None; None; None; None

Resúmenes

Objetivo: determinar el valor predictivo de la glucosa en ayunas, para identificar intolerancia a los carbohidratos en pacientes con síndrome de ovario poliquístico. Materiales y métodos: a 100 mujeres con diagnóstico de síndrome de ovario poliquístico, se les realizó una prueba de tolerancia a 75 g de glucosa. Resultados: la sensibilidad para una cifra umbral de 101 mg/dl, fue de un 41,7%, IC 95%: 23% - 63%, y la especificidad de un 92,1%, IC95 %:83% - 97%. Con un valor predictivo positivo del 62,5%, y negativo del 83,3%.El valor de corte óptimo fue de 93mg /dl, con una sensibilidad del 75%, IC 95%: 53%-89%, y una especificidad del 73,7%, IC 95%: 62%-83%. La cifra de corte umbral óptima de la glicemia en ayunas para el tamizaje de intolerancia en mujeres con SOPQ, fue de 93 mg/dl. Conclusiones: las recomendaciones actuales para diagnosticar intolerancia a los carbohidratos, en mujeres con síndrome de ovario poliquístico, no son apropiadas. las recomendaciones actuales para diagnosticar intolerancia a los carbohidratos, en mujeres con síndrome de ovario poliquístico, no son apropiadas.

intolerancia a los carbohidratos; síndrome de ovario poliquístico; tamizaje

Objective: To determine the predictive value of fasting glucose to identify abnormal carbohydrate tolerance in patients with polycystic ovary syndrome. Materials and methods: 100 women diagnosed with polycystic ovary syndrome underwent a tolerance test toa 75 gdose of glucose. Results: Sensitivity for a threshold value of 101 mg/dl was 41.7% (95% C.I.: 23% - 63%) and specificity 92.1% (95% C.I.: 83% - 97%); with a positive predictive value of 62.5% and a negative predictive value of 83.3%. The optimum cut-off value was 93 mg/dL, with a sensitivity of 75% (95% C.I.: 53% - 89%) and a specificity of 73.7% (95% C.I.: 62% - 83%). The optimum fasting plasma glucose cut-off value for intolerance in women with PCOS was 93md/dL. Conclusions: The current recommendations for diagnosing abnormal carbohydrate tolerance in women with polycystic ovary syndrome are not appropriate. The current recommendations for diagnosing abnormal carbohydrate tolerance in women with polycystic ovary syndrome are not appropriate.

abnormal carbohydrate tolerance; polycystic ovary syndrome; screening

Objective: To determine the predictive value of fasting glucose to identify abnormal carbohydrate tolerance in patients with polycystic ovary syndrome. Materials and methods: 100 women diagnosed with polycystic ovary syndrome underwent a tolerance test toa 75 gdose of glucose. Results: Sensitivity for a threshold value of 101 mg/dl was 41.7% (95% C.I.: 23% - 63%) and specificity 92.1% (95% C.I.: 83% - 97%); with a positive predictive value of 62.5% and a negative predictive value of 83.3%. The optimum cut-off value was 93 mg/dL, with a sensitivity of 75% (95% C.I.: 53% - 89%) and a specificity of 73.7% (95% C.I.: 62% - 83%). The optimum fasting plasma glucose cut-off value for intolerance in women with PCOS was 93md/dL. Conclusions: The current recommendations for diagnosing abnormal carbohydrate tolerance in women with polycystic ovary syndrome are not appropriate.

abnormal carbohydrate tolerance; polycystic ovary syndrome; screening

Determination of fasting plasma glucose cut-off valuefor the identification of abnormal carbohydrate tolerance in women with polycystic ovarian syndrome.

Yai-Linn Chang,Leonardo Orozco-Saborío, Ileana Azofeifa-Hernández,Gerardo Montiel-Larios

*^{Dirección para correspondencia}:

75 g de glucosa.

