Presentamos una mujer de 42 años quien consultó por parestesia lingual y ganancia de 10 Kg de peso, sin síntomas clásicos de hipoglucemia, a quién se le encontró una glucemia en ayunas de 46 mg/dl (2,6 mmol/L) con insulina y péptido C concomitantes de 10,2 µU/ml (73,2 pmol/L) y 2,14 ng/dl (79,2 nmol/L) respectivamente. Hallazgos similares fueron encontrados en una segunda ocasión. La resonancia magnética del páncreas mostró una lesión de 1,7 x 1,3 cm dependiente del reborde superior del cuerpo, la cual fue extirpada vía laparoscopia. Patología reveló un tumor neuroendocrino con inmunohistoquímica positiva para insulina, cromogranina y sinaptofisina. La parestesia lingual desapareció y la glucosa se normalizó. La tríada de Whipple no siempre está presente en pacientes con hipoglucemia, mientras que la parestesia lingual debe considerarse para la evaluación de estos pacientes.

Abstract
We report on a 42 years old female who consulted because of lingual paresthesia and 10 kg weight gain but without classic symptoms of hypoglycemia, who had a fasting blood glucose of 46 mg/dl (2.6 mmol/L) with a concomitant insulin a C-peptide of 10.2 µU/ml (73.2 pmol/L) and 2.14 ng/dl (79.2 nmol/L) respectively. Similar findings were obtained on a second occasion. Magnetic resonance of the pancreas revealed a 1.7 x 1.3 cm lesion dependent of the superior border of the body which was removed by laparoscopy.
Pathology showed a neuroendocrine tumor with positive immmunohistochemistry for insulin, chromogranin and synaptophysin. Lingual paresthesia disappeared and blood glucose was normalized. Patients with lingual paresthesia should be evaluated for hypoglycemia even in the absent of a classic Whipple triad.

1. Whipple. J InternatChir. 1938; 3: 237-276.
2. Cryer P 2001. The prevention and correction of hypoglycemia. In: Jefferson L, Cherrington A, Goodman H eds Handbook of Physiology ; Section7, the endocrine system. Volume 2. The endocrine pancreas and regulation of metabolism. New York : Oxford University Press; 1057-1092.
3. Service FJ, Dale AJ, Elveback LR et al. Insulinoma. Clinical and diagnostic features of 60 consecutive cases. Mayo Clinic proc 1976 Jul; 51(7): 417-429.
4. Jácome Roca A, Espinosa H, Echeverry G, Escallón A, Baena M. Insulinoma, demostración de hiperinsulinismo y localización preoperatoria: Manejo Quirurgico. Univmed 1983; 25 (1): 28-35.
5. Placzkowski KA, Vella A, Thompson GB et al. Secular trends in the presentation and management of functioning insulinoma at the Mayo Clinic, 1987- 2007. J ClinEndocrinolMetab 2009 Apr; 94(4): 1069-1073.
6. Cryer PE, Axelrod L, Grossman AB et al. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice Guide- line. J ClinEndocrinolMetab 2009 Mar; 94(3): 709-728.

Parestesia lingual
hipoglucemia
insulinoma

La tormenta tiroidea es una exacerbación aguda de hipertiroidismo que se presenta por una repentina liberación de hormonas tiroideas hacia la circulación sistémica. Es una afección potencialmente mortal que requiere tratamiento de emergencia. Se manifiesta por la descompensación de múltiples órganos, que a menudo se desencadena por estrés severo. Es una entidad poco común, con una incidencia reportada de 0,2 casos/100.000 habitantes y tasas de mortalidad alta de 10% a 30%(2). No obstante, el diagnóstico y el tratamiento oportunos pueden modificar ese desenlace al mejorar la supervivencia en los pacientes. Se ha descrito que la intervención temprana puede disminuir la mortalidad al 10% de los casos(3). En ese orden de ideas, es importante dar a conocer dicha patología, su presentación, el enfoque diagnóstico y el manejo oportuno para modificar el desenlace de los pacientes en nuestras instituciones, es el motivo de la presentación de dos casos de tormenta tiroidea en el Hospital de San José en Bogotá.

1. Parasa M, Chinthakunta BK, Vemuri NN, Shaik MS. Out of the blue! Thyroid crisis. Anesthesia, essays and researches. 2015;9(1):130-2.
2. Akamizu T, Satoh T, Isozaki O, Suzuki A, Wakino S, Iburi T, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nation- wide surveys. Thyroid : official journal of the American Thyroid Associa- tion. 2012;22(7):661-79.
3. Papi G, Corsello SM, Pontecorvi A. Clinical concepts on thyroid emergencies. Frontiers in endocrinology. 2014;5:102.
4. Rojas G W. Urgencias en tiroides: tormenta tiroidea y coma mixedematoso. En: Ardila A E, Barbosa M J, Dorado P L, et al, editores. Fascículo alteraciones endocrinas en urgencias. Bogotá: Producciones Científicas Ltda; 2012. p. 53 - 62.
5. Almanzar A., Mora L, Valderrama L, Barón G. Serie de casos: tirotoxicosis y tormenta tiroidea. Dovela científica (internet). 2011 (citado 09 Jul 2015); 1 (4): 1-8. Disponible en: http://www.hospitaloccidentekennedy.gov.co/ archivos/File/Dovela_Vol_1_No_/Casos_clinicos.html.
6. Hampton J. Thyroid gland disorder emergencies: thyroid storm and myx edema coma. AACN advanced critical care. 2013;24(3):325-32.
7. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinology and metabolism clinics of North America. 1993;22(2):263-77.
8. Rámiz M., Gutiérrez A., De la Guerra C. et al. Crisis tirotóxica (tormenta tiroidea). A propósito de dos observaciones. Gac Med Bilbao. 2010;107(2):64- 67.
9. Klubo-Gwiezdzinska J, Wartofsky L. Thyroid emergencies. The Medical clin ics of North America. 2012;96(2):385-403.
10. Angell TE, Lechner MG, Nguyen CT, Salvato VL, Nicoloff JT, LoPresti JS. Clinical features and hospital outcomes in thyroid storm: a retrospective cohort study. The Journal of clinical endocrinology and metabolism. 2015;100(2):451-9.
11. Bahn Chair RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, Klein I, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid : official journal of the American Thyroid Association. 2011;21(6):593-646.
12. Carroll R, Matfin G. Endocrine and metabolic emergencies: thyroid storm. Therapeutic advances in endocrinology and metabolism. 2010;1(3):139-45.
13. Duggal J, Singh S, Kuchinic P, Butler P, Arora R. Utility of esmolol in thyroid crisis. The Canadian journal of clinical pharmacology = Journal canadien de pharmacologie clinique. 2006;13(3):e292-5.
14. Uchida N, Suda T, Ishiguro K. Thyroidectomy in a patient with thyroid storm: report of a case. Surgery today. 2015;45(1):110-4.
15. Aulet RM, Wein RO, Siegel RD. Surgical management of an atypical presentation of a thyroid storm. International journal of endocrinology and metabolism. 2014;12(2):e13539.
16. Ahumada J.J. Terapia del hipertiroidismo. Acta Medica Colombiana Vol. 13 No. 1 (Enero-Febrero) 1988.
17. Muller C, Perrin P, Faller B, Richter S, Chantrel F. Role of plasma exchange in the thyroid storm. Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy. 2011;15(6):522-31.
18. Yoshihara A, Noh J, Yamaguchi T, Ohye H, Sato S, Sekiya K, et al. Treatment of graves’ disease with antithyroid drugs in the first trimester of pregnancy and the prevalence of congenital malformation. The Journal of clinical endocrinology and metabolism. 2012;97(7):2396-403.
19. Glinoer D. The systematic screening and management of hypothyroidism and hyperthyroidism during pregnancy. Trends in endocrinology and metabolism: TEM. 1998;9(10):403-11.
20. Restrepo O. Hipertiroidismo durante el embarazo: enfoque y manejo. Revista Colombiana de Obstetricia y Ginecología Vol. 52 No. 3 - 2001.

