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Abstract Disclosure: A. Garcia-Bautista: None. J. Panneflek: None. J. Garza: None. M. Twahirwa: None. M. Castillo: None. Introduction: Lymphocytic hypophysitis is a rare condition affecting the pituitary gland, causing hypopituitarism due to inflammation or a sellar mass lesion. It accounts for about two-thirds of primary hypophysitis cases and is more common in females, with a female-to-male ratio of 2-4:1. Patients often have a history of autoimmune diseases. Treatment involves observation for mild to moderate cases, while moderate to severe cases are typically treated with glucocorticoids. Case report A 43-year-old female with rheumatoid arthritis, diabetes mellitus presented with one month of worsening polyuria and polydipsia. She reported urinating >10 times daily and waking 4 times nightly. Associated symptoms included dry mouth, weakness, fatigue, and headaches which affected her workout routine. Nausea, tremors, and poor oral intake led to an emergency room visit. She denied head trauma or surgery. Medications included metformin, semaglutide, and adalimumab (last dose six months ago). She denied use of lithium, supplements, tobacco, alcohol, or drugs. Initial labs: sodium 150 mEq/L, serum osmolality 309 mOs/kg, urine osmolality 119 mOs/kg, specific gravity 1.003, ACTH 15 pg/mL, cortisol (4 PM) 4.4 µg/dL, prolactin 35.8 ng/mL, TSH 0.79 µIU/mL. Brain MRI showed an abnormal pituitary signal with loss of the normal T1 bright spot, hyperintense T2/FLAIR signal extending into the infundibulum, and post-contrast enhancement. The infundibulum measured 0.3 cm thick, and the gland measured 1 × 1 cm, without macroadenoma or optic chiasm compression. Gutenberg score: -5. Treatment began with oral and IV DDAVP, which was ineffective. Prednisone was subsequently initiated at 40 mg daily along with intranasal DDAVP (0.01%), resulting in resolution of polyuria within a day. After 10 days, prednisone was increased to 50 mg daily, leading to improved symptoms and stabilization of serum sodium at 134 mEq/L. Discussion: This case presents an atypical manifestation of lymphocytic infundibulo-neurohypophysitis, characterized by desmopressin-resistant central diabetes insipidus, in a patient with associated autoimmune comorbidities. Despite an initial lack of response to oral and intravenous DDAVP, the patient's symptoms demonstrated significant improvement following glucocorticoid therapy and intranasal DDAVP administration. This observation underscores the critical importance of early identification and tailored immunosuppressive treatment in managing these atypical cases. Presentation: Sunday, July 13, 2025

Thyroid hormone accelerates energy expenditure; thus, hypothyroidism is intuitively associated with obesity. However, studies failed to establish such a connection. In brown adipose tissue (BAT), thyroid hormone activation via type 2 deiodinase (D2) is necessary for adaptive thermogenesis, such that mice lacking D2 (D2KO) exhibit an impaired thermogenic response to cold. Here we investigate whether the impaired thermogenesis of D2KO mice increases their susceptibility to obesity when placed on a high-fat diet. To test this, D2KO mice were admitted to a comprehensive monitoring system acclimatized to room temperature (22°C) or thermoneutrality (30°C) and kept either on chow or high-fat diet for 60 days. At 22°C, D2KO mice preferentially oxidize fat, have a similar sensitivity to diet-induced obesity, and are supertolerant to glucose. However, when thermal stress is eliminated at thermoneutrality (30°C), an opposite phenotype is encountered, one that includes obesity, glucose intolerance, and exacerbated hepatic steatosis. We suggest that a compensatory increase in BAT sympathetic activation of the D2KO mice masks metabolic repercussions that they would otherwise exhibit. Thus, upon minimization of thermal stress, high-fat feeding reveals the defective capacity of D2KO mice for diet-induced thermogenesis, provoking a paradigm shift in the understanding of the role of the thyroid hormone in metabolism.

Hypothyroidism in humans is characterized by severe neurological consequences that are often irreversible, highlighting the critical role of thyroid hormone (TH) in the brain. Despite this, not much is known about the signaling pathways that control TH action in the brain. What is known is that the prohormone thyroxine (T4) is converted to the active hormone triiodothyronine (T3) by type 2 deiodinase (D2) and that this occurs in astrocytes, while TH receptors and type 3 deiodinase (D3), which inactivates T3, are found in adjacent neurons. Here, we modeled TH action in the brain using an in vitro coculture system of D2-expressing H4 human glioma cells and D3-expressing SK-N-AS human neuroblastoma cells. We found that glial cell D2 activity resulted in increased T3 production, which acted in a paracrine fashion to induce T3-responsive genes, including ectonucleotide pyrophosphatase/phosphodiesterase 2 (ENPP2), in the cocultured neurons. D3 activity in the neurons modulated these effects. Furthermore, this paracrine pathway was regulated by signals such as hypoxia, hedgehog signaling, and LPS-induced inflammation, as evidenced both in the in vitro coculture system and in in vivo rat models of brain ischemia and mouse models of inflammation. This study therefore presents what we believe to be the first direct evidence for a paracrine loop linking glial D2 activity to TH receptors in neurons, thereby identifying deiodinases as potential control points for the regulation of TH signaling in the brain during health and disease.

