Mortalidade hospitalar por covid-19 em crianças e adolescentes no Brasil em 2020–2021

OBJECTIVE: To describe cases, deaths, and hospital mortality from covid-19 in children andadolescents in Brazil, according to age group, during the evolving phases of the pandemic in2020 and 2021.METHODS: Census of patients aged up to 19 committed with severe acute respiratory syndrome, due to covid-19 or unspecified, notified to the Brazilian Influenza Epidemiological Surveillance Information System, from January 1, 2020, to December 31, 2021. The two years were divided into six phases, covering the spread of the disease—first, second and third wave—as well as the impact of vaccination. The pediatric population was categorized into infants, preschoolers, schoolchildren, and adolescents. Hospital mortality was assessed by pandemic phase and age group.RESULTS: A total of 144,041 patients were recorded in the two years, 18.2% of whom had confirmed cases of covid-19. Children under 5 years old (infants and preschoolers) accounted for 62.8% of those hospitalized. A total of 4,471 patients died, representing about 6.1 deaths per day. Infants were the ones who most progressed to the intensive care unit (24.7%) and had the highest gross number of deaths (n = 2,012), but mortality was higher among adolescents (5.7%), reaching 9.8% in phase 1. The first peak of deaths occurred in phase 1 (May/2020), and two other peaks occurred in phase 4 (March/2021 and May/2021). There was an increase in cases and deaths for younger ages since phase 4. Hospital mortality in the pediatric population washigher in phases 1, 4, and 6, following the phenomena of dissemination/interiorization of thevirus in the country, beginning of the second wave and beginning of the third wave, respectively.CONCLUSION: The absolute number of cases o f covid-19 in children and adolescents is significant. Although complete vaccination in descending order of age provided a natural deviation in age range, there was a greater gap between the curve of new hospitalized cases and the curve of deaths, indicating the positive impact of immunization.OBJETIVO: Descrever casos, óbitos e mortalidade hospitalar por covid-19 em crianças e adolescentes no Brasil, conforme faixa etária, durante as fases de evolução da pandemia em 2020 e 2021. MÉTODOS: Censo de pacientes de até 19 anos internados com síndrome respiratória aguda grave, por covid-19 ou não especificada, notificados ao Sistema de Informação de Vigilância Epidemiológica da Gripe do Brasil, entre 1 de janeiro de 2020 e 31 de dezembro de 2021. Os dois anos foram divididos em seis fases, abrangendo a disseminação da doença − primeira, segunda e terceira onda −, bem como o impacto da vacinação. A população pediátrica foi categorizada em lactentes, pré-escolares, escolares e adolescentes. A mortalidade hospitalar foi avaliada por fase da pandemia e faixa etária. RESULTADOS: Foram contabilizados 144.041 pacientes nos dois anos, sendo 18,2% casos de covid-19 confirmados. Menores de 5 anos (lactentes e pré-escolares) corresponderam a 62,8% dos hospitalizados. Evoluíram a óbito 4.471, representando cerca 6,1 óbitos por dia. Os lactentes foram os que mais evoluíram para unidade de terapia intensiva (24,7%) e apresentaram o maior número bruto de óbito (n = 2.012), porém a mortalidade foi maior entre os adolescentes (5,7%), chegando a 9,8% na fase 1. O primeiro pico de óbitos ocorreu na fase 1 (maio/2020), e outros dois picos ocorreram na fase 4 (março/2021 e maio/2021). Verificou-se avanço de casos e óbitos para as idades inferiores desde a fase 4. A mortalidade hospitalar na população pediátrica foi maior nas fases 1, 4 e 6, acompanhando os fenômenos de disseminação/interiorização do vírus no país, início da segunda onda e início da terceira onda, respectivamente. CONCLUSÃO: O número absoluto de casos de covid-19 em crianças e adolescentes é expressivo. Embora a vacinação completa em ordem decrescente de idade tenha proporcionado um desvio natural de faixa etária, ocorreu um distanciamento maior entre a curva de novos casos hospitalizados e a curva de óbitos, indicando o impacto positivo da imunização

