Niveles de vitamina D en pacientes con lesión medular traumática en Chile / Vitamin D levels in patients with traumatic spinal cord injury in Chile

Introducción. La vitamina D cumple un importante rol en el metabolismo óseo y en diversas funciones a nivel extraesquelético. El objetivo de este estudio es determinar la prevalencia de hipovitaminosis D en pacientes con lesión medular traumática (LMT) y describir su asociación con las características de la LMT y demográficas de los pacientes. Material y método. Estudio descriptivo prospectivo en 76 pacientes del Departamento de Rehabilitación del Hospital del Trabajador entre el 30 de julio 2015 y el 30 de julio de 2016. Se realizó la medición de 25-hidroxivitamina D (25-OH-D) en sangre mediante el método de radioinmunoanálisis y una encuesta estructurada a los pacientes. Los resultados se analizaron mediante estadística descriptiva, prueba de Kruskall Wallis, rangos signados de Wilcoxon, Chi cuadrado, Fisher y análisis de correlación de Spearman. Resultados. La mediana de la edad fue 49,5 años (±DE 15,05), el tiempo de evolución de LMT entre un mes hasta 36 años. El promedio de 25-OH-D fue 16,4ng/mL (4,2 - 45,9ng/mL). El 94,7% de los sujetos presentaban hipovitaminosis D (<30 ng/mL) y un 27,6% deficiencia severa (<10 ng/mL). No se encontraron diferencias significativas entre la asociación de hipovitaminosis con sexo, nivel y grado de compromiso de LMT, estación del año, tiempo de exposición al sol y zona donde habitan. Existe una correlación inversa con tendencia a disminuir los niveles de 25-OH-D por cada año de evolución de LMT (Ro=-0,33; p value=0,0040). Conclusión. La hipovitaminosis D es altamente prevalente en pacientes con LMT. Es importante diagnosticar oportunamente para su adecuada suplementación y disminuir la prevalencia de complicaciones (AU)

Introduction. Vitamin D plays an important role in bone metabolism and in various extra-skeletal functions. The aim of this study was to determine the prevalence of vitamin D deficiency in patients with traumatic spinal cord injury (TSCI) and to describe its association with the characteristics of TSCI and patients’ demographic characteristics. Material and method. A prospective descriptive study was conducted in 76 patients treated at the Rehabilitation Department of Hospital del Trabajador between July 30, 2015 and July 30, 2016. Blood measurement of 25-hydroxyvitamin D (25-OH-D) was performed by the radioimmunoassay method and a structured survey. The results were analysed using descriptive statistics, the Kruskall-Wallis test, Wilcoxon signed-rank test, chi-square test, Fisher test and Spearman rank correlation coefficient. Results. The median age was 49.5 years (SD 15.05) and the time from TSCI was between 1 month and 36 years. The mean 25-OH-D level was 16.4ng/mL (4.2-45.9ng/mL). Vitamin D deficiency (<30 ng/mL) was found in 94.7% of the participants and severe deficiency (<10ng/mL) in 27.6%. No significant differences were found between the association of vitamin deficiency with sex, neurologic level, or severity of TSCI, season, amount of time of sun exposure or geographical area of residence. There was s an inverse correlation with a tendency to decrease 25-OH-D for each year from the onset of TSCI (Ro=-0.33, p value=.0040). Conclusion. Vitamin D deficiency is highly prevalent in patients with TSCI. An early diagnosis is important to provide adequate supplementation in order to decrease the prevalence of complications (AU)

Estudio urodinámico en mujeres con síntomas de incontinencia urinaria de esfuerzo pura / Urodynamic study in women with pure stress urinary incontinence

