Introducción: La diabetes mellitus tipo 2 (DM2) es un problema sanitario importante en la actualidad, con alta morbilidad, mortalidad, costos directos e indirectos. Nuevas estrategias de manejo se han implementado para disminuir su impacto. Este estudio describe la experiencia del manejo con análogos GLP-1.
Métodos: Estudio retrospectivo, descriptivo, de pacientes con diagnóstico de DM2 en manejo con análogos GLP-1. Se describieron características clínicas al inicio de la terapia y control entre 3 -y 6 meses.
Resultados: De 69 pacientes, 55,1% eran mujeres, con edad promedio 57,1 años. La mediana de duración de DM2 fue 13 años. Se encontró reducción significativa del peso 3 kg (p=0,00), HbA1c 1,7% (p=0), glucemia en ayunas 41 mg/dL (p=0), colesterol total 14 mg/dL (p=0,0069) y triglicéridos 38 mg/dL (p=0,0247). No se presentaron cambios significativos en la tensión arterial, colesterol HDL y LDL.
Conclusión: Los análogos GLP-1 en pacientes con DM2 generan mejoría significativa en control glucémico, peso y colesterol. Es necesario un seguimiento a largo plazo para determinar mantenimiento del control glucémico, pérdida de peso e impacto en el riesgo cardiovascular.

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20. Buse, J, Drucker, D, Taylor K, Kim T, Walsh B, Hu H, et al. DURATION-1: ex- enatide once weekly produces sustained glycemic control and weight loss over 52 weeks. Diabetes Care. 2010; 33: 1255–1261.
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24. Russo G, Pintaudi B, Giorda C, Lucisano G, Nicolucci A, Cristofaro MR, et al. Age- and Gender-Related Differences in LDL-Cholesterol Management in Outpatients with Type 2 Diabetes Mellitus. Int J Endocrinol
2015;2015:957105.

análogos de GLP-1
diabetes mellitus tipo 2
incretinas

La caveolina 1 es una proteína estructural que interviene en diversos procesos metabólicos. En estudios de asociación genética, el gen que la codifica CAV1 (7q31.2) se ha asociado a resistencia a la insulina, hipertensión, hipertrigliceridemia y c-HDL bajo. Sin embargo, se desconoce si variantes en CAV1 se asocian a obesidad e incremento en el riesgo cardiovascular (RCV).

Objetivo: Analizar la posible asociación entre variantes en CAV1 con el RCV en población del caribe colombiano.
Metodología: Se realizó un estudio de asociación genética con 595 adultos de Cartagena de Indias. Se hizo la genotipificación de los polimorfismos de nucleótido simple (SNPs): rs3779512, rs926198, rs10207569, rs11773845, rs7804372, rs1049337. El RCV fue definido mediante el puntaje derivado del estudio de Framingham. Para estimar la asociación entre las variables de estudio se realizó un análisis de varianza ajustado y fueron construidos árboles de regresión. Se aplicó el ajuste de Bonferroni para pruebas múltiples, donde fuera necesario.
Resultados: La variante rs1049337 se encontró asociada con el incremento del RCV (p=0,0001). Los sujetos con el genotipo TT en este locus tuvieron un mayor puntaje de RCV, +4,1 IC95% [0,8-8,0] en comparación con CC (p=0,03) y +4,3 IC95% [0,3-8,4] con CT (p=0,03). El árbol mostró que en el grupo TT (rs1049337) presentaba un mayor puntaje si los sujetos además contaban con el genotipo TT para rs3779512.
Conclusiones: Las variantes rs1049337 y rs3779512 se encuentran asociadas a incremento en el puntaje de RCV.

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caveolina 1
enfermedades cardiovasculares
polimorfismo de nucleótido simple
estudios de asociación genética
Colombia
América Latina

