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S Beaulieu

Publications and source records attributed to S Beaulieu.

At least 19 recordsLinked to original sources
PubMed2004

Anal sphincter injury after forceps delivery: myth or reality? A prospective ultrasound study of 93 females.

PURPOSE: This study was designed to estimate the prevalence of anal sphincter injury after forceps delivery in a large population of females managed by trained obstetricians in a French hospital and to identify factors predictive for anal sphincter injury. METHODS: We performed a prospective study of healthy females older than 18 years with no history of anal incontinence, anorectal abnormalities, or anorectal surgery after their first vaginal delivery. All females were interviewed using a standardized questionnaire concerning intestinal transit and continence status. Physical examination and endoanal ultrasonography were performed after delivery. RESULTS: Between November 1999 and November 2000, 93 females were included in the study after their first forceps delivery. Eleven patients (11.8 percent) had a partial defect involving the external sphincter, visible on ultrasonography. One patient (1.1 percent) had a partial defect of external sphincter with complete defect of internal sphincter (sequelae of primary repair of a third-degree perineal tear). Seventeen patients (18.2 percent) had flatus incontinence, and four patients (4.3 percent) had liquid stool incontinence. A high daily number of stools was significantly associated with sphincter defect visible on ultrasonography (P=0.02). The development of anal incontinence was not related to sphincter defect on ultrasonography. There was a strong association between perineal tear and sphincter defect visible on ultrasonography (odds ratio, 4.5 (range, 1.2-16.7)). CONCLUSIONS: Anal sphincter injury after forceps delivery was identified in <13 percent of our large population of healthy females. Our study does not confirm previous observations that anal sphincter injury is common after forceps delivery; previously published studies may have overestimated the prevalence of this condition. The only factor with significant predictive value for anal sphincter injury was perineal tear. Anal endosonography should be recommended after obstetric perineal tear.

Adult↗
PubMed2004

Drug induced weight gain, an impediment to successful pharmacotherapy: focus on antipsychotics.

The antipsychotic drugs (APDs) are fundamental tools in current psychiatric practice. A new generation of agents, the atypical APDs, represents an important progress in the treatment of psychotic disorders. Unfortunately, some of them induce excessive body weight gain (BWG), obesity, hyperglycemia and dyslipidemia in the following order: clozapine approximately equal to olanzapine > quetiapine > risperidone > ziprasidone = aripiprazole. Appetite stimulation is probably the main mechanism of BWG and this is strongly correlated with the APD affinity for H1 (histaminergic) and alpha1 (adrenergic) receptors. A composed ratio of the APD affinity for diverse neurotransmitters involved in food intake (FI) regulation correlates with BWG as well. Endocrine/metabolic mechanisms, such as the activation of the hypothalamus-pituitary-adrenal axis, changes in insulin sensitivity (by conventional and atypical agents), hyperprolactinemia and gonadal dysfunction (by conventional APDs and risperidone) may also be involved. Importantly, patients with schizophrenia may have a genetically-based predisposition to appetite dysregulation, insulin resistance and endocrine imbalance involving gonadal steroids. Excessive BWG must be prevented or attenuated by proper drug selection, combining or switching agents, nutritional assistance and physical exercise. Amantadine. metformin and reboxetine proved to significantly lessen APD-induced BWG. Notwithstanding this, novel strategies are necessary to treat this side effect in a clinical population particularly prone to poor compliance and under a high risk of negative drug interaction.

Animals↗
PubMed2002

The effects of adrenalectomy and aldosterone replacement in transgenic mice expressing antisense RNA to the type 2 glucocorticoid receptor.

Bilateral adrenalectomy (ADX) either prevents or attenuates obesity in several animal models. Mice that express an antisense RNA to the glucocorticoid receptor (GCR) are obese. The present study was conducted to examine the effects of ADX and aldosterone (ALDO) replacement on the rate of weight gain and body composition of mice bearing an antisense GCR gene construct. Twenty-eight male transgenic mice bearing the antisense GCR construct and 16 male B6C/3F1 mice were either bilaterally ADX or given sham operations. At the time of surgery, some of the ADX mice and all of the sham-operated mice were implanted with 100-mg cholesterol (CHOL) pellets inserted subcutaneously in the subscapular region. The remaining ADX mice were implanted with 100-mg 1% w/w ALDO pellets using CHOL as vehicle. All mice were returned to their home cages for 2 weeks. They were then decapitated and the blood was collected for corticosterone, ALDO, insulin, and leptin radioimmunoassay. Carcasses were eviscerated and prepared for gravimetric analyses, including bomb calorimetry. ADX resulted in a significant drop in carcass fat in both transgenic and wildtype groups. ALDO prevented the decrease in carcass fat in both groups. Two weeks after ADX, transgenic mice were as fat as sham-operated wildtype controls, whereas both sham-operated and ALDO-treated transgenic groups were significantly fatter. Despite observing a reliable decrease in carcass fat following ADX, no corresponding decrease in circulating leptin was found.