Tormenta tiroidea
tormenta tirotóxica
hipertiroidismo

La acromegalia y el gigantismo hipofisiario son entidades de muy baja prevalencia pero a pesar de esto es sorprendente que en la historia de la humanidad hay en todas las épocas, descripciones de casos, sobre todo de gigantismo, que nos muestran que es una entidad que siempre nos ha acompañado.
Si revisamos desde cuando existen documentos o relatos sobre la existencia de gigantes, la sorpresa es que están descritos desde los relatos de la Biblia. Según las referencias que aparecen en los libros del Antiguo Testamento, en el Génesis (Génesis 6,1-2) y en el Deuteronomio (Deuteronomio 13,11) se hace referencia a la existencia de gigantes como una raza de seres nacidos de la unión entre hermosas mujeres y ángeles de Dios y se denominan nephilims. Al parecer, parte de la justificación bíblica para el diluvio universal fue que Dios quería acabar con esta raza de gigantes debido a sus orígenes y a sus comportamientos. Posteriormente, otra descripción bíblica que hace referencia a los gigantes es cuando al llegar los israelitas a la tierra de Canaan envían a un grupo por adelantado para observar el tipo de pobladores que había en estas tierras y al regresar estos exploradores relatan la presencia de gigantes que habitan las tierras de Canaan. A pesar de su presencia, los israelitas deciden invadir estos territorios con la convicción de que Dios está con ellos y no permitirá que nada le suceda a su pueblo.

1. Mitchell S, Conversations, Return of Gilgamesh, Archaeology 2005;58 (3):128.
2. Hoedl S, The disease of Akhenaton . Int J Dermatology 1989; 28(3):201-203.
3. Langebaeck Carl Henrick, Los Herederos del Pasado, Indigenas y pendamiento criollo en Colombia y Venezuela Tomo 1 Ediciones Uniandes Bogota DC., 2009 pags 105-112.
4. Charlier P, Tsigonaki C, A case of acromegaly (Greece, 7th century AD), European Journal of Endocrinology 2011; 165: 819–821.
5. Minozzi S et al, Pituitary Disease from the Past: A Rare Case of Gigantism in Skeletal Remains from the Roman Imperial Age J Clin Endocrinol Metab, 2012;97 (12):4302–4303.
6. Restrepo G, Memoria de la Historia. Historias Clínicas de la Corte de España, Ed Planeta 2000 pags 21-26.
7. Restrepo G. Memoria de la Historia. Historias Clinicas de la Corte de Francia. Ed Planeta 1997 pags 94-100.
8. Login I., Login J., Governor Pio Pico, the monster of California…no more: lessons in neuroendocrinology. Pituitary 2010;13: 80-86.
9. Martino E. Endocrinology and Art Drawing of a tooth to a giant.acromegalic man J. Endocrinol. Invest. 32: 293, 2009.
10. Toni R et al Endocrinology and Art. Acromegaly and Goiter in the precolumbian mesoamerican population J. Endocrinol. Invest. 2007; 30: 169-170.
11. Faglia G., Endocrinology and Art Was Caravaggio affected with y acromegaly?.J Endocrinol Invest 2011; 34:85.
12. Pozzilli P Leslie D, Endocrinology and Art, Louise Ou La servante Bretonne J. Endocrinol. Invest. 2003; 26: 1051.
13. Guaraldi F, Vannini F., Endocrinology and Art Cubist Portrait of acromegalic woman. J Endocrinol Invest 2013; 36:544.
14. Barbosa G, Wiesner C., Garavito G., Un Caso de acromegalia en el Instituto Nacional de Radium (1935) Revista Colombiana de Cancerologia 2004;
8(2): 52-56.
15. Muñoz L., Un caso de acromegalia en Zipaquira, Repertorios de Medicina y Cirugia 1942;2(12):150-156.
16. W de Herder W Acromegaly and gigantism in the medical literature. Case descriptions in the era before and the early years after the initial publication of Pierre Marie (1886) Pituitary (2009) 12:236–244.
17. De Herder W, Perie J Gnodde A Gigantism and Acromegaly in the 20th century, Published by Ipsen Pharma Boulogne-Billacourt, France.
18. http://www.thetallestman.com/asdrubalherreramora.htm

Acromegalia
gigantismo hipofisiario

Los mayores picos de mineralización se producen en los primeros 2 años de vida y la pubertad, en los que la masa ósea aumenta 40% y 60%; a los 20 años se estabiliza y, luego, se inicia una pérdida progresiva. El volumen de masa ósea es variable según la edad, el sexo y la raza, es afectado por factores ambientales, genéticos, hormonales y nutricionales. El objetivo del estudio fue conocer el impacto de los hábitos relacionados con el proceso de mineralización durante la etapa de la juventud. Los participantes completaron una ficha clínica. La densidad mineral ósea fue valorada por medio de densitometría, se midieron los niveles de calcio en orina para identificar posibles pérdidas, se calculó el índice de masa corporal (IMC) a partir del peso y la talla. El 5% de la población participante presentó un Z-score inferior a -2,0 y los factores relacionados fueron consumo de cafeína, alcohol y poca actividad física.

Abstract
The highest peaks of mineralization is in the first two years of life and puberty, bone mass increases 40% to 60%, at twenty stabilizes and begins a gradual loss. The volume of bone mass varies according to age, sex and race, which affect environmental, genetic, hormonal and nutritional factors. The aim of the study was to determine the impact of the habits related mineralization process during the stage of youth. Participants completed clinical record. BMD was assessed by densitometry; Calcium levels were measured in urine for loss, BMI was calculated from weight and height. 5% of the participating population present a Z-score less than -2,0 and related factors were caffeine, alcohol and little physical activity.

1. Caritat Bagur C, Ejercicio físico y masa ósea (I). Evolución ontogénica de la masa ósea e influencia de la actividad física sobre el hueso en las diferentes etapas de la vida. Apunts Med Esport. 2007;42:40-6. - Vol. 42 Núm.153.
2. Heaney RP, Abrams S, Lawson-Hughes B, Looker A, Marcus R, Matkovic V, et al. Peak bone mass. Osteoporos Int. 2000;11: 985-1009.
3. Shreyasee Amin, osteoporosis, 2012 American College of Rheumatology.
4. Balance control in elderly people with osteoporosis Wei-Li Hsu, Chao-Yin Chen, Jau-Yih Tsauo, Rong-Sen Yang Journal of the Formosan Medical Association - 20 March 2014 (10.1016/j.jfma.2014.02.006).
5. Caple C, Schub T, Pravikoff D, Osteoporosis: prevención, CINAHL Nursing Guide, 2011.
6. Schurman L, bagur a, claus-hermberg h, messina o, negri a, mastaglia s, et al. guías 2012 para el diagnóstico, la prevención y el tratamiento de la osteoporosis. (Spanish). Medicina (Buenos Aires) [serial on the Internet]. (2013, Jan), [cited March 28, 2014]; 73(1): 55-74. Available from: MedicLatina.
7. Aguilera-Barreiro M, Rivera-Márquez J, Trujillo-Arriaga H, Ruiz-Acosta J, Rodríguez-García M. Impacto de los factores de riesgo en osteoporosis sobre la densidad mineral ósea en mujeres perimenopáusicas de la Ciudad de Querétaro, Méxi- co. (Spanish). Archivos Latinoamericanos De Nutrición [serial on the Internet]. (2013, Mar), [cited March 28, 2014]; 63(1): 21-28. Available from: MedicLatina.
8. Strayer DA, Schub T, Pravikoff D, osteoporosis, CINAHL Nursing Guide, November 25, 2011.
9. Kanis JA, Melton LJ III, Christiansen C, Johnston CC, Khaltaev N. The diagnosis of osteoporosis. J Bone Miner Res 1994; 9: 1137-1141.
10. Bachrach LK, Hastie T, Wang MC, Narasimhan B, and Hispanick Black and Caucasian youth: a longitudinal study. J Clin Endocrinol Metab 84:4702-4712 2003.
11. S. Ferrari, M. L. Bianchi, J. A. Eisman, Show All (9), Osteoporosis in young adults: pathophysiology, diagnosis, and management, Osteoporosis International, 2012, Page 1.
12. M. Reyes Pérez-Fernández, Raquel Almazán Ortega, José M. Martínez Portela, M. Teresa Alves Pérez, M. Carmen Segura-Iglesias, Román Pérez-Fernández, Hábitos saludables y prevención de la osteoporosis en mujeres perimenopáusicas de un ámbito rural, Gaceta Sanitaria, Volume 28, Issue 2, March–April 2014, Pages 163- 165, ISSN 0213-9111, http://dx.doi.org/10.1016/j.gaceta.2013.09.006.