Clinical evaluation, biochemistry and genetic polymorphism analysis for the diagnosis of lactose intolerance in a population from northeastern Brazil

OBJECTIVE: This work aimed to evaluate and correlate symptoms, biochemical blood test results and single nucleotide polymorphisms for lactose intolerance diagnosis. METHOD: A cross-sectional study was conducted in Fortaleza, Ceará, Brazil, with a total of 119 patients, 54 of whom were lactose intolerant. Clinical evaluation and biochemical blood tests were conducted after lactose ingestion and blood samples were collected for genotyping evaluation. In particular, the single nucleotide polymorphisms C>;T-13910 and G>;A-22018 were analyzed by restriction fragment length polymorphism/polymerase chain reaction and validated by DNA sequencing. RESULTS: Lactose-intolerant patients presented with more symptoms of flatulence (81.4%), bloating (68.5%), borborygmus (59.3%) and diarrhea (46.3%) compared with non-lactose-intolerant patients (

VISITA DE INSPEÇÃO PREDIAL REALIZADA NO CONDOMÍNIO IRISVILLE

Este trabalho caracteriza-se pela inspeção predial como um “Check-up” da edificação, tendo como primordial um diagnóstico geral sobre o Residencial Irisville  região leste de Goiânia-Goiás , identificando as anomalias construtivas e falhas de manutenção – com a análise do risco oferecido aos usuários, ao meio ambiente e ao patrimônio – que interferem e prejudicam a saúde e habitabilidade, frente ao desempenho dos sistemas construtivos e elementos vistoriados da edificação, especialmente ao terreno, estrutura e fundações, instalações elétricas e hidro sanitárias. Neste contexto, a ANOMALIA representa a irregularidade relativa à construção e suas instalações, enquanto que a FALHA diz respeito à manutenção, operação e uso das casas do residencial

Efeito do bochecho com carboidrato associado com cafeína ou taurina sobre a performance de praticantes de atividade física de alta intensidade

The mouth rinse with carbohydrates and other substances has been studied as an ergogenic resource to improve physical performance, by stimulating receptors located in the oral cavity. During physical activity, the intake of certain nutrients becomes impractical because intestinal discomfort. Therefore, the use of mouth rinse in long-term sports would be an important application. This research evaluated the impact of the mouth rinse with carbohydrate combined or not with taurine or caffeine on the performance in high-intensity physical activity. This study was carried out with 12 physically active volunteers of both sexes (age 27.5 ±3.6; weight 69.8 ±11.4; BMI 24.8 ±2.32).  Each volunteer performed four tests, with different mouth rinse solutions: placebo, carbohydrate, carbohydrate associated with taurine or caffeine.  The test consisted of running on a treadmill for 30 minutes at 8 km/h. Subsequently, the volunteer performed the mouth rinse with the solution and then performed the maximum repetitions of burpees, for 3 minutes. Blood glucose, subjective perception of effort (SPE) was assessed using the Borg Scale, and the level of dehydration by the rate of sweating. Statistical differences were considered for p<0.05. There was no difference in the number of burps, SPE, dehydration, or blood glucose among tests. The caloric intake was below the recommended. The mouth rinse with carbohydrate alone or associated with taurine or caffeine did not affect the physical performance.O bochecho com carboidrato e outras substâncias vem sendo estudado como um recurso ergogênico, sendo este capaz de otimizar a performance física apenas por estímulo de receptores localizados na cavidade oral. Durante a atividade física a ingestão de determinados nutrientes torna-se inviável por causarem desconforto intestinal, logo, a utilização de bochechos em esportes de longa duração seria de importante aplicação. A presente pesquisa avaliou o impacto do bochecho com carboidrato combinado ou não com taurina ou cafeína sobre a performance de praticantes de atividade física de alta intensidade. Este foi estudo foi realizado com 12 voluntários fisicamente ativos de ambos os sexos (idade 27,5 ±3,6; peso 69,8 ±11,4 kg; IMC 24,8 ±2,32 kg/m2). Cada voluntário realizou quatro testes, com distintas soluções de bochecho, a saber: placebo, carboidrato, carboidrato associado à taurina ou à cafeína. O teste consistiu em corrida em uma esteira durante 30 minutos a 8 km/h. Posteriormente, o voluntário realizou o bochecho com a solução e em seguida, o máximo de repetições de “burpeesâ€, durante 3 minutos. Foi avaliada a glicemia, a percepção subjetiva de esforço (PSE) por meio da Escala de Borg e o nível de desidratação através taxa de sudorese. Diferenças estatísticas foram consideradas para o valor de p<0,05. Não houve diferença no número de "burpeeâ€, PSE, desidratação ou glicemia entre os testes. Observou-se uma ingestão calórica abaixo da recomendada entre os participantes. O bochecho de carboidrato isolado ou associado à taurina ou cafeína não tiveram efeito sobre a performance física dos indivíduos

