Las enfermedades cardiovasculares constituyen la primera causa de morbilidad y mortalidad en el mundo, tanto en los países desarrollados como en los que están en vías de desarrollo. La dislipidemia –asociada a la disfunción endotelial- y a los fenómenos inflamatorios vasculares, son los procesos iniciales en la patogénesis de la enfermedad arterial arterioesclerótica. Es evidente la asociación directa y lineal entre los niveles de colesterol de baja densidad y el riesgo de enfermedad arterial arterioesclerótica, al igual que el efecto benéfico de la intervención con fármacos que actúan en diferentes niveles (estatinas, ezetimibe, fibratos, anticuerpos monoclonales contra la PCSK9, entre otros).

Por su parte, la hipertrigliceridemia, y los niveles bajos de colesterol de alta densidad, al igual que otros parámetros como el colesterol no-HDL y otras lipoproteínas, también juegan un papel importante en la etiopatogenia de la enfermedad arterioesclerótica, y existe evidencia en favor de la modificación de dichos parámetros. Los nuevos fármacos han cambiado de forma sustancial los desenlaces cardiovasculares en individuos con alto riesgo cardiovascular, y en individuos con intolerancia a las estatinas. Las diferentes guías internacionales para el manejo de la dislipidemia comparten muchos aspectos respecto al manejo farmacológico y no farmacológico.

Sin embargo, existen algunas diferencias importantes entre ellas, incluso en la forma de abordar individuos con situaciones especiales de dislipidemia (embarazo, enfermedad renal crónica, entre otras).

