Los teratomas tiroideos son tumores raros, de características en la mayoría de los casos benignas y de presentación predominantemente en la infancia, su importancia radica en la confusión que causa sobre cuál es el tejido de origen del tumor, por lo que es de vital importancia sospecharlos para evitar demoras en el diagnóstico y manejos inadecuados. Presentamos el caso de un niño de 3 años con teratoma tiroideo benigno, la biopsia por aspirado con aguja fina fue sospechosa de teratoma. Se realizó biopsia por congelación y hemitiroidectomía izquierda, con diagnóstico de teratoma benigno constituido principalmente por elementos condroides. El paciente se encuentra vivo y sin recaídas seis años después del manejo quirúrgico.

Abstract
Thyroid teratomas are very rare tumors, most are benign and usually occur during childhood. The importance of these tumors relies in the common confusion generated by uncertainties about the origin of the lesion. An early diagnosis it is very important to avoid a late management. A case of thyroid benign teratoma in a 3-year-old boy is presented. The fine needle aspiration biopsy was suspicious for this disease. A frozen biopsy followed by left hemithyroidectomy was done and the diagnosis of benign teratoma was confirmed based on the findings of chondroid elements. The patient is alive without recurrence of the disease 6 years after the initial management.

1. Oak CY, Kim HK, Yoon TM, Lim SC, Park HB, Park HC, et al. Benign teratoma of the thyroid gland. Endocrinol Metab (Seoul). 2013;28(2):144-8.
2. Pérez-Mies B, Regojo Zapata RM, García-Fernández E, Serrano MN. Malignant teratoma of the thyroid in a pregnant woman. Ann Diagn Pathol.
2010;14(4):264-7.
3. Mohammad MA. Thyroid cervico-thoracic teratoma in a 14-month old child. Afr J Paediatr Surg. 2010;7(2):117-9.
4. Thompson LD, Rosai J, Heffess CS. Primary thyroid teratomas: a clinicopathologic study of 30 cases. Cancer. 2000;88(5):1149-58.
5. Kim E, Bae TS, Kwon Y, Kim TH, Chung KW, Kim SW, et al. Primary malignant teratoma with a primitive neuroectodermal tumor component in thyroid gland: a case report. J Korean Med Sci. 2007;22(3):568-71.
6. Deb M, Mohanty S, Ananthamurthy A, Garg I, Das K. Atypical extragonadal germ cell tumors. J Indian Assoc Pediatr Surg. 2012;17(1):9-15.
7. LaRiviere CA, Waldhausen JH. Congenital cervical cysts, sinuses, and fistulae in pediatric surgery. Surg Clin North Am. 2012;92(3):583-97, viii.
8. Fan SQ, Liang QC, Jiang Y. Thyroid teratoma in an 11-month-old infant. Int J Surg. 2008;6(6):462-4.
9. Riedlinger WF, Lack EE, Robson CD, Rahbar R, Nosé V. Primary thyroid teratomas in children: a report of 11 cases with a proposal of criteria for their diagnosis. Am J Surg Pathol. 2005;29(5):700-6.
10. Ranaldi R, Morichetti D, Goteri G, Martino A. Immature teratoma of the mediastinum arising in ectopic thyroid tissue: a case report. Anal Quant Cytol Histol. 2009;31(4):233-8.
11. DeLellis R, Lloyd R, Heitz P, C E. World Health Organization Classification of Tumours. Pathology and Genetics of Tumors of Endocrine Organs. Lyon: IARCS Press; 2004.
12. Hazama K, Miyoshi S, Ohta M, Matsuda H. Matured mediastinal teratoma extending into the cervical neck of an adult. Interact Cardiovasc Thorac Surg. 2003;2(3):265-7.
13. Kimler SC, Muth WF. Primary malignant teratoma of the thyroid: case report and literature review of cervical teratomas in adults. Cancer. 1978;42(1):311-7.
14. Zhang YZ, Li WH, Zhu MJ, Li YH, Gao Y. An unusual mature thyroid teratoma on CT and 99Tcm scintigraphy imaging in a child. Pediatr Radiol.
2010;40(11):1831-3.
15. Al-Sobhi S, Bazarbashi S, Al-Jiffry B, Akhtar M, Ingemansson S. Immature teratoma of the thyroid gland: A case report and review of the literature. Ann Saudi Med. 1998;18(3):254-6.
16. Nishihara E, Miyauchi A, Hirokawa M, Kudo T, Ohye H, Ito M, et al. Benign thyroid teratomas manifest painful cystic and solid composite nodules: three case reports and a review of the literature. Endocrine. 2006;30(2):231-6.
17. Martins T, Carrilho F, Gomes L, Mesquita C, Martins MJ, Carvalheiro M. Malignant teratoma of the thyroid: case report. Thyroid. 2006;16(12):1311-3.
18. Tsang RW, Brierley JD, Asa SL, Sturgeon JF. Malignant teratoma of the thyroid: aggressive chemoradiation therapy is required after surgery. Thyroid. 2003;13(4):401-4.
19. Majhi U. Primary malignant teratoma of the thyroid in a child with nodal metastases. Indian J Pathol Microbiol. 2009;52(2):234-6.
20. Craver RD, Lipscomb JT, Suskind D, Velez MC. Malignant teratoma of the thyroid with primitive neuroepithelial and mesenchymal sarcomatous components. Ann Diagn Pathol. 2001;5(5):285-92.

Teratoma
nódulo tiroideo
tiroides
neoplasia
thyroid nodule
thyroid

El panhipopituitarismo (PH) hace referencia a la pérdida total de la función de la hipófisis anterior (adenohipófisis) que incluye los ejes somatótropo, tirótropo, corticótropo, gonadótropo, entre otros. La diabetes insípida central (DIC) no está contemplada en la definición de PH y su asociación simultánea implica la destrucción o degeneración de las neuronas localizadas en los núcleos supraóptico y paraventricular a nivel hipotalámico, es decir, un compromiso más extenso, dicha asociación se ha reportado hasta en 27% de los casos de linfoma primario del sistema nervioso central (LPSNC), la presencia de esta alteración obliga siempre a descartar enfermedades de carácter hematológico, infiltrativo, infeccioso y autoinmune. Presentamos el caso de una paciente de 19 años quien debutó con PH y DIC en la que no se pudo esclarecer un diagnóstico definitivo en su abordaje inicial, luego de casi tres años de evolución, una segunda biopsia realizada a nivel cerebral permitió confirmar el diagnóstico de linfoma primario del SNC. El curso lento y progresivo observado en nuestra paciente es propio de dicha neoplasia; sin embargo, el efecto citorreductor de los corticoides utilizados para el manejo de su déficit hormonal, favoreció el retraso en la identificación de esta enfermedad hematológica.