Objetivo: Describir los resultados del estudio urodinámico en mujeres con síntomas de incontinencia urinaria de esfuerzo pura, incluyendo las características del detrusor hiperactivo, sin conocer otras evaluaciones clínicas. Material y métodos: Estudio retrospectivo de mujeres con incontinencia urinaria evaluadas con estudio urodinámico de forma consecutiva. De 710 mujeres evaluadas, se seleccionaron 108 con síntomas de incontinencia urinaria de esfuerzo pura (15%), excluyendo aquellas con cirugía de incontinencia urinaria previa, prolapso de órganos pélvicos en estadio ≥ iii, radioterapia pelviana, uso de fármacos uroselectivos y enfermedades neurológicas. La velocidad de infusión fue de 70 ml/min. La tos fue el único método utilizado para provocar la hiperactividad del detrusor. La prueba de esfuerzo se hizo estandarizada, con uso de tos de intensidad progresiva. Resultados: Se describen valores de referencia de las diferentes etapas del estudio urodinámico. Se demostró incontinencia urinaria de esfuerzo urodinámica en 79 mujeres (73,1%), detrusor hiperactivo en 4 (3,7%) y diagnóstico urodinámico mixto en 15 (13,8%). En 10 pacientes el examen no fue concluyente (9,2%). Dos mujeres presentaron incontinencia urinaria por detrusor hiperactivo (1,9%). Una paciente presentó detrusor hiperactivo inducido por tos sin incontinencia urinaria de esfuerzo urodinámica (0,9%). Hubo asociación entre detrusor hiperactivo y nicturia ≥ 2 (p = 0,002; odds ratio: 3,74; intervalo de confianza del 95%: 1,22-11,39). Una mujer presentó obstrucción de la salida de la vejiga (0,9%). Conclusiones: En mujeres con incontinencia urinaria de esfuerzo pura, sin conocer el resultado de otras evaluaciones clínicas, el estudio urodinámico puede proporcionar información útil para definir el tratamiento

Objective: To describe the results of urodynamic study in women with pure stress urinary incontinence symptoms, including the characteristics of the overactive detrusor. No other clinical assessments were taken into account. Material and methods: A retrospective study in women with urinary incontinence consecutively evaluated by urodynamic study. From a total of 710 women, only 108 (15%) with pure stress urinary incontinence symptoms were selected. Women with prior urinary incontinence surgery, pelvic organ prolapse (stage ≥ iii), pelvic radiotherapy, using medication active on the lower urinary tract and neurological diseases were excluded. Infusion rate was 70 ml/min. Detrusor overactivity was induced only by cough. A standardized cough stress test with progressive cough intensity was carried out. Results: Reference urodynamic values for stress incontinent women are described. Urodynamic stress incontinence was observed in 79 women (73.1%), detrusor overactivity in 4 (3.7%) and mixed urodynamic diagnosis in 15 (13.8%). Test was inconclusive in 10 patients (9.2%). Two women had detrusor overactivity incontinence (1.9%). One patient had detrusor overactivity induced by cough without urodynamic stress incontinence (0.9%). There was an association between detrusor overactivity and nocturia ≥ 2 (P = .002; odds ratio: 3.74; 95% confidence interval: 1.22-11.39). One woman had a bladder outlet obstruction (0.9%). Conclusions: In women with pure stress urinary incontinence, without knowing the outcome of other clinical assessments, urodynamic study can provide useful information to define the proper therapy

Urodynamic study in women with pure stress urinary incontinence.

OBJECTIVE: To describe the results of urodynamic study in women with pure stress urinary incontinence symptoms, including the characteristics of the overactive detrusor. No other clinical assessments were taken into account. MATERIAL AND METHODS: A retrospective study in women with urinary incontinence consecutively evaluated by urodynamic study. From a total of 710 women, only 108 (15%) with pure stress urinary incontinence symptoms were selected. Women with prior urinary incontinence surgery, pelvic organ prolapse (stage ≥iii), pelvic radiotherapy, using medication active on the lower urinary tract and neurological diseases were excluded. Infusion rate was 70 ml/min. Detrusor overactivity was induced only by cough. A standardized cough stress test with progressive cough intensity was carried out. RESULTS: Reference urodynamic values for stress incontinent women are described. Urodynamic stress incontinence was observed in 79 women (73.1%), detrusor overactivity in 4 (3.7%) and mixed urodynamic diagnosis in 15 (13.8%). Test was inconclusive in 10 patients (9.2%). Two women had detrusor overactivity incontinence (1.9%). One patient had detrusor overactivity induced by cough without urodynamic stress incontinence (0.9%). There was an association between detrusor overactivity and nocturia ≥2 (P=.002; odds ratio: 3.74; 95% confidence interval: 1.22-11.39). One woman had a bladder outlet obstruction (0.9%). CONCLUSIONS: In women with pure stress urinary incontinence, without knowing the outcome of other clinical assessments, urodynamic study can provide useful information to define the proper therapy.