Adrenal Cortex Hormones↗
PubMed2002

[Unusual association: hepatic peliosis and Crohn's disease].

INTRODUCTION: Hepatobiliary disorders occurs in about 10 to 30% of inflammatory bowel diseases. Fatty liver and gallstones are preferentially described with Crohn's disease. Conversely, peliosis hepatis has been only exceptionally reported in association with inflammatory bowel diseases. We describe here a case of peliosis hepatis complicating a misdiagnosed Crohn's disease. EXEGESIS: A 24-year-old woman was referred because of a hepatomegaly and a deterioration of the general state. The patient complained about diarrhea for 3 months and about an episode of bloody stools. There was an aphthous-like lesion on the tongue. X-ray pull-through revealed a typical aspect of terminal ileitis as seen in Crohn's disease. The liver was heterogeneous. Liver biopsy revealed a peliosis hepatis. No other possible cause of peliosis hepatis was found. Therefore, in this case, peliosis hepatis, revealed by the hepatomegaly, was associated with Crohn's disease. CONCLUSION: Association between Crohn's disease and peliosis hepatis has only exceptionally been described. A priori, this complication is not a pejorative feature in inflammatory bowel disease. The pathophysiological significance of this association remains unknown.

Adult↗
PubMed2002

Obesity and related metabolic abnormalities during antipsychotic drug administration: mechanisms, management and research perspectives.

Excessive body weight gain (BWG) is a common side effect of some typical and atypical antipsychotic drugs (APs). Convergent evidence suggests a hierarchy in the magnitude of BWG that may be induced by diverse agents, being very high for clozapine and olanzapine; high for quetiapine, zotepin, chlorpromazine, and thioridazine; moderate for risperidone and sertindole; and low for ziprazidone, amisulpiride, haloperidol, fluphenazine, pimozide, and molindone. BWG may be related to increased appetite that is due to drug interaction with the brain monoaminergic and cholinergic systems and to the metabolic/endocrine effects of hyperprolactinemia. Subjects with schizophrenia and bipolar disorders manifested a significantly high prevalence of diabetes, even before the introduction of atypical APs. However, clozapine and olanzapine appear to display a high propensity to induce glucose dysregulation and dyslipidemia. Sudden BWG, insulin resistance, increased appetite, and related endocrine changes also may be involved in the development of glucose intolerance and dyslipidemia in predisposed individuals. Patients should be informed of these side effects in order to prevent excessive BWG, and their blood glucose and lipids should be monitored before treatment and then at regular intervals. Nutritional advice must be given and regular physical exercise recommended. An appropriate selection of APs ought to be based on drug efficacy for specific patients and assessment of relevant risk factors such as propensity to gain weight; family or personal history of diabetes or hyperlipidemia; and elevated fasting serum glucose, lipid, or insulin levels. At present, there is no standardized pharmacological treatment for AP-induced BWG. Some studies have assessed the effects of agents such as amantadine, orlistat, metformin, nizatidine, and topiramate on AP-induced BWG. Further studies will provide tools to identify patients at high risk for obesity and metabolic abnormalities during AP administration. Excessive body weight gain (BWG), glucose intolerance, and dyslipidemia during treatment with antipsychotic drugs (APs) were reported in the late 1950s [14,101]. However, after 1990, interest in these problems increased noticeably, mainly because of the high propensity of some new atypical APs to induce these side effects (Fig.1). The APs are currently used in diverse mental disorders. Hence, excessive BWG and metabolic dysfunction are not exclusive of subjects with schizophrenia. In the case of bipolar disorders, AP-induced BWG may be additive to that induced by mood stabilizers [14,48,101]. The clinical features [2,14,24,133,139,140] and mechanisms [14,34,68,87,93,101,130] of BWG and metabolic dysfunction have been previously reviewed. In this article, we focus on a unified theory to explain these side effects, based on the interaction of APs with brain neurotransmitters involved in appetite regulation. This review comprises the following sections: 1) the clinical features of AP-induced BWG; 2) the effects of APs on carbohydrate and lipid metabolism in humans and experimental animals; 3) mechanisms involved in BWG, glucose, and lipid dysregulation; 4) strategies for prevention and treatment of these side effects; and 5) research perspectives in the field. The following sources were consulted: MEDLINE, Cochrane database system, and PsychINFO. Numerous articles referred to in leading articles also were consulted. The literature on this subject has increased so rapidly that it was impossible to include all the data recently published. For the first two sections, references that illustrate current controversies in the field were selected.

