The rate of progression to overt hyperthyroidism is higher in persons with thyroid-stimulating hormone levels less than 0. Subclinical hyperthyroidism is associated with an increased risk of atrial fibrillation and heart failure in older adults, increased cardiovascular and all-cause mortality, and decreased bone mineral density and increased bone fracture risk in postmenopausal women.
However, the effectiveness of treatment in preventing these conditions is unclear. A possible association between subclinical hyperthyroidism and quality-of-life parameters and cognition is controversial. The U. Preventive Services Task Force found insufficient evidence to assess the balance of benefits and harms of screening for thyroid dysfunction in asymptomatic persons.
The American Thyroid Association and the American Association of Clinical Endocrinologists recommend treating patients with thyroid-stimulating hormone levels less than 0. Subclinical hyperthyroidism is defined by a low or undetectable serum thyroid-stimulating hormone TSH level, with normal free thyroxine T 4 and total or free triiodothyronine T 3 levels. Since the most recent review on this topic, 2 studies have strengthened the association between subclinical hyperthyroidism and the risk of cardiovascular disease and bone fractures Table 1.
Enlarge Print. To reduce the risk of atrial fibrillation, heart failure, and mortality, physicians should treat adults with subclinical hyperthyroidism who are 65 years or older and have TSH levels less than 0. To decrease the risk of further bone loss, physicians should treat postmenopausal women with TSH levels less than 0. Do not order multiple tests in the initial evaluation of a patient with suspected thyroid disease.
Check thyroid-stimulating hormone level, and if abnormal, follow up with additional evaluation and treatment depending on the findings. Do not routinely order thyroid ultrasonography in patients with abnormal thyroid function tests if there is no palpable abnormality of the thyroid gland. Information from references 1 through 7. Subclinical hyperthyroidism may result from endogenous overproduction of thyroid hormone, administration of thyroid hormone to suppress malignancy, or excessive thyroid hormone replacement therapy in patients with hypothyroidism.
Common causes of endogenous subclinical hyperthyroidism include Graves disease, autonomous functioning thyroid adenoma, and multinodular toxic goiter.
Transient TSH suppression may occur during subacute, painless silent , or postpartum thyroiditis. The Third National Health and Nutrition Examination Survey evaluated TSH, free T 4 , and thyroid antibody levels in a sample population older than 12 years that represented the geographic and ethnic distribution of the U. A clinical history can distinguish subclinical hyperthyroidism from other causes of low TSH not related to thyroid overactivity, such as the use of certain drugs e.
In general, free T 4 and T 3 levels tend to be lower in persons with these conditions, whereas persons with subclinical hyperthyroidism may have free T 4 and T 3 levels in the mid to high reference range. Reassessment of TSH, free T 3 , and free T 4 levels is appropriate after two to four months to evaluate whether low TSH is persistent and whether subclinical thyroid disease has progressed to overt hyperthyroidism.
A suggested diagnostic approach is outlined in Figure 1. Algorithm for the diagnosis of suspected subclinical hyperthyroidism. Update on subclinical hyperthyroidism. Am Fam Physician.
Subclinical hyperthyroidism progresses to overt hyperthyroidism in a minority of patients. The disease course is less predictable in subclinical hyperthyroidism caused by Graves disease, with possible remission, progression, or no change in up to 36 months of follow-up. Cardiovascular effects of subclinical hyperthyroidism include an increased average heart rate, risk of atrial arrhythmias and heart failure, left ventricular mass and diastolic dysfunction, and reduced heart rate variability.
In a cohort of 2, adults older than 60 years, those with TSH levels less than 0. A pooled analysis of six prospective cohort studies that included 25, participants with a mean follow-up of 10 years found that those with TSH levels less than 0. A large Danish retrospective population-based study found that subclinical hyperthy-roidism is associated with increased all-cause mortality and major adverse cardiovascular events, with heart failure as the leading cause of increased cardiovascular mortality.
