A more recent article on hyperthyroidism is available. A handout on treating hyperthyroidismwritten by the authors of this article. The proper treatment of hyperthyroidism depends on recognition of the signs and symptoms of the disease and determination of the etiology.
Other common causes include thyroiditis, toxic multinodular goiter, ptu and atenolol for hyperthyroid, 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. 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. Clinical hyperthyroidism, ptu and atenolol for hyperthyroid, also called thyrotoxicosis, is caused by the effects of excess thyroid hormone and can be triggered by different disorders.
Etiologic diagnosis influences prognosis and therapy. The prevalence of hyperthyroidism in community-based studies has been estimated at 2 percent for women and 0.
Total thyroidectomy is recommended only for patients with severe disease or large goiters in whom recurrences would be more problematic. Nonselective beta blockers such as propranolol Inderal should be prescribed for symptom control because they have a more direct effect on hypermetabolism. For information about the SORT evidence rating system, see page or https: Hyperthyroidism presents with multiple symptoms that vary according to the age of the patient, duration of illness, magnitude of hormone excess, and presence of comorbid conditions, ptu and atenolol for hyperthyroid.
Common symptoms and signs are listed in Table 13 with attention to the differences in clinical presentation between younger and older patients. Older patients often present with a paucity of classic signs and symptoms, which can make the diagnosis more difficult. The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication. The causes of hyperthyroidism, and key clinical features that differentiate each condition, are outlined in Table 2.
Lymphocytic thyroiditis, postpartum thyroiditis, medication-induced thyroiditis. Iodine-induced hyperfunctioning of thyroid gland iodide ingestion, radiographic contrast, amiodarone [Cordarone]. Functioning pituitary adenoma thyroid-stimulating hormone ; trophoplastic tumors human chorionic gonadotropin. Information from references 6 and 7. It can be familial and associated with other autoimmune diseases. Toxic multinodular goiter causes 5 percent of the cases of hyperthyroidism in the United States and can be 10 times more common in iodine-deficient areas.
Toxic adenomas are autonomously functioning coconut oil antifungal antibacterial that are found most commonly in younger patients and in iodine-deficient areas. Subacute thyroiditis produces an abrupt onset of thyrotoxic symptoms as hormone leaks from an inflamed gland. It often follows a viral illness. Symptoms usually resolve within eight ptu and atenolol for hyperthyroid. This condition can be recurrent in some patients.
Postpartum thyroiditis can occur in up to 5 to 10 percent of women in the first three to six months after delivery. A transient hypothyroidism often occurs before resolution Figure 1 Reprinted with permission from Ross D. Medical diseases in women. Primary care of women. Iodine-induced hyperthyroidism can occur after intake of excess iodine in the diet, exposure to radiographic contrast media, ptu and atenolol for hyperthyroid, or medications.
Excess iodine increases the synthesis and release of thyroid hormone in iodine-deficient patients and in older patients with preexisting multinodular goiters. Amiodarone- Cordarone- induced hyperthyroidism can be found in up to 12 percent of treated patients, especially those in iodine-deficient areas, and occurs by two mechanisms.
Because amiodarone contains 37 percent iodine, type I is an iodine-induced hyperthyroidism see above. Amiodarone is the most common source of iodine excess in the United States. Type II is a thyroiditis that occurs in patients with normal thyroid glands. Medications such as interferon and interleukin-2 aldesleukin also can cause type II.
Factitial hyperthyroidism is caused by the intentional or accidental ingestion of excess amounts of thyroid hormone. Some patients may take thyroid preparations to achieve weight loss.
Rare causes of hyperthyroidism include metastatic thyroid cancer, ovarian tumors that produce thyroid hormone struma ovariitrophoblastic tumors that produce human chorionic gonadotrophin and activate highly sensitive TSH receptors, and TSH-secreting pituitary tumors. A diagnostic approach to patients who present with signs and symptoms of hyperthyroidism is summarized in Figure 2. Further testing is warranted if the TSH level is abnormal, ptu and atenolol for hyperthyroid. An undetectable TSH level is diagnostic of hyperthyroidism.
Nonspecific laboratory findings can occur in hyperthyroidism, including anemia, granulocytosis, lymphocytosis, hypercalcemia, transaminase elevations, and alkaline phosphatase elevation.
Algorithm for diagnosing hyperthyroidism. Information from references 5 and The goal of therapy is to correct the hypermetabolic state with the fewest side effects and the lowest incidence of hypothyroidism. Beta blockers and iodides are used as treatment adjuncts. Antithyroid drugs, radioactive iodine, and surgery are the main treatment options ptu and atenolol for hyperthyroid persistent hyperthyroidism Table 3.
Prompt control of symptoms; treatment of choice for thyroiditis; first-line therapy before ptu and atenolol for hyperthyroid, radioactive iodine, and antithyroid drugs; short-term therapy in pregnancy. Use with caution in older patients and in patients with pre-existing heart disease, chronic obstructive pulmonary disease, or asthma.
