Diferencias en las presiones del canal anal y la sensibilidad rectal en pacientes con incontinencia anal, estreñimiento crónico y sujetos sanos / No disponible

Introducción: Existe gran variabilidad en los hallazgos manométricos entre pacientes con incontinencia anal (IA) y sujetos sanos. La correlación entre las presiones del canal anal y la IA no es exacta por el amplio rango de valores normales. Objetivos: Estudio prospectivo para evaluar diferencias en las presiones del canal anal y en la sensibilidad rectal en pacientes con IA, estreñimiento crónico (EC) y sujetos sanos. Material y métodos: Noventa y cuatro pacientes con IA, 36 pacientes con EC y 15 sujetos sanos. Se obtuvieron: edad, sexo, presión de reposo, longitud del canal anal (LCA), presión de máxima contracción voluntaria (PMCV), duración de la contracción voluntaria, primera sensación, sensación de urgencia y máximo volumen tolerado (MVT). Estudio estadístico: test de Kruskal-Wallis, test de Mann-Whitney, regresión logística multinomial. Resultados: Se encontraron diferencias significativas en la edad (p < 0,001), la presión de reposo (p < 0,001), la LCA (p < 0,001) y la PMCV (p < 0,01) en el grupo de IA con respecto a los otros dos grupos. El volumen para la primera sensación fue significativamente más bajo en los sujetos sanos que en los otros dos grupos (p < 0,05). El volumen de urgencia y el MVT fueron menores en el grupo con IA con respecto a los otros dos grupos (p < 0,001). En el análisis multivariante la edad, la presión de reposo y el volumen de la primera sensación y de la urgencia aumentan el riesgo relativo de IA. Conclusiones: La mayor edad, la disminución presión basal del canal anal y la alteración del umbral sensorial rectal aumentan el riesgo de IA(AU)

Introduction: There exist a great variability in the manometric findings between patients with anal incontinence (AI) and healthy subjects. The correlation between the pressures of the anal canal and the AI is not exact by the wide rank of normal values. Objectives: Prospective study to evaluate differences in the pressures of the anal canal and in rectal sensitivity in patients with AI, chronic constipation (CC) and healthy subjects. Material and methods: Ninety four patients with AI, 36 patients with CC and 15 healthy subjects were included. The following data were obtained: age, sex, resting pressure, anal canal length (ACL), squeeze maximum pressure (SMP), squeeze pressure duration (SPD), first sensation, urge and maximum tolerated volume (MTV). Statistical study: test of Kruskal-Wallis, test of Mann-Whitney, and multinomial logistic regression test. Results: There were significant differences in the resting pressure (p < 0.001), the ACL (p < 0.001) and the SMP (p < 0.01) in the group of AI with respect to the other two groups. The volume for the first sensation was significantly lower in the healthy subjects than that in the other two groups (p < 0.05). The urge volume and the MVT were smaller in the group with AI with respect to the other groups (p < 0.001). In multivariate analysis the age, the resting pressure and the volume for the first sensation and urge increase the relative risk for AI. Conclusions: The greater age, the decrease in anal canal resting pressure and the alteration of rectal sensation increase the risk for AI(AU)

Differences in the pressures of canal anal and rectal sensitivity in patients with fecal incontinence, chronic constipation and healthy subjects.

INTRODUCTION: There exists a great variability in the manometric findings between patients with anal incontinence (AI) and healthy subjects. The correlation between the pressures of the anal canal and the AI is not exact by the wide rank of normal values. OBJECTIVES: Prospective study to evaluate differences in the pressures of the anal canal and in rectal sensitivity in patients with AI, chronic constipation (CC) and healthy subjects. MATERIAL AND METHODS: Ninety four patients with AI, 36 patients with CC and 15 healthy subjects were included. The following data were obtained: age, sex, resting pressure, anal canal length (ACL), squeeze maximum pressure (SMP), squeeze pressure duration (SPD), first sensation, urge and maximum tolerated volume (MTV). Statistical study: test of Kruskal-Wallis, test of Mann-Whitney, and multinomial logistic regression test. RESULTS: There were significant differences in the resting pressure (p < 0.001), the ACL (p < 0.001) and the SMP (p < 0.01) in the group of AI with respect to the other two groups. The volume for the first sensation was significantly lower in the healthy subjects than that in the other two groups (p < 0.05). The urge volume and the MVT were smaller in the group with AI with respect to the other groups (p < 0.001). In multivariate analysis the age, the resting pressure and the volume for the first sensation and urge increase the relative risk for AI. CONCLUSIONS: The greater age, the decrease in anal canal resting pressure and the alteration of rectal sensation increase the risk for AI.

