Diferencias clínicas entre los pacientes con dolor crónico primario y secundario atendidos por una unidad multidisciplinar de dolor crónico infantil / Clinical differences in a multidisciplinary pediatric pain unit between primary and secondary chronic pain

Introducción: El dolor crónico afecta a un porcentaje significativo de la población pediátrica en los países desarrollados, y puede tener una causa médica bien definida en el dolor crónico secundario (DCS), o desconocida en el dolor crónico primario (DCP). En España, hasta el momento, no existe información acerca de las diferencias clínicas de los pacientes atendidos en unidades multidisciplinarias. Métodos: Análisis retrospectivo de las historias clínicas de los pacientes atendidos en 2018 por la Unidad de Dolor Crónico Infantil del Hospital Universitario La Paz. Resultados: Se incluyeron los 92 pacientes atendidos, con edades comprendidas entre 2 y 19 años, y una edad media de 12,4 (SD=4,1) años, mayoritariamente de sexo femenino (55%) y una duración media del dolor de 11,3 (SD=10,4) meses. Los resultados de comparar pacientes con DCP (n=31) y DCS (n=61) mostraron que ambos grupos presentaban dolor medio con una gran intensidad (x=5,9; SD=2,2; rango=0-10), con duración y repercusión funcional similares, aunque el DCP se asoció menos a descriptores de tipo neuropático que el DCS (p=0,040) y era más extenso en su localización (p<0,001). Ambos grupos recibieron similar tratamiento basado en rehabilitación, psicoterapia, técnicas invasivas y tratamiento con medicación analgésica, aunque los pacientes del grupo DCP recibieron menos medicaciones analgésicas (gabapentinoides y opiáceos) que el DCS (p=0,011). Conclusión: Los pacientes con DCP o DCS, aunque tengan un perfil clínico similar, presentan diferencias en el número y tipo de analgésicos empleados, lo que avalaría la importancia del diagnóstico de la causa para adecuar el tratamiento farmacológico subsiguiente.(AU)

Introduction: Chronic pain affects an important part of the pediatric population in developed countries. secondary chronic pain (SCP) can have a well-defined medical cause, but primary chronic pain (PCP) can have an unknown etiology. In Spain, there is as yet no information on the clinical differences between patients treated in multidisciplinary units. Methods: Retrospective analysis of the clinical records of patients seen in 2018 at the Children's Chronic Pain Unit in University La Paz Hospital. Results: A total of 92 patients were included (age between 3 and 19 years), with a mean age of 12.4 (SD=4.1) years, mostly female (55%), with a mean duration of pain of 11.3 (SD=10.4) months. A comparison of patients with PCP (n=31) and SCP (n=61) showed that both groups, on average, presented intense pain (X=5.9; SD=2.2; range=0-10), with similar duration and functional repercussions, although PCP was less likely to be associated with neuropathic descriptors than SCP (p=.040), and was more extensive (p<.001). Both groups received similar treatment, based on rehabilitation, psychotherapy, invasive techniques and analgesic medication, although patients in the PCP group received less analgesic medication (gabapentinoids and opioids) than the SCP (p=.011). Conclusion: Patients treated in a multidisciplinary Child Pain Unit for PCP or SCP present a very similar clinical profile, though with differences in the number and type of analgesic drugs used. This shows the importance of etiologic diagnosis for adequate pharmacological treatment.(AU)

Clinical differences in a multidisciplinary pediatric pain unit between primary and secondary chronic pain.

