Simultaneously, cGMP contents of SMC were measured by radioimmunoassay. CCh-induced contraction was inhibited by 1 microM CGRP (maximum: 69+/-5% within 60 sec); similarly, exposure of cells to sodium nitroprussiate (SNP), 1 microM, fully inhibited contraction (maximum: 89+/-8% within 30 sec). In the same time-course as for relaxation, CGRP and sodium nitroprussiate caused significant increase in intracellular cGMP levels (2- and 10-fold that of the basal level, respectively, P < 0.01). The nitric oxide synthase (NOS) inhibitor, L-N5(I-iminoethyl)ornithine, dihydrochloride, (L-NIO), 1 microM, partly inhibited SMC relaxation induced by CGRP (78.26%); the protein kinase inhibitor, N-(2-aminoethyl)-5-isoquinolinesulfonamide hydrochloride (H9), 1 microM, and the selective cAMP-dependent protein kinase inhibitor, adenosine-3',5'-monophosphorothioate triethylammonium salt, Rp isomer, (Rp-cAMP(S)), 1 microM, also caused inhibition of relaxation (70.30% and 28.6%, respectively). In parallel, the increase in cGMP caused by CGRP was partly reduced by L-NIO (65.47%) and by H9 (55%). In conclusion, the nitric oxide generation following exposure of human colonic SMC to sodium nitroprussiate causes relaxation through the cGMP pathway; on the other hand, exposure of SMC to CGRP causes relaxation in part by activation of nitric oxide synthase and guanylate cyclase and in part through the cAMP pathway.

Sensitivity of human lymphocytes to acetaldehyde: comparison between alcoholic and control subjects.

The action of acetaldehyde (ACH), the first metabolite of ethanol, was studied on human lymphocytes stimulated in vitro by phytohemagglutinin (PHA) or Concanavalin A (Con A). ACH caused a dose-dependent decrease of [3H]thymidine uptake in lymphocytes from both alcoholic and control subjects. The area under the curve of [3H]thymidine incorporation as a function of ACH concentration was determined for each subject and referred to as the lymphocyte sensitivity index. Indexes for alcoholic subjects were found to be higher than those for controls, indicating a lower sensitivity to ACH of lymphocytes from alcoholics. We also found a wide range of sensitivity indexes within the same group. These results are consistent with the current hypothesis that not everybody is at equal risk to develop alcohol related disorders.

Effects of ethanol in vitro on some parameters of the immune response.

The action of ethanol (ETH) on murine lymphocyte subpopulations and on human peripheral blood mononuclear cells (PBMC) stimulated in vitro by mitogens was studied. ETH caused a concentration-dependent decrease in DNA synthesis in the different murine cell types. ETH was more immunosuppressive for T lymphocytes than for B lymphocytes. An enhancement of the blastogenic response was observed for B cells at 0.5% ETH. Interleukin 2 synthesis by murine splenocytes was inhibited by ETH in a concentration-related manner; the lowest concentrations of ETH caused an increase in interleukin 2 synthesis. The highest concentrations of ETH tested decreased the size of the cell clusters formed in cultures of mitogen-stimulated lymphocytes, whereas an increase in PBMC cluster size was observed in the presence of 0.5 and 1% ETH.

Flow cytometric analysis of oxidative product formation in phytohemagglutinin-stimulated ethanol-treated immune mononuclear cells.

Oxidative products formed by immune mononuclear cells were studied by flow cytometry. JURKAT T cells and peripheral blood mononuclear cells were incubated with 2,7-dichlorofluorescin diacetate. This substance was hydrolysed in the cells, leading to a non-fluorescent product which was oxidized into highly fluorescent 2,7-dichlorofluorescein by oxygen reactive species. These latter products were analysed by flow cytometry in phytohemagglutinin (PHA)-stimulated ethanol (ETH)-treated mononuclear cells. The level of fluorescence intensity (FI) was found higher in stimulated cells than in non-stimulated cells. ETH displayed two different effects on the cells: either a decrease of FI associated with a decrease of the number of fluorescent cells (FC) or an increase in FI. Both effects were dose-dependent. ETH is an effective scavenger of .OH radicals, but it is also oxidized by the microsomal ETH oxidizing system with production of oxygen reactive species, which probably explains the opposite effects of ETH. In the presence of desferal, an iron-chelating agent, and nordihydroguaiaretic acid, an inhibitor of the lipooxygenase pathway, the cells showed a decrease of FI and FC. These results suggest that .OH and other oxygen reactive species are involved in stimulation by PHA of ETH-treated immune mononuclear cells.

Does the short variant of the serotonin transporter linked polymorphic region constitute a marker of alcohol dependence?

The serotonin (5-hydroxytryptamine: 5-HT) system has been thought to play an important role in several steps of alcohol craving. A number of studies, including our own, have reported that alcohol dependence is associated with dysfunction of 5-HT transmission. Pharmacological and clinical studies have shown that the 5-HT transporter (5-HTT) and the 5-HT1A receptor appear to be candidate loci for the aetiology of alcohol dependence. We have analysed the presence of different 5-HTT and 5-HT1A variants in 104 alcohol-dependent patients and 38 controls for a possible association with alcohol dependence. In alcohol-dependent patients, we found a high frequency of the S allele of 5-HTTLPR (45.5% vs. 29%, chi2 = 6.33, p = 0.0081). No other significant differences were observed between the two populations for other polymorphisms. These results provide, for the first time, preliminary evidence that alcohol abuse disorders are associated with a genetic variant for 5-HT transmission. It might be possible to use this detection of the "S" allele as a clinical tool for pathology diagnosis and to advise recovering alcoholics and it could represent an aid to the prevention of relapse. Therapeutic actions could be envisaged to use this genotyping to help select the best therapeutic strategy.

