Prevalence and risk factors of posttraumatic stress disorder in COVID-19

Posttraumatic stress disorder (PTSD) has a prevalence of 2%–5% in the general population. COVID-19 is regarded as a traumatic agent that can increase the prevalence of this disorder to up to 30%. A documentary review was thus conducted, which included 13 studies on the presence of PTSD in patients who have survived COVID-19 infection and the possible associated factors. Female and young age, as well as other aspects associated with economic losses or living alone, could influence the appearance of this psychological sequela. A preventive mental healthcare program could be implemented during infection in such patients with COVID-19 who show the characteristics described in most studies

Hormona paratiroidea, aldosterona e hipertensión arterial ¿una amenaza infravalorada?

El Hiperparatiroidismo primario (HPTP) es un trastorno endocrino frecuente caracterizado por una secreción autónoma de hormona paratiroidea (PTH). Si bien, su variante asintomática es la más frecuentemente encontrada en la práctica clínica (la cual se diagnostica incidentalmente), las complicaciones óseas y renales afectan de forma importante la calidad de vida del paciente. Sin embargo, el espectro de manifestaciones de este trastorno no se limita al metabolismo mineral, puesto que las concentraciones elevadas de PTH se asocian a un mayor riesgo de alteraciones metabólicas como el síndrome metabólico, diabetes mellitus 2 y enfermedades cardiovasculares. En este ámbito, la hipertensión arterial (HTA), relacionada con aproximadamente 9,4 millones de muerte al año, ha sido considerada una manifestación no clásica del HPTP. La interacción PTH-Aldosterona ha surgido como un importante eslabón para tratar de explicar esta relación, planteándose diversos mecanismos teóricos que posicionan a la PTH como estimulador directo de la síntesis de aldosterona en las células de la zona glomerular. Sin embargo, estos mecanismos teóricos han estado rodeados de controversia en su aspecto epidemiológico y clínico, existiendo aún muy pocos estudios poblacionales explorando este vínculo y su relación con la morbimortalidad cardiovascular, por lo que es necesario mayor investigación en el área con el fin de conocer el verdadero impacto de estos mecanismos en la salud de los individuos. Esta revisión resume aspectos del metabolismo del calcio, al igual que los principales mecanismos subyacentes al vínculo HPTP-HTA, y los datos epidemiológicos disponibles sobre el tópico, a fin de brindar un mejor entendimiento sobre este novel planteamiento.Primary hyperparathyroidism (PHPT) is a common endocrine disorder characterized by autonomic parathyroid hormone secretion (PTH). Although its asymptomatic variant is the most frequently found in clinical practice (which is incidentally diagnosed), bone and kidney complications significantly affect the patient’s quality of life. However, the spectrum of manifestations of this disorder is not limited to mineral metabolism, since elevated concentrations of PTH are associated with an increased risk of metabolic syndrome, type 2 diabetes mellitus and cardiovascular disease. In this area, hypertension (AHT), related to approximately 9.4 million deaths per year, has been considered a non-classical manifestation of PHPT. The interaction PTH-Aldosterone has emerged as an important link to try to explain this relationship, posing various theoretical mechanisms that position PTH as a direct stimulator of aldosterone synthesis in the glomerular zone cells. However, these theoretical mechanisms have been surrounded by controversy in their epidemiological and clinical aspects, and there are still very few population studies exploring this link and its relation with cardiovascular morbimortality, which is why more research is needed in the area in order to know. The true impact of these mechanisms on the health of individuals. This review summarizes aspects of calcium metabolism, as well as the main mechanisms underlying the HPTP-HTA link, and available epidemiological data on the topic, in order to provide a better understanding of this novel approach

Alzheimer’s disease and type 2 diabetes mellitus: Pathophysiologic and pharmacotherapeutics links

At present, Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2DM) are two highly prevalent disorders worldwide, especially among elderly individuals. T2DM appears to be associated with cognitive dysfunction, with a higher risk of developing neurocognitive disorders, including AD. These diseases have been observed to share various pathophysiological mechanisms, including alterations in insulin signaling, defects in glucose transporters (GLUTs), and mitochondrial dysfunctions in the brain. Therefore, the aim of this review is to summarize the current knowledge regarding the molecular mechanisms implicated in the association of these pathologies as well as recent therapeutic alternatives. In this context, the hyperphosphorylation of tau and the formation of neurofibrillary tangles have been associated with the dysfunction of the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in the nervous tissues as well as the decrease in the expression of GLUT-1 and GLUT-3 in the different areas of the brain, increase in reactive oxygen species, and production of mitochondrial alterations that occur in T2DM. These findings have contributed to the implementation of overlapping pharmacological interventions based on the use of insulin and antidiabetic drugs, or, more recently, azeliragon, amylin, among others, which have shown possible beneficial effects in diabetic patients diagnosed with AD

