Endocannabinoid system and aggression across animal species.

This narrative review article summarizes the current state of knowledge regarding the relationship between the endocannabinoid system (ECS) and aggression across multiple vertebrate species. Experimental evidence indicates that acute administration of phytocannabinoids, synthetic cannabinoids, and the pharmacological enhancement of endocannabinoid signaling decreases aggressive behavior in several animal models. However, research on the chronic effects of cannabinoids on animal aggression has yielded inconsistent findings, indicating a need for further investigation. Cannabinoid receptors, particularly cannabinoid receptor type 1, appear to be an important part of the endogenous mechanism involved in the dampening of aggressive behavior. Overall, this review underscores the importance of the ECS in regulating aggressive behavior and provides a foundation for future research in this area.

CB1R chronic intermittent pharmacological activation facilitates amphetamine seeking and self-administration and changes in CB1R/CRFR1 expression in the amygdala and nucleus accumbens in rats.

Patterns of drug ingestion may have a dissimilar impact on the brain, and therefore also the development of drug addiction. One pattern is binge intoxication that refers to the ingestion of a high amount of drug on a single occasion followed by an abstinence period of variable duration. In this study, our goal was to contrast the effect of continuous low amounts with intermittent higher amounts of Arachidonyl-chloro-ethylamide (ACEA), a CB1R agonist, on amphetamine seeking and ingestion, and describe the effects on the expression of CB1R and CRFR1 in the central nucleus of the amygdala (CeA) and in the nucleus accumbens shell (NAcS). Adult male Wistar rats were treated with a daily administration of vehicle or 20 µg of ACEA, or four days of vehicle followed by 100 µg of ACEA on the fifth day, for a total of 30 days. Upon completion of this treatment, the CB1R and CRFR1 expression in the CeA and NAcS was evaluated by immunofluorescence. Additional groups of rats were evaluated for their anxiety levels (elevated plus maze, EPM), amphetamine (AMPH) self-administration (ASA) and breakpoint (A-BP), as well as AMPH-induced conditioned place preference (A-CPP). Results indicated that ACEA induced changes in the CB1R and CRFR1 expression in both the NAcS and CeA. An increase in anxiety-like behavior, ASA, A-BP and A-CPP was also observed. Since the intermittent administration of 100 µg of ACEA induced the most evident changes in most of the parameters studied, we concluded that binge-like ingestion of drugs induces changes in the brain that may make the subject more vulnerable to developing drug addiction.

Amapola, lindísima amapola: de los opiáceos y los opioides, utilidad y riesgos / Poppy, beautiful poppy: opiates and opioids, utility and risks

Resumen El opio y sus derivados, y recientemente los opioides, han acompañado a la humanidad desde las civilizaciones más antiguas hasta la actualidad. Sus efectos analgésicos, hipnóticos y placenteros no pasaron desapercibidos para los antiguos, los consideraron de utilidad médica y beneficiosa para el estado de ánimo. Hoy en día no existe otro tipo de medicamentos que puedan tratar el dolor más intenso tan eficientemente como estos potentes analgésicos. Sin embargo, el uso médico y recreativo de los opiáceos y los opioides conlleva riesgos para la salud, como la tolerancia, la hiperalgesia y la adicción. Actualmente, además de ser indiscutiblemente el tratamiento médico más poderoso para mitigar el sufrimiento ocasionado por el dolor, se ha convertido también en un problema de salud pública debido a la alta cantidad de personas con trastorno por uso de opioides y por las muertes ocasionadas por sobredosis. En esta revisión se hará mención de las bondades de los opiáceos y opioides, y también de los efectos no deseados que estos producen.

Abstract Opium and its derivatives, and recently the opioids have accompanied the humankind since the ancient civilizations to the present day. Its analgesic, hypnotic and pleasant effects did not go unnoticed by ancient people, which considered most of these effects of medical utility and noticed that they had remarkable mood benefits. Currently, there are no other kind of drugs that can palliate intense pain as efficiently as these powerful analgesics. However, the medical and recreational use of opiates and opioids may carry health risks such as tolerance, hyperalgesia, and addiction. Nowadays, in addition to being indisputably the most powerful medical treatment to alleviate the suffering caused by pain, it has also become a public health problem due to the high number of people with opioid use disorder that have facilitated deaths caused by opioids overdose. In this review we will discuss the medical benefits of opiates and opioids, as much as the unwanted effects they produce.

Role of cortical excitatory/inhibitory imbalance in autism spectrum disorders from a symptom severity trajectories framework: a study protocol.

