10. Isolated Addison's disease is unlikely to be caused by mutations in MC2R, MRAP or STAR, three genes responsible for familial glucocorticoid deficiency. METHODS: Forty patients with known AD without evidence of autoimmune disease were screened for mutations in MC2R, MRAP and STAR. In addition, patients were genotyped for the MC2R promoter polymorphism previously associated with reduced responsiveness to ACTH. RESULTS: No mutations in MC2R, MRAP or STAR were identified in any patient. The frequencies of the MC2R promoter polymorphism were similar to those reported in healthy controls. CONCLUSIONS: FGD does not appear to be underdiagnosed in the AD population. However, in approximately 50% of patients with FGD, no genetic cause has yet been identified and it is possible that the other, as yet unidentified, genes giving rise to FGD may be implicated in AD.
11. Isolated Addison's disease is unlikely to be caused by mutations in MC2R, MRAP or STAR, three genes responsible for familial glucocorticoid deficiency. APRECIACION DEL ARTICULO: La enfermedad de ADDISON es una enfermedad autonómica recesiva causada por la resistencia de ACTH y la deficiencia de glucocorticoides, el articulo nos da a entender que esta enfermedad parece desarrollar un patrón genético por la mutación de los genes encargados de la expresión de glucocorticoides causando así anomalías en la expresión de hormonas glucocorticoides
12. Autor: John Vane Science Centre Titulo: Eur J Endocrinol. 2010 Feb;162(2):357-9. Epub 2009 Nov 10. Isolated Addison's disease is unlikely to be caused by mutations in MC2R, MRAP or STAR, three genes responsible for familial glucocorticoid deficiency. Hospital de apoyo a la investigación: Centre for Endocrinology, John Vane Science Centre, Queen Mary University of London http://www.ncbi.nlm.nih.gov/pubmed
13. ENFERMEDAD DE ADDISON La enfermedad de Addison es poco probable que sea causado por mutaciones en MC2R, MRAP o STAR, tres genes responsables de la deficiencia de glucocorticoides familiar. Implicaciones genéticas que corresponden a los genes: Deficiencia de la Familia glucorticoidea (FGD) LA ENFERMEDAD DE ADDISON SE RELACIONA CON LA DEFICIENCIA DE LA FAMILIA GLUCOCORTICOIDEA PERO LAS MUTACIONES EN FGD NO SE RELACIONA CON LA ENFERMEDAD DE ADDISON MC2R MRAP START
14. La enfermedad de ADDISON es una enfermedad autonómica recesiva causada por la resistencia de ACTH y la deficiencia de glucocorticoides, el articulo nos da a entender que aun esta enfermedad no posee un patrón genético de desarrollo, pero si se relaciona con la deficiencia de la familia glucocorticoidea.
15. ADDISON DISEASE 2. ARTICULO Addison's disease induced by miliary tuberculosis and the administration of rifampicin. Abstract We herein report a rare occurrence of Addison's disease caused by acute adrenal gland tuberculosis occurring in association with miliary tuberculosis and the administration of rifampicin. An 82-year-old woman with miliary tuberculosis was treated with antituberculous chemotherapeutic agents including rifampicin (RFP), but she still demonstrated general malaise in addition to hyponatremia. Abdominal CT showed an enlargement of the right adrenal gland. However, after discontinuing RFP, the patient's symptoms improved. We carefully reinitiated the administration of RFP. The patient's condition thereafter did not worsen, and the treatment could thus be maintained. It is extremely important to immediately recognize adrenal crisis precipitated by the administration of RFP.
16. Addison's disease induced by miliary tuberculosis and the administration of rifampicin. APRECIACION DEL ARTICULO: Al parecer el patron de tubercolisis miliar, y su tratamiento no tiene que ver con el tratamiento para la enfermedad de addison pero si afecta la glandula suprarrenal por el tratamiento de TBC miliar y asi permitiendo el avance de la enfermedad.
17. Autores:Yokoyama T, Toda R, Kimura Y, Mikagi M, Aizawa H. Titulo: Addison's disease induced by miliary tuberculosis and the administration of rifampicin. http://www.ncbi.nlm.nih.gov/pubmed
18. ENFERMEDAD DE ADDISON La enfermedad de Addison y su complicacion por TBC miliar y la administración del antibiótico rifampicina Casos frecuentes reportan enfermedad de Addison y su complicación por la TBC miliar que se disemina a la glándula adrenal que es afectada por la rifampicina.