Abstract
The panhypopituitarism (PH) refers to total loss of function of the anterior pituitary (adenohypophysis), which ultimately can lead to commitment at differents endocrine axes involved at this level. Central diabetes insipidus (CDI) is not covered by the definition of PH and its simultaneous association involves the destruction or degeneration of neurons located in the supraoptic and paraventricular nuclei of the hypothalamus, it means a greater and more extent commitment. We present the case of a 19 years old female who debuted with PH and CDI in which failed to elucidate a definitive diagnosis in its initial approach. Finally, after nearly three years of evolution and a second biopsy performed in the brain the diagnosis of primary central nervous system lymphoma was confirmed.

1. Mohamad M, Cosi G,Genovese E, Manca-Bitti ML,Cohen A, Et all.Central diabetes insipidus in children and young adults.N Engl J Med. 2000 ;( 343):998-1007.
2. Akhtar S, Cheesman E,Jude EB. SIADH and partial hypopituitarism in a patient with intravascular large B-cell lymphoma: a rare cause of a common presentation. BMJ Case Rep. 2013 Jan 28; 2013.
3. Tanriverdi F, Dokmetas HS,Kebapc? N,Kilicli F, Atmaca H, Et all.Etiology of hypopituitarism in tertiary care institutions in Turkish population: analysis of 773 patients from pituitary study group database.Endocrine.2014;( 47):198–205.
4. Toogood AA,Stewart PM.Hypopituitarism: Clinical Features, Diagnosis, and Management. Endocrinol Metab Clin N Am. 2008; (37): 235-261.
5. Giustina A, Gola M, Doga M, Rosei EA. Clinical review 136: Primary lymphoma of the pituitary: an emerging clinical entity. J Clin Endocrinol Metab.2001; (86):4567-4575.
6. Layden BT, Dubner S, Toft DJ, Kopp P, Grimm S, Et al.Primary CNS Lymphoma with Bilateral Symmetric Hypothalamic Lesions Presenting with Panhypopituitarism and Diabetes Insipidus. Pituitary. 2011; 14(2): 194–197.
7. Kasenda B, Haug V, Schorb E, Fritsch K, Finke J, Et al. 18F-FDG PET Is an Independent Outcome Predictor in Primary Central Nervous System Lymphoma. THE JOURNAL OF NUCLEAR MEDICINE. 2013; 54(2):184-91.
8. Braaten KM, Betensky RA, de Leval L, et al. BCL6 expression predicts improved survival in patients with primary central nervous system lymphoma. Clin Cancer Res. 2003;(9):1063-1069.
9. Abla O, Weitzman S, Blay JY, et al. Primary CNS lymphoma in children and adolescents: a descriptive analysis from the International Primary CNS Lymphoma Collaborative Group (IPCG). Clin Cancer Res. 2011;(17):346-352.
10. Mohile NA, DeAngelis LM, Abrey LE. The utility of body FDG PET in staging primary central nervous system lymphoma. Neuro Oncol. 2008;10(2):223-228.
11. Coulter I, Garrioch S ,Toft A. An atypical cause of trigeminal neuralgia and Panhypopituitarism.The British Journal of Radiology.2010; (83): 1087–1089.
12. Singh AD, Lewis H, Schachat AP. Primary lymphoma of the central nervous system. Ophthalmol Clin North Am. 2005; (18): 199-207.
13. Mohile NA, Deangelis LM, Abrey LE. Utility of brain FDG-PET in primary CNS lymphoma. Clin Adv Hematol Oncol. 2008 ;6(11):818-20, 840.
14. Cote TR, Manns A, Hardy CR, Yellin FJ, Hartge P. Epidemiology of brain lymphoma among people with or without acquired immunodeficiency syndrome. AIDS/Cancer Study Group. J Natl Cancer Inst 1996; (88): 675-679.

Panhipopituitarismo
reporte de caso
diabetes insípida central
linfoma primario de sistema nervioso central
panhypopituitarism
Central diabetes insipidus
Primary Central Nervous System Lymphoma
Case report

La creación del radioinmunoanálisis o radioinmunoensayo supuso para la medicina y en especial para la endocrinología un extraordinario avance. Significó un fuerte empuje a la investigación de la diabetes, así como al diagnóstico y tratamiento de problemas hormonales relacionados con el crecimiento, la función tiroidea y la fertilidad. Se utilizó también para prevenir el retraso mental en los recién nacidos con hipotiroidismo. Todo ello se debe en buena medida a la labor desarrollada por Rosalyn Sussman Yalow y Salomon Berson, en los Estados Unidos, y al doctor Ekins, en Inglaterra.

1. Odell WD., Wilber JF., Paul WE. Radioimmunoassay of thyrotropin in human serum. J. Clin. Endocrinol. Metab. 1965. 25(9): 11-79-1188.
2. Berson SA., Yalow RS, Azulay A., Schreiber S., Bernard R., Roswit B. The biological decay curve of P32 tagged erythrocytes; application to the study of acute changes in blood volume. J. Clin. Invest. 1952. Jun, 31 (6): 581-591.
3. Friedman A. Remembrance: The Berson and Yalow Saga. J. Clin Endocrinol. Metab.2002. 87 (5): 1925-1928.
4. Un camp de margarides. L’ultra cara de www.biologiageologia.com Rosalyn Yalow desarrolló el radioinmunoensayo para analizar moléculas biológicas. Dissabte, 21 de febrero 2009.
5. Rosalyn Yalow- Biographical (internet) y Korin M. Dra. Rosalyn Yallow (nternet).
6. Gamez E. Historia del radioinmunoensayo. Dr.Salomon Berson (1918-1972). Un caballero del renacimiento. 12 feb. 2010. Sociedad Mexicana de Nutrición y Endocrinología. Clickderecho.com.mx.
7. Berson SA., Yalow RS., Bauman A., Rothschild MA., Newely K. Insulin I131 metabolism in humans subjects: demonstration of insulin binding globulin in the circulation of insulin treated subjects. J.Clin.Invest. 1956. Feb. 35 (2):170-190.
8. Berson SA-, Yalow RS. General principles of radioimmunossay 1968. Clin. Chim. Acta. 2006 Jul. 23. 369(2): 125-143.
9. Straus E. Rosalyn Yalow Nobel laureate: her life and work in medicine. New York Basic Books, 1990.
10. Reyes-Leal B. Diabetes mellitus. Bases experimentales de nuevos conceptos eti ológicos. Rev.Soc.Endocrinol. 1966. 4(1): 85-95.
11. Tafurt CA., Estrada de R., Garcia J. Niveles de proteína transportadora de hormonas sexuales (PTHS) y de testosterona en el embarazo en relación al sexo fetal. Rev.Soc.Colomb.Endocrinol. 1978. 11: 59-64.
12. Otero-Ruiz. E. Autoinmunidad tiroidea: Recuerdos personales (1957-1962). Medicina (Bogotá) Sept.2011. 33(3): 179-185.