Elastography improves accuracy of early hepato-biliary complications diagnosis after allogeneic stem cell transplantation

Significant morbidity and mortality have been associated with liver complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Causes and consequences of these hepato-biliary complications are various and might be life-threatening. A high misdiagnosis rate has been reported because of a weak correlation between clinical, laboratory and imaging data. Liver elastography, a liver stiffness measure, is able to assess liver fibrosis and portal hypertension in most liver diseases, but data after allo-HSCT are scarce. Our aim was to determine the interest of sequential liver stiffness measurements for the diagnosis of early hepatic complications after allo-HSCT. Over a two years period of time, 161 consecutive adult patients were included and 146 were analyzed. Ultrasonography and elastography measurements were performed before transplantation, at day+7 and day+14 by three different experienced radiologists unaware of patients'clinical status. Eighty-one (55%) patients had liver involvements within the first 100 days after allo-HSCT. Baseline elastography was not predictive for the occurrence of overall liver abnormalities. A significant increase in 2D real-time shearwave elastography (2D-SWE) was found in patients with sinusoidal obstruction syndrome (SOS). Fifteen patients (10%) fulfilled EBMT score criteria and twelve (8%) reached Baltimore criteria for SOS diagnosis, but only six (4%) had a confirmed SOS. 2D-SWE at day+14 allowed early detection of SOS (AUROC=0.84, p=0.004) and improved sensibility (75%), specificity (99%) and positive predictive value (60%) over the Seattle, Baltimore or EBMT scores. A 2D-SWE measurement above 8.1kPa at day+14 after allo-HSCT seems a promising, non-invasive, and reproducible tool for early and accurate diagnosis of SOS