mineralización ósea
calcio en huesos
osteoporosis
densidad mineral ósea
bone mineralization
calcium in bones
bone mineral density

Se presentan cinco casos de pacientes con hipotiroidismo primario y altos requerimientos de levotiroxina, que luego de haber tenido un abordaje convencional en el ajuste de las dosis necesarias de levotiroxina por el peso y etiología de hipotiroidismo, recomendación y educación para el consumo adecuado de levotiroxina, optimización de la calidad del medicamento recibido, eliminación de interferencias con la absorción por medicamentos o alimentos, reposición de deficiencia de vitamina B12, desparasitación, descartar enfermedad celíaca y gastritis autoinmune atrófica, persisten con TSH elevada pese al uso de dosis altas de levotiroxina (mayores de 2,5 µg/kg/día). Se les practicó prueba de absorción de levotiroxina con 1.000 µg en dosis única de carga y evaluación de los incrementos de T4 libre a las 2 y 4 horas en cuatro pacientes y en uno con suministro semanal de la dosis de levotiroxina y evaluación semanal de T4 libre. Se confirmó en los cinco pacientes la capacidad de absorción de levotiroxina, constituyendo cinco casos de pseudomalabsorción de levotiroxina.

Abstract
Five patients with primary hypothyroidism and high levothyroxine dose requirements (>2.5 µg/kg/day) are presented.

All patients had usual adjustment of the levothyroxine dose according to weight and hypothyroidism etiology. Patients were educated about the appropriate way of drug intake, the quality of the hormone replacement was assessed and withdrawal of all medications potentially interrupting with the levothyroxine absorption was done. All patients had vitamin B12 replacement, were treated for gastrointestinal parasites and celiac disease and autoimmune atrophic gastritis was ruled out. Despite correction of all this factors these patients had elevated TSH. To evaluate a potential mala-absorptive case all patients underwent a levothyroxine absorption test. In 4 cases, 1000 µg of levothyroxine was administered and free T4 was evaluated at 2 and 4 hours after intake of the drug. In 1 case, the levothyroxine was administered weekly with free t4 evaluation. Appropriate levothyroxine absorption was confirmed in all cases and the diagnosis of pseudo mal-absorption of levothyroxine was done.

1. Builes-Barrera CA, Palacios Bayona KL, Jaimes Barragán FA. Dosis de levotiroxina varía según la etiología del hipotiroidismo y el peso cororal. Revista Colombiana de Endocrinología, Diabetes y Metabolismo. 2014;1(1):27-32.
2. Lips DJ, van Reisen MT, Voigt V, Venekamp W. Diagnosis and treatment of levothyroxine pseudomalabsorption. Neth J Med. 2004;62(4):114-8.
3. Ain KB, Refetoff S, Fein HG, Weintraub BD. Pseudomalabsorption of levothyroxine. JAMA. 1991;266(15):2118-20.
4. Kubota S, Fukata S, Matsuzuka F, Kuma K, Miyauchi A. Successful management of a patient with pseudomalabsorption of levothyroxine. Int J Psychiatry Med. 2003;33(2):183-8.
5. Srinivas V, Oyibo SO. Levothyroxine pseudomalabsorption and thyroxine absorption testing with use of high-dose levothyroxine: case report and discussion. Endocr Pract. 2010;16(6):1012-5.
6. Ramadhan A, Tamilia M. Treatment-refractory hypothyroidism. CMAJ. 2012;184(2):205-9.
7. Robertson HM, Narayanaswamy AK, Pereira O, Copland SA, Herriot R, McKinlay AW, et al. Factors contributing to high levothyroxine doses in primary hypothyroidism: an interventional audit of a large community data- base. Thyroid. 2014;24(12):1765-71.
8. Liwanpo L, Hershman JM. Conditions and drugs interfering with thyroxine absorption. Best Pract Res Clin Endocrinol Metab. 2009;23(6):781-92.
9. Benoit A, Bouquegneau A, Petrossians P, Beckers A. [Malabsorption of thyroid hormones... or simply poor patient compliance?]. Rev Med Liege.
2013;68(3):118-21.
10. Checchi S, Montanaro A, Pasqui L, Ciuoli C, De Palo V, Chiappetta MC, et al. L-thyroxine requirement in patients with autoimmune hypothyroidism and parietal cell antibodies. J Clin Endocrinol Metab. 2008;93(2):465-9.
11. Collins D, Wilcox R, Nathan M, Zubarik R. Celiac disease and hypothyroidism. Am J Med. 2012;125(3):278-82.
12. Sun GE, Pantalone KM, Faiman C, Gupta M, Olansky L, Hatipoglu B. The clinical utility of free thyroxine in oral levothyroxine absorption testing. Endocr Pract. 2014;20(9):925-9.
13. Ogawa D, Otsuka F, Mimura U, Ueno A, Hashimoto H, Kishida M, et al. Pseudomalabsorption of levothyroxine: a case report. Endocr J. 2000;47(1):45- 50.
14. Pedrosa W, Santana G. [Pseudomalabsorption of levothyroxine: a case report]. Arq Bras Endocrinol Metabol. 2005;49(2):308-13.
15. Samuels MH. Psychiatric and cognitive manifestations of hypothyroidism. Curr Opin Endocrinol Diabetes Obes. 2014;21(5):377-83.
16. Jubiz W, Ramirez M. Effect of vitamin C on the absorption of levothyrox- ine in patients with hypothyroidism and gastritis. J Clin Endocrinol Metab. 2014;99(6):E1031-4.
17. Green WL. New questions regarding bioequivalence of levothyroxine prep arations: a clinician’s response. AAPS J. 2005;7(1):E54-8.
18. Walker JN, Shillo P, Ibbotson V, Vincent A, Karavitaki N, Weetman AP, et al. A thyroxine absorption test followed by weekly thyroxine administration: a method to assess non-adherence to treatment. Eur J Endocrinol. 2013;168(6):913-7.
19. Castellanos R. Altos requerimientos de levotiroxina. Tratado de Tiroides. 2014. Capítulo 9. p 73-77.