The US National Cholesterol Education Programme Adult Treatment Panel III (NCEP ATP III): prevalence of the metabolic syndrome in postmenopausal Latin American women.

BACKGROUND: Metabolic syndrome (METS) is a strong predictor of cardiovascular risk. Since the prevalence of METS increases after menopause, gynecological routine consultation offers an excellent screening opportunity. OBJECTIVES: To assess the prevalence of METS in Latin American postmenopausal women and factors modifying its risk; as well as to assess the role of simple routine care measurements in the diagnosis of the METS. METHODS: A total of 3965 postmenopausal women, aged 45-64 years, seeking health care at 12 gynecological centers in major Latin American cities were included in this cross-sectional study. The US National Cholesterol Education Programme Adult Treatment Panel III (NCEP ATP III) guidelines were applied to assess METS. This was present if three or more of the following conditions were present: waist circumference > or = 88 cm; blood pressure > or = 130/85 mmHg; fasting plasma triglycerides > or = 150 mg/dl; high density lipoprotein (HDL) cholesterol < 50 mg/dl; glucose > or = 110 mg/dl or subjects were receiving treatment for their condition. RESULTS: The prevalences of having at least two, three, four or five components were 62.5, 35.1, 13.5 and 3.2%, respectively. The prevalence increased from 28.1% in those aged 40-44 years to 42.9% in those aged 60-64 years. The risk of METS detection (multivariate analysis) increased with age (odds ratio (OR) 1.22, 95% confidence interval (CI) 1.03-1.43), time elapsed since menopause (OR 1.18, 95% CI 1.00-1.38), smoking cigarettes (OR 1.40, 95% CI 1.19-1.65), obesity (OR 13.01, 95% CI 10.93-15.49) and hypertension (OR 9.30, 95% CI 7.91-10.94). In contrast, hormone therapy reduces this risk (OR 0.59, 95% CI 0.51-0.70). CONCLUSION: There is a high prevalence of the metabolic syndrome in postmenopausal Latin American women seeking gynecologic health care. Age, years since menopause, obesity and hypertension are strong predictors of this condition.

Prevalencia de lesiones musculo-esqueléticas y factores de riesgo en trabajadores de plantas procesadoras de crustáceos en Chile / Prevalence of musculoskeletal disorders and risk factors in a crustacean proccessing plant workers in Chile

Una actividad económica de exportación importante para Chile es el procesamiento de crustáceos, que tiene la presencia de tareas repetitivas y de carga de materiales y cuyas empresas mantienen caracteristicas similares de tecnología y procesos de trabajo. En esta actividad no existe informacion epidemiologica ni programas ergonómicos establecidos en estos procesos.Este estudio se desarrollo en una empresa de procesamiento de crustáceos en la XII Región de Chile. Se senalaron las tareas criticas desde el punto de vista musculo-esqueletico, a las cuales se les determinó el riesgo de las lesiones de extremidad superior mediante la aplicacion de herramientas ergonómicas como Strain Index, RULA y OCRA. Por otro lado, se reunio la evidencia clinica de riesgo por movimientos repetitivos con un examen fisico y musculo-esqueletico. La percepcion subjetiva de los trabajadores se resgistro con la aplicacion de una encuesta basada en el cuestionario musculo-esqueletico nordico.Este estudio senala el precedente de la existencia de desórdenes musculo-esqueléticos en estas actividades, situación no descrita en la literatura, a partir de lo cual se pueden disenar criticas de formacion continua y vigilancia permanente, en la implementación de un Programa de Vigilancia Epidemiologica que establezca criterios comunes de evaluacion de estas actividades.