Dominance clonale dans les insuffisances médullaires

Les insuffisances médullaires sont maladies rares qui se manifestent principalement par pancytopénie. L'incapacité du tissu hématopoïétique à maintenir l'hématopoïèse peut être acquise, principalement l'aplasie médullaire idiopathique (AM), ou des défauts génétiques, tels que le déficit de réparation de l'ADN de l'anémie de Fanconi (AF). L'hématopoïèse clonale est très fréquente chez les patients atteints d'une insuffisance médullaire et l'évolution vers un syndrome myélodysplasique ou leucémie aiguë myéloïde (SMD/LAM) est un événement préoccupant. Certaines données publiées indiquent que l'hématopoïèse clonale affecterait le risque de progression. Notre travail s'est concentré sur l'émergence de clones avec des mutations somatiques chez AM et AF et leur effet clinique. Dans la première partie, nous nous sommes concentrés sur l'aplasie acquise. Près d'un tiers des patients AM présente une hémoglobinurie paroxystique nocturne (HPN) concomitante. La HPN est une maladie rare et monogénique qui se manifeste par une hémolyse intravasculaire. Elle est causée par des mutations somatiques du gène PIGA, entraînant une susceptibilité cellulaire au système du complément. Outre le gène PIGA, les anomalies du HLA de classe I sont fréquentes chez les patients AM. Ces deux groupes de cellules échapperaient à la destruction immunitaire, contribuant ainsi à soutenir l'hématopoïèse. De plus, certains allèles HLA de classe I sont surreprésentés dans l'AM. Cela pourrait indiquer que l'HLA joue un rôle dans la physiopathologie de l'AM. Jusqu'à présent, une prédisposition héréditaire à l'HPN est inconnue. Nous avons constaté que des variantes constitutionnelles du facteur H du complément étaient surreprésentées chez les patients atteints d'HPN. Certaines caractéristiques constitutionnelles semblent donc influencer la dominance clonale chez les patients atteints d'une aplasie acquise. Nous avons étudié comment les caractéristiques cliniques, cytogénétiques et moléculaires des patients AM/HPN affectent la transformation en SMD/LAM. Nous avons confirmé que l'absence de réponse aux traitements non-greffe, l'âge et les mutations myéloïdes conféraient un risque plus élevé de progression. Par ailleurs, nous avons observé que les mutations PIGA/HLA, prédominantes au départ, étaient remplacées par des mutations myéloïdes classiques lors de la transformation. Pour la deuxième partie, nous avons voulu explorer l'impact du mosaïcisme somatique dans l'AF sur la transformation en néoplasies myéloïdes. Près de 30% des patients atteints d'AF développeront un cancer du sang au cours de leur vie. Globalement, les complications hématologiques représentent près de 70 % des décès dus à l'AF. Diversement, certains patients présentent un phénotype hématologique moins grave : des cellules hématopoïétiques spontanément corrigées coexistent avec des cellules Fanconi, soutenant hématopoïèse. Notre équipe a précédemment étudié une cohorte de patients FA, décrivant les caractéristiques cliniques et moléculaires des révertants, et définissant les mécanismes génétiques expliquant la réversion. Jusqu'à présent, nous n'avons pas identifié de patient révertant évolué vers SMD/LAM. Inspirés par le mosaïcisme somatique, des essais cliniques ont montré des résultats prometteurs en utilisant des cellules souches hématopoïétiques corrigées génétiquement pour traiter l'insuffisance médullaire chez les patients AF. Cependant, l'effet sur le risque de transformation en SMD/LAM est inconnu pour l'instant. Nous avons travaillé sur le développement d'un modèle de réversion génétique chez des souris AF. Nous avons voulu tester des sous-clones corrigés génétiquement ou pré-leucémiques dans le contexte de Fanconi et le risque d'évolution. Ce travail contribuera à la compréhension des mécanismes qui participent de la progression vers les SMD/LAM dans les insuffisances médullaires, pouvant aider à adapter les stratégies de suivi et de traitement, réduisant ainsi la morbidité.Bone marrow failure syndromes (BMF) are a diverse group of rare diseases that manifest chiefly with pancytopenia. The incapacity of the haematopoietic tissue to sustain haematopoiesis can be acquired, chiefly immune-mediated aplastic anaemia (AA), or inherited intrinsic cellular defects, such as the DNA repair deficiency in Fanconi anaemia (FA). BMF severely impairs patients' quality of life and complications can be fatal. Besides, clonal haematopoiesis is very frequent among BMF patients, and progression into MDS/AML is a concerning event with a dismal prognosis. Despite a long-known association between BMF and myeloid malignancies, the precise mechanisms involved in clonal dominance are unclear. Some published data indicate that clonal haematopoiesis affects the MDS/AML progression risk. This work focused on the emergence of clones bearing somatic mutations in AA and FA and their clinical effect. In the first part of this work, we focused on acquired BMF. Nearly a third of AA patients have concomitant paroxysmal nocturnal haemoglobinuria (PNH). PNH is a rare, monogenic disease that manifests as intravascular haemolysis. It is caused by somatic mutations in the PIGA gene, resulting in impaired cellular defence against the complement system. Besides PIGA, HLA class I abnormalities are frequent among AA patients. Such cells would evade the immune-mediated destruction and expand, helping to sustain haematopoiesis. Moreover, some HLA class I alleles are overrepresented in aplastic anaemia irrespective of ethnic background. The overrepresentation of specific class I alleles among AA patients strongly supports its influence on AA pathophysiology. Thus far, an inherited predisposition to PNH is unknown. We found that rare germline complement factor H variants were overrepresented among PNH patients. Germline characteristics seem to influence clonal dominance among acquired BMF patients. We investigated how baseline clinical, cytogenetic, and molecular characteristics in AA/PNH patients affected AML/MDS transformation. We confirmed that lack of response to non-transplant treatments, older age, and myeloid driver mutations at marrow failure onset conferred a higher risk of progression. Besides, we observed that PIGA/HLA-mutations, predominant at baseline, were replaced by classic myeloid drivers at the transformation. For the second part of this work, we were interested in exploring the impact of somatic mosaicism in FA on AML/MDS transformation. Nearly 30% of FA patients will develop a myeloid malignancy during their lifetime. Overall, hematologic complications account for almost 70% of FA deaths. Diversely, a few patients present a milder hematologic phenotype: a mosaicism of spontaneously corrected cells coexist with FA-deficient cells. Our team has previously studied a cohort of FA patients, describing revertants' clinical and molecular characteristics, and defining the genetic mechanisms that explained reversion. Thus far, revertant patients have not progressed to MDS/AML. Allogeneic hematopoietic stem cell transplantation is the only curative treatment for haematologic FA manifestations. This modality carries high treatment-related mortality but abrogates the risk of AML/MDS. Inspired by revertant somatic mosaicism, clinical trials showed promising results using autologous ex vivo gene-corrected hematopoietic stem cells to rescue marrow failure in FA patients. However, the effect on AML/MDS transformation risk is unknown thus far. We worked on developing a model of genetic reversion in FA mice. We aimed to test the fitness of gene-corrected or preleukemic subclones in the Fanconi context. This work will contribute to understand the intrinsic and extrinsic mechanisms underlying clonal dominance and progression towards MDS/AML in BMF, helping to adapt follow-up and treatment strategies, reducing morbidity