The pathogenesis of primary biliary cirrhosis.

Primary biliary cirrhosis (PBC) would develop when the immune system comes across a microorganism with proteins similar to those in the piruvate dehydrogenase complex E2 (PDC-E2), or a neoantigen resulting from a xenobiotic-modified autoantigen. This would lead to an innate immune response where TLRs would play a pivotal mediating role, which would give rise to a local microenvironment favoring an adaptive immune response. Such response would be particularly strong in individuals with selected genetic characteristics. The genetic characteristics underlying this predisposition remain unknown, but they likely entail small numbers of scarcely-active regulatory T cells. The AE2 anion exchanger, which is deficient in patients with PBC, may reduce the number and activity of regulatory T cells. NK cells are also pivotal in the preparation of an adaptive response, as they release a number of cytokines and chemokines that favor and recruit antigen-presenting cells to activate B and T cells - CD4+ Th1 and CD8+. An activation of the former would increase the production of IgM and anti-mitochondrial IgG and IgA antibodies against PDC-E2. An activation of CD8+ cells, also sensitive to PDC-2 as aberrantly expressed on the surface of BECs and SECs, would result in apoptosis for these epithelial cells, and in small bile-duct destruction. Immune response is likely inadequately suppressed because of the small numbers of scarcely-active regulatory T cells, the latter resulting from low genetic expression and activity of the AE2 transporter.

The pathogenesis of primary biliary cirrhosis

Primary biliary cirrhosis (PBC) would develop when the immunesystem comes across a microorganism with proteins similarto those in the piruvate dehydrogenase complex E2 (PDC-E2), ora neoantigen resulting from a xenobiotic-modified autoantigen.This would lead to an innate immune response where TLRswould play a pivotal mediating role, which would give rise to a localmicroenvironment favoring an adaptive immune response.Such response would be particularly strong in individuals with selectedgenetic characteristics. The genetic characteristics underlyingthis predisposition remain unknown, but they likely entailsmall numbers of scarcely-active regulatory T cells. The AE2 anionexchanger, which is deficient in patients with PBC, may reducethe number and activity of regulatory T cells. NK cells arealso pivotal in the preparation of an adaptive response, as they releasea number of cytokines and chemokines that favor and recruitantigen-presenting cells to activate B and T cells – CD4+ Th1 andCD8+. An activation of the former would increase the productionof IgM and anti-mitochondrial IgG and IgA antibodies againstPDC-E2. An activation of CD8+ cells, also sensitive to PDC-2 asaberrantly expressed on the surface of BECs and SECs, would resultin apoptosis for these epithelial cells, and in small bile-duct destruction.Immune response is likely inadequately suppressed becauseof the small numbers of scarcely-active regulatory T cells,the latter resulting from low genetic expression and activity of theAE2 transporter(AU)

[An analysis of the causes, characteristics, and consequences of reexposure to a drug or compound responsible for a hepatotoxicity event]. / Análisis de las causas, características y consecuencias de la reexposición al fármaco o compuesto responsable de un episodio de hepatotoxidad.

INTRODUCTION: reexposure to a causal agent represents a potentially serious event in hepatotoxicity. OBJECTIVES: to assess the characteristics and outcome of cases with positive reexposure. MATERIAL AND METHODS: a retrospective study of cases with evidence of positive reexposure included in Registro Español de Hepatopatías Asociadas a Medicamentos, and an analysis of their relation to demographic and clinical variables, causality, course, and consequences. RESULTS: of a total of 520 cases 31 (6%) met reexposure criteria. Fatal outcomes, needs for admission, and mean recovery time were all higher for hepatocellular-type toxic injury. The most commonly identified drug class was antibiotics. On most occasions (73%) reexposure to the causal compound escaped notice because of: absence of index case diagnosis, lack of information to patients and their physicians, and (12%) development of cross reactions between structurally similar drugs. CONCLUSIONS: accidental reexposure to a drug or a structurally-related compound after an initial hepatotoxicity event is common and may have serious consequences, particularly in hepatocellular-type toxicity. Careful history taking and reflecting diagnostic suspicion in the initial episode s record may reduce the incidence of this iatrogenic event.