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131. Giugliano RP, Mach F, Zavitz K, et al. Cognitive function in a randomized trial of evolocumab. N Engl J Med. 2017;377:633-643.
132. Blom DJ, Hala T, Bolognese M, et al. A 52-week placebo-controlled trial of evolocumab in hyperlipidemia. N Engl J Med. 2014;370(19):1809-19.
133. Sabatine MS, Giugliano RP, Wiviott SD, et al. Efficacy and safety of evolocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015;372:1500-1509.
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136. Robinson JG, Nedergaard BS, Rogers WJ, et al. Effect of evolocumab or ezetimibe added to moderate- or high-intensity statin therapy on LDL-C lowering in patients with hypercholesterolemia: the LAPLACE-2 randomized clinical trial. JAMA. 2014;311(18):1870-1882.
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138. Sullivan D, Olsson AG, Scott R, et al. Effect of a monoclonal antibody to PCSK9 on low-density lipoprotein cholesterol levels in statin-intolerant patients: the GAUSS randomized trial. JAMA. 2012;308(23):2497-506.
139. Stroes E, Colquhoun D, Sullivan D, et al. Anti-PCSK9 antibody effectively lowers cholesterol in patients with statin intolerance: the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial of evolocumab. J Am Coll Cardiol. 2014;63(23):2541-2548.
140. Nissen SE, Dent-Acosta RE, Rosenson RS, et al. Comparison of PCSK9 Inhibitor Evolocumab vs Ezetimibe in Statin-Intolerant Patients: Design of the Goal Achievement After Utilizing an Anti-PCSK9 Antibody in StatinIntolerant Subjects 3 (GAUSS-3) Trial. Clin Cardiol. 2016;39:137-44.
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149. Bittner V. American College of Cardiology. Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab - ODYSSEY OUTCOMES. [Internet]. Available at: http://www.acc.org/latest-in-cardiology/clinical-trials/2018/03/09/08/02/odyssey-outcomes.
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153. Ginsberg HN, Rader DJ, Raal FJ, et al. Efficacy and safety of alirocumab in patients with heterozygous familial hypercholesterolemia and LDL-C of 160 mg/dl or higher. Cardiovasc Drugs Ther. 2016;30(5):473-483.
154. Kereiakes DJ, Robinson JG, Cannon CP, et al. Efficacy and safety of the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab among high cardiovascular risk patients on maximally tolerated statin therapy: the ODYSSEY COMBO I study. Am Heart J. 2015;169(6):906-915.
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157. Kastelein JJ, Kereiakes DJ, Cannon CP, et al. Effect of alirocumab dose increase on LDL lowering and lipid goal attainment in patients with dyslipidemia. Coron Artery Dis. 2017;28(3):190-197.
158. Jones PH, Bays HE, Chaudhari U, et al. Safety of alirocumab (a PCSK9 monoclonal antibody) from 14 randomized trials. Am J Cardiol. 2016;118(12):1805-1811.
159. Ray KK, Ginsberg HN, Davidson MH, et al. Reductions in atherogenic lipids and major cardiovascular events: a pooled analysis of 10 ODYSSEY trials comparing alirocumab with control. Circulation. 2016;134(24):1931-1943.
160. Zhang XL, Zhu QQ, Zhu L, et al. Safety and efficacy of anti-PCSK9 antibodies: a meta-analysis of 25 randomized, controlled trials. BMC Medicine. 2015;13(1):123.
161. Guedeney P, Giustino G, Sorrentino S, et al. Efficacy and safety of alirocumab and evolocumab: a systematic review and meta-analysis of randomized controlled trials. Eur Heart J. 2019. pii: ehz430. DOI: 10.1093/ eurheartj/ehz430.
162. Perry CM. Lomitapide: A Review of its Use in Adults with Homozygous Familial Hypercholesterolemia. Am J Cardiovasc Drugs. 2013;13(4):285-296.
163. Cuchel M, Meagher EA, du Toit Theron H, et al. Efficacy and safety of a microsomal triglyceride transfer protein inhibitor in patients with homozygous familial hypercholesterolaemia: a single-arm, open-label, phase 3 study. Lancet. 2013;381(9860):40-6.
164. Leipold R, Raal F, Ishak J, et al. The effect of lomitapide on cardiovascular outcome measures in homozygous familial hypercholesterolemia: A modelling analysis. Eur J Prev Cardiol. 2017;24(17):1843-1850.
165. Blom DJ, Fayad ZA, Kastelein JJ, et al. LOWER, a registry of lomitapidetreated patients with homozygous familial hypercholesterolemia: Rationale and design. J Clinical Lipidol. 2016;10(2):273-82.
166. Stefanutti C, Morozzi C, Di Giacomo S, et al. Management of homozygous familial hypercholesterolemia in real-world clinical practice: A report of 7 Italian patients treated in Rome with lomitapide and lipoprotein apheresis. J Clin Lipidol. 2016;10(4): 782-789.
167. Visser ME, Kastelein JJ, Stroes ES. Apolipoprotein B synthesis inhibition: results from clinical trials. Curr Opin Lipidol. 2010;21(4):319-323
168. Toth PP. Antisense therapy and emerging applications for the management of dyslipidemia. J Clin Lipidol. 2011;5(6):441-449.
169. Waldmann E, Vogt A, Crispin A, et al. Effect of mipomersen on LDL-cholesterol in patients with severe LDL-hypercholesterolaemia and atherosclerosis treated by lipoprotein apheresis (The MICA-Study). Atherosclerosis. 2017;259:20-25.
170. Duell PB, Santos RD, Kirwan BA, et al. Long-term mipomersen treatment is associated with a reduction in cardiovascular events in patients with familial hypercholesterolemia. J Clin Lipidol. 2016;10(4):1011-1021.
171. Panta R, Dahal K, Kunwar S. Efficacy and safety of mipomersen in treatment of dyslipidemia: A meta-analysis of randomized controlled trials. J Clin Lipidol. 2015;9(2):217-225.
172. Karalis DG, Hill AN, Clifton S, Wild RA. The risks of statin use in pregnancy: A systematic review. J Clin Lipidol. 2016;10(5):1081-1090.
173. Bateman BT, Hernandez-Diaz S, Fischer MA, et al. Statins and congenital malformations: cohort study. BMJ. 2015;350:h1035.
174. Haramburu F, Daveluy A, Miremont-Salamé G. Statins in pregnancy: new safety data are reassuring, but suspension of treatment is still advisable. BMJ. 2015;350:h1484.
175. Jacobson TA, Maki KC, Orringer CE, et al. National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia: Part 2. J Clin Lipidol. 2015;9(6 Suppl):S1-122.e1.
176. Catapano AL, Graham I, De Backer G, et al. 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. Eur Heart J. 2016;37(39):2999-3058.
177. Maggi P, Di Bagio A, Rusconi S, et al. Cardiovascular risk and dyslipidemia among persons living with HIV: a review. BMC Infect Dis. 2017;17(1):551.
178. Banach M, Dinca M, Ursoniu S, et al. A PRISMA-compliant systematic review and meta-analysis of randomized controlled trials investigating the effects of statin therapy on plasma lipid concentrations in HIV-infected patients. Pharmacol Res. 2016;111:343-356.
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183. Palmer SC, Navaneethan SD, Craig JC, et al. HMG CoA reductase inhibitors (statins) for dialysis patients. Cochrane Database Syst Rev. 2013;(9):CD004289.
184. Palmer SC, Navaneethan SD, Craig JC, et al. HMG CoA reductase inhibitors (statins) for kidney transplant recipients. Cochrane Database Syst Rev. 2014;(1):CD005019.
185. Su X, Zhang L, Lv J, et al. Effect of Statins on Kidney Disease Outcomes: A Systematic Review and Meta-analysis. Am J Kidney Dis. 2016;67(6):881-92.
186. Qin X, Dong H, Fang K, et al. The effect of statins on renal outcomes in patients with diabetic kidney disease: a systematic review and metaanalysis. Diabetes Metab Res Rev. 2017;33(6). DOI: 10.1002/dmrr.2901.
187. Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (study of heart and renal protection): a randomised placebo-controlled trial. Lancet. 2011;377(9784):2181-92.
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Cardiovascular
cLDL
estatinas
fibratos
riesgo
dieta
ezetimibe
PCSK9