Radioinmunoanálisis
radioinmunoensayo

Objetivo: Describir la relación existente entre el tamaño tumoral y el nivel de prolactina en pacientes con diagnóstico de prolactinoma manejados en el servicio de endocrinología en un centro de atención especializada de Costa Rica.
Diseño: Estudio retrospectivo, observacional y descriptivo con los datos de un único centro.
Marco de referencia: En la evaluación del prolactinoma existe consenso en la correlación entre el nivel de prolactina y el tamaño del adenoma, no obstante, son escasos los reportes sobre la magnitud de esta relación y la posibilidad de establecer una ecuación que genere una aproximación del diámetro tumoral.
Participantes: Se incluyeron los pacientes con diagnóstico de prolactinoma manejados en el servicio de endocrinología de un centro hospitalario costarricense entre los años 2008 y 2014, en quienes se contaba con una medición de prolactina y un estudio por imágenes que lograra determinar la presencia de un adenoma hipofisario.
Intervenciones y mediciones: Para la determinación de prolactina se recurrió al inmunoensayo por electroquimioluminiscencia, y el tamaño tumoral del prolactinoma se definió en estudio por resonancia magnética o tomografía axial computarizada, con un lapso de separación no mayor a seis meses entre ellos.
Resultados: Se reclutaron 32 casos de pacientes con prolactinomas. La edad promedio fue de 32,8 años, con un 75% de mujeres y un 56,2% de macroprolactinomas; el tamaño tumoral promedio fue de 15,6 ± 12,3 mm y la mediana de prolactina de 250,5 ng/mL. Se obtuvo un coeficiente de correlación de Pearson de 0,822 (p<0,001), el cual dio base para la creación de dos fórmulas para la predicción del diámetro mayor de la lesión tumoral corregidas por la edad, la primera para prolactinemias menores de 500 ng/mL y otra para valores iguales o mayores a esta cifra.
Conclusiones: El presente estudio permitió desarrollar dos ecuaciones mediante las cuales se puede predecir el diámetro mayor tumoral aproximado a partir del valor inicial hormonal.

Abstract
Introduction: In the clinical evaluation of patients with prolactinomas, there is a consensus on the literature regarding the correlation between prolactin levels and tumor size; however, there are few reports that detail about the magnitude of this relationship and the possibility of establishing an equation that may estimate the adenoma diameter.
Material and methods: We conducted a retrospective, observational and descriptive study with data from a single center, which intended to verify the relationship between tumor size and prolactinemia. All of the included patients had measurements for prolactin blood levels and pituitary imaging with at least one diameter measurement of the adenoma.
Measurements and interventions: prolactin blood levels were determined by electrochemicaluminiscense immunoassay, and the size of the adenoma was defined by magnetic resonance imaging or computerized axial tomography scan, each study taken within a maximum of 6 months.
Results: Thirty-two cases of patients with prolactinomas were assessed. The average age of the patients was of 32,8 ± 13,1 years, 75% were women and 56,2% were diagnosed with a macroprolactinoma. Mean tumor size was of 15,6 ± 12,3 mm and the median of prolactin level was 250,5 ng/mL. We report a Pearson’s correlation coefficient of 0,82 (p<0,001), showing a strong positive linear association between the prolactinemia and the tumor size. Through multiple linear regression analysis, we obtained two equations that allowed the prediction of the adenoma diameter given the prolactin level, adjusted by age.
Conclusion: We developed two equations that allowed us to estimate the largest tumoral diameter given the prolactin blood levels.

1. Chen-Ku C. Guías para el diagnóstico y tratamiento de acromegalia, prolactinomas y enfermedad de Cushing. Acta Médica Costarricense 2004; 46(1) 25-36.
2. Iglesias P et Diez J. Macroprolactinoma: a diagnostic and therapeutic update. QMJ 2013: 106(6) 495-504.
3. Klibanski A. Prolactinomas. New England Journal of Medicine 2010; 362: 1219-1222.
4. Rabinovich H. Clinical guidelines for diagnosis and treatment of prolactinoma and hyperprolactinemia. Endocrinología y Nutrición 2013; 60(6)
308-319.
5. Glezer A et Bronstein M. Prolactinomas. Endocrinology and Metabolism Clinics of North America 2015; 44(2): 71-78.
6. Iglesias P, Bernal C, Villabona C, Castro JC, Arrieta F, Díez J. Prolactinomas in men: a multicenter and retrospective analysis of treatment outcome. Clinical Endocrinology (Oxford) 2012; 77(2): 281-287.
7. Kars M. Update in prolactinomas. Netherlands: The Journal of Medicine 2010; 60(3): 104-112.
8. Colao A. The prolactinoma. Best Practice & Research: Clinical Endocrinology & Metabolism 2009; 23 (5): 575-596.
9. Cander, S. et al. Prolactin levels are correlated with tumor size and invasiveness in prolactinomas. Endocrine Abstracts 2012, 29: 1485.
10. Colao A, Sarno A, Cappabianca P, Briganti F, Pivonello R, Somma C, et al. Gender differences in the prevalence, clinical features and response to cabergoline in hyperprolactinemia. European Journal of Endocrinology 2003; 148 (3): 325-331.
11. Molitch M. Pharmacologic Resistance in Prolactinoma Patients. Pituitary 2005; 8:43-52.
12. Frieze, T. Mong, D. Koops, M. “Hook effect” in prolactinomas: case report and review of literature. Endocr Pract. 2002; 8 (4): 296-303.
13. Glezer, A. Brasil, C. Delano, M. Vieira, J. Macroprolactina e Incidentaloma Hipofisário. Arq Bras Endocrinol Metab. 2001; 45 (2): 190-198.

Prolactina
hiperprolactinemia
pro lactinoma
adenoma hipofisario
infertilidad
galactorrea
prolactin
hyperprolactinemia
prolactinoma
pituitary adenoma

Introducción: El pie diabético es un problema de salud pública debido a su elevada frecuencia, severidad y a su impacto económico. En la etapa prepatogénica, el pie presenta alteraciones funcionales y estructurales que de no detectarse a tiempo pueden progresar a la úlcera. Sin embargo, el examen de los pies no se realiza en la mayoría de las consultas. La prevención primaria y la detección oportuna deben tener lugar en el primer nivel de atención.
Objetivo: Desarrollar y validar un instrumento simple y práctico para clasificar de manera temprana el pie del paciente diabético en riesgo por parte de la enfermera entrenada antes de la visita a su médico tratante, teniendo en cuenta todos los elementos patogénicos.
Métodos: Estudio transversal. Se creó una escala a partir de la experiencia clínica en donde se califican ocho factores de riesgo para desarrollar ulceración: tiempo de diabetes desde el diagnóstico, control metabólico, presencia de síntomas de neuropatía diabética, diagnóstico de la neuropatía por monofi- lamento, presencia de claudicación intermitente y ausencia de pulsos periféricos, presencia de deformidades, presencia de infecciones locales e historia anterior de úlceras que sanaron, amputaciones menores o pie de Charcot. Los puntajes fueron asignados según gravedad. Esta herramienta fue aplicada a un grupo de 204 diabéticos con ulceración y 207 pacientes diabéticos sin ulceración.
Resultados: El promedio de edad fue de 65 años, el 42,8% de los pacientes eran hombres. La edad y todos los ítems de la escala, excepto hemoglobina glucosilada, fueron asociados con la presencia de úlcera. Usando un punto de corte de 10 puntos, la herramienta tuvo una sensibilidad del 100% y una especificidad del 73,4% para el diagnóstico de úlcera, con un área bajo la curva ROC de 0,992(IC 95%, 0,986 A 0,998).
Conclusión: La herramienta “pie risk” es útil para la calificación y valoración del riesgo de pie diabético.

