Magnification and Refocusing Comparison in Cataract Surgery Using a Heads-Up Three-Dimensional Visualization System versus Conventional Binocular Microscopy.

Purpose: To compare magnification and refocusing during phacoemulsification with the NGENUITY®â€¯3-D Visualization System (3-D) versus the conventional microscope (CM) OPMI LUMERA 700. Setting: This study was performed in the Department of Anterior Segment of the Fundación Hospital Nuestra Señora de la Luz. Design: Prospective, randomized, cross-sectional, multi-surgeon, and comparative study. Methods: This study enrolled 100 patients (eyes) scheduled for phacoemulsification to measure the number of times changes in focusing and magnification were needed during cataract surgery. Results: Our study included 100 patients. From the endpoints evaluated, "zoom-in" showed statistically significant differences for all of the four predefined cataract surgery steps (means: Step 1, 0.38 (CM) vs 0.08 (3-D); Step 2, 0.36 (CM) vs 0.06 (3-D); Step 3, 0.54 (CM) vs 0.22 (3-D); Step 4, 0.56 (CM) vs 0.24 (3-D); all comparisons, p <0.05). In Step 4, there was a statistically significant increased use of "focus-out" for the 3-D system (mean 0.16 (CM) vs 0.58 (3-D); p <0.05). "Focus-in" and "zoom-out" showed no group differences for all steps. The duration of surgery with the 3-D system was longer at each step and overall. The percentage of light intensity did not show a statistically significant difference between both systems, with a mean of 99.45 for CM vs 98.43% for the heads-up system. Conclusion: The heads-up 3-D system is a safe option that offers excellent magnification for anterior segment visualization. The surgical time is longer, but adjusting settings like light intensity and brightness may facilitate some surgical steps early in the learning curve.

The shaping of gut immunity in cirrhosis.

Cirrhosis is the common end-stage of chronic liver diseases of different etiology. The altered bile acids metabolism in the cirrhotic liver and the increase in the blood-brain barrier permeability, along with the progressive dysbiosis of intestinal microbiota, contribute to gut immunity changes, from compromised antimicrobial host defense to pro-inflammatory adaptive responses. In turn, these changes elicit a disruption in the epithelial and gut vascular barriers, promoting the increased access of potential pathogenic microbial antigens to portal circulation, further aggravating liver disease. After summarizing the key aspects of gut immunity during homeostasis, this review is intended to update the contribution of liver and brain metabolites in shaping the intestinal immune status and, in turn, to understand how the loss of homeostasis in the gut-associated lymphoid tissue, as present in cirrhosis, cooperates in the advanced chronic liver disease progression. Finally, several therapeutic approaches targeting the intestinal homeostasis in cirrhosis are discussed.

O uso do xilitol na prevenção da cárie dentária ­ Revisão de literatura

De acordo com a Organização Mundial da Saúde (OMS), a cárie é considerada a segunda maior doença do mundo, e afeta grande parte da população. A cárie é um­a doença multifatorial, influenciada principalmente pelo estilo de vida do paciente, através da dieta, hábitos de higiene bucal, entre outros fatores. O passo mais importante para prevenção da cárie, é ter um bom hábito de higiene bucal (escovação, utilização de fio dental e enxaguatórios bucais com a presença de flúor) associado a uma dieta balanceada com níveis de açúcares baixos, no qual pode ser substituído por algum adoçante, como o xilitol. O xilitol pode ser encontrado na Odontologia em dentifrícios, enxaguatórios bucais, entre outros. Pesquisas apontam que, a introdução desse substituto do açúcar nos produtos odontológicos diminuem a incidência da cárie, por ele não ser metabolizado pelas bactérias. Outro produto que podemos encontrar o xilitol é em gomas de mascar, no qual pesquisas clínicas comprovam que o uso de tais gomas, algumas vezes ao dia, produz o aumento da salivação, que promove o efeito tampão, impedindo que os microorganismos se alojem na superfície dentária. O objetivo deste trabalho foi realizar uma revisão de literatura para obter informações sobre o uso do xilitol na Odontologia e seu papel na prevenção da cárie dentária. Para a realização deste trabalho foi efetuada uma pesquisa bibliográfica por meio das seguintes bases de dados: Scielo, Pubmed, Lilacs e Periódicos Capes. Diante da literatura revisada, pôde-se elucidar as diversas aplicabilidades clínicas do xilitol na Odontologia, como em dentifrícios, gomas de mascar, soluções para bochechos e vernizes. Concluiu-se que o efeito do xilitol na prevenção da cárie é bastante controverso. Entretanto, seu uso parece ser um recurso promissor como coadjuvante dos procedimentos de higiene bucal, em pacientes de alto risco à cárie, carecendo de mais estudos.