Análisis de las causas, características y consecuencias de la reexposición al fármaco o compuesto responsable de un episodio de hepatotoxicidad / No disponible

Introducción: la reexposición al agente causal constituye unincidente potencialmente grave en hepatotoxicidad.Objetivos: evaluar las características y la evolución de los casoscon reexposición positiva.Material y métodos: estudio retrospectivo de una serie decasos con evidencia de reexposición positiva incluidos en el RegistroEspañol de Hepatopatías Asociadas a Medicamentos, analizandosu relación con variables demográficas y clínicas, causalidad,evolución y consecuencias.Resultados: de un total de 520 casos, 31 (6%) cumplían loscriterios de reexposición. La evolución fatal, la necesidad de hospitalizacióny el tiempo medio de recuperación fueron mayores enla lesión tóxica de tipo hepatocelular. El grupo farmacológicoidentificado con mayor frecuencia fue el de los antibióticos. En lamayoría de los casos la reexposición con el compuesto responsablefue inadvertida (73%) debido a: la ausencia de diagnóstico delcaso índice, la carencia de información al paciente o a su médicoy también (12%) por el desarrollo de una reacción cruzada entrefármacos estructuralmente similares.Conclusiones: la reexposición accidental a un mismo fármacoo a otro estructuralmente relacionado tras un primer episodiode hepatotoxicidad no es infrecuente y sus consecuencias puedenser graves, especialmente en el tipo de lesión hepatocelular. Unaminuciosa historia clínica y la sospecha diagnóstica reflejada en elinforme del primer episodio podrían disminuir la incidencia deeste evento iatrogénico

Introduction: reexposure to a causal agent represents a potentiallyserious event in hepatotoxicity.Objectives: to assess the characteristics and outcome of caseswith positive reexposure.Material and methods: a retrospective study of cases withevidence of positive reexposure included in Registro Español deHepatopatías Asociadas a Medicamentos, and an analysis of theirrelation to demographic and clinical variables, causality, course,and consequences.Results: of a total of 520 cases 31 (6%) met reexposure criteria.Fatal outcomes, needs for admission, and mean recovery timewere all higher for hepatocellular-type toxic injury. The most commonlyidentified drug class was antibiotics. On most occasions(73%) reexposure to the causal compound escaped notice becauseof: absence of index case diagnosis, lack of information topatients and their physicians, and (12%) development of cross reactionsbetween structurally similar drugs.Conclusions: accidental reexposure to a drug or a structurally-related compound after an initial hepatotoxicity event is commonand may have serious consequences, particularly in hepatocellular-type toxicity. Careful history taking and reflectingdiagnostic suspicion in the initial episode’s record may reduce the incidence of this iatrogenic event (AU)

Hidrotórax hepático refractario: tratamiento eficaz con octreótido / Refractory hepatic hydrothorax: successful treatment with octreotide

Describimos el caso de una paciente que presentó un hidrotórax como primera manifestación de una cirrosis hepática. Ante la ausencia de respuesta al tratamiento diurético, a la realización de una pleurodesis y a la colocación de una derivación portosistémica percutánea intrahepática, se inició tratamiento con octreótido conlo que se obtuvo la resolución del mismo. Se trata del tercer caso publicado en la literatura de hidrotórax hepático refractario con respuesta completa y mantenida al tratamiento con octreótido

We report the case of a patient that developed hepatic hydrothorax as the first complication of liver cirrhosis. Due to the lack of response to diuretics, pleurodesis and TIPS, treatment with octreotide was started with resolution of hydrothorax. To the best of our knowledge, this is the third reported case of refractory hepatic ;;hydrothorax with complete and sustained response to octreotide

IL-6 y remodelación de la matriz extracelular / IL-6 and extracellular matrix remodeling

No disponible

Refractory hepatic hydrothorax: successful treatment with octreotide.

We report the case of a patient that developed hepatic hydrothorax as the first complication of liver cirrhosis. Due to the lack of response to diuretics, pleurodesis and TIPS, treatment with octreotide was started with resolution of hydrothorax. To the best of our knowledge, this is the third reported case of refractory hepatic hydrothorax with complete and sustained response to octreotide.

Poliarteritis nodosa e infección por el virus de la hepatitis B / Polyarteritis nodosa and hepatitis B virus infection

No disponible

Clinical, anorectal manometry and surface electromyography in the study of patients with fecal incontinence.