Abstract
Background: The diabetic foot is a public health problem due to its frequency, severity and economic impact. In prepathogenic phases, the foot presents structural and functional alterations that, if not detected opportunely, will progress to an ulcer. However, a thorough examination of the diabetic patient’s feet is often eluded in routine health controls.
Objective: To develop and validate a simple and practical instrument for early classification of the diabetic foot risk that can be easily applied by a trained nurse before the medical visit.
Methods: Cross-sectional study. Based on clinical expertise, a scale with eight risk factors for foot ulcer was developed: time from diagnosis, glycosylated hemoglobin, neuropathy symptoms, monofilament test, absent pulses or claudication; deformities, local infection and history of either amputation, ulceration or Charcot foot. Item scores were assigned based on severity. The tool was tested in a group of 204 ulcerated diabetic patients and 207 of non-ulcerated diabetic patients.
Results: Median age was 65 years, 42.8% of patients were male. Age and all scale items except glycosylated hemoglobin were statically associated with ulcer presence. Using the proposed cut point of 10 points, the scale has 100% sensitivity and73.4% specificity for ulcer diagnosis, with an area under the ROC curve of 0.992 (95% CI 0.986 to 0.998).
Conclusions: ‘Pie risk’ is a useful tool for the evaluation and risk assessment of the diabetic patient.

1. International Consensus on the diabetic foot. Interactive version by the international Working group on the diabetic foot. A consultative section of the International Diabetes Federation 2011, Available from : http:// www. iwgdf.org.
2. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin dependent diabetes mellitus. N Engle J Med, 1993;329;977-86.
3. United Kingdom Prospective Diabetes Study Group. Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. Lancet 1998;352:837-53.
4. Aschner et al, Guias ALAD de diagnostico, control y tratamiento de la diabetes y sus complicaciones. Revista ALAS 2006 ; 4(3):1-78. Med 1994 : 11-166-169.
5. Aschner PJ, Ruiz AJ, Metabolic memory for vascular disease in Diabetes. Diabetes thecnol.Ther, 2012 Jun; 14 Suppl 1:s68-74.doi:10.1089/ dia.2012.0012.
6. Ragnarson Tennvall G, Apelqvist J. Health-related quality of life in patients with diabetes mellitus and foot ulcers. J Diabetes Complications [Internet]. 2000 Sep [cited 2015 Aug 26];14(5):235–41. Available from: http://linkin- ghub.elsevier.com/retrieve/pii/S1056872700001331.
7. Demet K, Martinet N, Guillemin F, Paysant J, André J-M. Health related quality of life and related factors in 539 persons with amputation of upper and lower limb. Disabil Rehabil [Internet]. Taylor & Francis; 2003 Jan 11 [cited 2015 Aug 26];25(9):480–6. Available from: http://www.tandfonline.com/ doi/full/10.1080/0963828031000090434.
8. Gilbert MP. Screening and Treatment by the Primary Care Provider of Common Diabetes Complications. Med Clin North Am [Internet]. 2015 Jan;99(1):201–19. Available from: http://linkinghub.elsevier.com/retrieve/pii/S0025712514001503
9. McCulloch DK. Evaluation of the diabetic foot. In: Post TW, editor. UpToDate [Internet]. Waltham, MA; 2014. Available from: http://www.uptodate.com/ contents/evaluation-of-the-diabetic-foot.
10. Weintrob AC, Sexton DJ. Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities. In: Post TW, editor. UpToDate [Internet]. Waltham, MA; 2014. Available from: http://www.uptodate.com/contents/clinical-manifestations-diagnosis-and-management- of-diabetic-infections-of-the-lower-extremities.
11. Alayón AN, Altamar-López D, Banquez-Buelvas C, Barrios-López K. Complicaciones crónicas, hipertensión y obesidad en pacientes diabéticos en Cartagena, Colombia. Rev Salud Pública (Bogota) [Internet]. 2009 Dec [cit- ed 2015 Aug 18];11(6):857–64. Available from: http://www.ncbi.nlm.nih. gov/pubmed/20379659.
12. Villegas Perrasse A, Abad SB, Faciolince S, Hernández N, Maya C, Parra L, et al. El control de la diabetes mellitus y sus complicaciones en Medellín, Colombia, 2001–2003. Rev Panam Salud Publica. 2006;20(6):393–402.
13. Pinilla AE, Sánchez AL, Mejía A, del Pilar Barrera M. Primary-care prevention activities in outpatients suffering from diabetic foot care. Rev Salud Pública [Internet]. Instituto de Salud Publica, Faculdad de Medicina - Universidad Nacional de Colombia; [cited 2015 Aug 27];13(2):262–73. Available from: http://www.scielosp.org/scielo.php?script=sci_arttext&pid=S0124- 00642011000200008&lng=en&nrm=iso&tlng.
14. Mythili A, Kumar KD, Subrahmanyam KA V, Venkateswarlu K, Butchi RG. A Comparative study of examination scores and quantitative sensory testing in diagnosis of diabetic polyneuropathy. Int J Diabetes Dev Ctries [Internet].
2010 Jan [cited 2015 Aug 26];30(1):43–8. Available from: http://www. pubmedcentral.nih.gov/articlerender.fcgi?artid=2859284&tool=pmcentre z&rendertype=abstract.
15. Peters EJ, Lavery LA. Effectiveness of the diabetic foot risk classification system of the International Working Group on the Diabetic Foot. Diabetes Care [Internet]. 2001 Aug [cited 2015 Aug 27];24(8):1442–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11473084.
16. Júbiz Y, Brugés J, Orduz A, Bohórquez L, Calderón C, Díaz A, Escobar I, et al. Guías colombianas para la prevención, diagnóstico y tratamiento del pie diabético: un manejo integral [Internet]. 1st ed. Bogotá: COLPEDIS Grupo Colombiano de Pie Diabético; 2012. 96 p. Available from: http://issuu.com/ presidenciafdc/docs/guias_pie_diabetico.
17. Jirkovská A, Bou?ek P, Wosková V, Bartoš V, Skibová J. Identification of patients at risk for diabetic foot: A comparison of standardized noninvasive testing with routine practice at community diabetes clinics. J Diabetes Complications. 2001;15(2):63–8.
18. Brownrigg JRW, Hinchliffe RJ, Apelqvist J, Boyko EJ, Fitridge R, Mills JL, et al. Effectiveness of bedside investigations to diagnose peripheral artery disease among people with diabetes mellitus: a systematic review [Internet]. London: International Working Group on the Diabetic Foot; 2015. p. 26. Available from: http://www.iwgdf.org/files/2015/PADdi- agnosis.pdf.
19. Driver VR, Fabbi M, Lavery LA, Gibbons G. The costs of diabetic foot: the economic case for the limb salvage team. J Vasc Surg [Internet]. Elsevier; 2010 Sep 9 [cited 2015 Apr 21];52(3 Suppl):17S – 22S. Available from: http:// www.jvascsurg.org/article/S0741521410013248/fulltext.
20. Tsourdi E, Barthel A, Rietzsch H, Reichel A, Bornstein SR. Current aspects in the pathophysiology and treatment of chronic wounds in diabetes mellitus [Internet]. BioMed Research International. 2013. p. 6. Available from: http://dx.doi.org.10.1144/2013/385641.
21. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJG, Armstrong DG, et al. 2012 infectious diseases society of America clinical practice guideline for the diagnosis and treatment of diabetic foot infections. Clinical Infectious Diseases. 2012. p. 1679–84.
22. Monteiro-Soares M, Boyko EJ, Ribeiro J, Ribeiro I, Dinis-Ribeiro M. Predictive factors for diabetic foot ulceration: A systematic review. Diabetes/Metabolism Research and Reviews. 2012. p. 574–600.
23. American Diabetes Association. Microvascular complications and foot care. Diabetes Care [Internet]. 2015;38(Suppl 1):S58–66. Available from: http:// care.diabetesjournals.org/content/38/Supplement_1/S58.full.
24. Dorresteijn J a N, Kriegsman DMW, Valk GD. Complex interventions for preventing diabetic foot ulceration. Cochrane Database Syst Rev.
2010;(1):CD007610.
25. Dorresteijn JAN, Kriegsman DMW, Assendelft WJJ, Valk GD. Patient education for preventing diabetic foot ulceration. Cochrane database Syst Rev [Internet]. 2014 Jan [cited 2015 Jul 28];12:CD001488. Available from: http:// www.ncbi.nlm.nih.gov/pubmed/25514250.
26. National Institute for Health and Care Excellence. Diabetic foot problems: prevention and management [Internet]. 2015. 46 p. Available from: nice. org.uk/guidance/ng19.
27. Fan L, y col , Feasibility, Acceptability and Effects of a Foot Self-Care Educa- tional Interventionon Minor Foot Problems in Adult Patients with Diabetes at Low Risk for Foot Ulceration: A Pilot Study . Canadian journal of diabetes. March 2013.Journal homepage: www.canadianjournalofdiabetes.com
28. Corbett C. y col . A rambdomized pilot study of improving foot care in home health patients with diabetes. The diabetes educator , vol 29 ,number 2, March 2003.