Reply.

We read with interest the letter by P Dey regarding our article which addresses the role of microbiome in driving intestinal inflammation, barrier disruption and bacterial translocation in CCl4 -cirrhosis (1). P Dey claims that dysbiosis and inflammation in this model can be attributed, rather than to cirrhosis, to the effects of CCl4 on the gut microbiome, and that the resultant dysbiosis becomes the major driver of CCl4 -liver damage. This article is protected by copyright. All rights reserved.

Intestinal Immune Dysregulation Driven by Dysbiosis Promotes Barrier Disruption and Bacterial Translocation in Rats With Cirrhosis.

In cirrhosis, intestinal dysbiosis, intestinal barrier impairment, and systemic immune system abnormalities lead to gut bacterial translocation (GBT) and bacterial infection. However, intestinal immune system dysfunction and its contribution to barrier damage are poorly understood. This study correlates immune system dysregulation in the intestines of rats at different stages of CCl4 -induced cirrhosis with barrier function and pathogenic microbiota. The following variables were addressed in the small intestine: intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) activation status and cytokine production (flow cytometry), cytokine mRNA and protein expression (quantitative real-time PCR and immunofluorescence), microbiota composition of ileum content (16S recombinant DNA massive sequencing), permeability (fecal albumin loss), and epithelial junctions (immunohistochemistry and immunofluorescence). The intestinal mucosa in rats with cirrhosis showed a proinflammatory pattern of immune dysregulation in IELs and LPLs, which featured the expansion of activated lymphocytes, switch to a T helper 1 (Th1) regulatory pattern, and Th17 reduction. In rats with cirrhosis with ascites, this state was associated with epithelial junction protein disruption, fecal albumin loss, and GBT. Direct correlations (P < 0.01) were observed between elevated interferon gamma (IFNγ)-expressing T cytotoxic LPLs and fecal albumin and between inflammatory taxa abundance and IFNγ-producing immune cells in the ileum. Bowel decontamination led to redistributed microbiota composition, reduced proinflammatory activation of mucosal immune cells, normalized fecal albumin levels, and diminished GBT; but there were no modifications in Th17 depletion. Conclusion: The intestinal mucosa of rats with cirrhosis acquires a proinflammatory profile of immune dysregulation that parallels the severity of cirrhosis; this impaired intestinal immune response is driven by gut dysbiosis and leads to disrupted barrier function, promoting GBT.

The firing frequency of spontaneous action potentials and their corresponding evoked exocytosis are increased in chromaffin cells of CCl4 -induced cirrhotic rats with respect to control rats.

High catecolamine plasma levels because of sympathetic nervous system over-activity contribute to cirrhosis progression. The aim of this study was to investigate whether chromaffin cells of the adrenal gland might potentiate the deleterious effect exerted by this over-activity. Electrophysiological patch-clamp and amperometric experiments with carbon-fibre electrodes were conducted in single chromaffin cells of control and CCl4 -induced cirrhotic rats. The spontaneous action potential firing frequency was increased in chromaffin cells of cirrhotic rats with respect to control rats. The exocytosis evoked by that firing was also increased. However, exocytosis elicited by ACh did not vary between control and cirrhotic rats. Exocytosis triggered by depolarizing pulses was also unchanged. Amperometric recordings confirmed the lack of increased catecholamine charge released in cirrhosis after ACh or depolarization stimuli. However, the amperometric spikes exhibited faster kinetics of release. The overall Ca2+ entry through voltage-dependent Ca2+ channels (VDCC), or in particular through Cav1 channels, did not vary between chromaffin cells of control and cirrhotic rats. The inhibition of VDCC by methionine-enkephaline or ATP was not either altered, but it was increased by adrenaline in cells of cirrhotic rats. When a cocktail composed by the three neurotransmitters was tested in order to approach a situation closer to the physiological condition, the inhibition of VDCC was similar between both types of cells. In summary, chromaffin cells of the adrenal gland might contribute to exacerbate the sympathetic nervous system over-activity in cirrhosis because of an increased exocytosis elicited by an enhanced spontaneous electrical activity.