INTRODUCTION: Chronic pain affects an important part of the pediatric population in developed countries. secondary chronic pain (SCP) can have a well-defined medical cause, but primary chronic pain (PCP) can have an unknown etiology. In Spain, there is as yet no information on the clinical differences between patients treated in multidisciplinary units. METHODS: Retrospective analysis of the clinical records of patients seen in 2018 at the Children's Chronic Pain Unit in University La Paz Hospital. RESULTS: A total of 92 patients were included, (age between 3 and 19 years), with a mean age of 12.4 (SD = 4.1) years, mostly female (55%), with a mean duration of pain of 11.3 (SD = 10.4) months. A comparison of patients with PCP (n = 31) and SCP (n = 61) showed that both groups, on average, presented intense pain (X = 5.9; SD = 2.2; range = 0-10), with similar duration and functional repercussions, although PCP was less likely to be associated with neuropathic descriptors than SCP (p = 0.040), and was more extensive (p < 0.001). Both groups received similar treatment, based on rehabilitation, psychotherapy, invasive techniques and analgesic medication, although patients in the PCP group received less analgesic medication (gabapentinoids and opioids) than the SCP (p = 0.011). CONCLUSION: Patients treated in a multidisciplinary Child Pain Unit for PCP or SCP present a very similar clinical profile, though with differences in the number and type of analgesic drugs used. This shows the importance of etiologic diagnosis for adequate pharmacological treatment.

MAOA genotype, social exclusion and aggression: an experimental test of a gene-environment interaction.

In 2002, Caspi and colleagues provided the first epidemiological evidence that genotype may moderate individuals' responses to environmental determinants. However, in a correlational study great care must be taken to ensure the proper estimation of the causal relationship. Here, a randomized experiment was performed to test the hypothesis that the MAOA gene promoter polymorphism (MAOA-LPR) interacts with environmental adversity in determining aggressive behavior using laboratory analogs of real-life conditions. A sample of 57 Caucasian male students of Catalan and Spanish origin was recruited at the University of Barcelona. Ostracism, or social exclusion, was induced as environmental adversity using the Cyberball software. Laboratory aggression was assessed with the Point Subtraction Aggression Paradigm (PSAP), which was used as an analog of antisocial behavior. We also measured aggressiveness by means of the reduced version of the Aggression Questionnaire. The MAOA-LPR polymorphism showed a significant effect on the number of aggressive responses in the PSAP (F(1,53) = 4.63, P = 0.03, partial η(2) = 0.08), as well as social exclusion (F(1,53) = 8.03, P = 0.01, partial η(2) = 0.13). Most notably, however, we found that the MAOA-LPR polymorphism interacts significantly with social exclusion in order to provoke aggressive behavior (F(1,53) = 4.42, P = 0.04, partial η(2) = 0.08), remarkably, the low-activity allele of the MAOA-LPR polymorphism carriers in the ostracized group show significantly higher aggression scores than the rest. Our results support the notion that gene-environment interactions can be successfully reproduced within a laboratory using analogs and an appropriate design. We provide guidelines to test gene-environment interactions hypotheses under controlled, experimental settings.

[The development of antisocial behavior: psychobiological and environmental factors and gene-environment interactions]. / Desarrollo del comportamiento antisocial: factores psicobiológicos, ambientales e interacciones genotipo-ambiente.

INTRODUCTION: Antisocial behavior is a complex phenomenon with strong implications in neurology and psychiatry. In order to study the ontogenetic development of antisocial behavior, we must check for the existence of physiological mechanisms related to it, and to understand its environmentally-modulated functioning. AIM: To review the state-of-the-art of the development of antisocial behavior, and especially, of the interaction between environmental and genetic factors. DEVELOPMENT: Recent research has highlighted certain brain alterations linked to violent behavior, either at structural, or functional or biochemical levels. Genetic research has also made some advances in this field, discovering some genes--i.e. monoamineoxidase A (MAOA)--related to antisocial behavior. However, the importance of environmental factors in its development must not be left behind. Recent studies have shown that individuals carrying a low transcriptional activity allele of the MAOA gene, and that also suffered severe maltreatment are more prone to antisocial behavior. This interaction is biologically relevant, as there are underlying biological mechanisms that may be able to explain the ethiopathogeny of antisocial behavior. CONCLUSIONS: Although the works herein presented pioneered the field, they are limited by the fact that all the reviewed variables are associated to antisocial behavior, but they lack direct causal evidence of their effects on antisocial behavior. Undoubtedly, future research on psychobiological mechanisms and the understanding of their environmental modulation will help finding therapeutic targets and preventive strategies for antisocial behavior.