Hipotiroidismo
TSH
pseudomalabsorción
levotiroxina
levothyroxine
pseudo malabsorption
hypothyroidism

Contexto: Los valores de referencia para pruebas tiroideas deben estandarizarse en la población local. En Colombia no tenemos datos propios.
Objetivo: Describir los niveles de hormonas tiroideas (TSH y T4 libre) en adultos de Medellín, Colombia.
Métodos: Estudio retrospectivo, con información obtenida de la base de datos electrónica de Dinámica IPS.
Criterios de inclusión: Adultos (18-50 años), con medición simultánea de TSH y T4 libre (T4L), ambos dentro del valor de referencia suministrado por el proveedor de la prueba (Abbott).
Criterios de exclusión: mujeres embarazadas, hipotiroidismo primario conocido y anticuerpos anti-TPO o antitiroglobulina positivos. Los datos se compararon con una curva normal. Se realizó un análisis de regresión lineal entre T4L y TSH o LogTSH.
Resultados: Se obtuvieron datos desde febrero 1 hasta abril 30 de 2015, n = 2.438 personas, el 80,5% eran mujeres, el promedio de edad 35,74±8,4 años. El promedio de TSH fue 2,19±1,10 mUI/L y el de T4L 1,00±0,11 ng/dl. Los valores de T4L se distribuyen de forma normal, pero los de TSH se distribuyeron como una curva asintótica hacia la izquierda. El 95% de los valores de T4L fueron entre 0,74-1,26 ng/dl y de TSH entre 0,36 y 4,55 mUI/L. No hubo diferencias entre TSH y T4 libre por sexo o por edad. El análisis de regresión lineal no mostró relación entre la T4L y TSH o LogTSH.
Conclusiones: En adultos entre 18 a 50 años, el 95% de los valores de TSH oscilan entre 0,36-4,55 mUI/ L y para T4 L entre 0,74-1,26 ng/dl. No hubo diferencias por sexo o décadas de edad. Tampoco entre valores de TSH y T4L.

Abstract
Context: Reference values for thyroid tests should be standardized in local adult people. In Colombia we do not have own data.
Objective: To describe serum levels of thyroid hormones (TSH and free T4) in adults from Medellin, Colombia.
Methods: Retrospective study based in information from an electronic database.
Inclusion criteria: Adults 18-50 years-old adults with simultaneous measurement of TSH and free T4 (FT4), both values within the reference value supplied by Abbot.
Exclusion criteria: pregnant women, primary hypothyroidism and positive TPO or thyroglobulin antibodies. Data were compared with a normal curve. Linear regression analysis between FT4 and TSH and between FT4 and LogTSH was performed.
Results: Data from February 1 to April 30 2015 were obtained, n=2.438 individuals, 80.5% were women, age mean±SD35.74±8.4 years. TSH values were mean±SD 2.19±1.10 mUI/L and FT4 1.00±0.11 ng/dl. FT4 were distributed as a normal curve, meanwhile TSH showed an asymptotic curve to the left. Ninety five percent of FT4 values were between 0.74-1.26 ng/dl and TSH 0.36-4.55 mUI/L. There was no difference between TSH and FT4 by gender or by age. Linear regression analysis do not showed any relationship between TSH and FT4.
Conclusions: In adult population 95% of serum TSH and FT4 ranging between 0.36-4.55 uUI/L and 0.74-1.26 ng/dl respectively. There were no differences by gender or age groups, or relationship between TSH and FT4.

1. Garber JR, Cobin RH, Gharib H, Hennessey JV, Klein I, Mechanick JI, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by The American Association of Clinical Endocrinologist and The American Thyroid Association. Endocr Pract. 2012 Nov-Dec;18(6):988-1028.
2. Baloch Z, Carayon P, Conte-Devolx B, Rasmussen U.F., Henry JF, LiVolsi V et al. Laboratory medicine practice guidelines. Laboratory support for the diagnosis and monitoring of thyroid disease. National Academy of Clinical Biochemistry. Thyroid. 2003 Jan;13(1):3-126.
3. Langén VL, Niiranen TJ, Mäki J, Sundvall J, Jula AM. Thyroid-stimulating hormone reference range and factors affecting it in a nationwide random sample. Clin Chem Lab Med. 2014 Dec; 52(12):1807-13.
4. Kratzsch J, Fiedler GM, Leichtle A, Brügel M, Buchbinder S, Otto L, et al. New reference intervals for thyrotropin and thyroid hormones based on National Academy of Clinical Biochemistry criteria and regular ultrasonography of the thyroid. Clin Chem 2005; 51:1480.
5. Vadiveloo T, Donnan PT, Murphy MJ, Leese GP. Age- and gender-specific TSH reference intervals in people with no obvious thyroid disease in Tayside, Scotland: the Thyroid Epidemiology, Audit, and Research Study (TEARS). J Clin Endocrinol Metab 2013; 98:1147.
6. Vanderpump MPJ, Tunbridge WMG, French JM, Appleton D, Bates D, Rodgers H et al. The incidence of thyroid disorders in the community; a twenty year follow up of the Whickham survey. Clin Endocrinol 1995; 43:55-68.
7. Biondi B. The Normal TSH Reference Range: ¿What Has Changed in the Last Decade? J Clin Endocrinol Metab, 2013 Sep;98(9):3584-7.
8. P. Laurberg, S. Andersen, A. Carl´e, J. Karmisholt, N. Knudsen, and I. B. Pedersen. The TSH upper reference limit: where are we at?. Nat Rev Endocrinol. 2011 Apr;7(4):232-9
9. Brabant G, Beck-Peccoz P, Jarzab B et al. Is there a need to redefine the upper normal limit of TSH? Eur J Endocrinol. 154; 5:633–637, 2006.
10. Wartofsky L, Dickey RA. The evidence for a narrower thyrotropin reference range is compelling. J Clin Endocrinol Metab, 90; 9: 5483–5488, 2005.
11. Dickey RA, Wartofsky L, Feld S. Optimal thyrotropin level: normal ranges and reference intervals are not equivalent. Thyroid. 15; 9: 1035–1039, 2005.
12. Surks MI. TSH reference limits: new concepts and implications for diagnosis of subclinical hypothyroidism. Endocrine Practice 2013, vol 19, No.6.
13. Hoermann R, Eckl W, Hoermann C, Larisch R. Complex relationship between free thy roxine and TSH in the regulation of thyroid function. Eur J Endocrinol, 162; 6: 1123– 1129, 2010.
14. Wardle CA, Fraser WD, Squire CR. Pitfalls in the use of thyrotropin concentration as a first-line thyroid-function test. Lancet 2001; 357:1013-4.
15. C. A. Spencer, J. G. Hollowell, M. Kazarosyan, and L. E. Braverman, National Health and Nutrition Examination Survey III Thyroid-StimulatingHormone (TSH)-thyro- peroxidase antibody relationships demonstrate that TSH upper reference limits may be skewed by occult thyroid dysfunction. J Clin Endocrinol Metab, vol. 92, no. 11, pp. 4236–4240, 2007.
16. Andersen S1, Bruun NH, Pedersen KM, Laurberg P. Biologic variation is important for interpretation of thyroid function tests. Thyroid. 2003 Nov; 13 (11):1069-78.
17. Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, et al. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANESIII). J Clin Endocri nol Metab.2002.87 ;( 2):489–499.
18. Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab 97:1554, 2012.
19. T. E. Hamilton, S. Davis, L. Onstad, and K. J. Kopecky, Thyrotropin levels in a population with no clinical, autoantibody, or ultrasonographic evidence of thyroid disease: implications for the diagnosis of subclinical hypothyroidism, J Clin Endocrinol Metab, vol. 93, no. 4, pp. 1224–1230, 2008.
20. Surks MI, Hollowell JG. Age-specific distribution of serum thyrotropin and antithyroid antibodies in the U.S. population: implications for the prevalence of subclinical hypothyroidism. The Journal of Clinical Endocrinology and Metabolism, 92; 12:4575–4582, 2007.
21. Boucai L, Hollowell JG, Surks MI. An approach for development of age-, gender-, and ethnicity-specific thyrotropin reference limits. Thyroid. 2011; 21: 5-11.
22. Surks M, Boucai L. Age and race- based serum thyrotropin reference limits. J Clin Endocrinol Metab 95: 496-502- 2010.
23. Hoermann R, Midgley J. TSH Measurement and Its Implications for Personalised Clinical Decision-Making. Journal of Thyroid Research. Volume 2012. doi: 10.1155/2012/438037.