Antecedentes

En diciembre de 2019, en Wuhan (Hubei, China) se reportaron 27 personas con neumonía de etiología desconocida; en enero de 2020 se identificó como agente a un virus zoonótico de la familia Coronaviridae (SARS-CoV-2). A su vez, la enfermedad producida por SARS-CoV-2 se denominó COVID-19; el virus se transmite de persona a persona por gotitas respiratorias, contacto directo o fómites. La COVID-19 tiene un período de incubación de 0-24 días. Algunos individuos no desarrollan síntomas y la mayoría se recupera, sin tratamiento específico. La COVID-19 se definió como pandemia en marzo de 2020 (1- 3). Los efectos de la COVID-19 sobre el sistema endocrino aún no están bien establecidos; sin embargo, los individuos con diabetes mellitus (DM) que sufren COVID-19 tienen una mayor tasa de letalidad (entre el 10% y el 11%), lo cual establece que la DM es un factor de riesgo para desenlaces fatales entre aquellos que padecen COVID-19, algo similar a lo que se ha presentado por otras infecciones por coronavirus, como el síndrome respiratorio agudo grave (SARS) y el síndrome respiratorio de Oriente Medio (MERS-CoV). En un modelo en ratones transgénicos, se encontró que la célula del alvéolo pulmonar expresa el receptor de la dipeptidil peptidasa IV (DPP-IV). Por su parte, el MERS-CoV se une a dicho receptor; por lo tanto, se ha hipotetizado (a partir de dicho modelo) que la expresión del receptor de DPP-IV en la célula del alvéolo pulmonar podría estar involucrada en la asociación entre DM y un compromiso pulmonar inflamatorio más grave y prolongado en aquellos infectados por COVID-19.

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Coronavirus
Covid-19
SARS-CoV-2

La enfermedad de Graves (EG) es una de las patologías más interesantes que competen al endocrinólogo. Siempre consideré que la orbitopatía (OG) era una rueda suelta en el manejo de la EG (además del más raro mixedema pretibial), y parecía que los oftalmólogos tampoco estaban muy familiarizados con ella. Algunos insistían en usar los epónimos de sus signos oculares, lo que nunca me pude aprender, y parece que ya se ha olvidado.

Los signos oculares aparecen aproximadamente en 1 de cada 4 pacientes, y cuando esto ocurre (además de encaminar al médico hacia el diagnóstico), generalmente son de naturaleza leve. Las OG moderadas y severas afortunadamente son menos frecuentes; el artículo de Gómez y colaboradores (1) nos actualiza en tan difícil tema.
La preferencia del endocrinólogo sobre el tratamiento de la EG ha variado a través del tiempo. La tiroidectomía fue la primera en desacreditarse porque, como se hacían subtotales, permitían la recurrencia del remanente tiroideo. Los antitiroideos, al principio muy de moda, empezaron a ser menos utilizados por el alto porcentaje de recurrencia. Algún autor recomendaba el uso concomitante de triyodotironina para disminuir los relapsos; sin embargo, el yodo radiactivo (I-131) empezó a posicionarse de primeras por su alta eficacia en la prevención de recurrencias, aunque había que manejar el hipotiroidismo de manera constante.