Dominance clonale dans les insuffisances médullaires

Bone marrow failure syndromes (BMF) are a diverse group of rare diseases that manifest chiefly with pancytopenia. The incapacity of the haematopoietic tissue to sustain haematopoiesis can be acquired, chiefly immune-mediated aplastic anaemia (AA), or inherited intrinsic cellular defects, such as the DNA repair deficiency in Fanconi anaemia (FA). BMF severely impairs patients' quality of life and complications can be fatal. Besides, clonal haematopoiesis is very frequent among BMF patients, and progression into MDS/AML is a concerning event with a dismal prognosis. Despite a long-known association between BMF and myeloid malignancies, the precise mechanisms involved in clonal dominance are unclear. Some published data indicate that clonal haematopoiesis affects the MDS/AML progression risk. This work focused on the emergence of clones bearing somatic mutations in AA and FA and their clinical effect. In the first part of this work, we focused on acquired BMF. Nearly a third of AA patients have concomitant paroxysmal nocturnal haemoglobinuria (PNH). PNH is a rare, monogenic disease that manifests as intravascular haemolysis. It is caused by somatic mutations in the PIGA gene, resulting in impaired cellular defence against the complement system. Besides PIGA, HLA class I abnormalities are frequent among AA patients. Such cells would evade the immune-mediated destruction and expand, helping to sustain haematopoiesis. Moreover, some HLA class I alleles are overrepresented in aplastic anaemia irrespective of ethnic background. The overrepresentation of specific class I alleles among AA patients strongly supports its influence on AA pathophysiology. Thus far, an inherited predisposition to PNH is unknown. We found that rare germline complement factor H variants were overrepresented among PNH patients. Germline characteristics seem to influence clonal dominance among acquired BMF patients. We investigated how baseline clinical, cytogenetic, and molecular characteristics in AA/PNH patients affected AML/MDS transformation. We confirmed that lack of response to non-transplant treatments, older age, and myeloid driver mutations at marrow failure onset conferred a higher risk of progression. Besides, we observed that PIGA/HLA-mutations, predominant at baseline, were replaced by classic myeloid drivers at the transformation. For the second part of this work, we were interested in exploring the impact of somatic mosaicism in FA on AML/MDS transformation. Nearly 30% of FA patients will develop a myeloid malignancy during their lifetime. Overall, hematologic complications account for almost 70% of FA deaths. Diversely, a few patients present a milder hematologic phenotype: a mosaicism of spontaneously corrected cells coexist with FA-deficient cells. Our team has previously studied a cohort of FA patients, describing revertants' clinical and molecular characteristics, and defining the genetic mechanisms that explained reversion. Thus far, revertant patients have not progressed to MDS/AML. Allogeneic hematopoietic stem cell transplantation is the only curative treatment for haematologic FA manifestations. This modality carries high treatment-related mortality but abrogates the risk of AML/MDS. Inspired by revertant somatic mosaicism, clinical trials showed promising results using autologous ex vivo gene-corrected hematopoietic stem cells to rescue marrow failure in FA patients. However, the effect on AML/MDS transformation risk is unknown thus far. We worked on developing a model of genetic reversion in FA mice. We aimed to test the fitness of gene-corrected or preleukemic subclones in the Fanconi context. This work will contribute to understand the intrinsic and extrinsic mechanisms underlying clonal dominance and progression towards MDS/AML in BMF, helping to adapt follow-up and treatment strategies, reducing morbidity.Les insuffisances médullaires