TSH
tiroxina
tirotropina
hormonas tiroideas
función tiroidea
thyroid function
thyroid function tests
thyroid hormones
thyrotropin
thyroxine
serum TSH levels

El tejido adiposo juega un papel central en la nutrición, el balance energético y la salud en los humanos. Existen dos tipos de tejido adiposo: el blanco (TAB) y el pardo (TAP). El TAB conserva la energía, mientras que el TAP la utiliza.
El exceso de nutrición y la inactividad física dan origen a un incremento del TAB y a la obesidad. En cambio el TAP es termogénico, debido a una proteína única desacopladora (UCP1).
Esta proteína localizada en la parte interna de la membrana mitocondrial desacopla la respiración mitocondrial, produciendo tanto energía como calor. Esta propiedad esencial protege a los animales de la hipotermia.
La creencia tradicional de que el TAP sólo existe en infantes y no en adultos retrasó la investigación en humanos. Pero el descubrimiento de que la grasa del adulto presentaba una alta actividad metabólica como lo demostraba la tomografía por emisión de positrones (TEP) hizo que los investigadores se interesaran nuevamente en el TAP y que se reiniciara la investigación sobre este tejido, su identificación, la prevalencia, regulación, localización, abundancia y su importancia en el humano.

1. Cannon B, Nedergaard J, Brown adipose tissue: function and physiological significance. Physio Rev. 2004;84:277-359.
2. Cypess AM, Lehman S, Williams G, et al. Identification and importance of brown adipose tissue in adult humans. N Engl J Med. 2009; 360:1059-1517.
3. Lee P, Greenfield JR, Ho KK, et al. A critical appraisal of the prevalence and metabolic significance of brown adipose tissue in adults humans. Am Physiol Endocrinol Metab. 200;299: E601- E 606.
4. Lee P, Zhas JT, Swarbrick MM, et al. High prevalence of brown adipose tissue in adults humans. J Clin En Endocrinol Metab. 2011;96:2450-2455.
5. Virtaner KA, Lindell ME, Orava J, et al. Functional brown adipose tissue in healthy adults. N Engl J MEd. 2009:360:1518-1525.
6. Zingaretti Mc, Crosta F,Vitali A, et al. The presence of UCP1 demostrates that active adipose tissue in the neck of adult humans truly represents brown adipose tissue. Faseb. 2009; 23: 3113-3120.
7. vanMarker Lichtenbelt WD, Vanhommerig JW,Smulders NM, et al. Cold activated brown adipose in healthy men. N Engl J Med. 2009;360: 1500-1508.
8. Bouillaud F, Villarroya F, Hentz E, et al. Detection of brown adipose tissue uncoupling protein mRNA in adults patients by a human genomic prole. Clin Sci(Lond) 1988; 75: 21-27.
9. Bouillaud F, Combes- George M, Ricquier D. Mitondria of adult human brown adipose tissue contains a 32.00.Mr uncoupling protein. Biosci Rep. 1983; 3: 775-780.
10. Hatai S. On the presence in human embroys of an interscapular gland corresponding to the so- called hibernating gland in the lower animals. Anatomischer Anzeiger. 1902; xxi: 369.
11. Bonnot E. The Interscapular gland. J Anat Physiol. 1908; 43:43-58.
12. Rasmussen A. The glandular status of brown multilocular adipose tissue. Endocrinology. 1922;6:760-770.
13. Smith RE, Hock RJ. Brown fat : thermogenic effector of arousal in hibernators. Science. 1963; 140: 199-200.
14. Dawkins MJ, Scopes JW. Non_ shiverning thermogenesis and brown adipose tissue in the human new- born infant. Nature. 1965;206:201-202.
15. Dawkins MJ, Hull D. Brown adipose tissue and the response of new-born rabbits to cold. J Physiol. 1964; 172:216-238.
16. Hull D. Th estructure and function of brown adipose tissue. Br Med Bull. 1966; 22: 92- 96.
17. Aherne W, Hull D. Brown adipose tissue and heat production in the new born infant. J Pathol Bacteriol. 1966;91:223-234.
18. Silverman WA;Zamelis A, Sinclair JC, et al. Warm nap of the newborn. Pediatrics. 1964;33:984-987.
19. Lee p, Swarbrick MM, Ken K Y. HO. Brown adipose tissue in adults humans: A metabolic renaissance. Endocrine Review. 2013;34:413-438.
20. Smalley RL, Dryer RL. Brown fat : thermogenic effect during arousal from hibernation in the bat. Science. 1963;140:1333-1334.
21. Heaton JM. The distribution of brown adipose tissue in the human. J Anat. 1972;122:35-39.
22. Himms- Hagen J. Obesity may be due to a malfunctioning of brown fat. Can Med Assoc J. 1979; 121: 1361-1364.
23. Do the lucky ones burn off their dietary excess? Lancet 1979;2: 115-116.
24. Elliot J. Blame It all on brown fat now. JAMA. 1980; 243: 1983-1985.
25. Lindley M. Nutrition and metabolism. Nature. 1980; 287:579-580.
26. Rothwell Nj, Stock MJ. Brown adipose tissue: does it play a role in the development of obesity? Diabetes Metab Rev. 1988;4: 595- 601.
27. Astrup A, Bulow J. Christensen NJ, et al. Ephedrine- induced thermogenesis in man: no role for interscapular brown adipose tissue. Clin Sci (Lond). 1984; 66: 179-186.
28. Himms-Hagen J. Brown adipose tissue thermogenesis and obesity. Prog Lipid Res. 1989; 28: 67-115.
29. Ravussin E, Kozak LP. Have we entered the brown adipose tissue renaissence? Obese Rev. 2009;10: 265-268.
30. Gesta S, Tseng YH, Kahn CR.Developmental origen of fat: tracking obesity to its source. Cell. 2007;131:242-256.
31. Rousseau V, Becker DJ, Ongemba LN, et al. Developmental and nutritional changes of ob and PPAR? 2 gene expressions in rat white adipose peroxisone tissue. Biochem J. 1997;321:451-456.
32. Braissant O, Wahli W. Differential expression of peroxisome proliferator activated receptor-?,-? and -? during rat embrionic development. Endocrinology. 1998;139:2748-2754.
33. Hansen JB, Kristiansen K. Regulatory circuits controling White versus brown adipocyte differentiation. Biochem J. 2006; 398; 153- 168.
34. Rosen ED. MacDougald OA. Adipocyte differentiation from the inside out. Nat Rev Moll Cell Biol. 2006;7:885-896.
35. Néchad M, Kuusela P, Carneheim C, et al. Development of brown fat cells in monolayer culture. Morphological and biochemical distinction from White fat cells in culture. Exp Cell Res. 1983;149:105-118.
36. Hu E, Tontonoz P, Spiegelman BM. Transdifferentiation of mioblast by the adipogenic transcription factors PPAR? and C/EBP?. Proc Natl Acad Sci U S A.1995;92:9856-9860.
37. Puigserver P, Wu Z, Park CW, et al. A cold imducible coactivador of nuclear receptors linked to adaptive thermogenesis. Cell. 1998;92:829-839.
38. Kleiner S, Mepani RJ,Laznik D, et al. Development of insulin resistance in mice lacking PGC-1? in adipose tissue. Proc Natl Acad Sci USA. 2012;109:9635-9640.
39. Pardo R,Enguix N, Lasheras J, et al. Rosiglitazone- induced mitocondrial biogenesis in White adipose is independent of peroxisome proliferator- activated receptor ? coactivator-1?. PLoS One. 2011;6: e 269 89.
40. Seale P, Kajimura S, Spiegelman BM. Transcriptional control of brown adipocyte development and physiological function: of mice and men.Genes Dev.2009;23:788-797.