Effects of aging on liver microcirculatory function and sinusoidal phenotype.

The socioeconomic and medical improvements of the last decades have led to a relevant increase in the median age of worldwide population. Although numerous studies described the impact of aging in different organs and the systemic vasculature, relatively little is known about liver function and hepatic microcirculatory status in the elderly. In this study, we aimed at characterizing the phenotype of the aged liver in a rat model of healthy aging, particularly focusing on the microcirculatory function and the molecular status of each hepatic cell type in the sinusoid. Moreover, major findings of the study were validated in young and aged human livers. Our results demonstrate that healthy aging is associated with hepatic and sinusoidal dysfunction, with elevated hepatic vascular resistance and increased portal pressure. Underlying mechanisms of such hemodynamic disturbances included typical molecular changes in the cells of the hepatic sinusoid and deterioration in hepatocyte function. In a specific manner, liver sinusoidal endothelial cells presented a dysfunctional phenotype with diminished vasodilators synthesis, hepatic macrophages exhibited a proinflammatory state, while hepatic stellate cells spontaneously displayed an activated profile. In an important way, major changes in sinusoidal markers were confirmed in livers from aged humans. In conclusion, our study demonstrates for the first time that aging is accompanied by significant liver sinusoidal deregulation suggesting enhanced sinusoidal vulnerability to chronic or acute injuries.

Obeticholic acid reduces bacterial translocation and inhibits intestinal inflammation in cirrhotic rats.

BACKGROUND & AIMS: In advanced cirrhosis, gut bacterial translocation is the consequence of intestinal barrier disruption and leads to bacterial infection. Bile acid abnormalities in cirrhosis could play a role in the integrity of the intestinal barrier and the control of microbiota, mainly through the farnesoid X receptor. We investigated the long-term effects of the farnesoid X receptor agonist, obeticholic acid, on gut bacterial translocation, intestinal microbiota composition, barrier integrity and inflammation in rats with CCl4-induced cirrhosis with ascites. METHODS: Cirrhotic rats received a 2-week course of obeticholic acid or vehicle starting once ascites developed. We then determined: bacterial translocation by mesenteric lymph node culture, ileum expression of antimicrobial peptides and tight junction proteins by qPCR, fecal albumin loss, enteric bacterial load and microbiota composition by qPCR and pyrosequencing of ileum mucosa-attached contents, and intestinal inflammation by cytometry of the inflammatory infiltrate. RESULTS: Obeticholic acid reduced bacterial translocation from 78.3% to 33.3% (p<0.01) and upregulated the expression of the farnesoid X receptor-associated gene small heterodimer partner. Treatment improved ileum expression of antimicrobial peptides, angiogenin-1 and alpha-5-defensin, tight junction proteins zonulin-1 and occludin, and reduced fecal albumin loss and liver fibrosis. Enteric bacterial load normalized, and the distinctive mucosal microbiota of cirrhosis was reduced. Gut immune cell infiltration was reduced and inflammatory cytokine and Toll-like receptor 4 expression normalized. CONCLUSIONS: In ascitic cirrhotic rats, obeticholic acid reduces gut bacterial translocation via several complementary mechanisms at the intestinal level. This agent could be used as an alternative to antibiotics to prevent bacterial infection in cirrhosis.

Defective thymopoiesis and poor peripheral homeostatic replenishment of T-helper cells cause T-cell lymphopenia in cirrhosis.