Descriptores

^1-4 Aunque usualmente son las manifestaciones de anovulación crónica e hiperandrogenismo las que hacen que estas pacientes consulten a su médico, la resistencia a la insulina y la hiperinsulinemia también son frecuentes en ellas,⁵^-11 y tienen un rol etiológico importante.^12-15

20 a 44 años en los EEUU.¹⁶ Con respecto a la diabetes mellitus (DM) tipo 2, su prevalencia oscila entre el 8–12% en esa población.^16-19 Estas variaciones podrían atribuirse a diferencias poblacionales correspondientes al origen de las pacientes, entre otros.²⁰ De igual forma, la asociación entre ITC y síndrome metabólico (SM) está claramente establecida.^21-23

La American Diabetes Association (ADA) indica pautas de tamizaje para la ITC en aquellas personas con algún factor de riesgo para DM tipo 2, como mujeres con SOPQ.²⁴ Se propone, únicamente, realizar la prueba de glucosa dos horas postcarga de 75 g de glucosa (G2–HPC), para identificar ITC en mujeres con SOPQ, cuando la glucosa en ayunas es mayor a 101 mg/dL (5,6 mmol/L).²⁵ Igualmente, la Canadian Diabetes Association recomienda el uso de esa prueba cuando la glucosa en ayunas es mayor a 103 mg/dL (5,7 mmol/L).²⁵ Sin embargo, aún cuando la evidencia demuestra que la medición de la glucosa en ayunas es un predictor poco confiable para identificar la ITC en mujeres con SOPQ,¹⁷, 25,26 las guías canadienses y norteamericanas basan su tamizaje en esta prueba,^25-28 y en consecuencia se realiza de igual forma en nuestro medio.

la Sociedad Europea de Embriología y Reproducción en la ciudad de Rotterdam, también llamados ‘Criterios de Rotterdam,²⁹ 1. Oligo y anovulación, 2. Signos clínicos y bioquímicos de hiperandrogenismo, 3. Ovarios poliquísticos por ultrasonido pélvico. De 109 mujeres con diagnóstico de SOPQ, nueve cumplieron con alguno de los criterios de exclusión, adolescentes con menos de 3 años de haber presentado la menarca, mujeres mayores de 40 años de edad con alteraciones del ciclo menstrual, antecedente personal de hiperplasia suprarrenal (no clásica congénita), hiperprolactinemia o hipotiroidismo, causas secundarias de hiperandrogenismo (ej. síndrome de Cushing o tumores secretores de andrógenos), y uso de anticonceptivos orales, hormonas sexuales o algún medicamento que afecte el metabolismo de la glucosa en los 3 meses previos a la captación.

la ADA, que las define como valores de glicemia entre 140–199 mg/dL en una G2–HPC con 75 g de glucosa, y ≥ 200 mg/dL, respectivamente.²⁴ Para todas la participantes se procesaron muestras sanguíneas en el laboratorio clínico del HOMACE, con el fin de obtener los niveles plasmáticos de la glicemia en ayunas y 2 hrs postprandial, hemoglobina glicosilada A1c, insulinemia en ayunas, colesterol total, lipoproteínas de alta densidad (HDL), lipoproteínas de baja densidad (LDL), triglicéridos, testosterona libre y total, sulfato de dehidroepiandrostenediona (DHEAS), hormona folículo estimulante (FSH), hormona luteinizante (LH), prolactina (PRL), hormona estimulante de la tiroides (TSH) y tiroxina (T₄). La química sanguínea (incluidos glicemia y lípidos) se procesó con un equipo OLYMPUS AU400®. La G2–HPC con 75 g de glucosa empleó dextrosa al 40%, donde 187.5 mL equivalen a 75 g de dextrosa anhidra, producido por Laboratorios Reactivos Químicos de la CCSS. El cálculo de hemoglobina glicosilada se realizó con una unidad BIORAD D10®, según un principio de cromatografía de alto rendimiento. La medición de los exámenes hormonales utilizó el INMULITE 1000®, el cual fundamenta dicha determinación inmunológica, en una reacción quimioluminiscente.