BACKGROUND: There is considerable evidence reporting an excitatory/inhibitory (E/I) cortical imbalance in autism spectrum disorders (ASD). However, previous findings on the direction of this imbalance and its relationship to ASD symptomatology are heterogeneous. Some factors contributing to these mixed results might be the methodological differences between studies assessing the E/I ratio and the intrinsic variability within the autistic spectrum. Studying the evolution of ASD symptoms and the factors that modulate it might help to explain and reduce this variability. Here we present a study protocol to explore the longitudinal role of E/I imbalance in ASD symptoms, combining different approaches to measure the E/I ratio and using the trajectories of symptom severity as a framework. METHODS: This observational two time-point prospective study assesses the E/I ratio and the evolution of the behavioural symptoms in a sample of at least 98 participants with ASD. Participants are enrolled at 12 to 72 months of age and followed from 18 to 48 months after. A comprehensive battery of tests is applied to evaluate ASD clinical symptoms. The E/I ratio is approached from electrophysiology, magnetic resonance, and genetics. We will calculate the individual change for the main ASD symptoms and, based on that, we will define the trajectories of symptom severity. Then, we will investigate the correlation between measures of excitation/inhibition balance and autistic symptomatology cross-sectionally, as well as the ability of these measurements to predict changes in symptoms over time. DISCUSSION: This study presents a robust multisystemic approach to the E/I imbalance theory in autism and its relation to divergent symptom trajectories. That setting will allow us to relate and compare the neurobiological information coming from different sources and its impact on behavioural symptoms while accounting for the high variability in ASD. The findings derived from this study could contribute to the ASD biomarkers research and might provide valuable evidence for the development of more personalized treatments in ASD.

Analysis of common genetic variation across targets of microRNAs dysregulated both in ASD and epilepsy reveals negative correlation.

Genetic overlap involving rare disrupting mutations may contribute to high comorbidity rates between autism spectrum disorders and epilepsy. Despite their polygenic nature, genome-wide association studies have not reported a significant contribution of common genetic variation to comorbidity between both conditions. Analysis of common genetic variation affecting specific shared pathways such as miRNA dysregulation could help to elucidate the polygenic mechanisms underlying comorbidity between autism spectrum disorders and epilepsy. We evaluated here the role of common predisposing variation to autism spectrum disorders and epilepsy across target genes of 14 miRNAs selected through bibliographic research as being dysregulated in both disorders. We considered 4,581 target genes from various in silico sources. We described negative genetic correlation between autism spectrum disorders and epilepsy across variants located within target genes of the 14 miRNAs selected (p = 0.0228). Moreover, polygenic transmission disequilibrium test on an independent cohort of autism spectrum disorders trios (N = 233) revealed an under-transmission of autism spectrum disorders predisposing alleles within miRNAs' target genes across autism spectrum disorders trios without comorbid epilepsy, thus reinforcing the negative relationship at the common genetic variation between both traits. Our study provides evidence of a negative relationship between autism spectrum disorders and epilepsy at the common genetic variation level that becomes more evident when focusing on the miRNA regulatory networks, which contrasts with observed clinical comorbidity and results from rare variation studies. Our findings may help to conceptualize the genetic heterogeneity and the comorbidity with epilepsy in autism spectrum disorders.

GPR55 activation prevents amphetamine-induced conditioned place preference and decrease the amphetamine-stimulated inflammatory response in the ventral hippocampus in male rats.

Inflammatory response in the Central Nervous System (CNS) induced by psychostimulants seems to be a crucial factor in the development and maintenance of drug addiction. The ventral hippocampus (vHp) is part of the reward system involved in substance addiction and expresses abundant G protein-coupled receptor 55 (GPR55). This receptor modulates the inflammatory response in vitro and in vivo, but there is no information regarding its anti-inflammatory effects and its impact on psychostimulant consumption. The aim of the present study was to investigate whether vHp GPR55 activation prevents both the inflammatory response induced by amphetamine (AMPH) in the vHp and the AMPH-induced conditioned place preference (A-CPP). Wistar adult male rats with a bilateral cannula into the vHp or intact males were subjected to A-CPP (5 mg/kg). Upon the completion of A-CPP, the vHp was dissected to evaluate IL-1ß and IL-6 expression through RT-PCR, Western blot and immunofluorescence. Our results reveal that AMPH induces both A-CPP and an increase of IL-1ß and IL-6 in the vHp. The GPR55 agonist lysophosphatidylinositol (LPI, 10 µM) infused into the vHp prevented A-CPP and the AMPH-induced IL-1ß increase. CID 16020046 (CID, 10 µM), a selective GPR55 antagonist, abolished LPI effects. To evaluate the effect of the inflammatory response, lipopolysaccharide (LPS, 5 µg/µl) was infused bilaterally into the vHp during A-CPP acquisition. LPS strengthened A-CPP and increased IL-1ß/IL-6 mRNA and protein levels in the vHp. LPS also increased CD68, Iba1, GFAP and vimentin expression. All LPS-induced effects were blocked by LPI. Our results suggest that GPR55 activation in the vHp prevents A-CPP while decreasing the local neuro-inflammatory response. These findings indicate that vHp GPR55 is a crucial factor in preventing the rewarding effects of AMPH due to its capacity to interfere with proinflammatory responses in the vHp.