Pie diabético
evaluación del riesgo
prevención primaria
enfermera entrenada
equipo de atención en salud
Diabetic Foot
Risk Assessment
Primary Prevention
Nurse Practitioners
Patient Care Team

Introducción: Las úlceras del pie son frecuentes en las personas con diabetes. Conocer los factores del comportamiento, y su relación con los factores biológicos y del ambiente puede favorecer el entendimiento de esta patología y sentar las bases para su intervención.
Métodos: Se realizó un estudio de casos y controles para determinar los factores asociados a la ocurrencia de úlceras en pacientes diabéticos. Los participantes fueron personas que asisten a una institución hospitalaria de nivel II y a una institución de nivel III de la ciudad de Cali. Los casos fueron pacientes diabéticos hospitalizados con diagnóstico de úlcera de miembros inferiores con o sin sobreinfección, y los controles pacientes hospitalizados con diagnóstico de diabetes pero sin úlceras.
Resultados: Se encontró en el análisis por regresión logística múltiple que hubo factores biológicos asociados a úlcera de miembros inferiores como la neuropatía periférica (OR: 3,95; IC: 2,01 – 7,71) y la presencia de dolor o calambres en las piernas (OR: 2,31; IC: 1,05 – 5,09), factores del comportamiento como no revisar nunca o revisar los pies una vez al mes (OR 2,78; IC: 1,16 -6,64) y factores del contexto social que fueron protectores como ir al parque a caminar o hacer ejercicio (OR 0,76; IC: 0,56- 1,04) y participar con frecuencia como voluntario en organizaciones locales como juntas de acción comunal, juntas de acción local (OR 0,68; IC: 0,44 – 1,07).
Discusión: El desarrollo de úlceras en los miembros inferiores tiene una base clínica ampliamente conocida, pero además se asocia a factores del comportamiento y del contexto social que implican autocuidado, adherencia, y dentro del modelo de creencias en salud claves para la acción y beneficios percibidos indirectos que deben evaluarse integralmente para impactar en la prevalencia y las complicaciones de esta patología.

Summary
Introduction: Foot ulcers are common in people with diabetes. Knowing behavioral factors and their relationship with biological and environmental factors can foster understanding of this disease, and set the stage for its intervention.
Methods: A study of cases and controls was conducted in order to determine the factors associated with the occurrence of ulcers in diabetic patients. Participants were people attending a Level 2 hospital and a Level 3 institution in the city of Cali. The cases were hospitalized diabetic patients diagnosed with lower limb ulcer with or without superinfection, and controls of hospitalized patients diagnosed with diabetes but without ulcers.
Results: In the analysis, it was found that biological factors were associated with lower limb ulcers and peripheral neuropathy by multiple logistic regression (OR: 3.95; IC: 2.01 – 7.71) and the presence of pain or cramps in the legs (OR: 2.31; IC: 1.05 –5.09), behavioral factors such as never checking or checking the feet once a month (OR 2.78; IC: 1.16 -6.64) and social context factors which were protective such as going to the park to walk or exercise (OR 0.76; IC: 0.56- 1.04) and frequently participate as a volunteer in local organizations such as communal action boards, local action boards (OR 0.68; IC: 0.44 – 1.07).
Discussion: The development of ulcer in the lower limbs has a well-known clinical basis, but also, it is associated with behavioral and social context factors which involve self-care, adherence, and within the model of key health beliefs for action and indirect benefits received that must be fully evaluated to decrease the prevalence and complications of this disease.