1,50 m de longitud, y tomó la presión (PA), sentada, con el esfigmomanómetro en el brazo derecho.

software Stata 10.0. Las variables fueron comparadas por medio de la estimación de la prueba de t Student para variables cuantitativas y de su homóloga Chi Cuadrado para variables cualitativas; se definió como estadísticamente significativo, un punto crítico de 0,05 (p ≤ 0,05). La especificidad, sensibilidad y los valores predictivos negativos y positivos, fueron generados con una cifra de corte umbral de 101 mg/dL. Una curva ROC (“receiver operating characteristic”) se elaboró para definir el más adecuado valor umbral de la glucosa en ayunas, con el fin de identificar tolerancia anormal a la glucosa.

75 g de glucosa iguales o mayores a 200 mg/dl (200 mg/dl, 203 mg/dl y 257 mg/dl, respectivamente). 16 de las 24 pacientes con ITC, cumplen con los criterios diagnósticos de SM, según la OMS (1999;³⁰); correspondientes a un 16,0% de las mujeres con SOPQ incluidas en esta investigación.

^{Cuadro 1}) comparado con las pacientes sin anormalidades en la tolerancia. Además, las concentraciones (medias) de hemoglobina A_1C e insulinemia en ayunas, fueron mayores en las mujeres con ITC, el 5,2 % vs el 6,3% y 12,2 µUI/ml vs 26,6 µUI/ml (valores normales 5-15 µUI/ml), respectivamente.

p> 0,05; ^{Cuadro 1}).

la Figura

Figura

¹Figura. Se demostró que un corte umbral de la glicemia en ayunas de 101 mg/dl tiene una sensibilidad del 41,7%, (IC 95%:23% - 63%) y una especificidad del 92,1%, (IC 95%: 83% - 97%), con valor predictivo negativo y positivo del 83,3% (IC 95%:73% - 90%) y del 62,5%, (IC 95%: 36% - 84%), respectivamente. En el ^{Cuadro 2} se resumen los demás valores de sensibilidad y especificidad, según el corte umbral de la glicemia en ayunas.

¹⁶ Dicha alteración metabólica ocurrió a una edad temprana en el estudio (29,7 años), sumándose a otras publicaciones que demuestran que las anormalidades metabólicas inician a edades tempranas en mujeres con SOPQ.¹⁷, ³¹ 14 pacientes de las 24 diagnosticadas con ITC, presentaron glicemias en ayunas por debajo de la cifra de corte umbral propuesta por la ADA de 101 mg/dl. Empleando este valor de corte umbral, no se habría diagnosticado la intolerancia a la glucosa en un 58,3% de las mujeres que la presentaban, de no haberse realizado la G2–HPC con 75 g de glucosa; esto debido a la baja sensibilidad de este corte umbral de la glicemia en ayunas en la muestra (41,7%).

^{32, 33}

³⁴ Dichos hallazgos, junto a las diferencias significativas en cuanto al IMC y las cifras tensionales para las mujeres con ITC y SOPQ, reiteran a ambas patologías como predisponentes a sufrir un mayor riesgo de enfermedad cardiovascular.

la ITC en mujeres con SOPQ.

²⁵, ³⁵ Además, utilizando este corte para realizar la G2–HPC en mujeres con SOPQ, aún se obtiene un inaceptable 25% de mujeres intolerantes que no se diagnosticarían. Asimismo, para alcanzar la sensibilidad del 80%, se tendría que aceptar un corte umbral de la glicemia en ayunas de 90 mg/dl, generando la posibilidad de elevar el porcentaje de falsos positivos, y un gasto innecesario de recursos.

¹⁷, ^25,26 la glicemia en ayunas no pareciera un factor predictivo importante para la identificación de la intolerancia a los carbohidratos en la población con SOPQ, lo que hace adecuado contemplar el costo-beneficio de realizar una G2–HPC al diagnosticar el SOPQ, y luego realizarla periódicamente, con el objetivo de prevenir el desarrollo de tolerancia anormal a los carbohidratos, o de diabetes mellitus tipo 2.

