HipotiroIdismo

bnormalities in the complete blood count and metabolic profile that may be found in patients with hypothyroidism include the following[2] :

Anemia
Dilutional hyponatremia
Hyperlipidemia
Reversible increases in creatinine [2]
Elevations in transaminases and creatinine kinase

¿Qué es este medicamento?

La LEVOTIROXINA es una hormona tiroidea. Este medicamento puede mejorar los síntomas de deficiencia tiroidea, tales como hablar con lentitud, falta de energía, aumento de peso, caída del cabello, piel seca y sensibilidad inusual al frío. También sirve para tratar una enfermedad llamada bocio (la dilatación de la glándula tiroides). Se utiliza también para tratar algunos tipos de cáncer tiroideo junto con la cirugía y otros medicamentos.

¿Cómo debo utilizar este medicamento?

Tome este medicamento por vía oral con agua abundante. Es mejor tomar este medicamento con el estómago vacío por lo menos 30 minutos antes o 2 horas después de una comida. Siga las instrucciones de la etiqueta del medicamento. Tómelo a la misma hora todos los días. No tome su medicamento con una frecuencia mayor que la indicada.

Hable con su pediatra para informarse acerca del uso de este medicamento en niños. Aunque este medicamento ha sido recetado a niños y bebés tan menores como unos pocos días de edad para condiciones selectivas, las precauciones se aplican. Para los bebés, puede triturar la tableta y mezclarla con una pequeña cantidad (5-10 ml o 1 a 2 cucharaditas) de agua, leche materna o formula del lactante sin soya. No lo mezcle con formula del lactante a base de soya.

¿Qué efectos secundarios puedo tener al utilizar este medicamento?

Efectos secundarios que debe informar a su médico o a su profesional de la salud tan pronto como sea posible:

reacciones alérgicas como erupción cutánea, picazón o urticarias, hinchazón de la cara, labios o lengua
dolor en el pecho
sudoración excesiva o intolerancia al calor
pulso cardiaco rápido o irregular
nerviosismo
erupción cutánea o urticaria
hinchazón de tobillos, pies o piernas
temblores
Efectos secundarios que, por lo general, no requieren atención médica (debe informarlos a su médico o a su profesional de la salud si persisten o si son molestos):

cambios en el apetito
cambios en los períodos menstruales
diarrea
caída del cabello
dolor de cabeza
problemas para dormir
pérdida de peso
¿Qué puede interactuar con este medicamento?

amiodarona
antiácidos
medicamentos antitiroideos
suplementos de calcio
carbamazepina
colestiramina
colestipol
digoxina
hormonas femeninas, incluyendo el contraconceptivo o las píldoras anticonceptivas
suplementos de hierro
ketamina
productos líquidos de nutrición, como Ensure
medicamentos para resfríos y problemas respiratorios
medicamentos para la diabetes
medicamentos para la depresión mental
medicamentos o productos a base de hierbas para bajar de peso o reducir el apetito
fenobarbital u otros barbitúricos
fenitoína
prednisona u otros corticosteroides
rifabutina
rifampicina
isoflavonas de soya
sucralfato
teofilina
warfarina

Ultrasonography of the neck and thyroid can be used to detect nodules and infiltrative disease. It has little use in hypothyroidism per se unless a secondary anatomic lesion in the gland is of clinical concern. Hashimoto thyroiditis is usually associated with a diffusely heterogeneous ultrasonographic image. In rare cases, it may be associated with lymphoma of the thyroid. Serial images with fine-needle aspiration (FNA) of suspicious nodules may be useful.

The use of color flow Doppler scanning allows assessment of vascularity, which can help to distinguish thyroiditis from Graves disease. Glands with the former will have decreased flow, whereas glands with the latter will have increased flow.

Any thyroid nodules noted on imaging studies should undergo standard evaluation.

