Unmasking the Mimic: Radionecrotic Lesion Masquerading as Brain Neoplasia on Magnetic Resonance Imaging.

Corpus callosotomy is a therapeutic approach for drug-resistant epilepsy, with positive outcomes observed in managing atonic seizures. Despite a decline in its usage, radiosurgical callosotomy remains a viable option for drug-resistant epilepsy due to its low risks of post-radiation neoplasia, albeit not with exceptions. Brain radionecrosis is characterized by tissue death and vascular endothelial damage following the procedure. Despite the low risk of intracranial secondary malignancy associated with radiation in some cases, post-radiation lesions might present with distinct characteristics needing a thorough diagnostic approach. Herein, we present a unique case of a patient with focal epilepsy who developed a radionecrotic lesion following radiosurgical callosotomy, affecting the anterior cingulate cortex, and mimicking a central nervous system (CNS) tumor. Molecular imaging techniques, including 18-fluorodeoxyglucose positron emission tomography/computed tomography (18-FDG PET/CT) and 11C-acetate PET/CT scans, were employed to differentiate the lesion from a tumor. This case underscores the importance of considering radionecrosis as a differential diagnosis in patients who undergo radiosurgical callosotomy presenting with ring-like enhancement lesions on magnetic resonance imaging (MRI).

Pathological Thoracic Vertebral Fractures Secondary to Achromobacter denitrificans: A Case Report.

Vertebral fractures remain a diagnostic challenge nowadays. The first and most common diagnosis needed to be ruled out is osteoporosis. Other diagnoses to rule out involve pathological fractures. Pathological fractures are a group of pathologies that result in a spine fracture as part of an underlying disease process that affects the spine. This group includes Paget's disease, tumors, osteomyelitis, and vertebral compression fractures. Fractures secondary to vertebral osteomyelitis are presented as collapsed vertebral bodies secondary to bone destruction and the formation of lytic lesions. Clinical presentation includes severe back pain refractory to analgesic therapy, persistent unexplained fever, and leukocytosis without any other obvious focus of infection. In cases like the one presented here, early biopsy and culture should be performed on every patient that fits these criteria. However, as it presents unspecific symptoms most of the time, it is not suspected, and therefore it is associated with high morbidity and mortality.

Ischemic Stroke as an Initial Manifestation of Antiphospholipid Syndrome in an Adolescent: A Case Report.

Cerebrovascular diseases in pediatric patients are relatively rare. Ischemic stroke in adolescents is associated with a poor prognosis. The most common causes include systemic diseases, such as heart disease and hypercoagulation disorders. It is important to mention that one of the most common acquired hypercoagulation states is the antiphospholipid syndrome (APS). Patients with this disease may present stroke as the first clinical manifestation, which not only increases morbidity in these patients but presents a diagnostic challenge. This case presents one example of how APS can present as a pediatric stroke. The diagnostic approach should always be through the presence of specific antibodies accompanied by the presence of a thromboembolic episode proven by catheterization or an imaging study. In the brain, the preferred imaging study is magnetic resonance imaging. Management is based on anticoagulation therapy and continuous monitoring in the intensive care unit.

Reactive Arthritis as a Consequence of Infection by Clostridium difficile in a Pediatric Patient.

Reactive arthritis (RA) is the development of a sterile inflammatory arthritis usually associated with a previously known infection, most commonly from the gastrointestinal or urogenital tract. The diagnosis is clinical, based on the presence of acute oligoarticular arthritis of larger joints developing within two to four weeks of the infection. However, in some cases where the infection is not clear, the diagnosis is a challenge, like in the case presented here. We must always rule out past infections as a cause of arthritis by directly asking about the presence of symptomatology associated with it, presented in the past few weeks. It's important to emphasize that human leukocyte antigen B27 (HLA-B27) should not be used as a diagnostic tool, and it always needs to be correlated with the clinical features. There is no confirmed evidence in the literature that is in favor of prescribing antibiotic therapy during an acute presentation of RA as it usually presents after the infection is cured.

Guillain-Barré Syndrome in an Immunocompromised Patient: A Case Report.

