A Synopsis of AFP's "Update on Subclinical Hyperthyroidism "

Update on Subclinical Hyperthyroidism 
INES DONANGELO, MD, PhD, and GLENN D. BRAUNSTEIN, MD, Cedars-Sinai Medical Center, Los Angeles, California
http://www.aafp.org/afp/2011/0415/p933.pdf
Am Fam Physician. 2011 Apr 15;83(8):933-938.

     Subclinical hyperthyroidism is low TSH with normal free T3 and T4.  The two categories of subclinical hyperthyroidism have either a TSH between 0.1-0.4 mIO/L or a TSH less than 0.1 mIO/L. The cause of subclinical hyperthyroidism is either endogenous (overproduction), due to Graves disease, multinodular goiter, or adenoma, or exogenous (excessive hormone therapy). Other causes of low TSH, besides subclinical hyperthyroidism, include medication (dopamine and glucocorticoids), pituitary TSH deficiency, euthyroid sick syndrome, hypothalamic disorders, and psychiatric illnesses. 
     According to the algorithm in this article, when a patient has suspected subclinical hyperthyroidism, a TSH is ordered. If it is normal, then it's probably not subclinical hyperthyroidism. If it is low, then a free T3/T4 should be ordered. If both are high, the patient has overt hyperthyroidism. If only the free T3 is high, then the patient has T3 toxicosis. If both are normal, then the patient has subclinical hyperthyroidism and more investigation is needed. A radioactive iodine uptake scan should be ordered to determine where the TSH is coming from. If the iodine uptake is increased (or normal) in a diffuse pattern, then the most likely diagnosis is Graves disease. If the uptake is increased in a localized pattern, then the diagnosis is a toxic nodular (or multinodular) goiter. If the uptake is decreased, a thyroglobulin is needed. If the thyroglobulin is decreased, then the diagnosis is exogenous thyroid hormone. If it is elevated, then the patient has subacute thyroiditis.
     Patients with subclinical hyperthyroidism will have elevated HR, more fibrillations, larger left ventricle, and lowered heart rate variability (so no nocturnal dipping). This will lead to an increased risk of cardiovascular events and atrial fibrillation. Treatment consists of methimazole or radioactive iodine. Methimazole help return the cardiovascular issues to normal after the  TSH level is fixed. Iodine does not have the same affect on the cardiovascular complications.
     Subclinical hyperthyroidism can also cause a decrease in cortical bone mineral density. It is more advanced in postmenopausal women. Elevated TSH will increase bone turnover. Treating the hyperthyroidism will stop the bone turnover. 
     Other symptoms of hyperthyroidism include palpitations, nervousness, tremor, heat intolerance, sweating, and lower well-being. There is also a relationship between TSH and cognitive function.
     There is no current recommendation to advise screening of subclinical hyperthyroidism. There is, however, a relationship between low TSH and atrial fibrillation in later life.