Referencias bibliográficas

1. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab. 2004 Jun; 89:2745-9.
2. Knochenhauer ES, Key TJ, Kahsar-Miller M, Waggoner W, Boots LR, Azziz R. Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: a prospective study. J Clin Endocrinol Metab. 1998 Sep; 83:3078-82.
3. Diamanti-Kandarakis E, Kouli CR, Bergiele AT, Filandra FA, Tsianateli TC, Spina GG, Zapanti ED, Bartzis MI. A survey of the polycystic ovary syndrome in the Greek island of Lesbos: hormonal and metabolic profile. J Clin Endocrinol Metab. 1999 Nov; 84:4006-11.
4. Asunción M, Calvo RM, San Millán JL, Sancho J, Avila S, Escobar-Morreale HF. A prospective study of the prevalence of the polycystic ovary syndrome in unselected Caucasian women from Spain. J Clin Endocrinol Metab. 2000 Jul; 85:2434-8.
5. Toprak S, Yönem A, Cakir B, Güler S, Azal O, Ozata M, Corakçi A. Insulin resistance in non obese patients with polycystic ovary syndrome. HormRes. 2001; 55:65-70.
6. Ciampelli M, Fulghesu AM, Cucinelli F, Pavone V, Caruso A, Mancuso S, Lanzone A. Heterogeneity in beta cell activity, hepatic insulin clearance and peripheral insulin sensitivity in women with polycystic ovary syndrome. Hum Reprod. 1997 Sep; 12:1897-901.
7. Sinagra D, Scarpitta AM, Brigandì M, D›Acquisto G. Feedback inhibition of insulin secretion and insulin resistance in polycystic ovarian syndrome with and without obesity. Eur Rev Med PharmacolSci. 1997 Sep-Oct; 1:167-71.
8. Dunaif A, Segal KR, Shelley DR, Green G, Dobrjansky A, Licholai T. Evidence for distinctive and intrinsic defects in insulin action in polycystic ovary syndrome. Diabetes. 1992 Oct; 41:1257-66.
9. Chang RJ, Nakamura RM, Judd HL, Kaplan SA. Insulin resistance in non obese patients with polycystic ovarian disease. J Clin Endocrinol Metab. 1983 Aug; 57:356-9.
10. Holte J, Bergh T, Berne C, Berglund L, Lithell H. Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance. J Clin Endocrinol Metab.1994 May; 78:1052-8.
11. Dunaif A, Segal KR, Futterweit W, Dobrjansky A. Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes. 1989 Sep; 38:1165-74.
12. Baillargeon JP. Use of insulin sensitizers in polycystic ovarian syndrome. Curr Opin InvestigDrugs 2005; 6:1012-22.
13. Baillargeon JP, Nestler JE. Polycystic ovary syndrome: a syndrome of ovarian hypersensitivity to insulin? J Clin EndocrinolMetab2006; 91:22-4.
14. Veldhuis JD, Zhang G, Garmey JC. Troglitazone, an insulin-sensitizing thiazolidinedione, represses combined stimulation by LH and insulin of de novo androgen biosynthesis by the cal cells in vitro. J Clin EndocrinolMetab2002; 87:1129-33.
15. Sekar N, Lavoie HA, Veldhuis JD. Concerted regulation of steroidogenic acute regulatory gene expression by luteinizing hormone and insulin (or insulin-like growth factor I) in primary cultures of porcine granulosa-luteal cells.Endocrinology 2000; 141:3983-92.
16. Legro RS, KunselmanAR, Dodson WC, Dunaif A. Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab. 1999; 84:165-9.
17. Ehrmann DA, Barnes RB, Rosenfield RL, CavaghanMK, Imperial J. Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome.
18. Diabetes Care. 1999; 22:141-6.
19. Gambineri A, Pelusi C, Manicardi E, Vicennati V, Cacciari M, Morselli-Labate AM, Pagotto U, Pasquali R. Glucose intolerance in a large cohort of Mediterranean women with polycystic ovary syndrome: phenotype and associated factors. Diabetes. 2004; 53:2353-8.
20. Dabadghao P, Roberts BJ, Wang J, Davies MJ, Norman RJ. Glucose tolerance abnormalities in Australian women with polycystic ovary syndrome. Med J Aust. 2007 Sep 17; 187:328-31.
21. Vrbíková J, Cibula D, Dvoráková K, Stanická S, Sindelka G, Hill M, Fanta M, Vondra K, Skrha J. Insulin sensitivity in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2004; 89:2942-5.
22. Vrbíková J, Vondra K, Cibula D, Dvoráková K, Stanická S, Srámková D, Sindelka G, Hill M, Bendlová B, Skrha J. Metabolic syndrome in young Czech women with polycystic ovary syndrome. Hum Reprod. 2005; 20:3328-32.
23. Teimuraz, A., Essah, P., Iuorno, M., Nestler, J. Prevalence and characteristics of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab2005; 90:1929-1935.
24. Sudhindra, B. Metabolic syndrome in females with polycystic ovary syndrome and International Diabetes Federation criteria. J Obstet GynaecolRes 2008; 34:62-66.
25. American Diabetes Association. Position Statement: Diagnosis and classification of diabetes mellitus. Diabetes Care 2007; 30:S42-7.
26. Gagnon, C., Baillargeon, J. Suitability of recommended limits for fasting glucose tests in women with polycystic ovary syndrome. CMAJ 2007; 176:933-8.
27. Palmert MR, Gordon CM, Kartashov AI, Legro RS, Emans SJ, Dunaif A. Screening for abnormal glucose tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol Metab.2002 Mar; 87:1017-23.
28. Möhlig M, Spranger J, Ristow M, Pfeiffer AF, Schill T, Schlösser HW, Moltz L, Brabant G, Schöfl C. Predictors of abnormal glucose metabolism in women with polycystic ovary syndrome. Eur J Endocrinol. 2006 Feb; 154:295-301.
29. Vrbikova J, Dvorakova K, Grimmichova T, Hill M, Stanicka S, Cibula D, Bendlova B, Starka L, Vondra K. Prevalence of insulin resistance and prediction of glucose intolerance and type 2 diabetes mellitus in women with polycystic ovary syndrome. Clin ChemLab Med. 2007; 45:639-44.
30. Rotterdam ESHRE/ASM–Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long–term health risks related to polycystic ovary syndrome. Fertil Steril2004; 81:19-25.
31. World Health Organization: Definition, Diagnosis, and Classification of Diabetes Mellitus and its Complications: Report of a WHO Consultation. Geneva, World Health Org., 1999.
32. Lo JC, Feigenbaum SL, Yang J, PressmanAR, Selby JV, Go AS. Epidemiology and adverse cardiovascular risk profile of diagnosed polycystic ovary syndrome. J Clin Endocrinol Metab. 2006 Apr; 91:1357-63. Epub2006 Jan 24.
33. Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M; Finnish Diabetes Prevention Study Group. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N EnglJ Med. 2001 May 3; 344:1343-50.
34. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N EnglJ Med. 2002 Feb 7; 346:393-403.
35. García-Romero G, Escobar-Morreale HF. Hyperandrogenism, insulin resistance and hyperinsulinemia as cardiovascular risk factors in diabetes mellitus. CurrDiabetes Rev. 2006 Feb; 2:39-49.
36. Greenhalgh T. How to read a paper. Papers that report diagnostic or screening tests. BMJ1997; 315:540-3.