Animals↗
PubMed2001

Dopaminergic activity in transgenic mice underexpressing glucocorticoid receptors: effect of antidepressants.

Transgenic mice bearing a transgene coding for a glucocorticoid receptor antisense mRNA, which partially blocks glucocorticoid receptor expression, were used to investigate the long-term effect of hypothalamic-pituitary-adrenal axis dysfunction on brain dopamine transmission. Compared to control mice, the transgenic animals showed increased amphetamine-induced locomotor activity and increased concentrations of striatal dopamine and its metabolites dihydroxyphenylacetic acid and homovanillic acid. Binding of [3H]SCH 23390 and [3H]spiperone to, respectively, D1 and D2 dopamine receptors was increased in transgenic mice. In contrast, autoradiography of striatal [3H]GBR 12935 binding to the dopamine transporter was decreased and the mRNA levels of this transporter, measured by in situ hybridization, remained unchanged in the substantia nigra pars compacta. The effect of chronic treatment for two weeks with amitriptyline or fluoxetine was compared in control and transgenic mice. No significant changes were observed in control mice following antidepressant treatment, whereas in transgenic mice both antidepressants reduced striatal [3H]SCH 23390 and [3H]raclopride specific binding to D1 and D2 receptors. Amitriptyline, but not fluoxetine, increased striatal [3H]GBR 12935 binding to the dopamine transporter, whereas its mRNA level in the substantia nigra pars compacta was decreased in fluoxetine, compared to vehicle- or amitriptyline-treated transgenic mice. From these results we suggest that hyperactive dopaminergic activity of the nigrostriatal pathway controls motor activity in the transgenic mice. Furthermore, antidepressant treatment corrected the increased striatal D1 and D2 receptors and decreased dopamine transporter levels in the transgenic mice.

Amitriptyline↗
PubMed2000

The immunodeficiency virus coreceptor, Bonzo/STRL33/TYMSTR, is expressed by macaque and human skin- and blood-derived dendritic cells.

Dendritic cells (DCs) have been shown to be important in the replication of human and simian immunodeficiency viruses (HIV and SIV, respectively) in vivo and in vitro. DCs express CD4 and several chemokine receptors, such as CCR5 and CXCR4, which are important for viral entry. In vivo, DCs are abundant at body surfaces, where they might be one of the first cells that encounter naturally transmitted virus. Furthermore, DCs pulsed with HIV or SIV in vitro can efficiently transmit virus to T cells, thereby propagating vigorous viral replication. Reports have implicated Bonzo/STRL33/TYMSTR to be an additional alternative coreceptor for HIV and especially SIV infection. However, at present there are no reports regarding the expression of Bonzo/STRL33/TYMSTR by human or macaque DCs. Here we demonstrate the presence of Bonzo/STRL33/TYMSTR transcripts in rhesus macaque and human skin-derived DCs, in immature and mature blood monocyte-derived DCs, and in T cells from both skin and blood. Therefore, Bonzo/STRL33/TYMSTR is expressed in DCs and T cells that can play a role in the transmission of immunodeficiency viruses.

Animals↗
PubMed2000

Fluorine-18 fluorodeoxyglucose positron emission tomography correlated with computed tomographic scan and magnetic resonance imaging in a case of hematometrocolpos.

A 12-year-old girl had intense abdominal pain that had increased in the past 3 months and was accompanied by weight loss. An ultrasound examination revealed large cystic masses in the abdomen. A computed tomographic scan could not conclusively rule out a malignant condition. The hymen was normal on physical examination, but magnetic resonance imaging confirmed that the abnormalities corresponded to dilated cavities of the vagina, uterus, and fallopian tubes, with an appearance suggestive of hematometrocolpos. Fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography was requested concurrently with the magnetic resonance image to assess the metabolic activity of the lesions and to exclude the presence of distant metastases. Large defects without FDG accumulation were noted in the areas corresponding to the cystic masses. Vaginal atresia with hematometrocolpos was confirmed at surgery. This rare case involving F-18 FDG positron emission tomographic imaging in hematometrocolpos illustrates that this diagnosis should be considered in the presence of symmetric hypometabolic masses in the pelvis.

Child↗
PubMed1999

Reliability of the Canadian emergency department triage and acuity scale: interrater agreement.