Dominance status is associated with a variation in cannabinoid receptor 1 expression and amphetamine reward.

The rewarding effects of psychostimulants appear to be distinct between dominant and subordinate individuals. In turn, the endocannabinoid system is an important modulator of drug reward in the nucleus accumbens and medial prefrontal cortex, however the connection with social dominance is yet to be established. Male rats were classified as dominant or subordinate on the basis of their spontaneous agonistic interactions and drug reward was assessed by means of conditioned place preference with amphetamine (AMPH). In addition, the expression of CB1R, CB2R, FAAH1, and DAGLa was quantified from accumbal and cortical tissue samples. Our findings demonstrate that dominant rats required a lesser dose of AMPH to acquire a preference for the drug-associated compartment, thereby suggesting a higher sensitivity to the rewarding effects of AMPH. Furthermore, dominants exhibited a lower expression of CB1R in the medial prefrontal cortex and nucleus accumbens. This study illustrates how CBR1 expression could differentiate the behavioral phenotypes associated to social dominance.

Función de la impulsividad en el trastorno por consumo de sustancias / Impulsivity`s role in substance use disorder

Resumen La proporción de usuarios de una sustancia de abuso que desarrolla problemas con su consumo (abuso o dependencia) representa solo una parte de esta población. En México, el 63.8 % de la población consume alcohol, y de ellos, el 15 % desarrolla algún trastorno por consumo de alcohol (TCA). Se ha observado una relación causal entre el trastorno por consumo de sustancias (TCS) y la falta de autocontrol. Es decir, satisfacer necesidades de manera impulsiva, v. gr., consumir una droga sin evaluar las consecuencias. La corteza prefrontal (CPF) es el principal sustrato neuroanatómico del autocontrol y característicamente la CPF alcanza la madurez alrededor de los 30 años, sugieriendo que el autocontrol se alcanza despues de esta edad. Se ha propuesto que todos los grupos etarios que no han consolidado el uso del autocontrol son vulnerables al TCS. Similarmente ocurre con aquellos sujetos que por algún trastorno psiquiátrico tienen como característica una limitada función prefrontal. La CPF coordina una red subcortical cuya interacción depende de distintos sistemas de neurotransmisión, entre ellos, endocanabinoides. En este trabajo se revisó la función de la CPF y del sistema de endocanabinoides (sECB) y su relación con la vulnerabilidad a la adicción y otros trastornos psiquiátricos.

Abstract The proportion of users of a substance of abuse who develop problems with its use (abuse or dependence) represents only a part of this population. In Mexico, 63.8% of the population consumes alcohol and only 15% of them develop an alcohol use disorder (AUD). A causal relation has been observed between substance use disorder (SUD) and the lack of self-control. Which means, satisfying needs in an impulsive way, v.gr. using a drug, without considering the consequences. The prefrontal cortex (PFC) is the main neuroanatomical substrate of self-control and characteristically reaches maturity around the age of 30, suggesting that self-control is reached after this age. We suggest that all age groups that have not consolidated the use of self-control are vulnerable to SUD. The same occurs with those who, due to a psychiatric disorder, have the characteristic of a limited prefrontal function. The PFC coordinates a subcortical network whose interaction depends on different neurotransmission systems among them, the endocannabinoids system (ECBs). In this work we will review the function of the PFC, the ECBs and its relationship with vulnerability to addiction and other psychiatric disorders.

ADHD: Reviewing the Causes and Evaluating Solutions.