Guillain-Barré syndrome (GBS) in post-transplant patients is a rare clinical presentation. Although in the literature this neurological condition has been mainly associated with viral infections secondary to immunosuppression, GBS should not only be suspected in patients with an acute condition. It is essential to always rule out a viral or bacterial cause, looking for the most common sources, i.e., urinary, respiratory, and gastrointestinal. The diagnosis of GBS is clinically based, and its management is based on the use of intravenous immunoglobulin (IVIG) or plasma exchange. Its timely diagnosis allows treatment to be started early, thus improving the prognosis of these patients and reducing the time of hospitalization and complications associated with it. This report shows how an interdisciplinary approach is vital in such cases, as both the precipitant and the disease must be managed to decrease the morbidity and mortality associated with this condition. It is crucial to evaluate the benefits and risks of withdrawing immunosuppressive treatment in post-transplant patients, and being able to recognize when restarting them is indicated.

Accuracy of Astigmatism Calculation with the Barrett, Panacea, and enVista Toric Calculators.

PURPOSE: To evaluate residual refractive astigmatism using the Panacea and enVista toric calculators, compared to the gold-standard Barrett toric calculator. DESIGN: A retrospective and comparative study was conducted in one center. METHODS: We reviewed the medical records of all patients with a diagnosis of senile cataracts and regular corneal astigmatism, without previous corneal or intraocular surgery, who underwent phacoemulsification with implantation of a toric intraocular lens, who had pre- and postoperative corneal topography, biometry, and refraction measurements. RESULTS: The frequency of preoperative astigmatism according to the axis was 70 (84%) eyes showing with-the-rule (WTR) astigmatism, 9 (14%) eyes with against-the-rule (ATR) astigmatism, and 1 (2%) eye with oblique astigmatism. Regarding astigmatism prediction errors, there were statistically significant differences between the enVista and Panacea calculators (median of 0.39, 0.18, and 0.52 for Barrett, enVista, and Panacea, respectively). The residual astigmatism prediction error centroid was similar for the Barrett and enVista toric calculators, and both were lower compared to the Panacea calculator (x-component p < 0.001). CONCLUSIONS: The enVista toric calculator incorporating the Emmetropia Verifying Optical (EVO) toric calculator provides similar results to the gold-standard Barrett calculator.

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.

Impacto de las exacerbaciones en la enfermedad pulmonar obstructiva crónica / Impact of Exacerbations on Chronic Obstructive Pulmonary Disease

La enfermedad pulmonar obstructiva crónica (EPOC) es la tercera causa de muerte en todo el mundo. Sin embargo, ante la falta de herramientas diagnósticas precisas en el primer nivel de atención médica, como la espirometría, es difícil determinar la prevalen-cia real de la EPOC.Por otro lado, la falta de una definición clara y precisa de las exacerbaciones de la EPOC hace que se subestime su impacto en la salud pública; habitualmente, los pacien-tes con EPOC que cursan una exacerbación retrasan la búsqueda de atención médica inmediata porque se acostumbran al deterioro asociado a la enfermedad o lo confun-den con cambios por la edad avanzada. Esto puede provocar un aumento de la mor-bilidad y la mortalidad, asimismo, mayor utilización de los recursos sanitarios y mayor carga económica. Por lo tanto, es importante sensibilizar sobre la importancia del diagnóstico temprano y el tratamiento adecuado de las exacerbaciones de la EPOC, del mismo modo que el mayor conocimiento público de los síntomas, las causas y los factores de riesgo de la EPOC. Con ello, se podrán aplicar estrategias de prevención, diagnóstico y tratamiento más eficaces que mejoren la calidad de vida de los pacientes y disminuyan la carga de la enfermedad para la sociedad.Esta revisión ofrece un análisis crítico de la definición más reciente y esboza las impli-caciones del comportamiento de las exacerbaciones, su impacto en los distintos ám-bitos del sistema sanitario, así como en las diferentes esferas de la vida de los pacien-tes con EPOC. (AU)

Chronic Obstructive Pulmonary Disease (COPD) is a common disease and the third leading cause of death worldwide. However, due to the lack of accurate diagnostic tools at the first level of care, such as spirometry, the true prevalence of COPD is difficult to determine.In addition, the lack of a clear definition of COPD exacerbations means that its pub-lic health impact is underestimated. Patients with COPD often do not seek immediate medical attention because they become used to the deterioration associated with the disease. This can lead to increased patient morbidity and mortality, as well as increased utilization of healthcare resources and higher economic costs. Therefore, it is important to promote greater awareness of the importance of early di-agnosis and proper management of COPD exacerbations, as well as increased public awareness of COPD symptoms, etiologic agents, and risk factors.By better understanding COPD exacerbations, more effective prevention, diagnosis and treatment strategies can be implemented to improve the quality of life of patients and reduce the burden of the disease on society.This review aims to provide a critical analysis of the most recent definition and to out-line the implications of the behavior of COPD exacerbations and their impact on the dif-ferent settings of the health care system, as well as on the different spheres of patients' lives. (AU)

Relationship between Helicobacter pylori and undifferentiated non-granulomatous anterior uveitis.