Unidad de Investigación Clínica del Hospital de las Mujeres “Dr. Adolfo Carit Eva”, CCSS.

Abreviaturas: ADA: American Diabetes Association, DM: Diabetes Mellitus, G2–HPC: glicemia dos horas postcarga, ITC: intolerancia a los carbohidratos, SM: síndrome metabólico, SOPQ: síndrome de ovario poliquístico

Fuentes de apoyo: Servicio de Ginecología Endocrinológica Hospital de las Mujeres “Dr. Adolfo Carit Eva”. Caja Costarricense de Seguro Social.

^*Correspondencia: lorozco@ihcai.org

Fecha aceptado: 25 de mayo de 2012

Determination of fasting plasma glucose cut-off valuefor the identification of abnormal carbohydratetolerance in women with polycystic ovarian syndrome.

Yai

Abbreviations: ADA, American Diabetes Association; DM, Diabetes Mellitus; G2–HAL, Glucose two hours afterload; CIT, Carbohydrate intolerance; SM, Metabolic Syndrome; PCOS, Polycystic Ovary Syndrome. Sources of support: Department of Endocrine Gynecology Women´s Hospital “Dr. Adolfo Carit Eva”. Costa Rican Social Insurance Fund.
Correspondence: lorozco@ihcai.org

Costa Rica.

