Painless lymphocytic thyroiditis

Thyrotoxicosis is associated with an increase in the number of beta-adrenergic receptors in many tissues. Beta-blockers therefore lessen many of the symptoms and signs of thyrotoxicosis, including tachycardia and tremulousness.[32]Geffner DL, Hershman JM. Beta-adrenergic blockade for the treatment of hyperthyroidism. Am J Med. 1992 Jul;93(1):61-8. http://www.ncbi.nlm.nih.gov/pubmed/1352658?tool=bestpractice.com They may also reduce the risk of atrial arrhythmia.

Non-selective beta-blockers (e.g., propranolol) reduce peripheral sympathomimetic symptoms. However, longer-acting beta-1-selective agents (e.g., atenolol) may increase compliance due to once-daily dosing and are associated with fewer adverse effects. Any beta-blocker may be used, but if there is concern about exacerbating underlying bronchospasm, shorter-acting agents should be given. Dose is increased until pulse is below 90 bpm, assuming that BP remains satisfactory and bronchospasm does not develop. As the thyrotoxicosis resolves, the dose can be tapered to avoid bradycardia and hypotension.

If patients cannot tolerate beta-blockers because of bronchospasm or other symptoms, calcium-channel blockers (verapamil or diltiazem) should be used to ameliorate tachycardia and possibly prevent tachyarrhythmias.[38]Nordin H, Galloe AM, Ladefoged SD, et al. The effects of propranolol and verapamil on hyperthyroid heart symptoms and function, assessed by systolic time intervals. Acta Endocrinol (Copenh). 1993 Apr;128(4):297-300. http://www.ncbi.nlm.nih.gov/pubmed/8498148?tool=bestpractice.com The dose is adjusted so as to reduce the heart rate to below 90 bpm if BP allows.

Addition of systemic corticosteroids may be considered in some patients with moderate thyrotoxicosis who cannot tolerate symptoms.

Thyrotoxicosis is associated with an increase in the number of beta-adrenergic receptors in many tissues. Beta-blockers therefore lessen many of the symptoms and signs of thyrotoxicosis, including tachycardia and tremulousness.[32]Geffner DL, Hershman JM. Beta-adrenergic blockade for the treatment of hyperthyroidism. Am J Med. 1992 Jul;93(1):61-8. http://www.ncbi.nlm.nih.gov/pubmed/1352658?tool=bestpractice.com They may also reduce the risk of atrial arrhythmia.

Non-selective beta-blockers (e.g., propranolol) may better reduce peripheral sympathomimetic symptoms; however, long-acting beta-1-selective agents (e.g., atenolol) may increase compliance and are associated with fewer adverse effects. Any beta-blocker may be used, but if there is a concern that beta blockade might exacerbate underlying bronchospasm, treatment should be initiated using shorter-acting agents. Dose is increased until pulse is below 90 bpm, assuming that BP remains satisfactory and the patient does not develop bronchospasm. As the thyrotoxicosis resolves, the dose may need to be tapered to avoid bradycardia and hypotension.

If beta-blockers are not tolerated because of bronchospasm or other symptoms, calcium-channel blockers (verapamil or diltiazem) may be used to ameliorate tachycardia and possibly prevent tachyarrhythmias.[38]Nordin H, Galloe AM, Ladefoged SD, et al. The effects of propranolol and verapamil on hyperthyroid heart symptoms and function, assessed by systolic time intervals. Acta Endocrinol (Copenh). 1993 Apr;128(4):297-300. http://www.ncbi.nlm.nih.gov/pubmed/8498148?tool=bestpractice.com The dose is adjusted so as to reduce the heart rate to below 90 bpm if BP allows.

In severe thyrotoxicosis or patients with complications (e.g., tachyarrhythmias, exacerbation of ischaemia), corticosteroids should be given. Towards the end of treatment, corticosteroids should be tapered to prevent symptoms of adrenal insufficiency.

Patients who have received high-dose glucocorticoid therapy may have suppression of the pituitary-adrenal axis and require glucocorticoid administration for physiological stresses that occur within several months of completing a course of treatment. The status of the pituitary-adrenal axis can be assessed by an ACTH stimulation test with administration of synthetic corticotrophin.

If thyroid-stimulating hormone is <10 milliunits/L (<10 microunits/mL) and the patient has absent or minimal symptoms, treatment may be deferred. Monitoring is recommended in this group.[33]Stuckey BG, Kent GN, Allen JR. The biochemical and clinical course of postpartum thyroid dysfunction: the treatment decision. Clin Endocrinol (Oxf). 2001 Mar;54(3):377-83. http://www.ncbi.nlm.nih.gov/pubmed/11298091?tool=bestpractice.com

The symptoms of hypothyroidism (e.g., fatigue, bloating, muscle cramps, weight gain, poor concentration, and cold intolerance) are easily reversed by administering levothyroxine.

Because hypothyroidism may reduce and correction of hypothyroidism may increase the metabolic clearance rate of other drugs, careful assessment of comorbid conditions and treatments is necessary before and during treatment.

In contrast to this effect, hypothyroidism reduces the metabolic clearance of vitamin K-dependent clotting factors, thereby increasing warfarin requirements during hypothyroidism and reducing them following treatment.[31]Woeber KA. Thyrotoxicosis and the heart. N Engl J Med. 1992 Jul 9;327(2):94-8. http://www.ncbi.nlm.nih.gov/pubmed/1603141?tool=bestpractice.com

To reduce long-term variability in dosing, many endocrinologists recommend using one brand of levothyroxine and avoiding multiple generic preparations.

Dose is adjusted at 6-week intervals until serum thyroid-stimulating hormone (TSH) concentrations are normalised.

After 6 months, therapy can be stopped or tapered to assess recovery of thyroid function. If TSH remains elevated after stopping levothyroxine treatment, hormone therapy should be re-started and continued indefinitely. Patient should be restarted at the same dose the patient was taking before attempted withdrawal/tapering and titrated to a normal serum TSH concentration.

Women who experience postnatal thyroiditis have a high risk of developing recurrent postnatal thyroiditis in subsequent pregnancies (69%).[19]Lazarus JH, Ammari F, Oretti R, et al. Clinical aspects of recurrent postpartum thyroiditis. Br J Gen Pract. 1997 May;47(418):305-8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1313006 http://www.ncbi.nlm.nih.gov/pubmed/9219408?tool=bestpractice.com

Up to 11% of patients with sporadic painless thyroiditis will have recurrent thyroiditis.[35]Nikolai TF, Coombs GJ, McKenzie AK. Lymphocytic thyroiditis with spontaneously resolving hyperthyroidism and subacute thyroiditis: long-term follow-up. Arch Intern Med. 1981 Oct;141(11):1455-8. http://www.ncbi.nlm.nih.gov/pubmed/7283556?tool=bestpractice.com Although it is rarely done, such patients may elect to have their thyroid gland ablated with radioiodine or surgically removed between episodes when they are euthyroid.[36]Duick DS. Management of thyrotoxicosis with a low radioactive iodine uptake. Arch Intern Med. 1980 Apr;140(4):469. http://www.ncbi.nlm.nih.gov/pubmed/7362371?tool=bestpractice.com [37]Ohye H. Recurrent severe painless thyroiditis requiring multiple treatments with radioactive iodine. Thyroid. 2008 Nov;18(11):1231-2. http://www.ncbi.nlm.nih.gov/pubmed/18925835?tool=bestpractice.com