Introducción: La folistatina es una proteína capaz de neutralizar varias hormonas de la familia del TGF-?, tales como la activina, las proteínas morfogénicas del hueso y la miostatina. Al inactivar la activina y la folistatina reduce la secreción de FSH. La folistatina se produce además de en el ovario en muchos otros tejidos, por ello se sospecha que tiene otros efectos. En ratones, la deleción genética de la folistatina se acompaña de resistencia a la insulina (RI). Sin embargo, la asociación entre la folistatina plasmática y RI medida directamente no ha sido evaluada en humanos.
Métodos: En 81 participantes entre 30 y 69 años (56% mujeres, 54% con sobrepeso, 13% con obesidad), determinamos antropometría, composición corporal, factores de riesgo cardiovascular y múltiples índices de RI: Área incremental bajo la curva de insulina, índice de sensibilidad a la insulina según Gutt, Homeostatic Model Assessment – Insulin Resistance (HOMA-IR) e insulinemia en ayuno. Un subgrupo de 21 participantes se sometió además a un clamp hiperinsulinémico-euglucémico. La folistatina y la miostatina se midieron en plasma de ayuno, empleando técnicas inmunométricas.
Resultados: La concentración promedio de folistatina fue 2.517±830 pg/mL, sin diferencia entre sexos (p=0,55). La folistatina tuvo una tendencia a correlación positiva con el porcentaje de masa magra (r=0,19, p=0,088) y negativa con el porcentaje de grasa corporal (r= -0,19, p=0,097). La folistatina no se correlacionó con índices de RI derivados de la PTOG pero sí con la captación corporal de glucosa en el clamp (r=0,42, p=0,031). No se halló asociación entre las concentraciones de folistatina y miostatina plasmáticas.
Conclusión: Los niveles de folistatina mostraron una tendencia hacia una correlación positiva con la masa muscular y negativa con adiposidad corporal. Esto concuerda con el efecto inhibitorio de la folistatina sobre la miostatina. Aunque la folistatina no correlacionó con índices indirectos de RI, sí lo hizo con la determinación directa de sensibilidad a la insulina en el clamp hiperinsulinémico-euglucémico.

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27. Teede H, Ng S, Hedger M, Moran L. Follistatin and activins in polycystic ovary syndrome: relationship to metabolic and hormonal markers. Metabolism. 2013;62:1394-400.
28. Wu H, Wu M, Chen Y, Allan CA, Phillips DJ, Hedger MP. Correlation between blood activin levels and clinical parameters of type 2 diabetes. Exp Diabetes Res. 2012;2012:410579.

folistatina
resistencia a la insulina
obesidad
adiposidad
miostatina
miocinas
TGF

Fragmento

Las alteraciones endocrinas en el paciente hospitalizado representan un reto desde su diagnóstico y manejo por la complejidad de la enfermedad en sí y por las múltiples variables que deben integrarse para optimizar su estabilidad fisiológica. Un aspecto fundamental que hay que considerar en el paciente hospitalizado es la homeostasis endocrina, de la que dependen un sinnúmero de vías de señalización intracelulares e intercelulares que se traducen en la sincronización de funciones metabólicas y orgánicas.

En los últimos años se han logrado avances en el conocimiento no solamente de la función endocrina, sino también de su disfunción y en la presentación de nuevas entidades endocrinológicas en el paciente internado, que no son exclusivamente una curiosidad fisiopatológica, ya que impactan en el comportamiento clínico, en el pronóstico y en la rehabilitación de este grupo especial de enfermos.

De las descripciones iniciales de la ya clásica respuesta metabólica al trauma y de las fases de flujo se ha alcanzado un elevado grado de conocimiento en el aspecto molecular y clínico de la disfunción endocrina en los enfermos hospitalizados. Por este motivo y por su gran interés en poner al día al grupo médico encargado del manejo del paciente hospitalizado, la Asociación Colombiana de Endocrinología, Diabetes y Metabolismo desarrolló un esfuerzo conjunto, bajo el liderazgo del doctor Alejandro Pinzón Tovar, para producir este libro de texto en el que se exponen los temas de más actualidad en relación a esta interesante e innovadora rama de la medicina endocrinológica, la disfunción endocrina del paciente hospitalizado.

homeostasis endocrina
alteraciones endocrinas
pacientes hospitalizados
función endocrina

Fragmento

Desde el aislamiento de la hormona tiroidea por Edward C. Kendall en la Clínica Mayo en 1914, a partir de un número importante de glándulas tiroides de cerdo(1), su molécula ha pasado por muchas etapas, tratando de suplir su deficiencia en los pacientes hipotiroideos.