WomenHospital “Dr. Adolfo Carit Eva” (HOMACE) in the period of February 1^st,2009 to May 31^st, 2010. The research protocol was approved by the Bioethics Local Committee of the HOMACE.

Rotterdam, also called Rotterdam Criteria 1. Olygo or Anovulation, 2.Clinical and biochemical signs of hyperaldoteronism, 3. Polycystic Ovaries by pelvic Ultrasound. Of 109 women with the diagnosis of PCOS, nine met any of the exclusion criteria, adolescents with less than three years of filing menarche, women over 40 years old with menstrual cycle alterations, personal history of suprarenal Hyperplasia (no classical congenital), Hyperprolactinemiaor Hypothyroidism, secondary causes of hyperandrogenism (Cushing Syndrome o Androgen-Secreting tumors), and the use of oral contraceptives, sex hormones or any medication that affects the metabolism of glucose in the three months prior recruitment.

ADA guidelines, which defined as glycemic values between 140-199 mg/dl in a G2–HAL with 75g of glucose, and ≥ 200 mg/dL respectively. For all the participants blood samples were processed in la HOMACE Clinical Laboratory, in order to obtain plasmatic levels of fasting glucose and 2 hour postprandial glucose, glycosy lated hemoglobin A1c, fasting insulinemia, total cholesterol, high density lipoproteins (HDL), Low density lipoproteins (LDL), Triglycerides, free testosterone and total, dehidroepiandrostenedione sulfate (DHEAS), follicle stimulating hormone (FSH), Luteinizing hormone (LH), prolactin (PRL), thyroid stimulating Hormone (TSH) and thyroxin (T4). The blood chemistry (including lipids and glycemic) was processed with OLYMPUS AU400® equipment. The G2-HAL with 75g of glucose used 40% of dextrose, where 187.5 ml equivalent to 75g of anhydride dextrose, produces by Chemical Reactive Laboratory of the CCSS. The calculation of glycosylated hemoglobin was performed using BIORAD D10® unit, according to the chromatographic principle of high performance. The measurement of the hormonal tests used INMULITE 1000®, which underlines said immunological determination, by a chemiluminescent reaction.

1.50 m long, and took blood pressure, sitting, with the sphygmomanometer in the right arm.

Table 1. In 24 of 100 women (24%), CIT was identified. Of these women, five showed enough alterations to realized DM type 2 diagnoses; two presented levels between 132 mg/dL to 147 mg/dL for fasting glycemia and postprandial between 202 mg/dL to 207 mg/dL, respectively. Other three women had showed fasting glycemic levels between normal limits, but G2-HAL with 75g of glucose higher or above 200 mg/dL(200 mg/dl, 203 mg/dl and 257 mg/dl, respectively). Sixteen of the 24 patients with CIT, meet the diagnosis criteria of MS, according to WHO (1999); corresponding a 16,0% of women with PCOS included in this research.

Thumbnail

Table

Table 1) compared with patients without abnormalities in tolerance. Furthermore, the Hemoglobin Aic (means) and fasting insulinemia concentrations, were higher in CIT women, 5,2% vs 6,3% and 12,2%μUI/ mlvs26,6 μUI/ml (normal values 5-15 μUI/ml) respectively.

Table 1).

. It was exposed that a cut threshold fasting glucose of 101mg/dl had a sensibility of 41,7%, (IC 95%:23% summarizes the others sensitivity and specificity values, according to the cut threshold fasting glycemia.

Figure 1

Thumbnail

Table 2

ADA of 101 mg/dl. Using this cutoff threshold number value, would not be diagnosed the glucose intolerance in 58,3% of women who had it, of the absence of the G2-HAL with 75g of glucose; this due to the low sensibility of this

en_bart08v54n4 Received: February 6^th, 2012 Accepted: May 25^th, 2012

Fechas de Publicación

Publicación en esta colección
12 Nov 2015
Fecha del número
Dic 2012

Histórico

Recibido
06 Feb 2012
Acepto
25 Mayo 2012

[1] 1. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab. 2004 Jun; 89:2745-9.