sont maladies rares qui se manifestent principalement par pancytopénie. L'incapacité du tissu hématopoïétique à maintenir l'hématopoïèse peut être acquise, principalement l'aplasie médullaire idiopathique (AM), ou des défauts génétiques, tels que le déficit de réparation de l'ADN de l'anémie de Fanconi (AF). L'hématopoïèse clonale est très fréquente chez les patients atteints d'une insuffisance médullaire et l'évolution vers un syndrome myélodysplasique ou leucémie aiguë myéloïde (SMD/LAM) est un événement préoccupant. Certaines données publiées indiquent que l'hématopoïèse clonale affecterait le risque de progression. Notre travail s'est concentré sur l'émergence de clones avec des mutations somatiques chez AM et AF et leur effet clinique. Dans la première partie, nous nous sommes concentrés sur l'aplasie acquise. Près d'un tiers des patients AM présente une hémoglobinurie paroxystique nocturne (HPN) concomitante. La HPN est une maladie rare et monogénique qui se manifeste par une hémolyse intravasculaire. Elle est causée par des mutations somatiques du gène PIGA, entraînant une susceptibilité cellulaire au système du complément. Outre le gène PIGA, les anomalies du HLA de classe I sont fréquentes chez les patients AM. Ces deux groupes de cellules échapperaient à la destruction immunitaire, contribuant ainsi à soutenir l'hématopoïèse. De plus, certains allèles HLA de classe I sont surreprésentés dans l'AM. Cela pourrait indiquer que l'HLA joue un rôle dans la physiopathologie de l'AM. Jusqu'à présent, une prédisposition héréditaire à l'HPN est inconnue. Nous avons constaté que des variantes constitutionnelles du facteur H du complément étaient surreprésentées chez les patients atteints d'HPN. Certaines caractéristiques constitutionnelles semblent donc influencer la dominance clonale chez les patients atteints d'une aplasie acquise. Nous avons étudié comment les caractéristiques cliniques, cytogénétiques et moléculaires des patients AM/HPN affectent la transformation en SMD/LAM. Nous avons confirmé que l'absence de réponse aux traitements non-greffe, l'âge et les mutations myéloïdes conféraient un risque plus élevé de progression. Par ailleurs, nous avons observé que les mutations PIGA/HLA, prédominantes au départ, étaient remplacées par des mutations myéloïdes classiques lors de la transformation. Pour la deuxième partie, nous avons voulu explorer l'impact du mosaïcisme somatique dans l'AF sur la transformation en néoplasies myéloïdes. Près de 30% des patients atteints d'AF développeront un cancer du sang au cours de leur vie. Globalement, les complications hématologiques représentent près de 70 % des décès dus à l'AF. Diversement, certains patients présentent un phénotype hématologique moins grave : des cellules hématopoïétiques spontanément corrigées coexistent avec des cellules Fanconi, soutenant hématopoïèse. Notre équipe a précédemment étudié une cohorte de patients FA, décrivant les caractéristiques cliniques et moléculaires des révertants, et définissant les mécanismes génétiques expliquant la réversion. Jusqu'à présent, nous n'avons pas identifié de patient révertant évolué vers SMD/LAM. Inspirés par le mosaïcisme somatique, des essais cliniques ont montré des résultats prometteurs en utilisant des cellules souches hématopoïétiques corrigées génétiquement pour traiter l'insuffisance médullaire chez les patients AF. Cependant, l'effet sur le risque de transformation en SMD/LAM est inconnu pour l'instant. Nous avons travaillé sur le développement d'un modèle de réversion génétique chez des souris AF. Nous avons voulu tester des sous-clones corrigés génétiquement ou pré-leucémiques dans le contexte de Fanconi et le risque d'évolution. Ce travail contribuera à la compréhension des mécanismes qui participent de la progression vers les SMD/LAM dans les insuffisances médullaires, pouvant aider à adapter les stratégies de suivi et de traitement, réduisant ainsi la morbidité