PURPOSE: The relationship of Helicobacter pylori infection with ocular diseases, including anterior uveitis, has been reported. The objective of this study was to determine the presence of anti-H. pylori IgG antibodies in patients with idiopathic non-granulomatous anterior uveitis and compare the results with a control group. METHODS: A prospective, comparative, and cross-sectional study was conducted. Patients with idiopathic granulomatous anterior uveitis and a group of control subjects were included. The presence of anti-H. pylori IgG antibodies was determined. The chi-square test was performed for comparative analysis with GraphPad Prism V5.0 software. RESULTS: Thirty patients with idiopathic non-granulomatous anterior uveitis and 35 control subjects were included. In the determination of anti-H. pylori IgG antibodies, 24 (80%) patients and 19 (54%) control subjects were positive. A significant difference (p = 0.0263) was found between the groups and an odds ratio (OR) of 3.37. CONCLUSIONS: A direct relationship was found between the presence of anti-H. pylori IgG antibodies and idiopathic non-granulomatous anterior uveitis. An association can be established between idiopathic non-granulomatous anterior uveitis and H. pylori infection, without this being a causal or physiopathogenic relationship.

Effect of Phosphate Binders and a Dietary Iron Supplement on the Pharmacokinetics of a Single Dose of Vadadustat in Healthy Adults.

Vadadustat is a hypoxia-inducible factor prolyl-hydroxylase inhibitor being developed for the treatment of anemia in patients with chronic kidney disease. Sequelae of chronic kidney disease include hyperphosphatemia and anemia, which are frequently treated with phosphate binders and iron supplements, respectively. Two studies evaluating the pharmacokinetics, safety, and tolerability of a single oral dose of vadadustat coadministered with a phosphate binder or iron supplement were conducted in healthy adult participants. In study 1, 54 healthy women and men were administered vadadustat (300 mg) alone and 1 hour before, concurrently with, or 2 hours after a phosphate binder (sevelamer carbonate 1600 mg, calcium acetate 1334 mg, or ferric citrate 2000 mg). In study 2, 10 healthy men were administered vadadustat (450 mg) alone and concomitantly with the oral iron supplement ferrous sulfate (325 mg [equivalent to 65 mg of elemental iron]). Vadadustat exposure was reduced by coadministration with sevelamer carbonate, calcium acetate, ferric citrate, or ferrous sulfate. Geometric least squares mean ratios for area under the concentration-time curve from time 0 to infinity were reduced 37% to 55% by phosphate binders and 46% by ferrous sulfate. However, when vadadustat was administered 1 hour before phosphate binders, 90% confidence intervals for vadadustat exposure were within the no-effect boundaries of +50% to -33%, indicating that drug-drug interactions can be reduced by administering vadadustat 1 hour before phosphate binders. Vadadustat was well tolerated when administered in conjunction with phosphate binders or an iron supplement.

Transcytosis of Bacillus subtilis extracellular vesicles through an in vitro intestinal epithelial cell model.

Bacterial EVs have been related to inter-kingdom communication between probiotic/pathogenic bacteria and their hosts. Our aim was to investigate the transcytosis process of B. subtilis EVs using an in vitro intestinal epithelial cell model. In this study, using Confocal Laser Scanning Microscopy, we report that uptake and internalization of CFSE-labeled B. subtilis EVs (115 nm ± 27 nm) by Caco-2 cells are time-dependent. To study the transcytosis process we used a transwell system and EVs were quantified in the lower chamber by Fluorescence and Nanoparticle Tracking Analysis measurements. Intact EVs are transported across a polarized cell monolayer at 60-120 min and increased after 240 min with an estimated average uptake efficiency of 30% and this process is dose-dependent. EVs movement into intestinal epithelial cells was mainly through Z axis and scarcely on X and Y axis. This work demonstrates that EVs could be transported across the gastrointestinal epithelium. We speculate this mechanism could be the first step allowing EVs to reach the bloodstream for further delivery up to extraintestinal tissues and organs. The expression and further encapsulation of bioactive molecules into natural nanoparticles produced by probiotic bacteria could have practical implications in food, nutraceuticals and clinical therapies.