[2] 2. Knochenhauer ES, Key TJ, Kahsar-Miller M, Waggoner W, Boots LR, Azziz R. Prevalence of the polycystic ovary syndrome in unselected black and white women of the southeastern United States: a prospective study. J Clin Endocrinol Metab. 1998 Sep; 83:3078-82.

[3] 3. Diamanti-Kandarakis E, Kouli CR, Bergiele AT, Filandra FA, Tsianateli TC, Spina GG, Zapanti ED, Bartzis MI. A survey of the polycystic ovary syndrome in the Greek island of Lesbos: hormonal and metabolic profile. J Clin Endocrinol Metab. 1999 Nov; 84:4006-11.

[4] 4. Asunción M, Calvo RM, San Millán JL, Sancho J, Avila S, Escobar-Morreale HF. A prospective study of the prevalence of the polycystic ovary syndrome in unselected Caucasian women from Spain. J Clin Endocrinol Metab. 2000 Jul; 85:2434-8.

[5] 5. Toprak S, Yönem A, Cakir B, Güler S, Azal O, Ozata M, Corakçi A. Insulin resistance in non obese patients with polycystic ovary syndrome. HormRes. 2001; 55:65-70.

[6] 6. Ciampelli M, Fulghesu AM, Cucinelli F, Pavone V, Caruso A, Mancuso S, Lanzone A. Heterogeneity in beta cell activity, hepatic insulin clearance and peripheral insulin sensitivity in women with polycystic ovary syndrome. Hum Reprod. 1997 Sep; 12:1897-901.

[7] 7. Sinagra D, Scarpitta AM, Brigandì M, D›Acquisto G. Feedback inhibition of insulin secretion and insulin resistance in polycystic ovarian syndrome with and without obesity. Eur Rev Med PharmacolSci. 1997 Sep-Oct; 1:167-71.

[8] 8. Dunaif A, Segal KR, Shelley DR, Green G, Dobrjansky A, Licholai T. Evidence for distinctive and intrinsic defects in insulin action in polycystic ovary syndrome. Diabetes. 1992 Oct; 41:1257-66.

[9] 9. Chang RJ, Nakamura RM, Judd HL, Kaplan SA. Insulin resistance in non obese patients with polycystic ovarian disease. J Clin Endocrinol Metab. 1983 Aug; 57:356-9.

[10] 10. Holte J, Bergh T, Berne C, Berglund L, Lithell H. Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance. J Clin Endocrinol Metab.1994 May; 78:1052-8.

[11] 11. Dunaif A, Segal KR, Futterweit W, Dobrjansky A. Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes. 1989 Sep; 38:1165-74.

[12] 12. Baillargeon JP. Use of insulin sensitizers in polycystic ovarian syndrome. Curr Opin InvestigDrugs 2005; 6:1012-22.

[13] 13. Baillargeon JP, Nestler JE. Polycystic ovary syndrome: a syndrome of ovarian hypersensitivity to insulin? J Clin EndocrinolMetab2006; 91:22-4.

[14] 14. Veldhuis JD, Zhang G, Garmey JC. Troglitazone, an insulin-sensitizing thiazolidinedione, represses combined stimulation by LH and insulin of de novo androgen biosynthesis by the cal cells in vitro. J Clin EndocrinolMetab2002; 87:1129-33.

[15] 15. Sekar N, Lavoie HA, Veldhuis JD. Concerted regulation of steroidogenic acute regulatory gene expression by luteinizing hormone and insulin (or insulin-like growth factor I) in primary cultures of porcine granulosa-luteal cells.Endocrinology 2000; 141:3983-92.

[16] 16. Legro RS, KunselmanAR, Dodson WC, Dunaif A. Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab. 1999; 84:165-9.

[17] 17. Ehrmann DA, Barnes RB, Rosenfield RL, CavaghanMK, Imperial J. Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome.

[18] 18. Diabetes Care. 1999; 22:141-6.

[19] 19. Gambineri A, Pelusi C, Manicardi E, Vicennati V, Cacciari M, Morselli-Labate AM, Pagotto U, Pasquali R. Glucose intolerance in a large cohort of Mediterranean women with polycystic ovary syndrome: phenotype and associated factors. Diabetes. 2004; 53:2353-8.