Euthyroid hyperthyroxinemia is defined as a condition in which the serum total thyroxine (T4) and triiodothyronine (T3) concentrations are increased, but the thyroid-stimulating hormone (TSH) concentration is normal and there are no clinical signs or symptoms of thyroid dysfunction. These changes may be transient or persistent.[1]

In the past, euthyroid hyperthyroxinemia was a diagnostic challenge and many patients were inappropriately treated for thyroid disease. Today, serum TSH is a screening test for thyroid function, and a normal TSH value should not be followed by measurement of total T4. In these circumstances, euthyroid hyperthyroxinemia frequently remains undetected with no harm to the patients.

Related Medscape topics include Hypothyroidism, Pediatric Hypothyroidism, Neurological Manifestations of Thyroid Disease, and Thyroid Dysfunction Induced by Amiodarone Therapy.

The term myxedema has been applied to several clinical entities and is often used interchangeably with severe hypothyroidism, the common clinical condition in which the thyroid gland produces abnormally low levels of hormones.

Myxedema also refers to 2 different dermatologic conditions. Pretibial myxedema, an uncommon skin disorder, occurs not in cases of hypothyroidism but in hyperthyroid states, including, most commonly, Graves disease. The term pretibial is somewhat misleading, because the condition can affect other areas of the body and could more accurately be called localized dermopathy.

The other skin condition, called myxedema, occurs in severe, long-standing hypothyroid states and is caused by the deposition of mucopolysaccharides within the dermis.

This article discusses myxedema coma, an uncommon but life-threatening form of untreated hypothyroidism with physiological decompensation.[1, 2, 3, 4] The condition occurs in patients with long-standing, untreated hypothyroidism and is usually precipitated by a secondary insult, such as climate-induced hypothermia, infection, or another systemic condition, or drug therapy. Patients with myxedema coma have changes in their mental status, including lethargy, stupor, delirium, or coma. A more appropriate term for myxedema coma is myxedema crisis; this article often uses the term myxedema coma/crisis.

Background
Riedel thyroiditis, or Riedel's thyroiditis (RT), is a rare, chronic inflammatory disease of the thyroid gland characterized by a dense fibrosis that replaces normal thyroid parenchyma. The fibrotic process invades adjacent structures of the neck and extends beyond the thyroid capsule. This feature differentiates RT from other inflammatory or fibrotic disorders of the thyroid. Extension beyond the thyroid also differentiates this from the fibosing variant of Hashimoto thyroiditis. Gross pathology is shown in the image below. (See Etiology and Workup.)

Gross pathology of Riedel thyroiditis. The cut edg
Gross pathology of Riedel thyroiditis. The cut edge is avascular, with a characteristic white color. Image courtesy of SL Lee.
Involvement in RT may be unilateral or bilobar. Thyroid function depends on the extent to which the normal thyroid gland has been replaced by fibrotic tissue. Most patients are euthyroid, but hypothyroidism is noted in approximately 30% of cases. Rarely, hyperthyroidism can occur, but this is probably secondary to a coexisting condition. (See Prognosis, Presentation, and Workup.)

Some experts have traditionally believed that RT is not primarily a thyroid disease but rather that it is a manifestation of the systemic disorder multifocal fibrosclerosis. Approximately one third of RT cases are associated with clinical findings of multifocal fibrosclerosis at the time of diagnosis. (See Etiology.)

In 1883, Professor Bernhard Riedel first recognized the disease. He published a description of 2 cases in 1896 and of a third case in 1897.[1] Riedel used the term eisenharte struma to describe the stone-hard consistency of the thyroid gland and its fixation to adjacent structures. He noted the presence of chronic inflammation with fibrosis and the absence of malignancy on microscopic examination. Simple wedge resection of the thyroid isthmus was used to alleviate tracheal obstruction and is still the preferred surgical therapy for RT.