Xanthine oxidase released from reperfused hind limbs mediate kupffer cell activation, neutrophil sequestration, and hepatic oxidative stress in rats subjected to tourniquet shock.

We have shown previously that rats subjected to tourniquet shock develop an acute form of remote organ injury of the liver that is both Kupffer cell (KC) and polymorphonuclear (PMN) leukocyte dependent. Circulating plasma xanthine oxidase (XO) has been shown to be responsible for the development of endothelial dysfunction and for remote organ injury of the lung and intestine after ischemia-reperfusion protocols. We now hypothesize that XO is released from rat hind limbs upon reperfusion and that it is responsible for KC and PMN leukocyte activation in this shock model. Our results show that about 30% of rat gastrocnemius muscle xanthine dehydrogenase (XD) is converted to XO during the 5-h tourniquet period and that it is released into the femoral vein within 10 min of reperfusion. Total muscle xanthine oxidoreductase activity (XO + XD) decreases within 30 min of reperfusion and is paralleled by a corresponding increase in femoral vein lactic dehydrogenase. In addition, liver tissue XO increases significantly within 30 min of reperfusion without a corresponding conversion of endogenous XD. Conversion of hepatic XD becomes evident 60 min after reperfusion is initiated, as does XO, and alanine aminotransferase (ALT) release into the hepatic vein, presumably from damaged hepatocytes as a consequence of oxidative stress. Tissue myeloperoxidase activity also increases significantly after the 60-min reperfusion period. That XO mediates KC and PMN activation is supported by the following observations: a) the close relationships between plasma XO and the time courses of tumor necrosis factor-alpha TNFalpha release into the hepatic vein and colloidal carbon clearance by KCs; b) that colloidal carbon clearance, TNFalpha and ALT release, loss of tissue free thiols, lipid peroxidation (TBARS), and liver infiltration by PMN neutrophils can also be induced by the administration of exogenous XO to normal rats; and c) pretreatment of rats with allopurinol inhibits KC activation and liver leukocyte infiltration. These results suggest that XO, released from the ischemic limb on reperfusion, is taken up by the liver were it mediates KC and PMN neutrophil activation and thus contributes to the development of multiple system organ failure after hind limb reperfusion.

Role of Küpffer cells and PMN leukocytes in hepatic and systemic oxidative stress in rats subjected to tourniquet shock.

Küpffer cells (KCs) have been implicated in leukocyte recruitment and microvascular dysfunction associated with liver inflammation. The overall objective of this study was to assess the role of KCs and polymorphonuclear (PMN) leukocytes on the oxidative stress elicited in the liver as a consequence of hind limb reperfusion in rats subjected to tourniquet shock, a shock model that differs from other models in that hepatic injury is a consequence of remote organ damage. Colloidal carbon clearance from blood and its incorporation into KCs demonstrate that these cells are activated after the 2 h hind limb reperfusion period and that they are responsible for the observed oxidative stress and for PMN leukocyte recruitment and activation. Liver oxidative stress in this model is evidenced by increased liver tissue GSSG/GSH ratio, thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, myeloperoxidase (MPO) activity, an index of tissue-associated neutrophil accumulation, and a significant loss in total tissue superoxide dismutase (SOD) activity. Mean arterial blood pressure (MAP), as well as plasma levels of alanine aminotransferase (ALT), an index of hepatic tissue injury, total SOD activity, plasma levels of alpha-tocopherol and beta-carotene, and total plasma nitrite are also affected as a consequence of KC activation after the 2 h hind limb reperfusion period. Inhibition of KC activity by gadolinium chloride (GdCl3) reverted most of the above alterations to values that do no differ from those found in control animals. These results support the hypothesis that hepatic and systemic oxidative stress elicited by hind limb reperfusion in rats subjected to tourniquet shock is both KC and PMN leukocyte dependent.

Inhibition of nitric oxide synthesis aggravates hepatic oxidative stress and enhances superoxide dismutase inactivation in rats subjected to tourniquet shock.