Overexpression of Lin28a delays Xenopus metamorphosis and down-regulates albumin independently of its translational regulation domain.

BACKGROUND: Lin28 regulates stem cell biology and developmental timing. At the molecular level Lin28 inhibits the biogenesis of the micro RNA let-7 and directly controls the transcription and translation of several genes. In Xenopus, Lin28 overexpression delays metamorphosis and affects the expression of genes of the thyroid hormone (TH) axis. The TH carrier albumin, synthesized by the liver, is down-regulated in limbs and tail after Lin28 overexpression. The molecular mechanisms underlying the interaction between Lin28, let-7, and the hypothalamus-pituitary-thyroid gland (HPT) axis are unknown. RESULTS: We found that precursor and mature forms of let-7 increase during Xenopus metamorphosis. In the liver, lin28b is down-regulated and albumin is up-regulated during metamorphosis. Overexpression of a truncated form of Lin28a (Lin28aΔC), which has been shown not to interact with RNA helicase A to regulate translation, delays metamorphosis, indicating that the translational regulation domain is not required to inhibit the HPT axis. Importantly, both full length Lin28a and Lin28aΔC block the increase of albumin mRNA in the liver independently of changes in TH signaling. CONCLUSIONS: These results suggest that Lin28 delays metamorphosis through regulation of let-7 and that the decrease of the TH carrier albumin is one of the early changes after Lin28 overexpression.

Benzoxaboroles as dynamic covalent receptors for bioconjugation and transport of nucleosides and related drugs: Proof of action in HeLa cells.

In this work we describe not previously explored binding studies on the reversible interaction of benzoxaborole with ligands of medical and pharmaceutical interest such as nucleosidic drugs gemcitabine and capecitabine, as well as the hydrophobic chemotherapeutic doxorubicin. We include functional derivatives of benzoxaborole such as a near infrared fluorescent boronolectine, Cy-Bx, The dynamic covalent interaction in physiological conditions was assessed by spectroscopic techniques yielding moderate to high binding affinities. The cytotoxic activity of the drugs upon conjugation to the boronolectins was evaluated revealing significant influence of the bioconjugation status on the cellular viability. The availability of the conjugate for cellular uptake and localization in the model cancer cell line HeLa was assessed by fluorescence imaging. Benzoxaborole and the fluorescent boronolectin Cy-Bx, proved to be versatile conjugation tools for 1,2 and 1,3-diol containing pharmacophores as well as bioisosteric forms such as 1,2-hydroxyamino, envisioning these small boronolectins as components in systems for drug release with tracking capability.

Toxicity of blue led light and A2E is associated to mitochondrial dynamics impairment in ARPE-19 cells: implications for age-related macular degeneration.

Age-related macular degeneration (AMD) is a multifactorial retinal disease characterized by a progressive loss of central vision. Retinal pigment epithelium (RPE) degeneration is a critical event in AMD. It has been associated to A2E accumulation, which sensitizes RPE to blue light photodamage. Mitochondrial quality control mechanisms have evolved to ensure mitochondrial integrity and preserve cellular homeostasis. Particularly, mitochondrial dynamics involve the regulation of mitochondrial fission and fusion to preserve a healthy mitochondrial network. The present study aims to clarify the cellular and molecular mechanisms underlying photodamage-induced RPE cell death with particular focus on the involvement of defective mitochondrial dynamics. Light-emitting diodes irradiation (445 ± 18 nm; 4.43 mW/cm2) significantly reduced the viability of both unloaded and A2E-loaded human ARPE-19 cells and increased reactive oxygen species production. A2E along with blue light, triggered apoptosis measured by MC540/PI-flow cytometry and activated caspase-3. Blue light induced mitochondrial fusion/fission imbalance towards mitochondrial fragmentation in both non-loaded and A2E-loaded cells which correlated with the deregulation of mitochondria-shaping proteins level (OPA1, DRP1 and OMA1). To our knowledge, this is the first work reporting that photodamage causes mitochondrial dynamics deregulation in RPE cells. This process could possibly contribute to AMD pathology. Our findings suggest that the regulation of mitochondrial dynamics may be a valuable strategy for treating retinal degeneration diseases, such as AMD.

Heme Oxygenase-1 protects astroglia against manganese-induced oxidative injury by regulating mitochondrial quality control.