Exogenous subclinical hyperthyroidism due to excessive levothyroxine replacement was also associated with increased cardiovascular and overall mortality in patients with fully suppressed TSH levels less than 0.
Some studies suggest that treatment of subclinical hyperthyroidism with antithyroid medication 18 or radioactive iodine 19 may improve symptoms, heart rate, and cardiovascular parameters.
However, no long-term prospective controlled studies have assessed whether treatment reduces the risk of arrhythmias, cardiovascular morbidity, or mortality. Overt hyperthyroidism is associated with increased bone turnover, decreased bone density particularly in cortical bone , and increased risk of fractures. Subclinical hyperthyroidism may exert similar effects in postmenopausal women. There is little evidence that subclinical hyperthyroidism has an effect on bone in men or premenopausal women.
In a cross-sectional study of women with endogenous subclinical hyperthyroidism TSH levels of 0. A meta-analysis of 13 prospective cohort studies 70, pooled participants, 3. Physical and mental aspects of quality of life may be affected in patients with subclinical hyperthyroidism. The association between low TSH levels and cognitive impairment is controversial.
A systematic review of 23 studies found evidence to support an association between cognitive impairment and subclinical hyperthyroidism or low TSH within the reference range.
In , a consensus panel representing members of the American Thyroid Association ATA , the American Association of Clinical Endocrinologists, and the Endocrine Society recommended against population-based screening for thyroid disease.
Preventive Services Task Force USPSTF and the American Academy of Family Physicians concluded that the current evidence is insufficient to assess the balance of benefits and harms of screening for thyroid dysfunction in non-pregnant, asymptomatic adults. Heart disease. Hyperthyroid symptoms. Postmenopausal no estrogen or bisphosphonate therapy. Treatment should be based on the underlying etiology of subclinical hyperthyroidism. In patients with toxic multinodular goiter or a solitary autonomous nodule, radioactive iodine ablation is a definitive treatment and is preferred because spontaneous remission is unlikely to occur.
It is caused by antibodies that attack the thyroid and turn it on. Genes: a molecular unit of heredity of a living organism. Living beings depend on genes, as they code for all proteins and RNA chains that have functions in a cell. Triiodothyronine T 3 : the active thyroid hormone, usually produced from thyroxine. TSH: thyroid stimulating hormone — produced by the pituitary gland that regulates thyroid function; also the best screening test to determine if the thyroid is functioning normally.
Radioactive iodine uptake RAIU : this is a measurement of activity of the thyroid gland and is reported as the percent of a dose of radioactive iodine that is retained in the thyroid gland 24 h after the dose is given. An increase in RAIU usually indicates hyperthyroidism. Braunstein, M.
Mutation: a permanent change in one of the genes. Occasionally, when screening a person who does not appear to have obvious thyroid disease, a TSH will be found to be very low or not detectable. In those cases, if the free T 4 is low, one might consider the diagnosis of central hypothyroidism a problem with the pituitary gland or the effect of another illness on TSH levels. If the free T 4 is normal or high, then a diagnosis of hyperthyroidism might be considered. However, this study illustrates a different diagnostic possibility, showing that the physician must keep an open mind when evaluating thyroid tests, especially when the patient does not have any symptoms.
In a prior study, a group of 20 patients who had a TSH that was not detectable by the commonly used assays, was found to have a mutation involving one of the chains that make up the TSH molecule.
The TSH with this mutation was found to have normal function, but almost half of the patients were inappropriately treated because their TSH levels were not detectable. The current article describes all studies done on a new family carrying the same mutation, and reports results that indicate that the mutation described changes only a very small portion of the molecule that is needed for the attachment of the TSH to the antibodies used in the assays, therefore TSH is not detected although is present in normal quantities and has normal function.
Thyroid ; Epub June 15, The first member of the family that was studied was a 4 year old boy. His 10 year old brother had identical thyroid tests.
Their mother, older brother and sister had a normal TSH.
0コメント