tejido adiposo
tejido adiposo blanco (TAB))
tejido adiposo pardo (TAP)

El carcinoma papilar de tiroides es un tumor frecuente en mujeres y el número de casos nuevos viene en crecimiento. La mayoría de estos casos de novo son tumores menores de 2 centímetros. Parte de la responsabilidad de este aumento es explicable por un uso mayor de ayudas diagnósticas. Esto ha permitido detectar el cáncer de tiroides temprano o clínicamente silente. En esta población, el manejo ha sido típicamente agresivo, incluyendo cirugías extensas (tiroidectomía total) seguidas por terapia con yodo radiactivo y supresión de TSH. Las próximas guías plantearán cuatro grandes modificaciones: 1. Estadificación dinámica del riesgo (respuesta completa, respuesta bioquímica incompleta, respuesta estructural incompleta e indeterminada) 2. Disminución de las indicaciones y de la dosis de ablación con yodo radiactivo, específicamente el uso de esta terapia debe estar ajustado al riesgo basal de recurrencia (bajo, intermedio, alto) del paciente y debe tenerse en cuenta el número de ganglios linfáticos afectados, el tamaño de las metástasis ganglionares, la histología y el tamaño del tumor. Una dosis de 30 mCi de 131yodo es igual de eficaz para negativizar la tiroglobulina que una dosis de 100 mCi. 3. Extensión de la cirugía (cirugía parcial en tumores menores de 4 cm con histología favorable) y 4. Terapia de supresión con levotiroxina con metas más laxas de TSH, dado el riesgo de osteoporosis y arritmias con una supresión exagerada de TSH, especialmente en la población de edad avanzada.

Abstract
Papillary thyroid carcinoma is a frequent cancer in women. An increase in the number of new cases has been detected in the last years. However, tumors smaller than 2 cms represent the largest sample in those new detected cancers. The cause of this increment is partially responsibility of an increased use of diagnostic aids such as ultrasound, even in asymptomatic patients. The management of these clinically silent tumors has been quite aggressive with extensive surgery (total thyroidectomy) followed by radioactive iodine therapy and TSH suppression. The next papillary thyroid carcinoma guidelines will address 4 important modifications: 1. Dynamic approach to risk stratification (Complete response, incomplete biochemical response, incomplete structural response and indeterminate response) 2. Decrease in the indication and dose of radioactive iodine. The use of this therapy must be adjusted to the basal risk of recurrence with consideration of the number of lymph node metastases, the size of the lymph node metastases, the histopathologic variant and the size of the primary tumor. A dose of 30mCi of 131I is as effective as a dose of 100 mCi for thyroid ablation. 3. Extension of the thyroidectomy (partial surgery in tumors smaller than 4 cms without unfavorable histopathology and 4. Higher TSH goal with levothyroxine suppression therapy. A strict TSH suppression has been associated with increased risk of osteoporosis and cardiac arrhythmias, especially in older population.