Desarrollo del comportamiento antisocial: factores psicobiológicos, ambientales e interacciones genotipo-ambiente / The deelopment of antisocial behavior: psychobiological and environmental factors and gene-environment interactions

Resumen. Introducción. El comportamiento antisocial es un fenómeno amplio y complejo con profundas implicaciones en neurología y psiquiatría. Para poder enfrentarse a una tarea tan compleja como estudiar el desarrollo ontogenético del comportamiento antisocial hace falta comprobar la existencia de mecanismos fisiológicos relacionados con él y entender cómo los factores ambientales pueden modular su funcionamiento. Objetivo. Revisar los conocimientos que tenemos acerca del desarrollo del comportamiento antisocial, y de la interacción entre factores ambientales y genéticos. Desarrollo. Investigaciones recientes han puesto de relieve alteraciones cerebrales que están asociadas al comportamiento violento, tanto desde el punto de vista estructural como funcional o bioquímico. La investigación genética también ha realizado avances en este terreno, como la detección de algunos genes –como el de la monoaminooxidasa A (MAOA)– relacionados con el comportamiento antisocial. Sin embargo, no debemos olvidar los factores ambientales en el desarrollo de éste. Estudios recientes indican que aquellos individuos portadores de una versión poco funcional del gen MAOA y que reciben un grave maltrato son más proclives al comportamiento antisocial. La significación biológica de esta interacción es relevante, ya que ciertos mecanismos biológicos subyacentes pueden explicar la etiopatogenia del comportamiento antisocial, aunque sea a un nivel muy elemental. Conclusiones. Los estudios mostrados, a pesar de ser pioneros, tienen una gran limitación, y es que a pesar de las evidencias de que todas las variables presentadas están asociadas al comportamiento antisocial, no hay una evidencia causal directa sobre su efecto en éste último. Sin duda, el estudio futuro de los mecanismos psicobiológicos y la comprensión de su modulación ambiental ofrecerán dianas terapéuticas y de prevención para el abordaje del comportamiento antisocial en todas sus vertientes (AU)

Summary. Introduction. Antisocial behavior is a complex phenomenon with strong implications in neurology and psychiatry. In order to study the ontogenetic development of antisocial behavior, we must check for the existence of physiological mechanisms related to it, and to understand its environmentally-modulated functioning. Aim. To review the state-of-the-art of the development of antisocial behavior, and especially, of the interaction between environmental and genetic factors. Development. Recent research has highlighted certain brain alterations linked to violent behavior, either at structural, or functional or biochemical levels. Genetic research has also made some advances in this field, discovering some genes –i.e. monoamineoxidase A (MAOA)– related to antisocial behavior. However, the importance of environmental factors in its development must not be left behind. Recent studies have shown that individuals carrying a low transcriptional activity allele of the MAOA gene, and that also suffered severe maltreatment are more prone to antisocial behavior. This interaction is biologically relevant, as there are underlying biological mechanisms that may be able to explain the ethiopathogeny of antisocial behavior. Conclusions. Although the works herein presented pioneered the field, they are limited by the fact that all the reviewed variables are associated to antisocial behavior, but they lack direct causal evidence of their effects on antisocial behavior. Undoubtedly, future research on psychobiological mechanisms and the understanding of their environmental modulation will help finding therapeutic targets and preventive strategies for antisocial behavior (AU)

Low-dose antihypertensive therapy with 1.5 mg sustained-release indapamide: results of randomised double-blind controlled studies. European study group.