Translation and cross-cultural adaptation of the arizona sexual scale (ASEX) into Portuguese

INTRODUCTION: Sexual dysfunction is common in individuals with psychiatric disorders and under psychotropic medication such as antidepressants and antipsychotics. Several scales have been developed to assess sexual function in these patients. The Arizona Sexual Scale (ASEX) is a five-item rating scale that quantifies sex drive, arousal, vaginal lubrication/penile erection, ability to reach orgasm, and satisfaction from orgasm. We describe the translation and cross-cultural adaptation of the ASEX into the Portuguese language, with the goal of contributing to the assessment of sexual function in Portuguese-speaking psychiatric patients under treatment with psychotropic drugs. METHODS: The translation and cross-cultural adaptation process thoroughly followed the steps recommended by the Task Force of the International Society for Pharmacoeconomics and Outcomes Research (ISPOR), namely: preparation, forward translation, reconciliation, back-translation, back-translation review, harmonization, cognitive debriefing, review of cognitive debriefing, finalization, proofreading, and final version. RESULTS: The process was successfully completed and no major differences were found between the translation, reconciliation and back-translation phases, with only small adjustments being made. CONCLUSION: The translation of the ASEX was completed successfully, following international reference guidelines. The use of these guidelines is a guarantee of a Portuguese version that is qualitatively and semantically equivalent to the original scale. This availability of this new scale version will enable studies evaluating the sexual function of Portuguese-speaking psychiatric patients. Future studies may assess the validity of the scale for Portuguese-speaking populations.info:eu-repo/semantics/publishedVersio