1. Gomez C, Imitola A, Taboada LB et al. Orbitopatía tiroidea: protocolo de manejo basado en revisión de la evidencia. Rev Col Endocrinol Diab Metab. 2019;6(3):210-217.
2. Bartalena L. Graves’ Disease: Complications. [acceso 20 de febrero de 2020]. En: Feingold KR, Anawalt B, Boyce A, et al., editores. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000. Disponible en: https://www.ncbi.nlm.nih.gov/books/NBK285551/
3. Rosetti S, Tanda ML, Veronesi G, Masiello E, Premoli P, Gallo D, et al. Oral steroid prophylaxis for Graves’ orbitopathy after radioactive iodine treatment for Graves’ disease is not only effective, but also safe. J Endocrinol Invest. 2020 Mar;43(3):381-383.

Orbitopatía tiroidea
enfermedad de Graves (EG)

Las enfermedades endocrinas han estado presentes en el arte desde tiempos inmemoriales, seguramente debido a la baja frecuencia de presentación de algunas de ellas, o por la dificultad de poder realizar un diagnóstico certero. En la antigüedad, por ejemplo, la glándula tiroides no se veía de la misma forma que en los tiempos contemporáneos. En el Renacimiento, los primero dibujos que nos hablan de ella son los realizados por Leonardo da Vinci en 1510, pero desafortunadamente sus cuadernos desaparecieron después de su fallecimiento en 1519.
En la antigüedad se pensaba que la tiroides era una glándula laríngea que humectaba la tráquea y los pulmones; pero en 1543 Vesalio en De Humani Corporis Fabrica hizo que esta glándula fuera visible para los médicos.
La primera vez que se utilizó el nombre de glandulee thyroideae fue en 1656 en la monografía publicada por Thomas Wharton sobre las glándulas del cuerpo; este nombre surgió por su cercanía al cartílago y su forma de escudo.
Así pues, en general el conocimiento de las glándulas endocrinas y de las hormonas es muy reciente dentro de la historia de la medicina, motivo por el cual muchos investigadores médicos, como historiadores y artistas, han tratado de encontrar dentro del arte pictórico algunos trastornos endocrinológicos que en el momento en que fueron plasmados no se conocían.

1. Fortoul van der Goes TI. La endocrinología en el arte. Entre la fantasía y la realidad. Rev. Fac. Med. (Méx.). 2017;60(4):58-60.
2. Vescia FG, Basso L. Goiters in the Renaissance. Vesalius. 1997 Jun;3(1):23-32.
3. Donnelly DE, Morrison PJ. Hereditary Gigantism-the biblical giant Goliath and his brothers. Ulster Med J. 2014 May;83(2):86-8.
4. Miranda M. Los médicos y el arte: una dualidad de beneficiosa reciprocidad. Rev.Med. Chile 2012;140(3):408-409.
5. Historiaum [Internet]. Víctor Hernández Ochando; 2015 [acceso 04 de marzo de 2020]. Los bufones de Velázquez. Disponible en:
https://www.historiarum.es/news/los-bufones-de-velazquez-por-victor-hernandez-ochando/
6. Ardila E. Historia clínica de Henri de Toulouse-Lautrec. Rev. Col. Endo. 2019;6(1):51-54.

Endocrinología
Arte

El carcinoma adrenocortical (CAC) es un tumor maligno poco frecuente. La presentación clínica, por lo general, es por exceso de producción hormonal. La afectación del sistema venoso con trombos en la vena cava inferior (VCI) solo se reporta en un tercio de los casos. El presente estudio informa un caso de CAC con producción hormonal con trombo tumoral con extensión a la VCI y aurícula derecha asociado a embolia pulmonar. Se trata de una paciente de género femenino de 63 años con diagnóstico reciente de hipertensión arterial en manejo, quien consulta a urgencias por dolor abdominal asociado a náuseas, vómitos y pérdida de peso. Imágenes convencionales con hallazgos de masa en fosa suprarrenal derecha irresecable sin plano de clivaje para realizar algún tipo de procedimiento. Patología con diagnóstico de neoplasia de la corteza suprarrenal con extensa necrosis. Se inicia mitotano y esquema ambulatorio de quimioterapia.