BACKGROUND & AIMS: Depletion of circulating CD4(+) T-helper (Th) lymphocytes, especially naive Th cells, is common in cirrhosis. Little is known about the pathogenetic mechanisms involved in Th-cell depletion in cirrhosis. We investigated the mechanisms involved in circulating Th-cell lymphopenia in cirrhosis. METHODS: Circulating naive and memory Th cells were analyzed by flow cytometry in 60 patients with cirrhosis and 40 sex- and age-matched healthy controls. Thymopoiesis, apoptosis, cell activation, and proliferation were assessed through CD31, annexin-V, HLA-DR and Ki-67 expression, respectively. Lipopolysaccharide (LPS)-binding protein (LBP) and spleen size were measured as indicators of bacterial translocation and splenic pooling, respectively. RESULTS: Compared to controls, patients showed reduced numbers of Th cells involving a greater depletion of the naive than memory Th-cell compartment (2.7- vs. 1.5-fold, respectively). Recent thymic emigrants were diminished (p < 0.01), and each patient had a lower number of CD31(+) naive Th cells than the matched-control. Spontaneous and induced apoptosis (Annexin-V(+)) of Th cells was increased in patients. Activated (HLA-DR(+)) and proliferating (Ki-67(+)) memory Th cells were increased in patients (p < 0.01), and they directly correlated with plasma LBP (p < 0.05) and negatively with naive Th cells (p < 0.01), respectively. Naive Th cells were inversely correlated (p < 0.01) with their frequencies of apoptosis and of activated memory Th cells, LBP, and spleen size. On multivariate analysis, defective thymic generation of naive Th cells, increased memory Th-cell activation, and splenomegaly were independently associated with Th-cell depletion. CONCLUSIONS: Th-cell immunodeficiency in cirrhosis is explained by a universal defect in thymopoiesis exacerbated by splenic pooling and activation-driven cell-death induced by bacterial translocation.

Interaction between intestinal dendritic cells and bacteria translocated from the gut in rats with cirrhosis.

UNLABELLED: Cirrhosis with ascites is associated with a high rate of gut bacterial translocation (GBT) and spontaneous bacterial infections of enteric origin. We addressed the activation state and role of intestinal dendritic cells (DCs) in experimental ascitic cirrhosis and their relationship with GBT. Cirrhosis with ascites was CCl(4) induced in rats. To examine their activation state and functions, DCs (CD103(+) RT1B(+) CD3(-) CD45RA(-) ) were isolated from the intestinal lamina propria and mesenteric lymph nodes (MLNs), and the following parameters were determined by flow cytometry: surface antigen expression; spontaneous or lipopolysaccharide-stimulated tumor necrosis factor alpha (TNF-α) production; and in vitro capacity to phagocytose latex beads and to migrate toward the chemokine (C-C motif) ligand 21. GBT was defined as the growth of bacteria in MLNs culture. Bacterial DNA (Bact-DNA) in MLNs was identified by polymerase chain reaction. In rats with Bact-DNA in MLNs without GBT, intestinal and MLNs CD103(+) -DCs showed features of activation, expansion of the proinflammatory CD4(+) -DC subpopulation, augmented TNF-α production, and increased phagocytic and migratory capacities. In contrast, in rats with GBT, CD103(+) -DCs showed the absence of an activated phenotype, lowered TNF-α production, and relatively deficient phagocytosis and migration capacities. The CD103(+) -DC of rats without Bact-DNA in MLNs or GBT were similar to controls. In cirrhotic rats, bowel decontamination with antibiotics eliminated Bact-DNA in MLNs and GBT, normalized the activation state and functions of CD103(+) -DCs, and increased their TNF-α production. CONCLUSION: In experimental cirrhosis with ascites, continuous pressure of gut bacteria shapes the phenotypic and functional profile of intestinal DCs to produce effects that range from their activation and enhanced functions to their exhaustion and tolerance.

Loss of surface antigens is a conserved feature of apoptotic lymphocytes from several mammalian species.

Human lymphocytes lose the expression of lineage antigens (LAgs) along apoptosis. Our aim was to extent our previous studies of LAg loss to rodent species, quantifying LAg expression on apoptotic murine lymphocytes using flow cytometry to measure alterations in cell permeability, phosphatidylserine exposure and caspase activation of CD3, CD5, CD4, CD8, CD19 and CD28 LAgs in highly purified lymphocyte populations. We found loss of expression by apoptotic cells of all LAgs studied in the three species analyzed except for CD3 antigen in mouse. We also found an early, rapid and dramatic reduction in the expression of CD28 by early apoptotic cells. We found several homologies across the three species in the kinetic of loss of several LAgs such as CD5, CD4 and CD28. These data suggest that the loss of expression of LAgs by apoptotic lymphocytes is a common and conserved feature of lymphocytes undergoing apoptosis in several mammalian species.

Modified checklist for autism in toddlers: cross-cultural adaptation and validation in Spain.

Early detection and treatment have been shown to be effective in reducing disability severity caused by Autistic Spectrum Disorders (ASDs). As Spanish pediatricians have no detection tool, the Modified Checklist for Autism in Toddlers (M-CHAT) was first translated into and culturally adapted to Spanish. Validity and reliability studies were carried out in two different geographical areas of Spain, where M-CHAT was administered to two different samples, namely: 2,480 high- and low-risk children; and 2,055 low-risk children. The results obtained were similar to those yielded by the original M-CHAT studies. Differences were found in positive predictive value, due to the low ASD frequency observed in this study. M-CHAT is still being studied in a large population-based screening program in Spain.