Ischemia-reperfusion histopathology alterations of the rabbit intestinal wall with and without exclusion of the collateral mesenteric circulation supply Alterações histopatológicas da parede intestinal de coelhos na isquemia-reperfusão com e sem exclusão da circulação mesentérica colateral

PURPOSE: To evaluate the histopathology alterations of the intestinal mucosa of rabbits submitted to different times of mesenteric artery ischemia and reperfusion with and without celiac artery collateral circulation supply. METHODS: Two groups of eight male New Zealand white rabbits (weight 2.2-3.5 kg) were used in this study. In the Group 1 animals, the proximal mesenteric artery was occluded for 60 min with an atraumatic vascular clamp, followed by reperfusion for 60 min. In the Group 2 animals the small bowel and mesentery were cut 30cm and 60cm far from the gastroduodenal pyloric transition before the proximal mesenteric artery occlusion. Small bowel biopsies were obtained before ischemia (control), after 30 min and 60 min of mesenteric ischemia and at 30 and 60 min. of mesenteric artery reperfusion. RESULTS: In the Group I animals, the followings histopathology grade results were observed: t1, mean 0.4 + 0.29; t2, mean 1.9 ± 0.38; t3, 1.9 ± 0.33; t4, 1.2 ± 0.36 and t5, 1.2 ± 0.32. Differences between t0 and t2 and between t3 and t4 were statistically significant (p<0.05). Differences between t2 and t3 and t4 and t5 were not significant (p>0.5). In the Group II animals, it was observed: t1, mean 1.6 ± 0.33; t2, 2.4 ± 0.36; t3, 3.0 ± 0.35; t4 3.4 ± 0.31; t5, 3 ± 031. Differences between t0 and t1, t1 and t2, and t2 and t3 were significant (p<0.05). Differences between histopathology grades results of samples t1 to t5 in Group 1 and 2 were statistically significant (p<0.5). CONCLUSION: Microscopic examination of the biopsies revealed significant evidence of worse small bowel wall ischemia-reperfusion lesions by exclusion of the celiac artery collateral circulation supply.<br>OBJETIVO: Avaliar as alterações histopatológicas da mucosa intestinal de coelhos submetidos à isquemia-reperfusão com e sem exclusão da circulação mesentérica colateral. MÉTODOS: Foram estudados dois grupos de oito coelhos Nova Zelândia machos com pesos variáveis entre 2,2 e 3,5 kg de peso corpóreo. Nos animais do Grupo 1, a artéria mesentérica proximal foi ocluida por pinçamento atraumático durante 60 min, seguido de reperfusão por 60 min. No Grupo 2 o intestino delgado e o mesentério foram seccionados 30 cm e 60 após a transição pilórica gastroduodenal antes da oclusão da artéria mesentérica cranial. Biópsias da parede intestinal foram obtidas antes da isquemia (controle), após 30 e 60 min. de isquemia. RESULTADOS: No Grupo I foram observados os seguintes graus de lesões: t1,média de 0.4 + 0.29; t2, média 1.9 ± 0.38; t3, 1.9 ± 0.33; t4, 1.2 ± 0.36 e t5, 1.2 ± 0.32. As diferenças entre t0 e t2 e entre t3 e t4 foram significantes (p<0.05). As diferenças entre t2 e t3 e t4 e t5 não foram significantes (p>0.5). No Group II observou-se: t1, média de 1.6 ± 0.33; t2, 2.4 ± 0.36; t3, 3.0 ± 0.35; t4 3.4 ± 0.31; t5, 3 ± 031. As diferenças entre t0 e t1, t1 e t2, e t2 e t3 foram significantes (p<0.05). As diferenças entre os resultados histopatológicos das biopsies de t1 a t5 dos Grupos 1 e 2 foram significantes (p<0.5). CONCLUSÃO: A exclusão da circulação mesentérica colateral agravou significantemente a degeneração histopatológica na isquemia-reperfusão da parede intestinal