Psycho-Neuro-Endocrine-Immunological Basis of the Placebo Effect: Potential Applications beyond Pain Therapy

The placebo effect can be defined as the improvement of symptoms in a patient after the administration of an innocuous substance in a context that induces expectations regarding its effects. During recent years, it has been discovered that the placebo response not only has neurobiological functions on analgesia, but that it is also capable of generating effects on the immune and endocrine systems. The possible integration of changes in different systems of the organism could favor the well-being of the individuals and go hand in hand with conventional treatment for multiple diseases. In this sense, classic conditioning and setting expectations stand out as psychological mechanisms implicated in the placebo effect. Recent advances in neuroimaging studies suggest a relationship between the placebo response and the opioid, cannabinoid, and monoaminergic systems. Likewise, a possible immune response conditioned by the placebo effect has been reported. There is evidence of immune suppression conditioned through the insular cortex and the amygdala, with noradrenalin as the responsible neurotransmitter. Finally, a conditioned response in the secretion of different hormones has been determined in different studies; however, the molecular mechanisms involved are not entirely known. Beyond studies about its mechanism of action, the placebo effect has proved to be useful in the clinical setting with promising results in the management of neurological, psychiatric, and immunologic disorders. However, more research is needed to better characterize its potential use. This review integrates current knowledge about the psycho-neuro-endocrine-immune basis of the placebo effect and its possible clinical applications

Specialized Pro-Resolving Lipid Mediators: The Future of Chronic Pain Therapy?

Chronic pain (CP) is a severe clinical entity with devastating physical and emotional consequences for patients, which can occur in a myriad of diseases. Often, conventional treatment approaches appear to be insufficient for its management. Moreover, considering the adverse effects of traditional analgesic treatments, specialized pro-resolving lipid mediators (SPMs) have emerged as a promising alternative for CP. These include various bioactive molecules such as resolvins, maresins, and protectins, derived from ω-3 polyunsaturated fatty acids (PUFAs); and lipoxins, produced from ω-6 PUFAs. Indeed, SPMs have been demonstrated to play a central role in the regulation and resolution of the inflammation associated with CP. Furthermore, these molecules can modulate neuroinflammation and thus inhibit central and peripheral sensitizations, as well as long-term potentiation, via immunomodulation and regulation of nociceptor activity and neuronal pathways. In this context, preclinical and clinical studies have evidenced that the use of SPMs is beneficial in CP-related disorders, including rheumatic diseases, migraine, neuropathies, and others. This review integrates current preclinical and clinical knowledge on the role of SPMs as a potential therapeutic tool for the management of patients with CP

Metabolic Syndrome: Is It Time to Add the Central Nervous System?

Metabolic syndrome (MS) is a set of cardio-metabolic risk factors that includes central obesity, hyperglycemia, hypertension, and dyslipidemias. The syndrome affects 25% of adults worldwide. The definition of MS has evolved over the last 80 years, with various classification systems and criteria, whose limitations and benefits are currently the subject of some controversy. Likewise, hypotheses regarding the etiology of MS add more confusion from clinical and epidemiological points of view. The leading suggestion for the pathophysiology of MS is insulin resistance (IR). IR can affect multiple tissues and organs, from the classic “triumvirate” (myocyte, adipocyte, and hepatocyte) to possible effects on organs considered more recently, such as the central nervous system (CNS). Mild cognitive impairment (MCI) and Alzheimer’s disease (AD) may be clinical expressions of CNS involvement. However, the association between MCI and MS is not understood. The bidirectional relationship that seems to exist between these factors raises the questions of which phenomenon occurs first and whether MCI can be a precursor of MS. This review explores shared pathophysiological mechanisms between MCI and MS and establishes a hypothesis of a possible MCI role in the development of IR and the appearance of MS

Efecto del consumo de alimentos preparados en el hogar y adquiridos en la escuela sobre el perfil lipídico de escolares en Maracaibo, Venezuela