1. Sharma E, Dahal S, Sharma P, et al. The Characteristics and Trends in Adrenocortical Carcinoma: A United States Population Based Study. J Clin Med Res. 2018;10(8):636–640.
2. Allolio B, Fassnacht M. Clinical review: Adrenocortical carcinoma: clinical update. J Clin Endocrinol Metab. 2006;91(6):2027–2037.
3. Luton JP, Cerdas S, Billaud L, et al. Clinical Features of Adrenocortical Carcinoma, Prognostic Factors, and the Effect of Mitotane Therapy. N Engl J Med. 1990;322:1195–1201.
4. Libé R. Adrenocortical carcinoma (ACC): diagnosis, prognosis, and treatment. Front Cell Dev Biol. 2015;3:45.
5. Bilimoria KY, Shen WT, Elaraj D, et al. Adrenocortical carcinoma in the United States: treatment utilization and prognostic factors. Cancer. 2008;113(11):3130–3136.
6. Yadav R, Dassi V, Kumar A. Adrenocortical carcinoma with inferior vena cava thrombus: Renal preserving surgery. Indian J Urol. 2016;32(2):161–163.
7. Pronio A, Piroli S, Ciambeerlano B, et al. Adrenocortical carcinoma with inferior vena cava, left renal vein and right atrium tumor thrombus extension. Int J Surg Case Rep. 2015;15:137–139.
8. Paragliola RM, Torino F, Papi G, et al. Role of Mitotane in Adrenocortical Carcinoma - Review and State of the art. Eur Endocrinol. 2018;14(2):62–66.
9. Creemers SG, Hofland LJ, Korpershoek E, et al. Future directions in the diagnosis and medical tretment of adrenocortical carcinoma. EndocrRelat Cancer. 2016;23(1):R43-R69.
10. Dinnes J, Bancos I, Ferrante di Ruffano L, et al. Management of endocrine disease: Imaging for the diagnosis of malignancy in incidentally discovered adrenal masses: a systematic review an meta-analysis. Eur J Endocrinol. 2016;175(2):R51-R64.
11. Cuevas C, Raske M, Bush WH, et al. Imaging Primary and Secondary Tumor Thrombus of the Inferior Vena Cava: Multi-Detector Computed Tomography and Magnetic Resonance imaging. Curr Probl Diagn Radiol. 2006;35(3):90-101.
12. Bancos I, Tamhane S, Shah M, et al. Diagnosis of endocrine disease: The diagnostic performance of adrenal biopsy: a systematic review and metaanalysis. Eur J Endocrinol. 2016;175(2):R65-R80. 13. Gaujoux S, Weinandt M, Bonnet S, et al. Surgical treatment of adrenal carcinoma. J Visc Suerg. 2017;154(5):335-343.

carcinoma corticosuprarrenal
trombosis
vena cava inferior
atrios cardíacos
mitotan

Los inhibidores del PCSK-9 se presentan como una excelente alternativa de tratamiento en aquellos casos de hipercolesterolemia que no alcanzan las metas con tratamiento usual con estatinas de alta potencia y ezetimiba, adicionalmente en los pacientes con intolerancia a estatinas que necesiten tener metas de colesterol LDL. En este caso exponemos la posibilidad de titular el tiempo de aplicación de PCSK-9i de acuerdo con las metas de los niveles de LDL.

1. Alenghat FJ, Davis AM. Management of blood cholesterol. JAMA. 2019;321(8):800-1.
2. Cicero AF, Bove M, Borghi C. Pharmacokinetics, pharmacodynamics and clinical efficacy of non-statin treatments for hypercholesterolemia. Expert Opin Drug Metab Toxicol. 2018;14(1):9-15.
3. American Diabetes Association. Cardiovascular disease and risk management: standards of medical care in diabetes. Diabetes Care. 2019;2(1):S103-23.

hipercolesterolemia
inhibidores de hidroximetilglutaril-CoA reductasas
evolocumab

El presente artículo de revisión tiene como objetivo presentar, de forma resumida, la evidencia que existe sobre las repercusiones metabólicas a nivel de obesidad y diabetes, que se genera como consecuencia de la exposición a sustancias químicas exógenas, denominadas disruptores endocrinos (DE), a las cuales nos exponemos de forma cotidiana y que afectan nuestra salud y la de nuestra descendencia. Adicionalmente, con la presente revisión hacemos un llamado no solo a la comunidad médica, sino a los sectores involucrados en la producción, distribución y reglamentación del uso de estas sustancias, pues cada vez hay más evidencia de los efectos nocivos que pueden generar y debemos evitar su uso.
Los datos se obtuvieron de estudios clínicos aleatorizados y de una revisión en idioma español e inglés de los últimos 15 años, que incluyó los términos DeCS: disruptores endocrinos, con alternativa DeCS: sustancias disruptoras endocrinas y efecto disruptor endocrino, así como términos MeSH: endocrine disruptors y alternativas MeSH: disruptors, endocrine; endocrine disrupting chemicals; chemicals, endocrine disrupting; endocrine disruptor effect; disruptor effect, endocrine; effect, endocrine disruptor; endocrine disruptor effects; disruptor effects, endocrine; effects, endocrine disruptor.