OBJECTIVE: In accordance with international recommendations on the need to decrease doses of antihypertensive drugs, a low-dose (1.5 mg) sustained-release (SR) formulation of indapamide was developed to optimize the drug's efficacy : safety ratio. The aim of this work was to evaluate the benefit of a low-dose diuretic by consolidating the efficacy and safety results of two clinical trials with a similar design. PATIENTS AND METHODS: Clinical data were obtained in two European randomized double-blind studies with 690 mild to moderate hypertensive patients (95 mmHg < or = supine diastolic blood pressure < or = 114 mmHg using a mercury sphygmomanometer) treated respectively for 2 and 3 months, with a mean age of 53 and 57 years, 44 and 57% males, mean supine diastolic blood pressure of 100.6 and 102.5 mmHg and mean supine systolic blood pressure of 161.0 and 164.5 mmHg. RESULTS: The first study, a dose-finding study with indapamide SR at 1.5, 2 and 2.5 mg versus placebo and the immediate-release (IR) formulation of indapamide, showed that the 1.5 mg dosage of the new indapamide formulation had an improved antihypertensive efficacy : safety ratio. The second study confirmed the equivalence of blood pressure reductions with 1.5 mg indapamide SR and 2.5 mg indapamide IR, and better acceptability with 1.5 mg indapamide SR, particularly in the number of patients with serum potassium levels < 3.4 mmol/l, which was reduced by more than 50%. The long-term efficacy of 1.5 mg indapamide SR was observed through a 9-month open-treatment follow-up to the second study. CONCLUSION: The 1.5 mg SR formulation of indapamide has an improved antihypertensive efficacy : safety ratio, which is in accordance with international recommendations for the use of low-dose antihypertensive drugs and diuretics in first-line therapy of hypertension.

Complement resistance of capsulated strains of Aeromonas salmonicida.

The complement resistance of Aeromonas salmonicida strains grown under conditions promoting capsule formation was investigated using well characterized strains and their isogenic mutants. Complement resistance was previously studied using the same strains growing under non-capsulating conditions. The serum resistant strains were found to activate complement, but rapidly degrade C3b preventing productive formation of the lytic complex C5b-9. Isogenic lipopolysaccharide rough mutants grown under non-capsulating conditions were serum sensitive, binding a large amount of C3b and leading to productive formation of C5b-9. When grown under conditions promoting capsule formation, these mutants were partially resistant to complement because less C3b is bound to them and also partially degraded, with a concomitant reduction in lytic C5b-9.

[Treatment of hypertension with indapamide 1.5 mg sustained-release form: synthesis of results]. / Traitement de l'hypertension artérielle par l'indapamide 1,5 mg comprimé enrobé à libération prolongée: synthèse des résultats.

In accordance with international recommendations on the need to decrease doses of antihypertensive drugs, a low-dose (1.5 mg) sustained-release form of indapamide was developed so as to optimize the safety/efficacy ratio, while maintaining a once-daily administration. The new formulation ensures that the active ingredient release occurs in a sustained manner over 24 hours, with mean concentrations close to the maximal concentration over a prolonged period, while avoiding peak plasma concentrations. Clinical data were obtained mainly through two European multicenter, randomized, double-blind trials, totalling 690 patients. Firstly, the antihypertensive efficacy' of the new indapamide 1.5 mg form was demonstrated by measuring blood pressure 24 hours after the last drug intake, using a mercury sphygmomanometer; the equivalence of its antihypertensive efficacy with the immediate-release form of indapamide 2.5 mg was then verified. Biochemical safety data showed better acceptability with indapamide 1.5 mg with in particular a reduction of more than 50% of the number of patients with kalemia < 3.4 mmol/l; clinical safety data confirmed the good acceptability observed with the 2.5 mg immediate-release form of indapamide since many years, especially regarding glucose and lipid neutrality. In conclusion, the 1.5 mg sustained-release form of indapamide has an improved antihypertensive efficacy/safety ratio which is in accordance with international recommendations for the usage of low doses of antihypertensive drugs and diuretics in the first-line treatment of hypertension.

The role of the capsular polysaccharide of Aeromonas salmonicida in the adherence and invasion of fish cell lines.