The role of nitric oxide (NO) on liver oxidative stress and tissue injury in rats subjected to tourniquet shock was investigated. This shock model differs from others in that injury is a consequence of remote organ damage. Liver oxidative stress becomes evident after hind limb reperfusion, as evidenced by the loss of total tissue thiols; by increases in tissue oxidized glutathione (GSSG), lipid peroxidation (LPO), plasma aminotransferases (alanine aminotransferase (ALT) and (aspartate aminotransferase (AST)), and plasma nitrites; and by a 36% loss in total superoxide dismutase (SOD) activity. Portal blood flow is reduced by 54.1% after 2 h of hind limb reperfusion. Inhibition of NO synthesis with Nomega-nitro-L-arginine methyl ester or L-arginine methyl ester increased mean arterial blood pressure; further reduced portal blood flow; and aggravated liver injury as assessed by further loss in total thiols, increased LPO and GSSG content, and further increases in plasma ALT and AST. Total plasma nitrites were lower than in control animals, and total tissue SOD activity decreased by more than 80%. Treatment with the NO donor sodium nitroprusside reverted the decrease in portal blood flow and also reverted tissue thiol loss, LPO, and GSSG increases, as well as the loss of ALT and AST to plasma and of SOD activity to levels comparable to untreated control shock animals. As expected, plasma nitrites were greater than in tourniquet control animals. These data support the hypothesis that endogenous NO formation protects the rat liver from the consequences of oxidative stress elicited by hind limb reperfusion in rats subjected to tourniquet shock.

Ibuprofen protects rat livers from oxygen-derived free radical-mediated injury after tourniquet shock.

Rats subjected to tourniquet shock suffer a severe form of circulatory shock, tissue and organ oxidative stress, and final multiple system organ failure (MSOF) and death of the animals within 24 h of tourniquet release. The oxidative damage observed in hind-limb muscle tissue after reperfusion does not by itself account for the final systemic and lethal MSOF. We have postulated that organ failure has its genesis in a primary perfusion abnormality, e.g. the hind limbs, which is followed by secondary hypoperfusion of other organs, such as the liver, as has been shown to be the case in several septic shock models. It has also been shown that injured or necrotic tissue can activate neutrophils, Küpffer cells, platelets, and both the complement and coagulation cascades. In turn, complement activation also leads to neutrophil and Küpffer cell activation as assessed by their capacity to generate oxyradicals. Herein we have evaluated the potential protective effect of ibuprofen on hepatic oxygen-derived free radical production, as well as its effects on both polymorphonuclear leucocyte (PMN) activation and liver infiltration. The protective effect of ibuprofen on hepatic oxidative injury was assessed by determining total thiol groups (SH), thiobarbituric acid-reactive substances (TBARS), and by the release of aspartic acid (AsT) and alanine (AIT) aminotransferases in control animals, in animals subjected to 5 h of tourniquets, and in animals after 2 h of hind-limb reperfusion. Liver infiltration by PMNs was determined by histology after staining with eosin-hematoxylin, and PMN activation by their capacity to reduce nitro blue tetrazolium (NBT).(ABSTRACT TRUNCATED AT 250 WORDS)

[The etiopathogenesis of the acute stress ulcer. The role of oxygen free radicals]. / Etiopatogenia de la úlcera aguda por estrés. Rol de los oxidantes derivados del oxígeno.

We evaluated the role of oxygen free radicals in the induction of acute stress gastric ulcer in rats. After 12 hr of immobility, ulcers of up to 4 mm were observed in the gastric mucosa. Pretreatment with allopurinol, a xanthine oxidase inhibitor, produced a significant reduction in the number and size of lesions (p < 0.0001). No protection was afforded by aluminum hydroxide or ranitidine alone, but enhanced protection was observed when given in association to allopurinol. A secondary role for H ions is suggested by these findings. Our results support the hypothesis of a role of oxygen free radicals in the pathogenesis of stress gastric ulcers. Allopurinol might be used in conditions predisposing to stress in patients.