19. La enfermedad de ADDISON es una enfermedad autonómica recesiva causada por la resistencia de ACTH y la deficiencia de glucocorticoides, como logramos observar en el articulo, al parecer una paciente que desarrolla TBC miliiar esta inmunocomprometida y para su tratamiento se suele administrar rimfapicina que genera una patología en la glandula adrenal permitiendo el avance patológico de la enfermedad de addison
20. ADDISON DISEASE 3. ARTICULO Emotions and features of temperament in patients with Addison's disease. Abstract INTRODUCTION: Patients with Addison's disease experience many somatic and psychic changes, which decrease their quality of life. The aim of the study was to evaluate the "psychological equipment" of these patients to cope with stress connected with this chronic disease and the challenge of constant treatment. MATERIAL AND METHODS: Fifteen patients (13 female, 2 male) were included in the study. Standard psychological tests were used to assess anxiety, temperament, depression, and emotional intelligence.
21. Emotions and features of temperament in patients with Addison's disease. RESULTS: The results show that patients with Addison's disease have not only increased levels of anxiety and fear, and over-reaction to stimuli, but decreased performance efficiency and need for social contact as well. Such psychological characteristics may result in difficulties in doctor-patient communication, aggravation of patients' feelings, limitation of patients' involvement in therapy, and, finally, a decrease the effectiveness of therapy. CONCLUSIONS: The temperamental characteristics and personal traits of patients with Addison's disease seem not to be useful in stressful events, and psychological support can be helpful in the effective therapy of these patients. (Pol J Endocrinol 2010; 61 (1): 90-92).
22. Emotions and features of temperament in patients with Addison's disease. APRECIACION DEL ARTICULO: En el articulo, se desarrolla un estudio acerca de loas consecuencias físicas y síquicas de las personas con enfermedad de addison y como afecta esta el desarrollo social y la calidad de vida del paciente.
23. AUTORES: Warmuz-Stangierska I, Baszko-Błaszyk D, Sowiński J. TITULO:Emotions and features of temperament in patients with Addison's disease. CENTRO DE APOYO A LA INVESTIGACION: Department of Endocrinology, Metabolism, and Internal Medicine, University of Medical Sciences, Poznań, Poland. http://www.ncbi.nlm.nih.gov/pubmed/20205110
24. Emociones y temperamentos en pacientes con enfermedad de Addison. Pacientes con enfermedad de addison presentan cambios somáticos y psíquicos Disminuyendo la calidad de vida del paciente
27. Decrecion en la interacción socialProblemas en: Comunicación Expresion de sentimientos Se presentan limitaciones en la terapia Y por ultimo deficiencia en la terapia
28. Los pacientes que presentan cualquier enfermedad y particularmente enfermedad de Adisson, deprimen su desarrollo social por tanto se afceta la calidad de vida del paciente, permitiendo que este se inmunodeprima y la terapia no sea eficaz para la enfermedad.
29. ADDISON DISEASE 4 ARTICULO Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone. Abstract Context Patients with primary adrenal insufficiency (Addison's disease) receive more glucococorticoids than the normal endogenous production, raising concern about adverse effects on bone. OBJECTIVE: To determine i) the effects of glucocorticoid replacement therapy on bone, and ii) the impact of glucocorticoidpharmacogenetics. DESIGN, SETTING AND PARTICIPANTS: A cross-sectional study of two large Addison's cohorts from Norway (n=187) and from UK and New Zealand (n=105). MAIN OUTCOME MEASURES: Bone mineral density (BMD) was measured; the Z-scores represent comparison with a reference population. Blood samples from 187 Norwegian patients were analysed for bone markers and common polymorphisms in genes that have been associated with glucocorticoid sensitivity.
30. Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone. RESULTS: Femoral neck BMD Z-scores were significantly reduced in the patients (Norway: mean -0.28 (95% confidence intervals (CI) -0.42, -0.16); UK and New Zealand: -0.21 (95% CI -0.36, -0.06)). Lumbar spine Z-scores were reduced (Norway: -0.17 (-0.36, +0.01); UK and New Zealand: -0.57 (-0.78, -0.37)), and significantly lower in males compared with females (P=0.02). The common P-glycoprotein (ABCB1) polymorphism C3435T was significantly associated with total BMD (CC and CT>TT P=0.015), with a similar trend at the hip and spine. CONCLUSIONS: BMD at the femoral neck and lumbar spine is reduced in Addison's disease, indicating undesirable effects of the replacement therapy. The findings lend support to the recommendations that 15-25 mg hydrocortisone daily is more appropriate than the higher conventional doses. A common polymorphism in the efflux transporter P-glycoprotein is associated with reduced bone mass and might confer susceptibility to glucocorticoid induced osteoporosis.
31. Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone. APRECIACION DEL ARTICULO: En el articulo se hace el análisis de la terapia para la enfermedad de addison puesto que ha estos pacientes se les administran muchos mas glucocorticoides que los que normalmente son producidos endógenamente y esto tiene altas repercusiones en los huesos.