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder in which patients present inattention, hyperactivity, and impulsivity. The etiology of this condition is diverse, including environmental factors and the presence of variants of some genes. However, a great diversity exists among patients regarding the presence of these ADHD-associated factors. Moreover, there are variations in the reported neurophysiological correlates of ADHD. ADHD is often treated pharmacologically, producing an improvement in symptomatology, albeit there are patients who are refractory to the main pharmacological treatments or present side effects to these drugs, highlighting the importance of developing other therapeutic options. Different non-pharmacological treatments are in this review addressed, finding diverse results regarding efficacy. Altogether, ADHD is associated with different etiologies, all of them producing changes in brain development, leading to the characteristic symptomatology of this condition. Given the heterogeneous etiology of ADHD, discussion is presented about the convenience of personalizing ADHD treatment, whether pharmacological or non-pharmacological, to reach an optimum effect in the majority of patients. Approaches to personalizing both pharmacological therapy and neurofeedback are presented.

Capsaicin intake and oral carcinogenesis: A systematic review / Ingesta de capsaicina y carcinogénesis oral: una revisión sistemática

Background: Chili is the most heavily and frequently consumed spice, either as a flavouring or colouring agent,and it is also a major source of pro-vitamin A, vitamin E and C. The main capsaicinoid found in chili peppers iscapsaicin. It has been demonstrated that capsaicin acts as a cancer-suppressing agent through its antioxidant andanti-inflammatory effects, by blocking several signal transduction pathways. Oral squamous cell carcinoma isone of the most prevalent cancer worldwide. It is noteworthy that in countries where populations of diverse ethnicgroups co-exist, differences have been observed in terms of incidence of oral cancer. The variances in their dietcould explain, at least in part, these differences. The objective of this systematic review is to explore if there isevidence of a possible relationship between capsaicin intake and the incidence of oral squamous cell carcinoma,and discuss such association.Material and Methods: A bibliographical search was made in PubMed, Scopus and Web of Science databases, andfinally 7 experimental studies were included; OHAT risk of bias tool was used to assess their quality.Results: All the studies confirm that capsaicin is a chemopreventive agent that prevents the development of oralcancer, through inhibition of malignant cell proliferation and increase of apoptosis.Conclusions: More human studies are needed in order to clarify the real link between consumption of chili (cap-saicin) and the prevalence of oral cancer.(AU)

Fragility of reward vs antifragility of defense brain systems in drug dependence.

Drug dependence is a debilitating disorder, affecting 30 million people worldwide. In this short review we discuss about the plasticity changes in the reward and defense brain systems induced by early-life psychosocial stressful experiences. Such changes may render persons more vulnerable to illicit drugs use, facilitating behaviors of abuse and development of addiction. We propose that underlying plasticity changes render brain reward system as increasingly fragile because of tolerance and other physiological effects that reduce responsiveness with repeated use. In contrast, we propose that brain defense system makes maintain antifragile mechanisms that generate more robust responses with the prolonged consumption of drugs. Investigating the underlying mechanisms of these brain plasticity changes may advance the development of more efficacious pharmacologic and psychotherapeutic approaches to rehabilitate patients and more efficacious prevention policies to protect children from stressful experiences.

Author Correction: Hesperidin and capsaicin, but not the combination, prevent hepatic steatosis and other metabolic syndrome-related alterations in western diet-fed rats.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Marihuana: legalización y atención médica / Marihuana: Legalization and Medical Care

Resumen A pesar de que el uso de marihuana se considera ilegal en la mayoría de los países del mundo, es una de las drogas más utilizadas. El 8,6% de la población mexicana, entre 12 y 65 años, ha probado la marihuana alguna vez (2017). Este porcentaje ha aumentado significativamente en los últimos años. Casos fatales asociados con el consumo de cannabis no se documentaron durante mucho tiempo; sin embargo, recientemente se ha informado de muertes causada por un síndrome de hiperémesis de cannabis (CHS) y muerte por automutilación. Si bien se ha documentado que la marihuana sintetiza sustancias activas con potenciales propiedades terapéuticas, en la actualidad, el mayor uso de la marihuana en nuestro país y en el mundo es recreativo. Esta revisión analiza las consecuencias del uso recreativo de marihuana, el contexto social y de salud con respecto a la legalización y los posibles usos terapéuticos de compuestos extraídos de la planta, de acuerdo a estudios reportados en la literatura científica. La contribución que hacemos es alertar sobre el impacto negativo en la salud del uso recreativo de marihuana y la urgencia de favorecer la investigación sobre sus efectos en el cerebro. Asimismo, identificar los principios activos que tengan potencial para el uso terapéutico.