1. Kweon SS, Shin MH, Chung IJ, Kim YJ, Choi JS. Thyroid cancer is the most common cancer in women, based on the data from population-based cancer registries, South Korea. Japanese journal of clinical oncology. Oct 2013;43(10):1039-1046.
2. Davies L, Welch HG. Current thyroid cancer trends in the United States.JAMA otolaryngology-- head & neck surgery. Apr 2014;140(4):317-322.
3. Ezzat S, Sarti DA, Cain DR, Braunstein GD. Thyroid incidentalomas. Prevalence by palpation and ultrasonography. Archives of internal medicine. Aug 22 1994;154(16):1838-1840.
4. Riesco-Eizaguirre G, Santisteban P. New insights in thyroid follicular cell biology and its impact in thyroid cancer therapy. Endocrine-related cancer. Dec 2007;14(4):957-977.
5. Mehanna H, Al-Maqbili T, Carter B, et al. Differences in the recurrence and mortality outcomes rates of incidental and nonincidental papillary thyroid microcarcinoma: a systematic review and meta-analysis of 21 329 person- years of follow-up. The Journal of clinical endocrinology and metabolism. Aug 2014;99(8):2834-2843.
6. Roh JL, Kim JM, Park CI. Central cervical nodal metastasis from papillary thyroid microcarcinoma: pattern and factors predictive of nodal metastasis. Annals of surgical oncology. Sep 2008;15(9):2482-2486.
7. Shindo M, Wu JC, Park EE, Tanzella F. The importance of central compartment elective lymph node excision in the staging and treatment of papillary thyroid cancer. Archives of otolaryngology--head & neck surgery. Jun 2006;132(6):650-654.
8. So YK, Son YI, Hong SD, et al. Subclinical lymph node metastasis in pap illary thyroid microcarcinoma: a study of 551 resections. Surgery. Sep 2010;148(3):526-531.
9. Wada N, Duh QY, Sugino K, et al. Lymph node metastasis from 259 papillary thyroid microcarcinomas: frequency, pattern of occurrence and recurrence, and optimal strategy for neck dissection. Annals of surgery. Mar 2003;237(3):399-407.
10. American Thyroid Association Guidelines Taskforce on Thyroid N, Differentiated Thyroid C, Cooper DS, et al. Revised American Thyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid : official journal of the American Thyroid Association. Nov 2009;19(11):1167-1214.
11. Mazzaferri EL, Young RL. Papillary thyroid carcinoma: a 10 year follow-up report of the impact of therapy in 576 patients. The American journal of medicine. Mar 1981;70(3):511-518.
12. Mazzaferri EL, Young RL, Oertel JE, Kemmerer WT, Page CP. Papillary thyroid carcinoma: the impact of therapy in 576 patients. Medicine. May 1977;56(3):171-196.
13. Farrar WB, Cooperman M, James AG. Surgical management of papillary and follicular carcinoma of the thyroid. Annals of surgery. Dec 1980;192(6):701- 704.
14. Hay ID, Grant CS, Taylor WF, McConahey WM. Ipsilateral lobectomy versus bilateral lobar resection in papillary thyroid carcinoma: a retrospective analysis of surgical outcome using a novel prognostic scoring system. Surgery. Dec 1987;102(6):1088-1095.
15. Shlossberg AH, Jacobson JC, Ibbertson HK. Serum thyroglobulin in the diagnosis and management of thyroid carcinoma. Clinical endocrinology. Jan 1979;10(1):17-27.
16. Hay ID, Grant CS, van Heerden JA, Goellner JR, Ebersold JR, Bergstralh EJ. Papillary thyroid microcarcinoma: a study of 535 cases observed in a 50- year period. Surgery. Dec 1992;112(6):1139-1146; discussion 1146-1137.
17. Hay ID, Grant CS, Bergstralh EJ, Thompson GB, van Heerden JA, Goellner JR. Unilateral total lobectomy: is it sufficient surgical treatment for patients with AMES low-risk papillary thyroid carcinoma? Surgery. Dec 1998;124(6):958-964; discussion 964-956.
18. Tuttle RM, Leboeuf R, Martorella AJ. Papillary thyroid cancer: monitoring and therapy. Endocrinology and metabolism clinics of North America. Sep 2007;36(3):753-778, vii.
19. Vaisman F, Tala H, Grewal R, Tuttle RM. In differentiated thyroid cancer, an incomplete structural response to therapy is associated with significantly worse clinical outcomes than only an incomplete thyroglobulin response. Thyroid : official journal of the American Thyroid Association. Dec 2011;21(12):1317-1322.
20. Ibrahimpasic T, Nixon IJ, Palmer FL, et al. Undetectable thyroglobulin after total thyroidectomy in patients with low- and intermediate-risk papillary thyroid cancer--is there a need for radioactive iodine therapy? Surgery. Dec 2012;152(6):1096-1105.
21. Nixon IJ, Ganly I, Patel SG, et al. The results of selective use of radioactive iodine on survival and on recurrence in the management of papillary thyroid cancer, based on Memorial Sloan-Kettering Cancer Center risk group stratification. Thyroid : official journal of the American Thyroid Association. Jun 2013;23(6):683-694.
22. Ghossein R, Ganly I, Biagini A, Robenshtok E, Rivera M, Tuttle RM. Prognostic factors in papillary microcarcinoma with emphasis on histologic subtyping: a clinicopathologic study of 148 cases. Thyroid : official journal of the American Thyroid Association. Feb 2014;24(2):245-253.
23. Cady B. Hayes Martin Lecture. Our AMES is true: how an old concept still hits the mark: or, risk group assignment points the arrow to rational therapy selection in differentiated thyroid cancer. American journal of surgery. Nov 1997;174(5):462-468.
24. Hay ID, Bergstralh EJ, Goellner JR, Ebersold JR, Grant CS. Predicting outcome in papillary thyroid carcinoma: development of a reliable prognostic scoring system in a cohort of 1779 patients surgically treated at one institution during 1940 through 1989. Surgery. Dec 1993;114(6):1050-1057; discussion 1057-1058.
25. Shah JP, Loree TR, Dharker D, Strong EW, Begg C, Vlamis V. Prognostic factors in differentiated carcinoma of the thyroid gland. American journal of surgery. Dec 1992;164(6):658-661.
26. Tuttle RM, Tala H, Shah J, et al. Estimating risk of recurrence in differentiated thyroid cancer after total thyroidectomy and radioactive iodine remnant ablation: using response to therapy variables to modify the initial risk estimates predicted by the new American Thyroid Association staging system. Thyroid : official journal of the American Thyroid Association. Dec 2010;20(12):1341-1349.
27. Schlumberger M, Borget I, Nascimento C, Brassard M, Leboulleux S. Treatment and follow-up of low-risk patients with thyroid cancer. Nature reviews. Endocrinology. Oct 2011;7(10):625-628.
28. Schlumberger M, Catargi B, Borget I, et al. Strategies of radioiodine ablation in patients with low-risk thyroid cancer. The New England journal of medicine. May 3 2012;366(18):1663-1673.
29. Mallick U, Harmer C, Yap B, et al. Ablation with low-dose radioiodine and thyrotropin alfa in thyroid cancer. The New England journal of medicine. May 3 2012;366(18):1674-1685.
30. Remy H, Coulot J, Borget I, et al. Thyroid cancer patients treated with 131I: radiation dose to relatives after discharge from the hospital. Thyroid : official journal of the American Thyroid Association. Jan 2012;22(1):59-63.
31. Christensen SB, Ljungberg O, Tibblin S. Surgical treatment of thyroid carcinoma in a defined population: 1960 to 1977. Evaluation of the results after a conservative surgical approach. American journal of surgery. Sep 1983;146(3):349-354.
32. Wanebo H, Coburn M, Teates D, Cole B. Total thyroidectomy does not enhance disease control or survival even in high-risk patients with differentiated thyroid cancer. Annals of surgery. Jun 1998;227(6):912-921.
33. Haigh PI, Urbach DR, Rotstein LE. Extent of thyroidectomy is not a major determinant of survival in low- or high-risk papillary thyroid cancer. Annals of surgical oncology. Jan 2005;12(1):81-89.
34. Lefevre JH, Tresallet C, Leenhardt L, Jublanc C, Chigot JP, Menegaux F. Reoperative surgery for thyroid disease. Langenbeck’s archives of surgery / Deutsche Gesellschaft fur Chirurgie. Nov 2007;392(6):685-691.
35. Alzahrani AS, Al Mandil M, Chaudhary MA, Ahmed M, Mohammed GE. Frequency and predictive factors of malignancy in residual thyroid tissue and cervical lymph nodes after partial thyroidectomy for differentiated thyroid cancer. Surgery. Apr 2002;131(4):443-449.
36. Pacini F, Elisei R, Capezzone M, et al. Contralateral papillary thyroid cancer is frequent at completion thyroidectomy with no difference in low- and high-risk patients. Thyroid : official journal of the American Thyroid Association. Sep 2001;11(9):877-881.
37. Cooper DS, Specker B, Ho M, et al. Thyrotropin suppression and disease progression in patients with differentiated thyroid cancer: results from the National Thyroid Cancer Treatment Cooperative Registry. Thyroid : official journal of the American Thyroid Association. Sep 1998;8(9):737-744.
38. Pujol P, Daures JP, Nsakala N, Baldet L, Bringer J, Jaffiol C. Degree of thyrotropin suppression as a prognostic determinant in differentiated thyroid cancer. The Journal of clinical endocrinology and metabolism. Dec 1996;81(12):4318-4323.
39. Klein Hesselink EN, Klein Hesselink MS, de Bock GH, et al. Long-term cardiovascular mortality in patients with differentiated thyroid carcinoma: an observational study. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. Nov 10 2013;31(32):4046-4053.
40. Wang LY, Smith AW, Palmer FL, et al. Thyrotropin Suppression Increases the Risk of Osteoporosis Without Decreasing Recurrence in ATA Low- and Intermediate-Risk Patients with Differentiated Thyroid Carcinoma. Thyroid: official journal of the American Thyroid Association. Nov 11 2014.
41. Roswarski TE, Murray MD. Supervision of students may protect academic physicians from cognitive bias: a study of decision making and multiple treatment alternatives in medicine. Medical decision making : an international journal of the Society for Medical Decision Making. Mar-Apr 2006;26(2):154-161.
42. Fandel TM, Pfnur M, Schafer SC, et al. Do we truly see what we think we see? The role of cognitive bias in pathological interpretation. The Journal of pathology. Oct 2008;216(2):193-200.

Carcinoma de tiroides
yodo radiactivo
tiroidectomía
TSH
levotiroxina
thyroid carcinoma
radioactive iodine
thyroidectomy
levothyroxine

Ya no contaremos más con la presencia del Dr. Álvaro Duque García. Tuve el privilegio de conocer al Dr. Alvarito en las reuniones de la entonces “Sociedad Colombiana de Endocrinología”, estando inicialmente separados por la distancia geográfica y por más de cuatro generaciones, pues yo vivía en Bogotá y él en Cúcuta.
Recién graduado hizo su medicatura rural, en Ulloa, Valle del Cauca, en una época plagada de violencia. Contaba que se enfrentó entonces a los bandos diciendo que él “no podía participar con uno u otro porque era médico y su deber era con la vida, independientemente del color del trapo que estuviera luciendo el gamonal de turno”.
Hizo su especialización en el Hospital San José de Bogotá, como discípulo del Dr. Antonio Ucrós Cuéllar, graduado 1976 de la Universidad del Rosario. Colaboró con varias de las investigaciones sobre bocio, en Mariquita, en la época donde también asistieron Julio Gómez, Rafael Almanzar y Luis Callejas (qedp). Junto con los doctores Gustavo Sánchez y Antonio Ucrós realizaron un original estudio radiológico de la microangiopatía diabética en el pabellón de la oreja, en 91 pacientes con descripciones detalladas.