32. AUTORES:Løvås K, Gjesdal CG, Christensen M, Wolff AB, Almås B, Svartberg J, Fougner KJ, Syversen U, Bollerslev J, Falch JA, Hunt PJ, Chatterjee VK, Husebye ES TITULO:Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone. CENTRO DE APOYO A LA INVESTIGACION:Institute of Medicine, University of Bergen, 5020 Bergen, Norway Department of Medicine, Haukeland University Hospital, 5021 Bergen, Norway. kristian.lovas@med.uib.no http://www.ncbi.nlm.nih.gov/pubmed/19282465
33. Terapia de reemplazo de glucocorticoides y de la farmacogenética en la enfermedad de Addison: efectos sobre el hueso. Los pacientes con enfermedad de Addison recibe n una carga de Glucocorticoides mucho mas alta que la producción endógena, esto conlleva a efectos en el hueso Efectos específicamente en la espina dorsal
34. LA ENFERMEDAD DE ADDISON Y SU ADMINISTRACION DE GLUCOCORTICIDES EXOGENAMENTE TIENE SERIAS REPERCUSIONES EN LOS DEPOSITO DE CALCIO DEL HUESO, ADEMAS DE QUE HAY UN EFECTO CELULAR QUE AFECTA LA MEDULA OSEA.
35. ADDISON DISEASE 5. ARTICULO Addison's disease in women is a risk factor for an adverse pregnancy outcome. Abstract CONTEXT: Autoimmune Addison's disease (AAD) tends to affect young and middle-aged women. It is not known whether the existence of undiagnosed or diagnosed AAD influences the outcome of pregnancy. OBJECTIVE: The aim of the study was to compare the number of children and pregnancy outcomes in individuals with AAD and controls. DESIGN AND SETTING: We conducted a population-based historical cohort study in Sweden. PATIENTS: Through the Swedish National Patient Register and the Total Population Register, we identified 1,188 women with AAD and 11,879 age-matched controls who delivered infants between 1973 and 2006.
36. ADDISON DISEASE Addison's disease in women is a risk factor for an adverse pregnancy outcome. MAIN OUTCOME MEASURES: We measured parity and pregnancy outcome. RESULTS: Adjusted odds ratios (ORs) for infants born to mothers with deliveries 3 yr or less before the diagnosis of AAD were 2.40 [95% confidence interval (CI), 1.27-4.53] for preterm birth (≤37 wk), 3.50 (95% CI, 1.83-6.67) for low birth weight (<2500 g), and 1.74 (95% CI, 1.02-2.96) for cesarean section. Compared to controls, women who gave birth after their AAD diagnosis were at increased risk of both cesarean delivery (adjusted OR, 2.35; 95% CI, 1.68-3.27) and preterm delivery (adjusted OR, 2.61; 95% CI, 1.69-4.05). Stratifying by isolated AAD and concomitant type 1 diabetes and/or autoimmune thyroid disease in the mother did not essentially influence these risks. There were no differences in risks of congenital malformations or infant death. Women with AAD had a reduced overall parity compared to controls (P<0.001). CONCLUSION: Clinically undiagnosed and diagnosed AAD both entail increased risks of unfavorable pregnancy outcomes. AAD also influences the number of childbirths.
37. Addison's disease in women is a risk factor for an adverse pregnancy outcome. APRECIACION DEL ARTICULO: Al parecer el diagnostico de enfermedad de Addison afecta el desarrollo de un embarazo normal en una mujer, este diagnostico es muy importante para tener cuidados de prevención en una mujer que presenta enfermedad de Addison.
38. AUTORES:Björnsdottir S, Cnattingius S, Brandt L, Nordenström A, Ekbom A, Kämpe O, Bensing S. TITULO: Addison's disease in women is a risk factor for an adverse pregnancy outcome. CENTRO DE APOYO A LA INVESTIGACION:I Department of Molecular Medicine and Surgery, KarolinskaInstitutet, 171 76 Stockholm, Sweden. Sigridur.Bjornsdottir@karolinska.se http://www.ncbi.nlm.nih.gov/pubmed/20861125
39. La enfermedad de Addison en las mujeres es un factor de riesgo para un resultado adverso del embarazo La enfermedad de Addison en mujeres jovenes y de mediana edad, ya sea diagnosticada o no, esta enfermedad afecta el desarrollo de un embarazo normal. Conllevando a un parto por cesaria puesto que se compromete la salud del niño, teniendo un parto normal.
40. AL PARECER EL DIAGNOSTICO DE ENFERMEDAD DE ADDISON EN MUEJERES QUE PUEDEN ESTAR EMBARAZADAS O PIENSAN ESTARLO, ES BASTANTE MPORTANTE PARA TOMAR MEDIDAS PREVENTIVAS QUE FACILITEN UN PARTO CASI NORMAL, Y ASI NO ENTREN EN RIESGO LA VIDA DE LA PACIENTE NI DEL NEONATO.
