Hipotiroidismo espontáneo en 4 pacientes con enfermedad de Graves-Basedow
ABSTRACT Presentamos los casos de 4 pacientes con enfermedad de Graves- Basedow que, durante el curso de su proceso patológico, sufrieron hipotiroidismo espontáneo. Los dos mecanismos fisiopatológicos más probables para explicar esta evolución son la destrucción autoinmunitaria progresiva del epitelio folicular tiroideo y la predominancia de anticuerpos inhibidores de los receptores de tirotropina (TSH) frente a anticuerpos estimulantes en un mismo paciente con enfermedad de Graves-Basedow. La exposición de estos 4 casos ilustra la heterogeneidad de esta enfermedad, así como la interrelación de las distintas formas clínicas de la enfermedad tiroidea autoinmunitaria.
Article: Metamorphic Thyroid AutoimmunityThyroid: official journal of the American Thyroid Association 11/2008; 18(10):1035-7. DOI:10.1089/thy.2008.1551 · 3.84 Impact Factor
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ABSTRACT: The course and severity of autoimmune thyroid disease are altered during pregnancy and in the postpartum period. The thyroidal response to a fluctuating immune status, combined with changes in thyroid economy during pregnancy, may result in a need to adjust the treatment regimen for thyroid disease during pregnancy. Patients with Hashimoto's hypothyroidism on thyroid hormone replacement are frequently observed to have an increased requirement for levothyroxine early in pregnancy, although this is not a universal finding. Hashimoto's hypothyroidism does not typically remit during pregnancy, although further progression of thyroiditis may be seen in the postpartum period. Graves' disease usually improves during pregnancy and flares after delivery, again necessitating monitoring of thyroid status and possible adjustments in thionamide therapy. However, spontaneous transformation from Hashimoto's hypothyroidism to Graves' disease during pregnancy is rare. We report a case of transient Graves' hyperthyroidism during the late second trimester in a patient on levothyroxine replacement for Hashimoto's hypothyroidism. This resulted in a need to discontinue the patient's thyroid hormone entirely to avoid exacerbation of her hyperthyroidism. This interesting case is presented, along with a discussion of how the expression of autoimmune thyroid disease may be altered during pregnancy.Thyroid 08/2005; 15(7):725-9. DOI:10.1089/thy.2005.15.725 · 3.84 Impact Factor
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ABSTRACT: Three patients with Graves' disease who spontaneously developed hypothyroidism after treatment with antithyroid drugs are described herein. Patient 1 developed a painful tender thyroid enlargement with a fever and accelerated erythrocyte sedimentation rate when she was receiving maintenance therapy with methimazole, and she progressed to persistent hypothyroidism with increased titers of antithyroglobulin and antimicrosomal antibodies and marked reduction of goiter size within the subsequent 2 months. Thyroid-stimulating hormone-binding inhibitory immunoglobulins (TBIIs) and thyroid stimulation-blocking antibody (TSBAb) were absent when she was hypothyroid. Hypothyroidism probably resulted from autoimmune thyroid destruction due to subacute aggravation of Hashimoto's thyroiditis. During the clinical course of patient 2, accelerated erythrocyte sedimentation rate and later transient increases of antimicrosomal and antithyroglobulin antibody titers were observed repeatedly (four times), and she finally fell into overt hypothyroidism. She also had negative results of tests for TBII and TSBAb. Her hypothyroidism appeared to result from repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis. Patient 3 fell into hypothyroidism when receiving a small dosage of methimazole. The TBII and TSBAb were strongly active when she developed hypothyroidism, which thus seemed to be due to blocking antibody. Patients with Graves' hyperthyroidism may eventually progress to hypothyroidism later by several different mechanisms. Severe and sudden or slowly repeated thyroid destruction due to aggravation of Hashimoto's thyroiditis is one mechanism. Another may be the appearance of a blocking antibody to the TSH receptor.Archives of Internal Medicine 06/1990; 150(5):1105-9. · 13.25 Impact Factor