STUDY OBJECTIVE: To determine the rate of interobserver reliability of the Canadian Emergency Department Triage and Acuity Scale (CTAS). METHODS: Ten physicians and 10 nurses were randomly selected to review and assign a triage level on 50 ED case summaries containing presenting complaint, mode of arrival, vital signs, and a verbatim triage note. The rate of agreement within and between groups of raters was determined using kappa statistics. One-way, 2-way analysis of variance (ANOVA) and combined ANOVA were used to quantify reliability coefficients for intraclass and interclass correlations. RESULTS: The overall chance-corrected agreement kappa for all observers was.80 (95% confidence interval [CI] .79 to .81), and the probability of agreement between 2 random observers on a random case was.539. For nurses alone, kappa=.84 (95% CI .83 to .85, P = .598), and for doctors alone, kappa= .83 (95% CI .81 to .85, P = .566). The 1-way, 2-way ANOVA and combined ANOVA showed that the reliability coefficients (84%) for both nurses and physicians were similar to the kappa values. A combined ANOVA showed there was a. 2-point difference with physicians assigning a higher triage level. CONCLUSION: The high rate of interobserver agreement has important implications for case mix comparisons and suggests that this scale is understood and interpreted in a similar fashion by nurses and physicians.

Analysis of Variance↗
PubMed1998

Differentiation of monocytes into dendritic cells in a model of transendothelial trafficking.

Essential to the dendritic cell system of antigen-presenting cells are the veiled dendritic cells that traverse afferent lymph to enter lymph nodes, where they initiate immune responses. The origin of veiled cells, which were discovered 20 years ago, is unclear. Monocytes cultured with endothelium differentiated into dendritic cells within 2 days, particularly after phagocytosing particles in subendothelial collagen. These nascent dendritic cells migrated across the endothelium in the ablumenal-to-lumenal direction, as would occur during entry into lymphatics. Monocytes that remained in the subendothelial matrix became macrophages. Therefore, monocytes have two potential fates associated with distinct patterns of migration.

Antigens, CD↗
PubMed1998

A physiologic function for p-glycoprotein (MDR-1) during the migration of dendritic cells from skin via afferent lymphatic vessels.

P-glycoprotein (MDR-1) is a well-known transporter that mediates efflux of chemotherapeutic agents from the intracellular milieu and thereby contributes to drug resistance. MDR-1 also is expressed by nonmalignant cells, including leukocytes, but physiologic functions for MDR-1 are poorly defined. Using an initial screening assay that included >100 mAbs, we observed that neutralizing mAbs MRK16, UIC2, and 4E3 against MDR-1 specifically and potently blocked basal-to-apical transendothelial migration of mononuclear phagocytes, a process that may mimic their migration into lymphatic vessels. Antagonists of MDR-1 then were used in a model of authentic lymphatic clearance. In this model, antigen-presenting dendritic cells (DC) migrate out of explants of cultured human skin and into the culture medium via dermal lymphatic vessels. DC and T cells derived from skin expressed MDR-1 on their surfaces. Addition of anti-MDR-1 mAbs MRK16, UIC2, or the MDR-1 antagonist verapamil to skin explants at the onset of culture inhibited the appearance of DC, and accompanying T cells, in the culture medium by approximately 70%. Isotype-matched control mAbs against other DC molecules including CD18, CD31, and major histocompatibility complex I did not block. In the presence of MDR-1 antagonists, epidermal DC were retained in the epidermis, in contrast to control conditions. In summary, this work identifies a physiologic function for MDR-1 during the mobilization of DC and begins to elucidate how these critical antigen-presenting cells migrate from the periphery to lymph nodes to initiate T lymphocyte-mediated immunity.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Characterization of the cytotoxic factor(s) released from thymic dendritic cells upon human immunodeficiency virus type 1 infection.

We previously demonstrated that infection of primary human thymic dendritic cells (DCs) with laboratory strains of HIV leads to the release of soluble factor(s) which induced thymocyte killing. In the present paper, we extend the characterization of this process. Our results reveal that primary HIV-1 isolates are similarly able to induce the production of cytotoxic factor(s) from thymic DCs and that the release of such factor(s) is dependent on viral infection. Interestingly, we observed that CD4+ and CD8+ purified thymocyte subsets, and activated PBMCs are susceptible to the cytotoxic activity, whereas freshly isolated resting PBMCs are resistant to this effect. Cycloheximide treatment prevents the killing of thymocytes exposed to HIV-infected DC supernatant, revealing that this form of cell death is an active biological process requiring protein synthesis. Finally, our data suggest that FasL and TNF alpha could both participate in the killing process. These in vitro observations provide a plausible model, whereby HIV-infected DCs can play a role in vivo in the induction of uninfected thymocyte killing.

Animals↗