endocrinología en Colombia
Dr. Álvaro Duque García

La tiroiditis es un fenómeno inflamatorio de la tiroides, de causas diversas, incluyendo raramente traumas de la región anterior del cuello. Se presenta el caso de un paciente con depresión mayor de curso crónico, con síntomas sicóticos y farmacodependencia, quien intenta suicidarse mediante ahorcamiento. Ingresa con un Glasgow de 3/15, por lo cual requiere intubación orotraqueal inmediata, posterior traslado a unidad de cuidados intensivos y ventilación mecánica durante diez días. Durante este periodo desarrolla taquicardia persistente, diaforesis y alteraciones del sensorio, se encontró TSH en 0,00 (0,4- 4 mUI/ml); una T3 total en 2,42, (0,8-2,0 ng/ml) y T4 libre >6 (0,93-1,70 ng/dL), la gammagrafía de tiroides con tecnecio 99 mostró bloqueo de la captación. Se sospechó tormenta tiroidea y recibió propranolol 80 mg vía oral cada 8 horas en forma continua e hidrocortisona 50 mg intravenosa cada 8 horas durante
5 días. Los controles, dos semanas después, muestran TSH en 0,00 (0,4-4 uUI/ml) y una T4 libre de 1,78 (0,93-1,70 ng/dl) y cuatro días después normalización de la T4 libre (1,45 ng/dl), acompañado de mejoría clínica de los síntomas adrenérgicos.
Se presenta el caso de un paciente con tiroiditis postrauma, entidad que debe ser sospechada en pacientes con trauma en el cuello que presenten síntomas de tirotoxicosis.

Abstract

Thyroiditis is an inflammatory disorder of the thyroid, which stems from a variety of causes including in some rare cases trauma to the neck. We present the case of a male patient with chronic depression associated with psychotic symptoms and drug abuse that tried to commit suicide through hanging. The patient had a Glasgow Coma Scale 3/15 requiring orotracheal intubation, a stay in the intensive care unit and mechanical ventilation for 10 days. While in the ICU the patient developed persistent tachycardia, diaphoresis and changes in mental status. A suppressed TSH was found with a level of 0,00 (0,4-4 uUI/ml) and high thyroid hormone level (total T 2,42, (normal value 0,8-2,0 ng/ml) and free T >6 (normal value 0,93-1,70 ng/dL). A technetium-99 thyroid scintygraphy showed blocked uptake. With those findings, a thyroid storm was suspected and management was begun with propranolol 80 mg per mouth every 8 hours and IV hydrocortisone 50 mg every 8 hours for 5 days. Two weeks later, the TSH was 0,00 (0,4-4 uUI/ ml) and the free T4 was 1,78 (normal value 0,93-1,70 ng/dl). Four days later, the free T4 concentration was normal (1,45 ng/dl) with a clinical improvement of the adrenergic symptoms. Inconclusion, thyroiditis should be suspected in patients with neck trauma with compatible clinical manifestations.

1. Meurisse M, Gollogly L, Degauque C, Fumal I, Defechereux T, Hamoir E. Iatrogenic thyrotoxicosis: causal circumstances, pathophysiology, and principles of treatment-review of the literature. World J Surg. 2000;24(11):1377-85.
2. Blum M, Schloss MF. Martial-arts thyroiditis. N Engl J Med. 1984;311(3):199- 200.
3. Stang MT, Yim JH, Challinor SM, Bahl S, Carty SE. Hyperthyroidism after parathyroid exploration. Surgery. 2005;138(6):1058-64; discussion 64-5.
4. Lederer SR, Schiffl H. Transient hyperthyroidism after total parathyroidectomy for tertiary hyperparathyroidism: a report of two cases.Wien Klin Wochenschr. 2008;120(13-14):432-4. doi: 10.1007/s00508-008-0996-3.
5. Salazar Thieroldt E, Boado Lama J, Molinero Abad S, Miján de la Torre A. Transient hyperthyroidism after total laryngectomy for laryngeal cancer. Nutr Hosp. 2014 Oct 24;31(n01):380-383.
6. Yoon SJ, Kim DM, Kim JU, Kim KW, Ahn CW, Cha BS, et al. A case of thyroid storm due to thyrotoxicosis factitia. Yonsei Med J. 2003;44(2):351-4.
7. Leckie RG, Buckner AB, Bornemann M. Seat belt-related thyroiditis documented with thyroid Tc-99m pertechnetate scans. Clin Nucl Med. 1992;17(11):859-60.
8. Nishihara E, Miyauchi A, Matsuzuka F, Sasaki I, Ohye H, Kubota S, et al. Acute suppurative thyroiditis after fine-needle aspiration causing thyrotoxicosis. Thyroid. 2005;15(10):1183-7.
9. Kobayashi A, Kuma K, Matsuzuka F, Hirai K, Fukata S, Sugawara M. Thyrotoxicosis after needle aspiration of thyroid cyst. J Clin Endocrinol Metab. 1992;75(1):21-4.
10. Carney JA, Moore SB, Northcutt RC, Woolner LB, Stillwell GK. Palpation thyroiditis (multifocal granulomatour folliculitis). Am J Clin Pathol. 1975;64(5):639-47.
11. Ramirez JI, Petrone P, Kuncir EJ, Asensio JA. Thyroid storm induced by strangulation. South Med J. 2004;97(6):608-10.
12. Wartofsky L. Clinical criteria for the diagnosis of thyroid storm. Thyroid. 2012;22(7):659-60.
13. Bergenfelz A, Ahren B. Hyperthyroxinemia after surgery for primary hyperparathyroidism. Langenbecks Arch Chir. 1994;379(3):178-81.
14. Lindblom P, Valdemarsson S, Westerdahl J, Tennvall J, Bergenfelz A. Hyperthyroidism after surgery for primary hyperparathyroidism. Langenbecks Arch Surg. 1999;384(6):568-75.
15. Musi N, Braverman LE, Norris CM, Jr. Severe thyrotoxicosis after parathyroid surgery for hyperparathyroidism. Am J Med. 2000;108(6):519-20.
16. Calle RA, Cohen KL. Transient thyroiditis due to surgical trauma. Am J Med. 1993;95(5):546-8.
17. Yoshida D. Thyroid storm precipitated by trauma. J Emerg Med. 1996;14(6):697-701.
18. Hwang TS, Park SH. Histopathologic study of the so called ‘palpation thyroiditis’. J Korean Med Sci. 1988;3(1):27-9.
19. Jacobs RR. Acute hyperthyroidism precipitated by trauma. South Med J. 1979;72(7):890-1.
20. Doussin JF, Dubost J, Banssillon V. [Post-traumatic hyperthyroxinemia or hyperthyroidism]. Ann Fr Anesth Reanim. 1985;4(1):72-4.
21. Blenke EJ, Vernham GA, Ellis G. Surgery-induced thyroiditis following laryngectomy. J Laryngol Otol. 2004;118(4):313-4.
22. McDermott A, Onyeaka CV, Macnamara M. Surgery-induced thyroiditis: fact or fiction? Ear Nose Throat J. 2002;81(6):408-10.
23. Delikoukos S, Mantzos F. Thyroid storm induced by trauma due to spear fishing-gun trident impaction in the neck. Emerg Med J. 2007;24(5):355-6.
24. Kanbay M, Sengul A, Güvener N. Trauma induced thyroid storm complicated by multiple organ failure. Chin Med J (Engl). 2005;118(11):963-5.
25. Hagiwara A, Murata A, Matsuda T, Sakaki S, Shimazaki S. Thyroid storm after blunt thyroid injury: a case report. J Trauma. 2007;63(3):E85-7.

Tiroiditis
estrangulación
trauma
suicidio
gammagrafía
thyroid scan
suicide
strangulation
Thyroiditis