El hipotiroidismo es una entidad de las más frecuentes en endocrinología y especialmente en los países como Colombia en los cuales se conjugaron durante mucho tiempo, además de la altura sobre el nivel del mar en ciertas regiones, la deficiencia de yodo en la dieta, factor de riesgo superado desde hace ya varios años con la administración de yodo en la sal, faltando por supuesto, seguimiento de parte de las autoridades sanitarias nacionales en relación a su concentración. En este momento, su origen está relacionado con problemas inmunológicos, como sucede en la mayoría de los países del mundo.

La hormona tiroidea es una sustancia que por su misma composición es una molécula inestable y en la cual se conjugan varios factores en ocasiones relacionados: problemas en su fabricación, bioequivalencia, eficacia de ciertos lotes e inclusive su almacenamiento, lo cual podría llevar a no suplir las necesidades de los pacientes, obligando a los fabricantes de diferentes marcas y presentación a agregar nuevos excipientes.

1. Kendall EC The isolation in crystalline form of the compound containing iodin, which occurs in the thyroid: its chemical nature and physiologic activity. J Am Med Ass 1915. 64:2042-3.
2. J Jácome A, Terapia de suplencia tiroidea: una historia del siglo XIX que aún genera noticias en el siglo XXI. Revista Colombiana de Endocrinología, Diabetes y Metabolismo. 2018; Vol.5(1): 38-41.
3. Levothyrox: L'ANSM admet un défault d'infomation. Le Monde 2 septiembre 2017. P.11

Hipotiroidismo
hormona tiroidea
Endocrinología

La osteomalacia tumoral (OT) es un síndrome paraneoplásico poco frecuente caracterizado por una alteración en la tasa de reabsorción del fósforo a nivel renal, causado por la producción tumoral de la proteína fosfatúrica, llamada factor de crecimiento fibroblástico 23 (FGF-23). Las manifestaciones clínicas son consecuencia de los niveles bajos de fósforo sérico que llevan a dolor musculoesquelético y fracturas por fragilidad ósea. Usualmente se trata de un tumor de origen mesenquimal de pequeño tamaño que puede ser difícil de localizar, pero en los casos en los que se logra realizar la extirpación quirúrgica del mismo, los síntomas y las anomalías bioquímicas revierten rápidamente(1).
Presentamos un caso de un paciente con un tumor de gran tamaño y una enfermedad de larga evolución, que tuvo un desenlace exitoso luego de la cirugía.

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5. Portillo MR. Nefrología al día. 2012th ed. Víctor Lorenzo JML-G, editor. Vol. 25. Madrid: Revista Nefrología; 2010. 201-219 p.
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osteomalacia tumoral (OT)
síndrome paraneoplásico
factor de crecimiento fibroblástico 23 (FGF-23)

La asociación entre la obesidad y la densidad mineral ósea ha sido un punto controversial al momento de establecer si existe una asociación positiva o negativa entre las mismas. Diversos estudios han propuesto que la obesidad es un factor protector del hueso, debido a la tensión mecánica dada por el peso corporal en la remodelación ósea. Otros estudios plantean que la relación es mucho más compleja debido a que el tejido adiposo y los osteoblastos provienen de líneas germinales comunes. Además, el adipocito tiene la capacidad de secretar diversas moléculas, entre ellas las adipocinas. Adicionalmente, el tejido adiposo es una de las principales fuentes de aromatasa, esto lo involucra en la conversión de andrógenos a estrógenos, que juegan un papel importante en el mantenimiento de la homeostasis ósea. Por lo tanto, se ha planteado el hueso como órgano blanco de diversas vías endocrinas y, a su vez, se considera un órgano endocrino que puede afectar otros órganos cuando está alterado. Por otra parte, se ha visto que la resistencia a la insulina en el contexto de la obesidad está asociada con inflamación crónica de bajo grado, deterioro funcional de órganos y alteración del metabolismo energético, que impacta la remodelación ósea.

Abstract

There is controversy over the effect of obesity in bone mineral density. Several studies have proposed that obesity is a protective factor of the bone by the mechanical tension that favors the bone remodeling. However, other studies suggest that this relationship is more complex because both tissues come from a common germ line; emphasizing that the adipocyte secretes diverse molecules, among them adipocinas. In addition, adipose tissue has aromatases that convert androgens into estrogens, having an importance in bone homeostasis. Therefore, the bone has been raised as a target organ of various endocrine pathways, which may affect other organs when it is altered. On the other hand, it has been shown that insulin resistance in the context of obesity is associated with chronic low-grade inflammation, functional impairment of organs and impaired energy metabolism, which impacts bone remodeling.