Heme Oxygenase-1 (HO-1), a stress- responsive enzyme which catalyzes heme degradation into iron, carbon monoxide, and biliverdin, exerts a neuroprotective role involving many different signaling pathways. In Parkinson disease patients, elevated HO-1 expression levels in astrocytes are involved in antioxidant defense. In the present work, employing an in vitro model of Mn2+-induced Parkinsonism in astroglial C6 cells, we investigated the role of HO-1 in both apoptosis and mitochondrial quality control (MQC). HO-1 exerted a protective effect against Mn2+ injury. In fact, HO-1 decreased both intracellular and mitochondrial reactive oxygen species as well as the appearance of apoptotic features. Considering that Mn2+ induces mitochondrial damage and a defective MQC has been implicated in neurodegenerative diseases, we hypothesized that HO-1 could mediate cytoprotection by regulating the MQC processes. Results obtained provide the first evidence that the beneficial effects of HO-1 in astroglial cells are mediated by the maintenance of both mitochondrial fusion/fission and biogenesis/mitophagy balances. Altogether, our data demonstrate a pro-survival function for HO-1 in Mn2+-induced apoptosis that involves the preservation of a proper MQC. These findings point to HO-1 as a new therapeutic target linked to mitochondrial pathophysiology in Manganism and probably Parkinson´s disease.

Alpha-synuclein mitochondrial interaction leads to irreversible translocation and complex I impairment.

α-synuclein is involved in both familial and sporadic Parkinson's disease. Although its interaction with mitochondria has been well documented, several aspects remains unknown or under debate such as the specific sub-mitochondrial localization or the dynamics of the interaction. It has been suggested that α-synuclein could only interact with ER-associated mitochondria. The vast use of model systems and experimental conditions makes difficult to compare results and extract definitive conclusions. Here we tackle this by analyzing, in a simplified system, the interaction between purified α-synuclein and isolated rat brain mitochondria. This work shows that wild type α-synuclein interacts with isolated mitochondria and translocates into the mitochondrial matrix. This interaction and the irreversibility of α-synuclein translocation depend on incubation time and α-synuclein concentration. FRET experiments show that α-synuclein localizes close to components of the TOM complex suggesting a passive transport of α-synuclein through the outer membrane. In addition, α-synuclein binding alters mitochondrial function at the level of Complex I leading to a decrease in ATP synthesis and an increase of ROS production.

A Highly Sensitive Fluorogenic Probe for Imaging Glycoproteins and Mucine Activity in Live Cells in the Near-Infrared Region.

A novel fluorescent molecular probe is reported, which is able to detect glycoproteins, especially mucins, with high sensitivity and with a turn-on response along with a large Stokes shift (>130 nm), within the biologically active window. The probe contains an aminotricarbocyanine as the fluorescent reporter with a linked benzoboroxole as the recognition unit, which operates through a dynamic covalent reaction between the boronic hemiester residue of the receptor and cis-diols of the analyte. The superior selectivity of the probe is displayed by the labeling of mucins present in Calu-3 cells. The new benzoboroxole fluorescent derivative gathers together key properties to make it a highly rated molecular probe: specificity, excellent solubility in water, and off-on near infrared emission. This probe is expected to be an excellent tool for imaging intracellular mucin to evaluate mucus-related diseases as well as a sensing strategy towards glycosylated structures with a high potential for theranostics approaches in biological samples.

Drp-1 dependent mitochondrial fragmentation and protective autophagy in dopaminergic SH-SY5Y cells overexpressing alpha-synuclein.

Parkinson's disease is a neurodegenerative movement disorder caused by the loss of dopaminergic neurons from substantia nigra. It is characterized by the accumulation of aggregated α-synuclein as the major component of the Lewy bodies. Additional common features of this disease are the mitochondrial dysfunction and the activation/inhibition of autophagy both events associated to the intracellular accumulation of α-synuclein. The mechanism by which these events contribute to neural degeneration remains unknown. In the present work we investigated the effect of α-synuclein on mitochondrial dynamics and autophagy/mitophagy in SH-SY5Y cells, an in vitro model of Parkinson disease. We demonstrated that overexpression of wild type α-synuclein causes moderated toxicity, ROS generation and mitochondrial dysfunction. In addition, α-synuclein induces the mitochondrial fragmentation on a Drp-1-dependent fashion. Overexpression of the fusion protein Opa-1 prevented both mitochondrial fragmentation and cytotoxicity. On the other hand, cells expressing α-synuclein showed activated autophagy and particularly mitophagy. Employing a genetic strategy we demonstrated that autophagy is triggered in order to protect cells from α-synuclein-induced cell death. Our results clarify the role of Opa-1 and Drp-1 in mitochondrial dynamics and cell survival, a controversial α-synuclein research issue. The findings presented point to the relevance of mitochondrial homeostasis and autophagy in the pathogenesis of PD. Better understanding of the molecular interaction between these processes could give rise to novel therapeutic methods for PD prevention and amelioration.