Complications
Because of the encroachment beyond the thyroid capsule, nonthyroid problems can be associated with RT. Complications of Riedel thyroiditis can include the following:

Airway obstruction
Dysphonia
Hoarseness - Due to recurrent laryngeal involvement
Hypothyroidism
Hypoparathyroidism
Dysphagia
Stridor - Due to tracheal compression

Deficiency of thyroid hormone leads to a state called hypothyroidism. Common causes of hypothyroidism include the following:

Treatment with radioactive iodine (I 131) for Graves disease
Hashimoto disease - An autoimmune process in which lymphocytic infiltration and fibrous tissue accumulation cause replacement of normal thyroid tissue
Drug-induced hypothyroidism - Known to occur with amiodarone and iodine (ie, Wolff-Chaikoff effect)
Hereditary disorders of the iodothyronine synthesis pathway (thyroxine [T4] and triiodothyronine [T3])
Pituitary tumors and related surgical resections
Hypothyroidism can cause several symptoms, ranging from mild (eg, fatigue, weight gain, cold intolerance, mental slowing, muscle cramping) to severe (eg, heart enlargement, myxedema coma [rare]).

Without regard to the cause of hypothyroidism, neuromuscular and musculoskeletal manifestations can be observed in many patients with the condition.[1] These manifestations can occur at any time in the hypothyroidism disease process. Usually mild, they include weakness, pain, aching, and stiffness.

Hypothyroid myopathy typically manifests as polymyositis-like myopathy with proximal muscle weakness and an increased creatine kinase level.[2, 3] However, it sometimes manifests as muscle enlargement (pseudohypertrophy); in adults, this condition is called Hoffman syndrome.[4, 5, 6] In children with hypothyroid disease (cretinism), a pattern of proximal weakness and diffuse muscle enlargement is known as Kocher-Debr é -S é m é laigne syndrome.

Several case reports describe rhabdomyolysis associated with hypothyroidism.[7] In these cases, the hypothyroidism is thought to have predisposed individuals to rhabdomyolysis.

Related Medscape Reference topics:

Endocrine Myopathies

Hypothyroidism [Endocrinology]

Pediatric Hypothyroidism

Myopathies

Neurological Manifestations of Thyroid Disease

Related Medscape resources:

Resource Center Hypothyroidism

Resource Center Thyroid Disease

Hypothyroidism is a common endocrine disorder resulting from deficiency of thyroid hormone. In the United States and other areas of adequate iodine intake, autoimmune thyroid disease (Hashimoto disease) is the most common cause of hypothyroidism; worldwide, iodine deficiency remains the foremost cause.

The image below depicts the hypothalamic-pituitary-thyroid axis.

The hypothalamic-pituitary-thyroid axis. Levels of
The hypothalamic-pituitary-thyroid axis. Levels of circulating thyroid hormones are regulated by a complex feedback system involving the hypothalamus and pituitary gland.
Signs and symptoms
Hypothyroidism commonly manifests as a slowing in physical and mental activity but may be asymptomatic. Symptoms and signs are often subtle and neither sensitive nor specific.

The following are symptoms of hypothyroidism:

Fatigue, loss of energy, lethargy
Weight gain
Decreased appetite
Cold intolerance
Dry skin
Hair loss
Sleepiness
Muscle pain, joint pain, weakness in the extremities
Depression
Emotional lability, mental impairment
Forgetfulness, impaired memory, inability to concentrate
Constipation
Menstrual disturbances, impaired fertility
Decreased perspiration
Paresthesia and nerve entrapment syndromes
Blurred vision
Decreased hearing
Fullness in the throat, hoarseness
The following are symptoms more specific to Hashimoto thyroiditis:

Feeling of fullness in the throat
Painless thyroid enlargement
Exhaustion
Transient neck pain, sore throat, or both
Physical signs of hypothyroidism include the following:

Weight gain
Slowed speech and movements
Dry skin
Jaundice
Pallor
Coarse, brittle, straw-like hair
Loss of scalp hair, axillary hair, p***c hair, or a combination
Dull facial expression
Coarse facial features
Periorbital puffiness
Macroglossia
Goiter (simple or nodular)
Hoarseness
Decreased systolic blood pressure and increased diastolic blood pressure
Bradycardia
Pericardial effusion
Abdominal distention, ascites (uncommon)
Hypothermia (only in severe hypothyroid states)
Nonpitting edema (myxedema)
Pitting edema of lower extremities
Hyporeflexia with delayed relaxation, ataxia, or both
Myxedema coma is a severe form of hypothyroidism that most commonly occurs in individuals with undiagnosed or untreated hypothyroidism who are subjected to an external stress. Features are as follows:

Altered mental status
Hypothermia

HIPERTIROIDISMO. Revisión de la evidencia actual sobre la prevención, diagnóstico y tratamiento del hipertiroidismo.