Abstract Despite the fact that the use of marihuana is illegal in most countries of the world, it still is one of the most commonly used drugs worldwide. 8.6% of the Mexican population, between 12-65 years old, has smoked marihuana at least once in their lifetime (2017). There has been a significant increase in the number of consumers in the last few years. Fatal cases associated with cannabis use had not been recognized for a long time, however, lately, deaths due to a cannabis hyperemesis syndrome (CHS) and deaths from self-mutilation have been reported. Although marihuana synthesizes several active substances with potential therapeutic properties, nowadays, the greatest use of marihuana in our country and in the world is recreational. This review discusses the consequences of using marihuana for recreational use, the social and health contexts regarding legalization and potential therapeutic uses of compounds isolated from the plant based on the scientific literature. Our contribution is to warn people about the potential negative impact on the health of recreational use marihuana and the urgency of supporting the research of its effects on the brain. Similarly, we aim to identify the active principles with potential therapeutic use.

Relationship between Changes in Microbiota and Liver Steatosis Induced by High-Fat Feeding-A Review of Rodent Models.

Several studies have observed that gut microbiota can play a critical role in nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) development. The gut microbiota is influenced by different environmental factors, which include diet. The aim of the present review is to summarize the information provided in the literature concerning the impact of changes in gut microbiota on the effects which dietary fat has on liver steatosis in rodent models. Most studies in which high-fat feeding has induced steatosis have reported reduced microbiota diversity, regardless of the percentage of energy provided by fat. At the phylum level, an increase in Firmicutes and a reduction in Bacteroidetes is commonly found, although widely diverging results have been described at class, order, family, and genus levels, likely due to differences in experimental design. Unfortunately, this fact makes it difficult to reach clear conclusions concerning the specific microbiota patterns associated with this feeding pattern. With regard to the relationship between high-fat feeding-induced changes in liver and microbiota composition, although several mechanisms such as alteration of gut integrity and increased permeability, inflammation, and metabolite production have been proposed, more scientific evidence is needed to address this issue and thus further studies are needed.

Sexual Behavior and Synaptic Plasticity.

Although sex drive is present in many animal species, sexual behavior is not static and, like many other behaviors, can be modified by experience. This modification relies on synaptic plasticity, a sophisticated mechanism through which neurons change how they process a given stimulus, and the neurophysiological basis of learning. This review addresses the main plastic effects of steroid sex hormones in the central nervous system (CNS) and the effects of sexual experience on the CNS, including effects on neurogenesis, intracellular signaling, gene expression, and changes in dendritic spines, as well as behavioral changes.

Effects of Quercetin Metabolites on Triglyceride Metabolism of 3T3-L1 Preadipocytes and Mature Adipocytes.

Quercetin (Q) has rapid metabolism, which may make it worthwhile to focus on the potential activity of its metabolites. Our aim was to evaluate the triglyceride-lowering effects of Q metabolites in mature and pre-adipocytes, and to compare them to those induced by Q. 3T3-L1 mature and pre-adipocytes were treated with 0.1, 1 and 10 µM of Q, tamarixetin (TAM), isorhamnetin (ISO), quercetin-3-O-glucuronide (3G), quercetin-3-O-sulfate (3S), as well as with 3S and quercetin-4-O-sulfate (4S) mixture (3S+4S). Triglyceride (TG) content in both cell types, as well as free fatty acid (FFA) and glycerol in the incubation medium of mature adipocytes were measured spectrophotometrically. Gene expression was assessed by RT-PCR. In mature adipocytes, Q decreased TG at 1 and 10 µM, 3S metabolite at 1 and 10 µM, and 3S+4S mixture at 10 µM. 3S treatment modified the glucose uptake, and TG assembling, but not lipolysis or apoptosis. During differentiation, only 10 µM of ISO reduced TG content, as did Q at physiological doses. In conclusion, 3S metabolite but not ISO, 3G, 4S and TAM metabolites can contribute to the in vivo delipidating effect of Q.

Endocannabinoids as Therapeutic Targets.

Most of the drugs of abuse affect the brain by interacting with naturally expressed molecular receptors. Marihuana affects a series of receptors including cannabinoid receptor 1 (CB1R) and CB2R, among others. Endogenous molecules with cannabinoid activity interact with these receptors naturally. Receptors, ligands, synthesizing and degrading enzymes, as well as transporters, have been described. This endocannabinoid system modulates behaviors and physiological processes, i.e. food intake, the sleep-waking cycle, learning and memory, motivation, and pain perception, among others. The rather broad distribution of endocannabinoids in the brain explains the different effects marihuana induces in its users. However, this very same anatomical and physiological distribution makes this system a useful target for therapeutic endeavors. In this review, we briefly discuss the potential of small molecules that target the endocannabinoids as therapeutic tools to improve behaviors and treat illnesses. We believe that under medical supervision, endocannabinoid targets offer new advantages for patients for controlling multiple medical disorders.