Propósito: En décadas recientes, ha aumentado en la poblacióninfantil la prevalencia de enfermedades como obesidady dislipidemias, de manera atribuible a prácticas propiasde la sociedad occidentalizada. Esto incluye sobreingestacalórica, incluso en el desayuno, una particularmenteimportante para ésta demografía. Por lo tanto, el objetivode este estudio fue analizar efecto del consumo de alimentospreparados en el hogar (APH) o alimentos adquiridos enla institución educativa (AIE) y la ingesta nutricional diariaen el perfil lipídico de escolares normopeso de la parroquiaRaúl Leoni del Municipio Maracaibo, Venezuela.Materiales y Métodos: Estudio cuantitativo, transversaly de campo en 52 escolares de ambos sexos pertenecientesa 2 colegios privados de la Parroquia Raúl Leoni delMunicipio Maracaibo, Estado Zulia; con edades comprendidasentre 8-10 años, e Índice de Masa Corporal clasificadonormopeso para su edad y sexo. Se determinaronlos parámetros antropométricos y perfil lipídico de losparticipantes; y se obtuvo la frecuencia de consumo dealimentos y el contenido nutricional de su desayuno e ingestadiaria mediante un recordatorio de 24 horas tipoencuesta, cuyos datos fueron procesados según la Tablade Composición de Alimentos de Venezuela.Resultados: Las proporciones de adecuación nutricionalde calorías, grasas y carbohidratos fueron excesivas en losniños que desayunan AIE, y significativamente superioresa los que desayunan APH (p<0,011; p<0,002 y p<0,002,respectivamente). No se objetivaron diferencias entre losparámetros bioquímicos. Los alimentos más frecuentementeconsumidos en ambos grupos incluyeron frituras.No se encontró relación entre los valores de perfil lipídicoy la proporción de adecuación nutricional de calorías, proteínas,carbohidratos o grasas en ningún grupo (p>0,05).Conclusiones: En la población estudiada, los escolaresque desayunan AIE reciben un aporte excesivo de calorías,grasas y carbohidratos; no obstante, este excedente noparece influir significativamente sobre su perfil lipídico

The Role of Metformin in Metabolic Disturbances during Pregnancy: Polycystic Ovary Syndrome and Gestational Diabetes Mellitus

Maintenance of gestation implicates complex function of multiple endocrine mechanisms, and disruptions of the global metabolic environment prompt profound consequences on fetomaternal well-being during pregnancy and postpartum. Polycystic Ovary Syndrome (PCOS) and gestational diabetes mellitus (GDM) are very frequent conditions which increase risk for pregnancy complications, including early pregnancy loss, pregnancy-induced hypertensive disorders, and preterm labor, among many others. Insulin resistance (IR) plays a pivotal role in the pathogenesis of both PCOS and GDM, representing an important therapeutic target, with metformin being the most widely prescribed insulin-sensitizing antidiabetic drug. Although traditional views neglect use of oral antidiabetic agents during pregnancy, increasing evidence of safety during gestation has led to metformin now being recognized as a valuable tool in prevention of IR-related pregnancy complications and management of GDM. Metformin has been demonstrated to reduce rates of early pregnancy loss and onset of GDM in women with PCOS, and it appears to offer better metabolic control than insulin and other oral antidiabetic drugs during pregnancy. This review aims to summarize key aspects of current evidence concerning molecular and epidemiological knowledge on metformin use during pregnancy in the setting of PCOS and GDM

Depression as a Neuroendocrine Disorder: Emerging Neuropsychopharmacological Approaches beyond Monoamines

Depression is currently recognized as a crucial problem in everyday clinical practice, in light of ever-increasing rates of prevalence, as well as disability, morbidity, and mortality related to this disorder. Currently available antidepressant drugs are notoriously problematic, with suboptimal remission rates and troubling side-effect profiles. Their mechanisms of action focus on the monoamine hypothesis for depression, which centers on the disruption of serotonergic, noradrenergic, and dopaminergic neurotransmission in the brain. Nevertheless, views on the pathophysiology of depression have evolved notably, and the comprehension of depression as a complex neuroendocrine disorder with important systemic implications has sparked interest in a myriad of novel neuropsychopharmacological approaches. Innovative pharmacological targets beyond monoamines include glutamatergic and GABAergic neurotransmission, brain-derived neurotrophic factor, various endocrine axes, as well as several neurosteroids, neuropeptides, opioids, endocannabinoids and endovanilloids. This review summarizes current knowledge on these pharmacological targets and their potential utility in the clinical management of depression