El hipertiroidismo es un estado clínico caracterizado por la concentración excesiva de tiroxina (T4), triyodotironina (T3), o ambas en el suero, con la supresión de la hormona estimulante del tiroides (TSH). Algunos observadores prefieren denominar a esta condición tirotoxicosis y reservar el término hipertiroidismo a los tipos de tirotoxicosis que se producen cuando la glándula tiroides sintetiza y secreta demasiada hormona tiroidea. Para evitar confusiones, los autores consideran que hipertiroidismo y tirotoxicosis son lo mismo y por lo tanto, solo utilizarán el término hipertiroidismo.

Se considera hipertiroidismo manifiesto (“overt”) cuando el nivel de TSH en el suero es bajo y se asocia con niveles elevados de T4 libre o total y/o T3 libre o total. Se denomina hipertiroidismo “subclínico" a la combinación de niveles bajos de TSH sérica con niveles séricos de T4 y T3 dentro de los límites de referencia de la población. Por lo tanto, los términos manifiesto y subclínico se definen por lo datos bioquímicos, sin hacer referencia a las características clínicas. Aunque los síntomas y signos suelen ser preponderantes en el hipertiroidismo manifiesto, pueden estar presentes o no en el hipertiroidismo subclínico. Se calcula que en Estados Unidos la prevalencia de hipertiroidismo es de alrededor de 0,4%-1,2%; casi el 40% de los casos es de hipertiroidismo manifiesto y 60% de hipertiroidismo subclínico.

¿Quién tiene un riesgo elevado de hipertiroidismo?

Las personas con mayor riesgo de hipertiroidismo son aquellas con bocio difuso o nodular, diabetes mellitus tipo 1, enfermedades endocrinas y autoinmunes no endocrinas y, personas con antecedentes familiares de hipertiroidismo o hipotiroidismo. Los medicamentos que aumentan el riesgo de hipertiroidismo son la amiodarona, el interferón α, la interleucina-2, el litio y el yoduro. Los agentes de contraste yodado usados para obtener imágenes también aumentan el riesgo de hipertiroidismo en los individuos con enfermedad autoinmune preexistente o enfermedad nodular tiroidea.

¿Cuál prueba debería usarse para el cribado del hipertiroidismo?

La mejor manera de detectar el hipertiroidismo es mediante la determinación de los niveles séricos de TSH. La TSH está baja tanto en el hipertiroidismo manifiesto como en el subclínico, debido a la retroalimentación negativa de los niveles elevados de la hormona tiroidea en la hipófisis, además de que los análisis están estandarizados, son precisos y ampliamente disponibles.

¿Qué síntomas despiertan la sospecha de hipertiroidismo?

Los síntomas que sugieren hipertiroidismo son: nerviosismo, hipersudoración, intolerancia al calor, palpitaciones, fatiga, pérdida de peso, taquicardia, disnea, debilidad, edema de las piernas, síntomas oculares, labilidad emocional y defecación frecuente sin aumento del peso de las heces (hiperdefecación).

Los pacientes ancianos con hipertiroidismo a menudo tienen síntomas menos típicos, más leves y sutiles, que suelen estar dominados por la fatiga, la depresión, la pérdida de peso y la fibrilación auricular. Esta presentación clínica se describe como hipertiroidismo apático. Algunos elementos de la historia también pueden sugerir una causa específica de hipertiroidismo. El dolor o la inflamación ocular, la visión doble o un trastorno de la piel de la cresta tibial sugieren la enfermedad de Graves.

El embarazo reciente aumenta la posibilidad de tiroiditis posparto. El dolor anterior del cuello, el malestar general, la fiebre y el dolor de garganta son característicos de la tiroiditis subaguda. La amiodarona, el litio, el interferón α, la interleucina-2 o el antecedente de haber usado yoduro de potasio o haber estado expuesto a agentes de contraste radiológico yodados aumentan la probabilidad de hipertiroidismo inducido por fármacos o yodo.