Critical role of the liver in the induction of systemic inflammation in rats with preascitic cirrhosis.

UNLABELLED: Systemic activation of the inflammatory immune system contributes to the progression of cirrhosis with ascites. Immune cells become activated after interacting at the mesenteric lymph nodes (MLNs) with bacteria translocated from the gut, and thereafter reach the bloodstream through recirculation. It is unknown whether systemic activation of the immune system is present in pre-ascitic cirrhosis, in which gut bacterial translocation has not been described. The purpose of this study was to determine whether systemic activation of the immune system initiates in rats with compensated carbon tetrachloride (CCl(4))-induced cirrhosis, and if so to establish the activation site of immune cells. We studied the activation status of immune cells in peripheral blood, MLNs, and hepatic lymph nodes (HLNs). Systemic inflammation was present in rats with cirrhosis, as shown by expansion (P < 0.01) of circulating total and inflammatory monocytes and recently activated CD134(+) T helper (T(h)) cells. The same populations of cells were increased (P < 0.01) in MLNs and HLNs. Bacterial translocation was absent in rats with cirrhosis or control rats, but bacterial DNA fragments were present in the MLNs of 54% of rats with cirrhosis. The liver was the source of activated immune cells present in the blood, as shown by the direct correlation between activated T(h) cells in the blood and HLNs, but not in MLNs, and the normalization by gut decontamination with antibiotics of activated cells in MLNs, but not in the blood or HLNs. CONCLUSION: In experimental cirrhosis, systemic activation of the immune system occurs before ascites development and is driven by recirculation of cells activated in HLNs. In addition, in compensated cirrhosis, bacterial DNA fragments reach the MLNs, where they elicit a local inflammatory response.

The biological response modifier AM3 attenuates the inflammatory cell response and hepatic fibrosis in rats with biliary cirrhosis.

BACKGROUND: An inflammatory immune system response ensues in the liver and in the systemic circulation in cirrhosis, where it contributes to hepatic fibrosis and peripheral vasodilation. Modulation of the inflammatory response without increasing susceptibility to infection is a therapeutic target in cirrhosis. AM3 is a low-toxicity biological response modifier with regulatory effects on innate and adaptative immunity, and the ability to normalise the production of tumour necrosis factor alpha (TNFalpha). AIMS: This was an experimental study to investigate the effects of oral AM3 on the systemic and hepatic inflammatory response, liver fibrosis and on the haemodynamic abnormalities of portal hypertension in rats with biliary cirrhosis. DESIGN: Bile-duct ligated rats received a 3-week oral course of AM3 or placebo. RESULTS: In cirrhotic rats, AM3 blunted the inflammatory switch of circulating and intrahepatic monocytes and T-cells to TNFalpha and interferon gamma (IFNgamma) production, respectively. AM3 modified the intrahepatic polarisation pattern of the regulatory cytokines, decreasing the mRNA expression of transforming growth factor beta1 (TGFbeta1), interleukin 4 (IL4), and IFNgamma, and increasing that of IL10. Total and IFNgamma-producing natural killer (NK) cells were lowered by AM3 in the peripheral blood and liver of cirrhotic rats. The immunomodulatory effects of AM3 led to reduced hepatic fibrogenesis in cirrhotic rats, as shown by decreased area of liver fibrosis, hydroxyproline content and mRNA expression of procollagen alpha1(I). Besides, AM3 lowered portal pressure and systemic hyperaemia. CONCLUSIONS: The biological response modifier AM3 reverses the concurrent inflammatory immune system activation in peripheral blood and liver of experimental established cirrhosis, which results in reductions of hepatic fibrosis, portal pressure and peripheral vasodilation.

[Trends in studies on autism in Spain: Publications and authorship networks (1974-2007)]. / Evolución de los estudios sobre autismo en España: publicaciones y redes de coautoría entre 1974 y 2007.