1. Association AD. Classification and Diagnosis of Diabetes. Diabetes Care 2015;38:S8–16.
2. Soto C, Vergara W, Neciosup P. Prevalencia y factores de riesgo de sindrome metabolico en poblacion adulta del departamento de lambayeque, Peru - 2004. Rev Peru Med Exp Salud Publica 2005;22:254–61.
3. Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. Jama 2015;314:1021– 9.
4. Barceló A, Rajpathak S. Incidence and prevalence of diabetes mellitus in the Americas. Rev Panam Salud Publica 2001;10:300–8.
5. Buckley R. South and Central America. Int Diabetes Fed 2015:86–9.
6. Ulbrecht JS, Cavanagh PR, Caputo GM. Foot problems in diabetes: an over view. Clin Infect Dis 2004;39 Suppl 2:S73–82.
7. Clayton W, Elcasy T. A review of the pathophysiology, classification and treatment of foot ulcers in diabetics patients. Clin Diabetes 2009;27:52–8.
8. Sumpio BE. FOOT ULCERS. N Engl J Med 2000;343:787–93.
9. Potier L, Abi Khalil C, Mohammedi K, Roussel R. Use and utility of Ankle brachial index in patients with diabetes. Eur J Vasc Endovasc Surg 2011;41:110–6.
10. Hokkam EN. Assessment of risk factors in diabetic foot ulceration and their impact on the outcome of the disease. Prim Care Diabetes 2009;3:219–24.
11. Rocha R, Zanetti ML, Dos Santos MA. Behavior and knowlege?: basis for prevention of diabetic foot *. Acta Paul Enferm 2009;22:17–23.
12. Crawford F, Mccowan C, Dimitrov BD, Woodburn J, Wylie GH, Booth E, et al. The risk of foot ulceration in people with diabetes screened in community settings: Findings from a cohort study. Qjm 2011;104:403–10. doi:10.1093/ qjmed/hcq227.
13. Ciechanowski PS, Katon WJ, Russo JE. Depression and diabetes: impact of depressive symptoms on adherence, function, and costs. Arch Intern Med 2000;160:3278–85.
14. Dorresteijn JAN, Kriegsman DMW, Assendelft WJ, Valk GD. Patient education for preventing diabetic foot ulceration. Cochrane Database Syst Rev
2010:1–48. doi:10.1002/14651858.CD001488.pub3.
15. Eakin EG, Reeves MM, Bull SS, Riley KM, Floyd S, Glasgow RE. Validation of the Spanish-language version of the chronic illness resources survey. Int J Behav Med 2007;14:76–85.
16. Lavery L, Hunt N, Lafontaine J, Baxter C, Ndip A, Boulton A. Diabetic Foot Prevention. Diabetes Care 2010;33:1460–2.
17. Lustman PJ, Anderson RJ, Freedland KE, De Groot M, Carney RM, Clouse RE. Depression and poor glycemic control: A meta-analytic review of the literature. Diabetes Care 2000;23:934–42. doi:10.2337/diacare.23.7.934.
18. Suico JG, Marriott DJ, Vinicor F, Litzelman DK. Behaviors Predicting Foot Lesions in Patients with Non-Insulin-Dependent Diabetes Mellitus. J Gen Intern Med 1998;13:482–4.
19. Glasgow Russell E FE. Behavioral Science in Diabetes Contributions and opportunities. Diabetes Care 1999;22:832–43.
20. Hosmer D, Lemshow S. Applied Logistic Regression. 2002.

Pie diabético
Diabetic foot

Estudios epidemiológicos y estadísticas de cada país muestran un aumento en la prevalencia de la diabetes en el mundo. Recientes informes y datos epidemiológicos estiman que para el año 2030, 552 millones de personas tendrán diabetes y estos, por lo tanto, estarán en riesgo de desarrollar complicaciones macrovasculares y microvasculares. La retinopatía diabética (RD) es una de las complicaciones microvasculares que potencialmente desarrollan estos pacientes, la cual puede llevar a ceguera y, por tanto, deteriorar la calidad de vida, sobre todo en personas en edad productiva, generando un impacto en su entorno familiar y social. El propósito de este trabajo es realizar una revisión de los datos disponibles sobre la prevalencia de diabetes y de algunos de los estudios epidemiológicos más importantes de la retinopatía diabética. La importancia del tema radica en lograr un diagnóstico temprano de la patología retiniana para realizar una intervención oportuna en los factores de riesgo y disminuir así la progresión de la enfermedad.

Abstract
Epidemiological studies and statistics reports from countries have shown that the prevalence of diabetes is increasing worldwide. Recent reports and epidemiological data estimate that more than 552 million people will be affected by diabetes by 2030, and those affected will therefore be at risk of developing macrovascular and microvascular complications. Diabetic retinopathy is a microvascular complication which can lead to blindness and thus impair the quality of life, especially in the working-age population and a subsequent impact on family and social environment. The objective of this paper is to review available data on the prevalence of diabetes and some epidemiological studies of diabetic retinopathy. The importance of the issue is to obtain an earlier diagnosis for an intervention in risk factors resulting in a slower progression of the disease.