The ability of several Aeromonas salmonicida strains grown under different conditions (capsulated and non-capsulated) to adhere to and invade two fish cell lines was compared. The level of adherence was slightly higher when the strains were grown under conditions promoting capsule formation than when the same strains were grown under conditions which did not promote capsule formation. However, the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines, which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation. From these results we conclude that the capsular polysaccharide, in these strains, is an important factor for intracellular invasion.

The presence of capsular polysaccharide in mesophilic Aeromonas hydrophila serotypes O:11 and O:34.

Mesophilic Aeromonas hydrophila from serotypes O:11 and O:34 grown in a glucose-rich medium produce a capsule that can be seen under light and electron microscopy. The purified capsular polysaccharide has a composition qualitatively similar for strains O:11 and O:34, but quantitatively different. The capsular polysaccharides were immunogenic in rabbits, and did not cross-react with specific antibodies against either purified lipopolysaccharide from strains O:34 or O:11 or against the S-layer characteristic of strains from serotype O:11.

Production and Rheological Properties of the Extracellular Polysaccharide Synthesized by Pseudomonas sp. Strain EPS-5028.

During batch aerobic submerged fermentation, the exopolysaccharide synthesis by Pseudomonas sp. strain EPS-5028 occurred in growth- and non-growth-linked processes. Polysaccharide formation increased when the pH was controlled at 7 during fermentation. Exopolysaccharide production depended on the phosphate content of the medium. The polymer exhibited a pseudoplastic nature, had good thermostability, and was affected neither by pH nor by high concentrations of salt.

Farmacodermia simil lupus eritematoso durante terapeutica con captopril. / Pharmacodermia in lupus erythematosus like-syndrome during captopril therapy

Captopril es una droga utilizada en el tratamiento de la hipertension arterial.Actua inhibiendo a la enzima convertidora de la angiotensina. Es capaz de producir lesiones cutaneas variadas, probablemente inducidas por un mecanismo de potenciacion de las quininas. Se presenta un caso de Sindrome Simil Lupus Eritematosos y Eritema Polimorfo observado en un paciente durante la terapeutica con captopril. Se analizan las lesiones cutaneas registradas en el seguimiento de un total de 22 pacientes. Asimismo se puntualizan las caracteristicas del Sindrome Simil Lupus Eritematoso y las drogas que se han reportado como capaces de inducirlo, entre las que posiblemente se deba incluir captopril. No hemos hallado mencion en la bibliografia de las manifestaciones dermatologicas por captopril de cuadros Simil Lupus como el de nuestro paciente

Farmacodermia simil lupus eritematoso durante terapeutica con captopril. / Pharmacodermia in lupus erythematosus like-syndrome during captopril therapy

Captopril es una droga utilizada en el tratamiento de la hipertension arterial.Actua inhibiendo a la enzima convertidora de la angiotensina. Es capaz de producir lesiones cutaneas variadas, probablemente inducidas por un mecanismo de potenciacion de las quininas. Se presenta un caso de Sindrome Simil Lupus Eritematosos y Eritema Polimorfo observado en un paciente durante la terapeutica con captopril. Se analizan las lesiones cutaneas registradas en el seguimiento de un total de 22 pacientes. Asimismo se puntualizan las caracteristicas del Sindrome Simil Lupus Eritematoso y las drogas que se han reportado como capaces de inducirlo, entre las que posiblemente se deba incluir captopril. No hemos hallado mencion en la bibliografia de las manifestaciones dermatologicas por captopril de cuadros Simil Lupus como el de nuestro paciente

Effect of two organophosphorus insecticides on the phosphate-dissolving soil bacteria.

Dimethoate and malathion added to soil at 10 and 100 microgram/g caused an initial stimulation of CO2 production. Total counts of bacterial propagules were increased. All insecticide applications increased bacteria producing phospholipases from week 1 until week 4 after the application; bacteria then returned to the original levels.