*Acceso exclusivo para profesionales registrados en IntraMed: http://www.intramed.net/76989

Euthyroid sick syndrome can be described as abnormal findings on thyroid function tests that occur in the setting of a nonthyroidal illness (NTI), without preexisting hypothalamic-pituitary and thyroid gland dysfunction. After recovery from an NTI, these thyroid function test result abnormalities should be completely reversible.

Multiple alterations in serum thyroid function test findings have been recognized in patients with a wide variety of NTI without evidence of preexisting thyroid or hypothalamic-pituitary disease. The most prominent alterations are low serum triiodothyronine (T3) and elevated reverse T3 (rT3), leading to the general term "low T3 syndrome." Thyroid-stimulating hormone (TSH), thyroxine (T4), free T4 (FT4), and free T4 index (FTI) also are affected in variable degrees based on the severity and duration of the NTI. As the severity of the NTI increases, both serum T3 and T4 levels drop and gradually normalize as the patient recovers, as shown in the image below.

Euthyroid sick syndrome. Relationship between seru
Euthyroid sick syndrome. Relationship between serum thyroid hormone concentrations and severity of nonthyroidal illness (NTI). Abbreviations: reverse triiodothyronine (rT3), thyroid-stimulating hormone (TSH), free thyroxine (FT4), thyroxine (T4), triiodothyronine (T3).
TSH is affected in variable degrees, but, in the overwhelming majority of patients, TSH is above 0.05 μ IU/mL. In severe, critical illness, most patients have reduced T4 levels. In patients hospitalized for NTI, about 10% have abnormally low TSH values; the highest incidence occurs in the most severely ill group. In the sickest patients who manifest low T4, TSH elevates to hypothyroid levels at the recovery phase, returning to reference range levels with complete recovery, as shown in the image below.

Euthyroid sick syndrome. Relationship between seve
Euthyroid sick syndrome. Relationship between severity and duration of nonthyroidal illness (NTI) and thyroid hormone levels. Abbreviations: reverse triiodothyronine (rT3), free thyroxine (free T4), thyroxine (T4), triiodothyronine (T3).
These changes in thyroid function test results are observed in most of the acute and chronic illnesses. Examples of illness include the following:

Gastrointestinal diseases
Pulmonary diseases
Cardiovascular diseases
Renal diseases
Infiltrative and metabolic disorders
Inflammatory conditions
Myocardial infarction
Starvation
Sepsis
Burns
Trauma
Surgery
Malignancy
Bone marrow transplantation
Alterations in thyroid function test findings may reflect changes in production of thyroid hormone by effects on the thyroid itself, on the hypothalamic-pituitary-thyroid axis, or on peripheral tissue metabolism of the hormones, or by a combination of these effects.

A general conviction exists that patients with thyroid function test result abnormalities do not have hypothyroidism despite the low serum hormone levels in blood and low T3 in most of the tissues. Many patients with NTI also receive drugs that affect thyroid hormone regulation and metabolism. This discussion does not consider pharmacologic interference an intrinsic part of the spectrum of changes in hypothalamic-pituitary-thyroid function that occur in NTI. Consider pharmacologic interferences as part of the evaluation of a patient who has thyroid function test result abnormalities.

Recent studies
Coceani et al investigated whether low levels of T3 in euthyroid patients are associated with the presence of and prognosis for coronary artery disease (CAD). The authors assessed data from 1047 euthyroid patients who had undergone coronary angiography for suspected CAD. The results, before and after multivariate logistic regression analysis, indicated that a link exists between low levels of free T3 (FT3) and the presence of either single-vessel or multivessel CAD. By mean 31-month follow-up, the total and cardiac mortality rates, before and after multivariate Cox regression analysis, were higher in patients with low T3 syndrome (Cox analysis: total mortality HR = 1.80; cardiac mortality HR = 2.58). The authors concluded that within the study cohort, low FT3 levels and low T3 syndrome, even in patients with no history of myocardial infarction or chronic heart failure, were associated, respectively, with the presence of and an adverse prognosis for CAD.[1]