La enfermedad de Graves-Basedow, que es la causa más frecuente de hipertiroidismo en la edad pediátrica, es muy infrecuente en el niño preescolar. El hipertiroidismo es poco frecuente en la infancia y aparece, en general, en el contexto de la enfermedad de Graves. La mejor forma de tratamiento continúa. Download scientific diagram | Enfermedad de Graves-Basedow: facies. from publication: Hyperthyroidism. Concept. Classification. Description of principal types.
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Download Citation on ResearchGate | On Dec 31, , J.J. Corrales Hernández and others published Hipertiroidismo en la enfermedad de Graves-Basedow. Hipertiroidismo por enfermedad de Graves Basedow en mujer Document downloaded from tombdetercomi.cf, day 11/07/ This copy is for personal. RESUMENSe realizó una revisión narrativa rigurosa de la literatura inglesa y en español sobre diferentes aspectos de la Enfermedad de Graves-Basedow.
Management of infants born to mothers with HT Studies published in recent years have recommended followup of these children with protocols that require collection of multiple blood samples and several visits to a hospital. The presence of hypothyroidism in pregnant women does not warrant a different approach to neonatal screening for thyroid dysfunction. Infants born to mothers with Graves-Basedow disease Children born to mothers with Graves disease GD are at significant risk of morbidity and mortality and thus require the use of appropriate protocols for their identification and management.
At present, two methods are available for the measurement of TRAb. Second-generation methods measure immunoglobulin levels and do not discriminate between thyroid-stimulating or thyroid-blocking antibodies, but they are inexpensive and widely available. Third-generation methods are less available, more complicated and more expensive, but can discriminate between blocking and stimulating antibodies. The presence of stimulating antibodies is associated with a high risk of neonatal hyperthyroidism.
They should be measured between weeks 20 and 24 of gestation 6 ; if the results are negative, the newborn can be considered to be at low risk, but if they are positive, the newborn should be considered to be at high risk.
It manifests with tachycardia, heart failure, non-immune hydrops fetalis, goitre, intrauterine growth restriction, preterm birth, accelerated bone maturation and craniosynostosis.
These symptomatic cases may be treated with administration of antithyroid medication to the pregnant patient. If this were not possible, it is preferable to use PTU during this trimester and, given the risk of liver failure, switch to MMI in the second and third trimesters.
Possible findings include goitre, tracheal compression, low weight, periorbital oedema, retraction of the eyelid, hyperthermia, diarrhoea, irritability, skin redness and warmth, difficulty feeding, stagnant weight gain, tachycardia, heart failure, hypertension, splenomegaly, cholestasis, thrombocytopenia and hyperviscosity.
These symptoms are non-specific and could be attributed to congenital infection or sepsis. Children of mothers with GD that are euthyroid at birth usually have a normal cognitive development, but children that have neonatal hyperthyroidism may experience neurodevelopmental impairment.
If maternal hyperthyroidism is poorly controlled during pregnancy, the high levels of thyroid hormones hinder the normal development and maturation of the thyroid gland and the hypothalamic—pituitary—thyroid axis in the foetus.
This is a transient condition that usually improves in 3—19 months. It usually manifests in the first 4—5 days after birth, and followup of hyperthyroidism may be indicated depending on TRAb levels. Figure 1. Approach to the management of an infant born to a mother with GD or hyperthyroidism current or past.
Pregnant mother: measure TRAb levels in the second to third trimester of pregnancy. Inform the neonatologist of results. In newborns, FT4 and TSH levels should be measured between days 3 and 5 post birth or before if patient is symptomatic , and again between days 10 and 14 post birth use age-specific reference ranges.
Infectious trigger[ edit ] Since Graves' disease is an autoimmune disease which appears suddenly, often later in life, a viral or bacterial infection may trigger antibodies which cross-react with the human TSH receptor, a phenomenon known as antigenic mimicry. Thyroxine receptors in the pituitary gland are activated by the surplus hormone, suppressing additional release of TSH in a negative feedback loop.
The result is very high levels of circulating thyroid hormones and a low TSH level.
Pathophysiology[ edit ] Histopathological image of diffuse hyperplasia of the thyroid gland clinically presenting as hyperthyroidism Graves' disease is an autoimmune disorder, in which the body produces antibodies to the receptor for thyroid-stimulating hormone. Antibodies to thyroglobulin and to the thyroid hormones T3 and T4 may also be produced.
These antibodies cause hyperthyroidism because they bind to the TSHr and chronically stimulate it. The TSHr is expressed on the follicular cells of the thyroid gland the cells that produce thyroid hormone , and the result of chronic stimulation is an abnormally high production of T3 and T4. This, in turn, causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goiter.
The infiltrative exophthalmos frequently encountered has been explained by postulating that the thyroid gland and the extraocular muscles share a common antigen which is recognized by the antibodies. Antibodies binding to the extraocular muscles would cause swelling behind the eyeball.
The "orange peel" skin has been explained by the infiltration of antibodies under the skin, causing an inflammatory reaction and subsequent fibrous plaques. The three types of autoantibodies to the TSH receptor currently recognized are: Thyroid stimulating immunoglobulins: these antibodies mainly IgG act as long-acting thyroid stimulants, activating the cells in a longer and slower way than TSH, leading to an elevated production of thyroid hormone.
Thyroid growth immunoglobulins: these antibodies bind directly to the TSH receptor and have been implicated in the growth of thyroid follicles. Thyrotrophin binding-inhibiting immunoglobulins: these antibodies inhibit the normal union of TSH with its receptor. Some actually act as if TSH itself is binding to its receptor, thus inducing thyroid function. Other types may not stimulate the thyroid gland, but prevent TSI and TSH from binding to and stimulating the receptor.
Another effect of hyperthyroidism is bone loss from osteoporosis, caused by an increased excretion of calcium and phosphorus in the urine and stool. The effects can be minimized if the hyperthyroidism is treated early.
This can cause stomach upset, excessive urination, and impaired kidney function. Goiter is an enlarged thyroid gland and is of the diffuse type i. Diffuse goiter may be seen with other causes of hyperthyroidism, although Graves' disease is the most common cause of diffuse goiter.
A large goiter will be visible to the naked eye, but a small one mild enlargement of the gland may be detectable only by physical examination. Occasionally, goiter is not clinically detectable, but may be seen only with computed tomography or ultrasound examination of the thyroid. Another sign of Graves' disease is hyperthyroidism, i.
Normal thyroid levels are also seen, and occasionally also hypothyroidism , which may assist in causing goiter though it is not the cause of the Graves' disease. Hyperthyroidism in Graves' disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free unbound T3 and T4.
Other useful laboratory measurements in Graves' disease include thyroid-stimulating hormone TSH, usually undetectable in Graves' disease due to negative feedback from the elevated T3 and T4 , and protein-bound iodine elevated.
Serologically detected thyroid-stimulating antibodies, radioactive iodine RAI uptake, or thyroid ultrasound with Doppler all can independently confirm a diagnosis of Grave's disease. Biopsy to obtain histiological testing is not normally required, but may be obtained if thyroidectomy is performed. Discussion Sarcoidosis is a multisystemic, chronic granulomatous disease with unknown etiology, characterized by non-caseating granuloma formation.
Sarcoid involvement of the thyroid gland has been detectedupon autopsy or fine needle aspiration biopsy and thyroidectomy. Goiter, subacute thyroiditis and thyroid cancer have been reported among other thyroid disorders accompanying sarcoidosis.
Further studies on this topic are required. References R. Baughman, A. Teirstein, M. Judson, M.