Block the conversion of T 4 to T 3 and inhibit hormone release. Rapid decrease in thyroid hormone levels; preoperatively when other medications are ineffective or contraindicated; during pregnancy when antithyroid drugs are not tolerated; with antithyroid drugs to treat amiodarone- Cordarone- induced hyperthyroidism. Paradoxical increases in hormone release with prolonged use; common side effects of sialadenitis, conjunctivitis, or acneform rash; interferes with the response to radioactive iodine; prolongs the time to achieve euthyroidism with antithyroid drugs.
Interferes with the organification of ptu and atenolol for hyperthyroid PTU can block peripheral conversion of T 4 toT 3 in large doses. High relapse rate; relapse more likely in smokers, patients with large goiters, and patients with positive thyroid-stimulating antibody levels at end of therapy; major side effects red yeast rice and tricor polyarthritis 1 to 2 percentagranulocytosis 0, ptu and atenolol for hyperthyroid.
Treatment of choice for patients who are pregnant and children who have had major adverse reactions to antithyroid drugs, toxic nodules in patients younger than 40 years, and large goiters with compressive symptoms; can be used for patients who are noncompliant, refuse radioactive iodine, ptu and atenolol for hyperthyroid, or fail antithyroid drugs, and in patients with severe disease who could not tolerate recurrence; may be done for cosmetic reasons.
Risk of hypothyroidism 25 percent or hyperthyroid relapse 8 percent ; temporary or permanent hypoparathyroidism orlaryngeal paralysis less than 1 percent ; higher morbidity and cost than radioactive iodine; requires patient to be euthyroid preoperatively with antithyroid drugs or iodides to avoid thyrotoxic crisis.
Information from references 589and 14 through Beta blockers offer prompt relief of the adrenergic symptoms of hyperthyroidism such as tremor, palpitations, heat intolerance, and nervousness.
Propranolol Inderal has been used most widely, but other beta blockers can be used. Nonselective beta blockers such as propranolol, are treatment plan and objectives because they have a more direct effect on hypermetabolism. The dose should be increased progressively until symptoms are controlled. In most cases, a dosage of 80 to mg per day is sufficient. Iodides block the peripheral conversion of thyroxine T4 to triiodothyronine T3 and inhibit hormone release.
Organic iodide radiographic contrast agents e. The dosage of either agent is 1 g per day for up to 12 weeks. Antithyroid drugs act principally by interfering with the organification of iodine, thereby suppressing thyroid hormone levels. Remission rates vary with the length of treatment, but rates of 60 percent have been reported when ptu and atenolol for hyperthyroid is continued for two years. A recent randomized trial 27 indicated that relapse was more likely in patients who smoked, had large goiters, or had elevated thyroid-stimulating antibody levels at the end of therapy.
Methimazole usually is the drug of choice in nonpregnant patients because of its lower cost, longer half-life, and lower incidence of hematologic side effects.
The starting dosage is 15 to 30 mg per day, and it can be given in conjunction with a beta blocker. At one year, ptu and atenolol for hyperthyroid, if the patient is clinically and biochemically euthyroid and a thyroid-stimulating antibody level is not detectable, therapy can be discontinued.
If the thyroid-stimulating antibody level is elevated, continuation of therapy for another year should be considered. Once antithyroid drug therapy is discontinued, the patient should be monitored every three months for the first year, because relapse is more likely to occur during this time, and then annually, because relapse can occur years later.
If relapse occurs, radioactive iodine or surgery generally is recommended, although antithyroid drug therapy can be restarted. PTU is preferred for pregnant women because methimazole has been associated with rare congenital abnormalities.
The starting dosage of PTU is mg three times per day with a maintenance dosage of to mg daily. Agranulocytosis is the most serious complication of antithyroid drug therapy and is estimated to occur in 0. Routine monitoring of white cell counts remains controversial, but results of one study 29 showed that close monitoring of white cell counts allowed for earlier detection of agranulocytosis.
In this study, patients had white cell counts every two weeks for the first two months, then monthly. In most cases, agranulocytosis is reversible with supportive treatment. It is inexpensive, highly effective, easy to administer, and safe. There has been reluctance to use radioactive iodine in women of childbearing years because of the theoretical risk of cancer of the thyroid, leukemia, or genetic damage in future offspring.
Long-term follow-up of patients has not validated these concerns. The treatment dosage of radioactive iodine has been a topic of much debate. A gland-specific dosage based on the estimated weight of the gland and the hour uptake may allow a lower dosage and result in a lower incidence of hypothyroidism but may have a higher recurrence rate, ptu and atenolol for hyperthyroid.
Some studies 818 have shown that the eventual incidence of hypothyroidism is similar regardless of the radioactive iodine dosage. The high-dose regimen is clearly favored in older patients, those with cardiac disease, and other groups who need prompt control of hyperthyroidism to avoid complications. Patients with toxic nodular goiter or toxic adenomas are more radio resistant and generally need high-dose therapy to achieve remission.
They have a lower incidence of eventual hypothyroidism because the rest of the gland has been suppressed by the toxic nodules and protected from the effects of radioactive iodine. Using antithyroid drugs to achieve a euthyroid ptu and atenolol for hyperthyroid before treatment with radioactive iodine is not recommended for most patients, but it may improve safety for patients with severe or complicated hyperthyroidism.