1. Mbanya, J, Ben-Nakhi, A, Borch-Johnsen, K. Federación Internacional de Diabetes (FID), Plan mundial contra la diabetes 2011 – 2021, reunión de expertos de la septiembre de 2010. Pag.1-5.
2. Simó R, Hernández C. Novel approaches for treating diabetic retinopathy based on recent pathogenic evidence. Prog Retin Eye Res. 2015 Sep;48:160–80.
3. Diabetic Retinopathy PPP - 2014, OCT 2014 from AAO Retina/Vitreous PPP panel, Hoskins Center for Quality Eye Care.
4. OMS. Diabetes mellitus. Hoja de datos N° 138, Abril 2002 Diabetes: El coste de la diabetes. Hoja de datos N° 236, Sept. 2002 www.who.int/mediacentre/ factsheets
5. Federación Internacional de Diabetes, Atlas de la diabetes de la FID, 2013, Sexta edición. Páginas 9 – 17. www.idf.org/diabetesatlas
6. Harjutsalo V, Forsblom C, Groop P-H. Time trends in mortality in patients with type 1 diabetes: nationwide population based cohort study. BMJ. 2011;343:364.
7. Miller RG, Secrest AM, Sharma RK, Songer TJ, Orchard TJ. Improvements in the life expectancy of type 1 diabetes: the Pittsburgh Epidemiology of Diabetes Complications study cohort. Diabetes. 2012;61(11):2987–92.
8. Writing Group for the DCCT/EDIC Research Group, Orchard TJ, Nathan DM, Zinman B, Cleary P, Brillon D, et al. Association between 7 years of intensive treatment of type 1 diabetes and long-term mortality. JAMA. 2015; 313(1):45–53.
9. Litwak L, Goh S-Y, Hussein Z, Malek R, Prusty V, Khamseh ME. Prevalence of diabetes complications in people with type 2 diabetes mellitus and its association with baseline characteristics in the multinational Archieve study. Diabetol Metab Syndr. 2013; 5(1):57.
10. White, Neil H. Long-term Outcomes in Youths witj Diabetes Mellitus, Pediatr Clin North Am 2015; 62 (4)889-909.
11. Fangueiro JF, Silva AM, Garcia ML, Souto EB. Current nanotechnology approaches for the treatment and management of diabetic retinopathy. Eur J Pharm Biopharm Off J Arbeitsgemeinschaft Für Pharm Verfahrenstechnik EV. 2015; (95):307–22.
12. Wan T-T, Li X-F, Sun Y-M, Li Y-B, Su Y. Recent advances in understanding the biochemical and molecular mechanism of diabetic retinopathy. Biomed Pharmacother Bioméd Pharmacothérapie. 2015;74:145–7
13. Wu L, Fernandez-Loaiza P, Sauma J, Hernandez-Bogantes E, Masis M. Classification of diabetic retinopathy and diabetic macular edema. World J Diabetes. 2013 Dec 15;4(6):290–4.
14. Ciulla TA, Amador AG, Zinman B. Diabetic Retinopathy and Diabetic Macular Edema Pathophysiology, screening, and novel therapies. Diabetes Care. 2003;26(9):2653–64.
15. Zheng, Y., He, M., & Congdon, N. The worldwide epidemic of diabetic retinopathy, Indian J Ophthalmol 2012; 60(5), 428.
16. Von-Bischhoffshausen, F. B., & Castro, F. M. Guía práctica clínica de retinopatía diabética para latinoamérica. Revista Médico Oftalmólogo, 2011.
17. Lagani, V., Chiarugi, F., Thomson, S., Fursse, J. Development and validation of risk assessment models for diabetes-related complications based on the DCCT/EDIC data. J Diabetes Complications, 2015; 29(4):479-487.
18. Limburg H, von-Bischhoffshausen FB, Gomez P, Silva JC, Foster A. Review of recent surveys on blindness and visual impairment in Latin America. Br J Ophthalmol. 2008 Mar 1;92(3):315–9.
19. Varma R, Torres M, Peña F, Klein R, Azen SP, Los Angeles Latino Eye Study Group. Prevalence of diabetic retinopathy in adult Latinos: the Los Angeles Latino eye study. Ophthalmol. 2004;111(7):1298–306.
20. Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care.
2004;27(5):1047–53.
21. Klein, R., Klein, B. E., Moss, S. E., Davis, M. D., & DeMets, D. L. The Wisconsin Epidemiologic Study of Diabetic Retinopathy: III. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Arch Ophthalmol, 1984;(4), 527-532.
22. The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the diabetes control and complications trial. Diabetes. 1995;(8):968–83.
23. Nathan DM, DCCT/EDIC Research Group. The diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: overview. Diabetes Care. 2014;37(1):9–16.
24. Hendrick AM, Gibson MV, Kulshreshtha A. Diabetic Retinopathy. Prim Care. 2015 Sep;42(3):451–64.
25. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet Lond Engl. 1998;(9131):837–53.
26. Nordwall M, Abrahamsson M, Dhir M, Fredrikson M, Ludvigsson J, Arnqvist HJ. Impact of HbA1c, followed from onset of type 1 diabetes, on the development of severe retinopathy and nephropathy: the VISS Study (Vascular Diabetic Complications in Southeast Sweden). Diabetes Care. 2015;38(2):308– 15.
27. Goff DC, Gerstein HC, Ginsberg HN, Cushman WC, Margolis KL, Byington RP, et al. Prevention of cardiovascular disease in persons with type 2 diabetes mellitus: current knowledge and rationale for the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. Am J Cardiol. 2007;18;99(12):4 – 20.
28. Patel.A, MacMahon.S, Chalmers.J, Intensive Blood Glucose Control and Vascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2008;12;358(24):2560–72.
29. Bailey .K, Gohdes.D, Haffner.S, Hiss.R. Effects of Intensive Glucose Lowering in Type 2 Diabetes. N Engl J Med. 2008 Jun 12;358(24):2545–59Lyons TJ, Jenkins AJ, Zheng D, Lackland DT, McGee D, Garvey WT, et al. Diabetic retinopathy and serum lipoprotein subclasses in the DCCT/EDIC cohort. Invest Ophthal- mol Vis Sci. 2004;45(3):910–8.
30. Lyons, T. J., Jenkins, A. J., Zheng, D., Lackland, D. T., McGee, D., Garvey, W. T., & Klein, R. L. (2004). Diabetic retinopathy and serum lipoprotein subclasses in the DCCT/EDIC cohort. Investigative ophthalmology & visual science, 45(3), 910-918.
31. Gardner TW, Sander B, Larsen ML, Kunselman A, Tenhave T, Lund-Andersen H, et al. An extension of the Early Treatment Diabetic Retinopathy Study (ET- DRS) system for grading of diabetic macular edema in the Astemizole Retinopathy Trial. Curr Eye Res. 2006;31(6):535–47.
32. Keech, AC; Mitchell, P; Summanen, PA; O’Day, J; Davis, TME et al .Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomised controlled trial. The Lancet. 2007;370 (9600)1687- 1697.

Retinopatía diabética
epidemiología
patogénesis
clasificación de retinopatía diabética
factores de riesgo
complicaciones de la diabetes
diabetic retinopathy
epidemiology
pathogenesis
Diabetic retinopathy classification
risk factors
diabetes complications

Es muy grato para mí, como endocrinóloga y cartagenera, darles la bienvenida a este magno evento, nuestro VI Curso Internacional de Endocrinología, Diabetes y Metabolismo, donde podremos conjugar el deber con el placer.

La consolidación de este curso como un evento que convoca la asistencia masiva de médicos generales y especialistas afines nos impone la necesidad ineludible de mantener la actualización como atractivo principal y, por ende, la extensión de las fronteras de lo conocido, interactuando con otras especialidades, retroalimentándonos mutuamente para el bien de nuestros pacientes.

VI Curso Internacional de Endocrinología, Diabetes y Metabolismo

Se presenta el caso de un paciente con diagnóstico de novo de hipopituitarismo, cuya manifestación inicial fue con hiponatremia grave, secundaria a una insuficiencia suprarrenal central. Adicionalmente se documentó hipotiroidismo e hipogonadismo centrales. El paciente tuvo una lesión cerebral traumática cuatro décadas atrás y se encontraron en la resonancia nuclear de hipófisis hallazgos de hipoplasia hipofisaria y aracnoidocele selar, apoyando el diagnóstico de hipopituitarismo anterior. El caso resalta la presentación de hipopituitarismo diagnosticado décadas después de una lesión cerebral traumática. Se propone un enfoque para el diagnóstico, tratamiento y seguimiento de estos pacientes en nuestro medio.