All the papers on autism published in journals by Spanish authors until 2007 were reviewed in order to identify changes and trends in studies, journals and authorship networks. A total of 567 works were analyzed. Results showed a continuous increase in the total number of publications and collaborative works (especially from 1999 onwards), as well as coincidence of the general framework of papers with the guidelines for research and treatment on autism that were published in the Anglo-Saxon arena for the same period. Some weak points were also identified, such as the low proportion of empirical and funded studies, low impact of the journals, and low author continuity, which have also been noted for other domains of research in Spain. We conclude that psychological and biomedical research on autism is currently a growing field in our country. However, important changes are needed, both in the way the authors conduct and communicate their studies, and in the commitment of some institutions (specially, universities and parent advocacy groups). Lastly, some proposals are suggested to improve the scientific quality of future studies and their usefulness for people with autism.

Evolución de los estudios sobre autismo en España: publicaciones y redes de coautoría entre 1974 y 2007 / Trends in studies on autism in Spain: publications and authorship networks (1974-2007)

Se revisaron todos los trabajos sobre autismo publicados en revistas por autores españoles hasta 2007 para analizar la evolución de los estudios, las revistas y las redes de coautoría en este ámbito. En total, se analizaron 567 trabajos. Se observó un incremento progresivo del total de artículos publicados y de los investigadores que trabajan en colaboración, especialmente en los últimos diez años, así como una notable coincidencia entre el enfoque general de los trabajos y las recomendaciones publicadas en el ámbito anglosajón sobre la investigación y el tratamiento del autismo para ese periodo. También se identificaron puntos débiles, como la baja proporción de trabajos empíricos y financiados, el bajo impacto de las revistas y la falta de continuidad de los autores, detectados también en otras áreas de investigación. Se concluye que los estudios psicológicos y biomédicos del autismo en España están actualmente en expansión, pero que se requerirían cambios importantes en el modo en que los autores desarrollan y comunican sus trabajos y una mayor implicación de las instituciones (especialmente, universidades y asociaciones de padres). Finalmente, se sugieren algunas propuestas para mejorar la calidad y visibilidad de los futuros estudios y su utilidad real para las personas afectadas(AU)

All the papers on autism published in journals by Spanish authors until 2007 were reviewed in order to identify changes and trends in studies, journals and authorship networks. A total of 567 works were analyzed. Results showed a continuous increase in the total number of publications and collaborative works (especially from 1999 onwards), as well as coincidence of the general framework of papers with the guidelines for research and treatment on autism that were published in the Anglo-Saxon arena for the same period. Some weak points were also identified, such as the low proportion of empirical and funded studies, low impact of the journals, and low author continuity, which have also been noted for other domains of research in Spain. We conclude that psychological and biomedical research on autism is currently a growing field in our country. However, important changes are needed, both in the way the authors conduct and communicate their studies, and in the commitment of some institutions (specially, universities and parent advocacy groups). Lastly, some proposals are suggested to improve the scientific quality of future studies and their usefulness for people with autism(AU)

Deteccion precoz y atencion de los niños con trastornos generalizados del desarrollo / Early detection and management of children with pervasive developmental disorders

Los Trastornos Generalizados del Desarrollo (TGD) o Trastornosdel Espectro Autista (TEA) conforman un amplio grupode alteraciones del neurodesarrollo que afectan a la personadurante toda su vida, produciendo discapacidad con diferentegrado de severidad. Aunque actualmente no hay un tratamientocurativo, diversos estudios han mostrado la importancia de la deteccion e intervencion precoz para la mejora del pronostico y la calidad de vida de estos niños y sus familias. A pesarde esto, no existen programas de cribado especificos para estostrastornos en el Sistema de Salud, por lo que la formacion e informacion a cerca de los mismos cobra una especial relevancia.Los profesionales enfermeros, como integrantes delequipo de Atencion Primaria, pueden ejercer una importantelabor en la deteccion de estos trastornos a traves de los programasde control del niño sano y en la derivacion y coordinacion con los servicios especializados (AU)

Pervasive developmental disorders (PDD) or Autism SpectrumDisorders (ASD) encompass a wide group of neurodevelopmentdisorders that affect the patient throughout life,producing different degrees of disability. Although at the presenttime there is no curative treatment, several studies haveshown the importance of early detection and intervention in orderto improve prognosis and the quality of life of these childrenand their families. In spite of this, there are no specificscreening programmes for these disorders in the HealthcareSystem, making education and information on these conditionsespecially relevant. Nursing professionals, as membersof a Primary Care team, can greatly increase the detection ofthese disorders via healthy children management programmesand referral and coordination with specialised services (AU)