Some people pursue medical interventions as part of the process of expressing their gender, and an increasing number of gender affirmation surgeries are being performed.This book, which provides comprehensive coverage of the subject, is edited by three well-respected and experienced authors with over 20 contributors from around the world.

Background University dropout in health sciences programs threatens the stability of the future healthcare workforce, particularly in Latin American public universities facing structural and institutional constraints. Dropout intention is a strong predictor of actual dropout and reflects the interaction of personal, relational, and institutional factors. However, integrative models that examine these factors simultaneously and their mediating mechanisms remain limited. This study aimed to evaluate an explanatory model of university dropout intention among health sciences students, considering the mediating role of academic burnout and satisfaction with education. Methods A cross-sectional observational study was conducted between March and September 2025 among undergraduate health sciences students at a public university in Cali, Colombia. A proportionate stratified random sample was obtained. Data were collected using validated self-report instruments assessing personal, relational, and institutional risk factors, academic burnout, satisfaction with education, and university dropout intention. Structural equation modeling was applied using the weighted least squares mean and variance adjusted (WLSMV) estimator to examine direct and indirect (mediated) effects. Results The sample comprised 320 undergraduate health sciences students (69.1% female; mean age = 22.46 ± 3.47 years). The final structural model demonstrated adequate fit and explained 86.3% of the variance in university dropout intention. Academic burnout emerged as the strongest predictor of dropout intention, whereas satisfaction with education showed a significant protective effect. Several personal, relational, and institutional factors were directly and indirectly associated with dropout intention. Dysfunctional support networks and vocational decision-making were positively associated with dropout intention directly and through academic burnout and satisfaction with education, whereas curricular support and functional support networks were negatively associated with dropout intention primarily through higher satisfaction with education. Conclusions University dropout intention among health sciences students is a multidimensional phenomenon mediated by personal, relational, and institutional factors. Interventions aimed at enhancing satisfaction with education and preventing academic burnout are essential to strengthen student retention and well-being in health sciences education.

The construction of knowledge from the exchange of knowledge between patients, families, and healthcare teams is a felt need that can impact health education and adherence to treatment. To develop a social appropriation strategy that enables innovation in the health care of people with ischemic heart disease and their families through the use of an MHealth tool. Exploratory study that allowed the design of a strategy for the social appropriation of knowledge to improve the cardiovascular health of people suffering from myocardial ischemia. Thirty-one people participated, including patients, family members, and health professionals. Two virtual workshops were held in June, and follow-up phone calls were made between August and September. The participant's experiences and knowledge enabled the construction of the MHealth tool. The critical reflection of the stakeholders facilitated the construction and development of the MHealth tool (webpage/app) named \"Cuidando tu corazón\" (Taking care of your heart). Social appropriation strategies are a relevant tool for knowledge creation in health. The strategy implemented made it possible to recognize the importance of developing cardiovascular healthcare tools from stakeholders' needs, perspectives, and beliefs to improve education and care.

Introducción: La construcción de conocimiento a partir del intercambio de saberes entre pacientes, familias y equipo de salud es una necesidad sentida que puede impactar en la educación en salud y la adherencia a los tratamientos. Objetivo: Desarrollar una estrategia de apropiación social que permita innovar en el cuidado de la salud de las personas con enfermedad isquémica cardiaca y sus familias mediante el uso de la herramienta MHealth. Materiales y Métodos: Estudio exploratorio que permitió el diseño de una estrategia de apropiación social de conocimiento para mejorar la salud cardiovascular de personas que sufren isquemia cardiaca. Participaron 31 personas entre pacientes, familiares, profesionales de la salud. Se desarrollaron dos talleres virtuales en el mes de junio y seguimientos telefónicos entre agosto y septiembre. Las experiencias y saberes de los participantes, permitió la construcción de la herramienta MHealth. Resultados: La reflexión crítica entre los actores facilitó la construcción y desarrollo de la herramienta tipo MHealth (página web/app) titulada “Cuidando tu corazón”, que permite el acceso a información relacionada con el cuidado durante la isquemia cardiaca y articula información a partir del diálogo de saberes y la evidencia reportada en la literatura. Discusión: Las estrategias de apropiación social son una herramienta relevante para la generación de conocimiento en el área de la salud. Conclusiones: La estrategia implementada permitió reconocer la importancia de contar con herramientas para el cuidado de la salud cardiovascular elaboradas desde las necesidades, perspectivas y creencias de sus actores para mejorar la educación y el cuidado.