Abstract
We present the case of a patient with previously undiagnosed hypopituitarism, it presents whose initial manifestation was a severe hyponatremia secondary to a central adrenal insufficiency, and besides this deficit he had central hypothyroidism and hypogonadism. In his past medical history he had a moderate traumatic brain injury almost 40 years before. The case highlights the presentation of hypopituitarism decades after a traumatic brain injury. An approach to the diagnosis, treatment and follow-up of these patients in our environment is proposed.

1. Coronado VG, Xu L, Basavaraju SV, et al. Surveillance for traumatic brain injury-related deaths--United States, 1997-2007. MMWR SurveillSumm. 2011; 60:1-32.
2. Schneider HJ, Kreitschmann-Andermahr I, Ghigo E, Stalla GK, Agha A. Hy- pothalamus pituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review. JAMA. 2007; 298: 1429-1438.
3. Agha A, Rogers B, Sherlock M, et al. Anterior pituitary dysfunction in survivors of traumatic brain injury. J ClinEndocrinolMetab. 2004; 89(10):4929–4936.
4. Aimaretti G, Ambrosio MR, Di Somma C, et al. Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study. J ClinEndocrinolMetab. 2005; 90(11):6085–6092.
5. Schneider HJ, Schneider M, Saller B, et al. Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury. Eur J Endocrinol. 2006; 154(2):259–265.
6. Tanriverdi F, Senyurek H, Unluhizarci K, Selcuklu A, Casanueva FF, Kelestimur F. High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma. J ClinEndocrinolMetab. 2006;91(6): 2105–2111.
7. Tanriverdi F, Ulutabanca H, Unluhizarci K, Selcuklu A, Casanueva FF, Kele- stimur F. Three years prospective investigation of anterior pituitary function after traumatic brain injury: a pilot study. ClinEndocrinol (Oxf ). 2008; 68(4):573–579.
8. Tanriverdi F, De Bellis A, Ulutabanca H, et al. A five year prospective investigation of anterior pituitary function after traumatic brain injury: is hypopituitarism long-term after head trauma associated with autoimmunity? J Neurotrauma. 2013; 30(16):1426–1433.
9. Lauzier F, Turgeon AF, Boutin A, et al. Clinical outcomes, predictors, and prevalence of anterior pituitary disorders following traumatic brain injury: a systematic review. CritCareMed. 2014;42:712-721.
10. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974; 2(7872):81–84.
11. Cryan E. Pituitary damage due to skull base fracture. DtschMedWochenschr. 1918; 44:1261.
12. Streetz-van der Werf C, Karges W, Blaum M, ..Kreitschmann-Andermahr. Addisonian Crisis after Missed Diagnosis of Posttraumatic Hypopituitarism. J Clin Med. 2015 May; 4(5): 965–969.
13. Tanriverdi F, Schneider HJ, Aimaretti G, Masel BE, Casanueva FF, Kelestimur F. Pituitary dysfunction after traumatic brain injury: a clinical and patho- physiological approach. Endocr Rev. 2015 Jun;36(3):305-42.
14. Tanriverdi F,Kelestimur F. Pituitary dysfunction following traumatic brain injury: clinical perspectives Neuropsychiatr Dis Treat. 2015; 11: 1835– 1843.
15. Tritos N, Yuen K, Kelly D. A neuroendocrine approach to patients with traumatic brain injury. EndocrPract. 2015;21: 823-831.

Lesión cerebral traumática
hipopituitarismo
hiponatremia
disfunción neuroendocrina
traumatic brain injury
hypopituitarism
hyponatremia
neuroendocrine dysfunction

El hipotiroidismo primario es la patología tiroidea más frecuente. El manejo estándar de esta enfermedad es con levotiroxina, cuya absorción puede verse afectada por distintas condiciones médicas, medicamentos e incluso la dieta del paciente. Los requerimientos de levotiroxina podrían variar debido a factores sobre agregados como la tiroiditis subaguda, la deficiencia de vitamina B12 y el uso de medicamentos, elementos que afectan el control del hipotiroidismo. Se presenta el caso de una paciente con hipotiroidismo primario con necesidad de ajuste en la dosis de levotiroxina a través del tiempo debido a comorbilidades agregadas. Se presentan claves para la evaluación del paciente con dificultad para lograr una TSH dentro del rango normal.

Abstract
Hypothyroidism is the most common thyroid disease. This disease is managed with hormonal replacement therapy using levothyroxine, whose absorption can be affected by various medical conditions, drugs and even patient´s diet. Levothyroxine requirements could vary according to co-morbidities such as subacute thyroiditis, vitamin B12 deficiency and the use of drugs, factors that can affect the control of hypothyroidism. The case of a patient with primary hypothyroidism who required dose adjustments of levothyroxine over time due to added co-morbidities is presented. Clues are given for evaluation of the patient with difficulty in achieving maintenance of TSH within the normal range. 

1. Almandoz JP, Gharib H. Hypothyroidism: Etiology, Diagnosis, and Management. Med Clin North Am. 2012;96(2):203–21.
2. Seo HM, Kim M, Bae J, Kim J-H, Lee JW, Lee SA, et al. A Case of Painful Hashimoto Thyroiditis that Mimicked Subacute Thyroiditis. Chonnam Med J. 2012;48(1):69.
3. Umut M, Alptekin G, Cuneyd A. Should neck pain in a patient with Hashimoto?s thyroiditis be underestimated? A case and review of the literature. Indian J Endocrinol Metab. 2012;16(3):444.
4. Lazarus J, Hennesey J. Subacute thyroiditis. In: De Groot L, Beck-Peccoz P, Chrousos G, editors. Endotext. South Darmouth, MA: MDText.com, Inc;
2012.
5. Brunton L, Chabner B, Knollman B. Goodman & Gilman: Las Bases Farmacológicas de la Terapéutica. 12 Ed. México: McGraw-Hill Interamericana Editores S.A.; 2011. 2035 p.
6. Ianiro G, Mangiola F, Di Rienzo T a., Bibbò S, Franceschi F, Greco a. V., et al. Levothyroxine absorption in health and disease, and new therapeutic perspectives. Eur Rev Med Pharmacol Sci. 2014;18(4):451–6.
7. Builes Barrera CA, Palacios K, Barragán F. Dosis de levotiroxina varía según la etiología del hipotiroidismo y el peso corporal. Revista Colombiana de Endocrinología y Metabolismo. 2014;27–32.
8. Liwanpo L, Hershman JM. Conditions and drugs interfering with thyroxine absorption. Best Pract Res Clin Endocrinol Metab. 2009;23(6):781–92.
9. Biondi B, Wartofsky L. Treatment with thyroid hormone. Endocr Rev. 2014;35(3):433–512.
10. Cutolo M. Autoimmune polyendocrine syndromes. Autoimmunity reviews. 2014. 13:85-89.

Levotiroxina
tiroiditis
hipotiroidismo
interacciones de comida y medicamentos
levothyroxine
thyroiditis
hypothyroidism
food-drug interactions