ITEMS IN AFP WITH MESH TERM:
ABSTRACT: Subclinical hyperthyroidism is an increasingly recognized entity that is defined as a normal serum free thyroxine and free triiodothyronine levels with a thyroid-stimulating hormone level suppressed below the normal range and usually undetectable. The thyroid-stimulating hormone value is typically measured in a third-generation assay capable of detecting approximately 0.01 microU per mL (0.01 mU per L). Subclinical hyperthyroidism may be a distinct clinical entity, related only in part to Graves' disease or multinodular goiter. Persons with subclinical hyperthyroidism usually do not present with the specific signs or symptoms associated with overt hyperthyroidism. A detailed clinical history should be obtained, a physical examination performed and thyroid function tests conducted as part of an assessment of patients for subclinical hyperthyroidism and to evaluate the possible deleterious effects of excess thyroid hormone on end organs (e.g., heart, bone). A reasonable treatment option for many patients is a therapeutic trial of low-dose antithyroid agents for approximately six to 12 months in an effort to induce a remission. Further research regarding the etiology, natural history, pathophysiology, and treatment of subclinical hyperthyroidism is warranted.
Diagnosing Night Sweats - Article
ABSTRACT: Night sweats are a common outpatient complaint, yet literature on the subject is scarce. Tuberculosis and lymphoma are diseases in which night sweats are a dominant symptom, but these are infrequently found to be the cause of night sweats in modern practice. While these diseases remain important diagnostic considerations in patients with night sweats, other diagnoses to consider include human immunodeficiency virus, gastroesophageal reflux disease, obstructive sleep apnea, hyperthyroidism, hypoglycemia, and several less common diseases. Antihypertensives, antipyretics, other medications, and drugs of abuse such as alcohol and heroin may cause night sweats. Serious causes of night sweats can be excluded with a thorough history, physical examination, and directed laboratory and radiographic studies. If a history and physical do not reveal a possible diagnosis, physicians should consider a purified protein derivative, complete blood count, human immunodeficiency virus test, thyroid-stimulating hormone test, erythrocyte sedimentation rate evaluation, chest radiograph, and possibly chest and abdominal computed tomographic scans and bone marrow biopsy.
Subclinical Thyroid Disease - Article
ABSTRACT: Subclinical thyroid dysfunction is defined as an abnormal serum thyroid-stimulating hormone level (reference range: 0.45 to 4.50 microU per mL) and free thyroxine and triiodothyronine levels within their reference ranges. The management of subclinical thyroid dysfunction is controversial. The prevalence of subclinical hypothyroidism is about 4 to 8.5 percent, and may be as high as 20 percent in women older than 60 years. Subclinical hyperthyroidism is found in approximately 2 percent of the population. Most national organizations recommend against routine screening of asymptomatic patients, but screening is recommended for high-risk populations. There is good evidence that subclinical hypothyroidism is associated with progression to overt disease. Patients with a serum thyroid-stimulating hormone level greater than 10 microU per mL have a higher incidence of elevated serum low-density lipoprotein cholesterol concentrations; however, evidence is lacking for other associations. There is insufficient evidence that treatment of subclinical hypothyroidism is beneficial. A serum thyroid-stimulating hormone level of less than 0.1 microU per mL is associated with progression to overt hyperthyroidism, atrial fibrillation, reduced bone mineral density, and cardiac dysfunction. There is little evidence that early treatment alters the clinical course.
Hyperthyroidism: Diagnosis and Treatment - Article
ABSTRACT: The proper treatment of hyperthyroidism depends on recognition of the signs and symptoms of the disease and determination of the etiology. The most common cause of hyperthyroidism is Graves' disease. Other common causes include thyroiditis, toxic multinodular goiter, toxic adenomas, and side effects of certain medications. The diagnostic workup begins with a thyroid-stimulating hormone level test. When test results are uncertain, measuring radionuclide uptake helps distinguish among possible causes. When thyroiditis is the cause, symptomatic treatment usually is sufficient because the associated hyperthyroidism is transient. Graves' disease, toxic multinodular goiter, and toxic adenoma can be treated with radioactive iodine, antithyroid drugs, or surgery, but in the United States, radioactive iodine is the treatment of choice in patients without contraindications. Thyroidectomy is an option when other treatments fail or are contraindicated, or when a goiter is causing compressive symptoms. Some new therapies are under investigation. Special treatment consideration must be given to patients who are pregnant or breastfeeding, as well as those with Graves' ophthalmopathy or amiodarone-induced hyperthyroidism. Patients' desires must be considered when deciding on appropriate therapy, and dose monitoring is essential.
Thyroiditis - Article
ABSTRACT: Thyroiditis is an inflammation of the thyroid gland that may be painful and tender when caused by infection, radiation, or trauma, or painless when caused by autoimmune conditions, medications, or an idiopathic fibrotic process. The most common forms are Hashimoto's disease, subacute granulomatous thyroiditis, postpartum thyroiditis, subacute lymphocytic thyroiditis, and drug-induced thyroiditis (caused by amiodarone, interferon-alfa, interleukin-2, or lithium). Patients may have euthyroidism, hyperthyroidism, or hypothyroidism, or may evolve from one condition to another over time. Diagnosis is by clinical context and findings, including the presence or absence of pain, tenderness, and autoantibodies. In addition, the degree of radioactive iodine uptake by the gland is reduced in most patients with viral, radiation-induced, traumatic, autoimmune, or drug-induced inflammation of the thyroid. Treatment primarily is directed at symptomatic relief of thyroid pain and tenderness, if present, and restoration of euthyroidism.
Hyperthyroidism - Clinical Evidence Handbook
Update on Subclinical Hyperthyroidism - Article
ABSTRACT: Subclinical hyperthyroidism is defined by low or undetectable serum thyroid-stimulating hormone levels, with normal free thyroxine and total or free triiodothyronine levels. It can be caused by increased endogenous production of thyroid hormone (as in Graves disease or toxic nodular goiter), administration of thyroid hormone for treatment of malignant thyroid disease, or unintentional excessive thyroid hormone therapy. The rate of progression to overt hyperthyroidism is higher in persons who have suppressed thyroid-stimulating hormone levels compared with those who have low but detectable levels. Subclinical hyperthyroidism is associated with an increased risk of atrial fibrillation in older adults, and with decreased bone mineral density in postmenopausal women; however, the effectiveness of treatment in preventing these conditions is unknown. There is lesser-quality evidence suggesting an association between subclinical hyperthyroidism and other cardiovascular effects, including increased heart rate and left ventricular mass, and increased bone turnover markers. Possible associations between subclinical hyperthyroidism and quality of life parameters, cognition, and increased mortality rates are controversial. Prospective randomized con- trolled trials are needed to address the effects of early treatment on potential morbidities to help determine whether screening should be recommended in the asymptomatic general population.
Gynecomastia - Article
ABSTRACT: Gynecomastia is defined as benign proliferation of glandular breast tissue in men. Physiologic gynecomastia is common in newborns, adolescents, and older men. It is self-limited, but can be treated to minimize emotional distress and physical discomfort. Nonphysiologic gynecomastia may be caused by chronic conditions (e.g., cirrhosis, hypogonadism, renal insufficiency); use of medications, supplements, or illicit drugs; and, rarely, tumors. Discontinuing use of contributing medications and treating underlying disease are the mainstay of treatment. Medications, such as estrogen receptor modulators, and surgery have a role in treating gynecomastia in select patients. Treatment should be pursued early and should be directed by the patient.