Hesperidin and capsaicin, but not the combination, prevent hepatic steatosis and other metabolic syndrome-related alterations in western diet-fed rats.

We aimed to assess the potential effects of hesperidin and capsaicin, independently and in combination, to prevent the development of obesity and its related metabolic alterations in rats fed an obesogenic diet. Three-month-old male Wistar rats were divided into 5 groups: Control (animals fed a standard diet), WD (animals fed a high fat/sucrose (western) diet), HESP (animals fed a western diet + hesperidin (100 mg/kg/day)), CAP (animals fed a western diet + capsaicin (4 mg/kg/day)), and HESP + CAP (animals fed a western diet + hesperidin (100 mg/kg/day) + capsaicin (4 mg/kg/day)). Hesperidin and capsaicin were administered by gavage. Capsaicin decreased body fat gain and prevented insulin resistance, whereas hesperidin showed little effect on body fat gain and no apparent effects on insulin resistance. No additive effects were observed with the combination. Capsaicin and hesperidin, separately, improved blood lipid profile, diminished hepatic lipid accumulation, and prevented non-alcoholic steatohepatitis in western diet-fed rats, but the combination showed lower effects. Hesperidin alone, and to a lesser extent capsaicin or the combination, displayed hypotensive effects in western diet-fed rats. In conclusion, capsaicin and hesperidin, separately, exhibit health beneficial effects on metabolic syndrome-related alterations in western diet-fed rats, but the effects are mitigated with the combination.

Combination of Capsaicin and Hesperidin Reduces the Effectiveness of Each Compound To Decrease the Adipocyte Size and To Induce Browning Features in Adipose Tissue of Western Diet Fed Rats.

We explored the potential of hesperidin and capsaicin, separately and in combination, to induce white adipose tissue (WAT) browning and to help body weight management in Western diet-fed rats. Adult male Wistar rats were fed for 8 weeks with Western diet and treated daily with hesperidin (100 mg/kg/day), capsaicin (4 mg/kg/day), hesperidin (100 mg/kg/day) + capsaicin (4 mg/kg/day), or the vehicle. Hesperidin and capsaicin separately, but not (or to a lesser extent) the combination, resulted in a decreased size of adipocytes and induced emergence of multilocular brown-like adipocytes positive for UCP1 and CIDEA in retroperitoneal WAT. Expression levels of browning markers, such as Prdm16, in inguinal WAT also increased with capsaicin treatment compared with the vehicle (145% ± 17% vs 92% ± 21%, P < 0.05), but no significant effects were found with the combination (106% ± 12%). Thus, the combination of both bioactives reduces the effectiveness of each compound to decrease the adipocyte size and induce WAT browning.

Ambulatory blood pressure monitoring in school children with a history of extreme prematurity. / Monitorización ambulatoria de presión arterial en escolares con antecedente de prematurez extrema.

INTRODUCTION: Extremely premature children have a higher incidence of High Blood Pressure (HBP) and risk of renal damage due to decreased glomerular count with consequent hyperfiltration of the remnants. OBJECTIVES: To assess the prevalence of altered blood pressure values in outpatient measurement and ambulatory blood pressure monitoring (ABPM) in preterm infants ≤ 32 weeks and/ or ≤ 1,500 g birth weight between 5 and 7 years of age, as well as the presence of early renal damage markers. PATIENTS AND METHODS: An isolated measurement of blood pressure, ABPM and laboratory tests (microalbuminuria/creatininuria ratio in an isolated urine sample, serum creatinine, blood urea nitrogen and urinalysis) were performed. RESULTS: 30 patients were recruited, of whom valid measu rements of ABPM were obtained in 19 cases, of which nine (47,4%) presented some abnormalities, principally nocturnal day/night difference or DIP absent. No abnormal laboratory tests were found. DISCUSSION: Our study detected a high prevalence of abnormalities in ABPM principally DIP absence, which has been related to an increased risk of progression to hypertension. The importance of per forming ABPM in the study is emphasized in patients with risk factors for developing hypertension in order to detect early alterations and close management and follow-up.