Proteins as Nano-Carriers for Bioactive Compounds. The Case of 7S and 11S Soy Globulins and Folic Acid Complexation.

Isolated 7S and 11S globulins obtained from defeated soy flour were complexated with folic acid (FA) in order to generate nano-carriers for this important vitamin in human nutrition. Fluorescence spectroscopy and dynamic light scattering were applied to follow the nano-complexes formation and for their characterization. Fluorescence experimental data were modeled by the Stern-Volmer and a modified double logarithm approach. The results obtained confirmed static quenching. The number of binding sites on the protein molecule was ~1. The values obtained for the binding constants suggest a high affinity between proteins and FA. Particle size distribution allowed to study the protein aggregation phenomenon induced by FA bound to the native proteins. Z-average manifested a clear trend to protein aggregation. 11S-FA nano-complexes resulted in more polydispersity. ζ-potential of FA nano-complexes did not show a remarkable change after FA complexation. The biological activity of nano-complexes loaded with FA was explored in terms of their capacity to enhance the biomass formation of Lactobacillus casei BL23. The results concerning to nano-complexes inclusion in culture media showed higher bacterial growth. Such a result was attributed to the entry of the acid by the specific receptors concomitantly by the peptide receptors. These findings have technological impact for the use of globulins-FA based nano-complexes in nutraceutical, pharmaceutical and food industries.

Trastorno por atracón, depresión, ansiedad y gen del neuropéptido relacionado con Agouti en pacientes con cirugía bariátrica / Binge eating disorder, depression, anxiety and Agouti gen related neuropeptide in patients with bariatric surgery

Resumen El objetivo de este estudio retroprospectivo fue analizar la relación de la sintomatología de depresión, de ansiedad y el trastorno por atracón (TPA) con el gen del neuropéptido relacionado con Agouti en pacientes sometidos a cirugía bariátrica. Participó una cohorte de 249 adultos (edad media = 41.1, DE =11.3), 64.1% mujeres y 35.9% hombres. La evaluación de la sintomatología depresiva, de ansiedad y de TPA se llevó a cabo a través de una entrevista semiestructurada. Además, se calculó el índice de masa corporal y se tomaron muestras de sangre para realizar un análisis de discriminación alélica. Del total de pacientes, un 20.2% fueron diagnosticados con TPA, encontrando una asociación de este trastorno con una menor pérdida de peso posterior a la cirugía bariátrica a los 6,12, 18 y 24 meses. Las medidas de depresión y de ansiedad no difirieron entre pacientes con TPA vs. sin TPA. Los pacientes con un alelo mutante en el gen del neuropéptido relacionado con Agouti tuvieron un riesgo 2.6 veces mayor de presentar TPA (IC 95% 1.0-6.8; p = 0.04). Además, el TPA parece ser más frecuente en pacientes con el gen del neuropéptido relacionado con Agouti mutado. Destaca la necesidad de que en el estudio de la obesidad se aborden tanto los aspectos psicológicos como los genéticos.

Abstract The objective of this retrospective study was to analyze the relationship between the symptoms of depression, anxiety and binge eating disorder (BED) with the gene related to the Agouti neuropeptide in patients undergoing bariatric surgery. A cohort of 249 adults (average age = 41.1, SD = 11.3), 64.1% women and 35.9% men, were included. The assessment of depression, anxiety and BED symptoms was carried out through a semi-structured interview. In addition, the body mass index was calculated, and blood samples were taken for an allelic discrimination analysis. Of the total number of patients 20.2% were diagnosed with BED, finding an association of this disorder with a lower weight loss after bariatric surgery at 6, 12, 18 and 24 months. The measures of depression and anxiety did not differ between patients with BED vs. without BED. Patients with a mutant allele in the gene related to the Agouti neuropeptide were 2.6 times more likely to present BED (95% C11.0-6.8, P = 0.04). In addition, BED appears to be more frequent in patients with a gene related to the Agouti neuropeptide mutated. When obesity is studied, it is emphasized the need to address both psychological and genetic factors.