[Impaired fibrinolytic response to the venous occlusion test in patients with cryptogenic colitis]. / Réponse anormale au test d'occlusion veineuse chez les patients atteints de colite cryptogénique.

The fibrinolytic response to venous occlusion was studied in 17 patients with inflammatory bowel disease: 7 with Crohn's disease, 10 with ulcerative colitis and compared with those obtained in 20 controls. Patients with inflammatory bowel disease showed decreased tissue-type plasminogen activator antigen release (t-PA Ag), no significant Von Willebrand antigen release (vWF Ag), and a residual plasminogen activator inhibitor activity (PAI activity) after venous occlusion. These modifications were more important in the evolutive colitis group compared with the remission group. Hypofibrinolysis, as defined by a defective t-PA release, and a residual PAI activity after venous occlusion might contribute to digestive and/or extra digestive thrombotic manifestations observed during the course of inflammatory bowel diseases.

Primary sinusoidal lymphoma of the liver revealed by autoimmune hemolytic anemia.

Primary liver lymphomas usually present with the clinical picture of a liver tumor, and are characterized by a predominantly portal invasion by lymphoid cells of the B-cell phenotype. We report a case of primary sinusoidal lymphoma of the liver, in a 36 year-old male patient, revealed by homogeneous hepatosplenomegaly and infiltration of liver sinusoids by morphologically normal lymphocytes, without destruction of the parenchyma. Immunohistochemistry in paraffin-embedded tissue sections was positive for the pan T-cell marker MTI, weakly positive for UCHLI, and negative for CD3, and B-cell markers were negative; these findings were consistent with the diagnosis of T-cell lymphoma. The clinical, histological and immunological presentation of this lymphoma was similar to that of hepatosplenic gamma delta T-cell lymphoma. Autoimmune hemolytic anaemia preceded the lymphoma. Despite chemotherapy, the patient died 24 months after the initial presentation in the leukemic phase. A better understanding of this exceptional but characteristic entity is required for an accurate and early diagnosis.

[Primary prevention of digestive hemorrhage, caused by rupture of esophageal varices, by endoscopic sclerotherapy in patients with liver cirrhosis. Multicenter randomized controlled study]. / Prophylaxie primaire des hémorragies digestives par rupture de varices oesophagiennes par sclérothérapie endoscopique chez le malade atteint de cirrhose. Etude contrôlée randomisée multicentrique.

The severity of esophageal variceal bleeding in cirrhotic patients justifies prophylactic therapy. A multicenter controlled study was carried out in Languedoc in 116 cirrhotic patients with esophageal varices and no history of bleeding. Patients were randomly assigned to two groups: 60 control patients without therapy; 56 patients treated by endoscopic sclerotherapy (209 sessions). The mean follow-up was 20 +/- 11 months. Esophageal varices disappeared in 35 patients (62.5%) or became smaller in 10 other patients (18%). Varices reappeared in 9 of these 35 patients within 3 months. Minor (fever, dysphagia, stenosis) or major complications (variceal bleeding, bacterial peritonitis) were noted in 26 patients (46%). Esophageal variceal bleeding occurred in 13 of the treated patients and in 10 control patients. Actuarial curves of bleeding and survival were similar for both groups. Twenty controls and 21 treated patients died during the study. In conclusion, prophylactic sclerotherapy of esophageal varices should not be performed in cirrhotic patients, considering lack of efficacy and high rate of side effects.

[Highly elevated alphafetoprotein and hepatic cirrhosis. It is not always hepatocarcinoma]. / Alpha-foetoprotéine très élevée et cirrhose hépatique. Ce n'est pas toujours un hépatocarcinome.

BACKGROUND: Alphafetoprotein assay contributes considerably to the diagnosis of hepatocarcinoma in patients with hepatic cirrhosis. We report the case of a cirrhotic patient whose elevated alphafetoprotein level was not associated with liver disease. CASE REPORT: Alphafetoprotein level was followed in a 64-year-old man with hepatic cirrhosis. A rise from 415 to 7690 ng/ml between June and November 1997 led to the discovery of adenocarcinoma of the cardia with liver metastasis. This extrahepatic adenocarcinoma was probably the cause of inappropriate secretion of alphafetoprotein. DISCUSSION: Primary liver tumors are obviously not the only source of elevated alphafetoprotein levels. High levels can also be observed in certain, notably digestive tract and embryonary, cancers. Gastric hepatoid adenocarcinoma is a recently described histological entity first described in 1970. Typically, there is an inappropriate secretion of alphafetoprotein due to a secondary liver tumor.

[Percutaneous hepatic puncture biopsy in ambulatory care. 231 patients]. / Ponction biopsie hépatique transpariétale en aveugle et en ambulatoire. 231 patients.

OBJECTIVES: The aim of this study was to verify that percutaneous liver biopsy does not require prolonged hospitalization over 24 hours and can be performed in a day care clinic without increased morbidity. PATIENTS AND METHODS: Two hundred thirty-one outpatients underwent percutaneous liver biopsies in a day care clinic from November 1, 1994 to June 30, 1996. There were 136 men and 95 women, mean age 39.5 years, age range 16-72 years. Liver biopsy was performed as part of the work-up for hepatitis C in 183 patients. The biopsy was a repeat procedure in 43 patients. RESULTS: The procedure was uneventful in 230 patients. Hospitalization for 24 hours was required in one patient with a biliodigestive anastomosis who developed chills and fever due to Eschericia coli bacteremia. Two procedures were unsuccessful. CONCLUSION: This series confirms that when performed in compliance with standard rules for strictly controlled indications, morbidity after percutaneous liver biopsy is not greater in an outpatient than a classical inpatient setting.