OBJECTIVE: to demonstrate the role of the clinical, anorectal manometry and surface electromyography in the assessment of patients with fecal incontinence. PATIENTS AND METHODS: ninety-three patients with fecal incontinence are retrospectively reviewed and the data obtained from the directed clinical history, physical examination of the anal region, digital rectal examination, anorectal manometry and surface electromyography are analyzed. A treatment was administered in accordance with the alterations encountered and the results evaluated at 3 and 12 months. RESULTS: fecal incontinence was predominant (91.4%) in women age 59.7+/-11. A background of obstetric risks (48.2%) was frequent in women. Also, 73.1% of the patients presented diarrhea. The anorectal manometry (ARM) demonstrated some alterations in 90.3% of the patients, whereas a hypotonic sphincter was the most common finding (85.7%). Rectal sensitivity or distensibility alterations were present in the rest of the patients. In 79.2% ofthe cases, hypotonic sphincter was associated with rectal sensitivity or distensibility alterations. In 65.2% of patients with hypotonic external anal sphincter, damage of the pudendal nerve was found and therefore biofeedback was indicated in 41.9% of them. CONCLUSIONS: the clinical study of the patients, together with the anorectal manometry and surface electromyography enables the identification of the cause of FI and its treatment. These studies demonstrate that in most cases the origin of the incontinence is due to multiple etiologies, however the treatment of some of the factors involved frequently improves the symptomatology.

Collagen alpha1(I) gene contains an element responsive to tumor necrosis factor-alpha located in the 5' untranslated region of its first exon.

The aims of the present study were to identify the cis-acting element through which tumor necrosis factor-alpha (TNFalpha) inhibits collagen alpha1(I) gene transcription and the trans-acting factors involved in this effect in cultured hepatic stellate cells. Deletion analysis of the collagen alpha1(I) promoter demonstrated that TNFalpha inhibited gene expression through an element located between -59 and + 116 bp relative to the transcription start site. DNase I protection assays revealed a footprint between +68 and +86 bp of the collagen first exon, the intensity of which decreased when the DNA probe was incubated with nuclear protein from TNFalpha-treated hepatic stellate cells. This footprint contained a G+C-rich box. Transfection experiments demonstrated that mutations in this G+C-rich element abrogated the inhibitory effect of TNFalpha on the collagen alpha1(I) promoter. Gel retardation experiments using a radiolabeled oligonucleotide containing sequences of this region confirmed that TNFalpha treatment decreased the formation of two complexes between nuclear proteins and DNA. These complexes were efficiently blocked with an oligonucleotide containing an Spl-binding site and were supershifted with specific Spl and Sp3 antibodies. These results suggest that TNFalpha inhibits collagen alpha1(I) gene expression by decreasing the binding of Spl to a G+C-rich box in the 5' untranslated region of its first exon.

Sp family of transcription factors is involved in iron-induced collagen alpha1(I) gene expression.

The purpose of this study was to identify the cis-acting elements and the trans-acting factors involved in the iron-induced expression of the collagen alpha1(I) (COL1aI) gene. Rat hepatic stellate cells were cultured in the presence of 50 microM ferric chloride, 50 microM ascorbic acid, and 250 microM citric acid (Fe/AA/CA), and the effects on collagen gene expression and the binding of nuclear proteins to the COL1aI promoter were measured. The Fe/AA/CA treatment induced a time- and dose-dependent increase in the cellular levels of COL1aI mRNA that was abrogate by pretreating cells with cycloheximide, antioxidants, and inhibitors of aldehyde-protein adduct formation. Transient transfection experiments showed that Fe/AA/CA exerted its effect through regulatory elements located between -220 and -110 bp of the COL1aI promoter. Gel retardation assays showed that Fe/AA/CA increased the binding of nuclear proteins to two elements located between -161 and -110 bp of the COL1aI promoter. These bindings were blocked by unlabeled consensus Sp1 oligonucleotide and supershifted with Sp1 and Sp3 antibodies. Finally, Fe/AA/CA increased cellular levels of the Sp1 and Sp3 proteins and Sp1 mRNA. Treatment with Fe/AA/CA stimulates COL1aI gene expression by inducing the synthesis of Sp1 and Sp3 and their binding to two regulatory elements located between -161 and -110 bp of the COL1aI promoter.