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Obesidad
Densidad ósea
Insulina
Factor de crecimiento similar a la insulina
Vitamina D
Leptina
Adiponectina
Estradiol
Testosterona
obesity
bone density
insulin
Insulin-like growth factor
vitamin D
leptin
Adiponectin
testosterone

Fragmento.

La relación entre la glándula tiroides, cretinismo, mixedema del adulto y caquexia estrumipriva solo fue definida hacia finales del siglo XIX. El concepto de hipotiroidismo, que hoy nos parece obvio y sencillo, no existía. Habría que esperar a que —a finales del siglo XX— se descubriera el radioinmunoanálisis, se midieran las hormonas tiroideas y la TSH ultrasensible en suero, y se encontraran las desyodasas que en últimas regularían también la función tiroidea a través de la producción periférica de triyodotironina.
Antes de tocar el tema que nos ocupa, es conveniente conocer los antecedentes que se refieren al conocimiento del bocio endémico y su tratamiento en la antigüedad, las primeras descripciones anatómicas de la glándula tiroides, la relación de ésta con el yodo, al hipotiroidismo congénito o cretinismo, y al descubrimiento del hipotiroidismo como tal, dejando para otra ocasión el tema de su tratamiento.

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hipotiroidismo
bocio endémico
tiroides
yodo y tiroides
cretinismo

Las enfermedades crónicas no transmisibles son las entidades que tienen mayor repercusión en el sector salud a nivel global. Quizá una de las circunstancias que más se encuentra relacionada con el aumento progresivo en muchas de estas entidades es la obesidad. Las causas y posibles planes terapéuticos para la obesidad son complejos, por tal motivo deben ser enfocados desde diferentes tejidos en el organismo. Uno de estos enfoques sería la regulación del centro del hambre y la saciedad a nivel central, especialmente en el hipotálamo, otro es la forma como el individuo gasta su energía en las células musculares y un aspecto adicional es la forma en que las células adiposas almacenan y ahorran energía. En los últimos años se ha observado que los individuos adultos cuentan con diferentes tipos de células adiposas con origen germinal divergente. La presencia de estas células adiposas puede tener una variación fenotípica y en determinadas circunstancias podría presentar una función más termogénica de acuerdo con diferentes circunstancias ambientales. La influencia del ambiente se realiza mediante la modificación de genes específicos, que pueden determinar una variación funcional del hipotálamo, el músculo y el tejido adiposo. Estas modificaciones son denominadas epigenéticas, dado que no influyen sobre la estructura del ADN, pero cambian completamente su funcionalidad. En el presente trabajo hemos realizado un estudio de las circunstancias a través de las cuales el ambiente puede tener influencia en la aparición de la obesidad. Se ha realizado una búsqueda mediante las bases de datos de Pubmed, Evidencia Based Medicine, Science direct, Ovid, EBSCO, Proquest, Springer, desde enero del año 2012 hasta marzo del año 2017, buscando como palabras clave, obesidad, adipocito y los términos epigenética y ambiente.

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Obesidad
Epigenética
Tejido adiposo
Expresión genética

El feocromocitoma y el paraganglioma son tumores neuroendocrinos derivados de la cresta neural. Son tumores infrecuentes en la práctica clínica diaria. El feocromocitoma está localizado en la médula suprarrenal y el paraganglioma es un tumor localizado en los paraganglios del sistema nervioso autónomo, por ende, su localización es extraadrenal. Existen predictores clínicos de malignidad como el tamaño, la localización y las mutaciones en SHDB. La presencia de predictores clínicos y la supervivencia según el compromiso metastásico en aquellos casos con feocromocitoma/ paraganglioma maligno ha permitido por primera vez crear la clasificación TNM para esta enfermedad. Adicionalmente, la evaluación genética se ha establecido como el paradigma de manejo. Los resultados del análisis del genoma del feocromocitoma confirman una alta heredabilidad de esta enfermedad y descubren nuevos genes que pueden convertirse en objetivosterapéuticos para el futuro.

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feocromocitoma
paraganglioma
neuroendocrinología