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disruptores endocrinos
diabetes mellitus tipo 1
diabetes mellitus tipo 2
dibutil ftalato
fitoestrógenos
obesidad
parabenos

La energía necesaria para la regulación de las funciones fisiológicas depende del equilibrio entre el aporte y el gasto energético. Un disbalance entre estas condiciones, donde se vea favorecido el consumo sobre el gasto, lleva a un incremento de la reserva, el cual, a su vez, favorece la hipertrofia e hiperplasia del tejido adiposo; en condiciones crónicas, este reservorio energético lleva a la obesidad. A través del uso de fórmulas, se ha tratado calcular la tasa metabólica basal para considerar el aporte óptimo energético y, por ende, la individualización en la prescripción de estrategias nutricionales en el paciente sano y con enfermedades crónicas no transmisibles (ECNT). Sin embargo, estas fórmulas no han sido evaluadas ni validadas para todas las poblaciones y menos en obesidad, que es, de forma coincidente, la población donde más se usan en la práctica clínica, además del poco conocimiento en medicina y la mayor aplicación por nutrición. El propósito de este artículo es revisar los elementos que constituyen las fórmulas de cálculo de la tasa metabólica basal (TMB) y la población de estudio para evidenciar la usabilidad de estas fórmulas en la práctica clínica en pacientes sanos y con ECNT, como la obesidad y diabetes mellitus, dada la importancia que esto representa en el contexto del balance energético.

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metabolismo basal
metabolismo energético
obesidad
hipertensión
diabetes mellitus

Diversos genes pueden desencadenar la diabetes mellitus gestacional (DMG), considerada como un problema de salud pública de etiología compleja y multifactorial.
Objetivo: presentar una revisión de tema de la evidencia científica disponible sobre el impacto de la expresión de los genes omentina-1, quemerina y miR-1013p, implicados en el desarrollo de la DMG.
Materiales y métodos: se realizó una búsqueda de estudios electrónicos transversales a través de la base de datos registrados en MEDLINE y PUBMED, publicados durante 2010-2019, que valoraran mediciones de los tres genes en mujeres con DMG.
Resultados: ocho artículos cumplieron con los criterios de inclusión, cuatro artículos midieron los niveles de quemerina, tres de omentina-1 y uno de miR-103p. Entre los niveles de quemerina se mostró que la circulación de quemerina y miR103p se correlacionó positivamente con las variables metabólicas durante el primer y tercer trimestre del embarazo. Se demostró que la liberación de omentina-1 fue mayor en el tejido adiposo vs. placenta cuando se presenta obesidad.
Conclusión: la expresión de genes y la presencia de obesidad están relacionados con el desarrollo de la diabetes mellitus gestacional.

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Diabetes gestacional
genes
obesidad
tejido adiposo
glucosa

La deficiencia de vitamina D es considerado un problema de salud pública. Aunque algunos estudios han evaluado la deficiencia de vitamina D en poblaciones de riesgo (adultos mayores, posmenopáusicas), existen pocos datos en población adulta joven y mucho menos en poblaciones latinoamericanas. Se realizó un estudio de corte transversal con 205 universitarios entre 18 y 45 años en 2 ciudades colombianas para establecer la prevalencia y los factores asociados con la deficiencia de vitamina D. Se consideró como deficiencia de vitamina D un valor menor o igual de 20 ng/mL de 25-hidroxivitamina-D. Se estableció una prevalencia de deficiencia de vitamina D del 22,4 % (IC 95 % 17- 29). Se encontró que el género masculino y fototipo Fitzpatrick IV se asociaron de manera independiente con mayor riesgo de deficiencia de vitamina D, mientras el consumo de pescado y la exposición al sol de miembros inferiores al hacer ejercicio lo disminuyeron.

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vitamina D
deficiencia de vitamina D
estudios transversales
prevalencia
adulto joven