[20] 20. Dabadghao P, Roberts BJ, Wang J, Davies MJ, Norman RJ. Glucose tolerance abnormalities in Australian women with polycystic ovary syndrome. Med J Aust. 2007 Sep 17; 187:328-31.

[21] 21. Vrbíková J, Cibula D, Dvoráková K, Stanická S, Sindelka G, Hill M, Fanta M, Vondra K, Skrha J. Insulin sensitivity in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2004; 89:2942-5.

[22] 22. Vrbíková J, Vondra K, Cibula D, Dvoráková K, Stanická S, Srámková D, Sindelka G, Hill M, Bendlová B, Skrha J. Metabolic syndrome in young Czech women with polycystic ovary syndrome. Hum Reprod. 2005; 20:3328-32.

[23] 23. Teimuraz, A., Essah, P., Iuorno, M., Nestler, J. Prevalence and characteristics of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab2005; 90:1929-1935.

[24] 24. Sudhindra, B. Metabolic syndrome in females with polycystic ovary syndrome and International Diabetes Federation criteria. J Obstet GynaecolRes 2008; 34:62-66.

[25] 25. American Diabetes Association. Position Statement: Diagnosis and classification of diabetes mellitus. Diabetes Care 2007; 30:S42-7.

[26] 26. Gagnon, C., Baillargeon, J. Suitability of recommended limits for fasting glucose tests in women with polycystic ovary syndrome. CMAJ 2007; 176:933-8.

[27] 27. Palmert MR, Gordon CM, Kartashov AI, Legro RS, Emans SJ, Dunaif A. Screening for abnormal glucose tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol Metab.2002 Mar; 87:1017-23.

[28] 28. Möhlig M, Spranger J, Ristow M, Pfeiffer AF, Schill T, Schlösser HW, Moltz L, Brabant G, Schöfl C. Predictors of abnormal glucose metabolism in women with polycystic ovary syndrome. Eur J Endocrinol. 2006 Feb; 154:295-301.

[29] 29. Vrbikova J, Dvorakova K, Grimmichova T, Hill M, Stanicka S, Cibula D, Bendlova B, Starka L, Vondra K. Prevalence of insulin resistance and prediction of glucose intolerance and type 2 diabetes mellitus in women with polycystic ovary syndrome. Clin ChemLab Med. 2007; 45:639-44.

[30] 30. Rotterdam ESHRE/ASM–Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long–term health risks related to polycystic ovary syndrome. Fertil Steril2004; 81:19-25.

[31] 31. World Health Organization: Definition, Diagnosis, and Classification of Diabetes Mellitus and its Complications: Report of a WHO Consultation. Geneva, World Health Org., 1999.

[32] 32. Lo JC, Feigenbaum SL, Yang J, PressmanAR, Selby JV, Go AS. Epidemiology and adverse cardiovascular risk profile of diagnosed polycystic ovary syndrome. J Clin Endocrinol Metab. 2006 Apr; 91:1357-63. Epub2006 Jan 24.

[33] 33. Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M; Finnish Diabetes Prevention Study Group. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N EnglJ Med. 2001 May 3; 344:1343-50.

[34] 34. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N EnglJ Med. 2002 Feb 7; 346:393-403.

[35] 35. García-Romero G, Escobar-Morreale HF. Hyperandrogenism, insulin resistance and hyperinsulinemia as cardiovascular risk factors in diabetes mellitus. CurrDiabetes Rev. 2006 Feb; 2:39-49.

[36] 36. Greenhalgh T. How to read a paper. Papers that report diagnostic or screening tests. BMJ1997; 315:540-3.

Determinación del valor umbral de tamizaje de la glicemia en ayunas, para identificar la intolerancia a los carbohidratos, en mujeres con síndrome de ovarios poliquísticos

Determination of fasting plasma glucose cut-off valuefor the identification of abnormal carbohydrate tolerance in women with polycystic ovarian syndrome

Resúmenes

Referencias bibliográficas

Fechas de Publicación

Histórico