eMedicine Specialties > Endocrinology > Thyroid

Hashimoto Thyroiditis: Follow-up

Author: Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Coauthor(s): Sylvester Odeke, MD, FACE, Clinical Assistant Professor of Medicine, Division of Endocrinology and Metabolism, The Brody School of Medicine at East Carolina University; Steven B Nagelberg, MD, Clinical Professor, Department of Medicine, Division of Endocrinology and Metabolism, Drexel University College of Medicine
Contributor Information and Disclosures

Updated: Apr 10, 2009

Follow-up

Further Outpatient Care

  • Upon the initiation of the levothyroxine replacement therapy, check thyroid function tests, specifically TSH, initially every 6-8 weeks as dose adjustments are made. After the attainment of the clinical euthyroid state and a normal TSH level, patients and the TSH levels may be checked every 6-12 months. More frequent follow-up and TSH checks may need to be performed when patients start taking medications, such as ferrous sulphate, calcium supplementation, and multivitamins, which have a potential to impair the absorption of levothyroxine and therefore to affect the TSH level. Patients need to be advised to separate these medications from levothyroxine by at least 4 hours.
    • Follow-up care should include clinical evaluation for symptoms of hypothyroidism or iatrogenic hyperthyroidism.
    • Physical examination should routinely include weight measurement, pulse and blood pressure determinations, and thyroid examination for the presence of nodules.
    • Yearly thyroid ultrasonographic evaluation is important in patients with Hashimoto's thyroiditis because of the increased risk of thyroid nodules in these patients and for follow-up of patients with existing benign thyroid nodules.

Deterrence/Prevention

  • Although it is not deemed cost-effective to screen whole populations for hypothyroidism, the following groups deserve special consideration and should be evaluated with an annual TSH screening:
    • Elderly patients - Hypothyroidism in elderly patients may be characterized by only a few subtle symptoms, which may include voice hoarseness, confusion, depression, memory changes, and dementia. Up to 15% of patients older than 65 years may have subclinical hypothyroidism or mild thyroid failure, with these individuals feeling better following treatment.
    • Patients with a history of medical or surgical treatment of thyroid disease
    • Patients with diabetes mellitus
    • Patients with other autoimmune disorders
    • Patients with dementia or depression
    • Patients with hypercholesterolemia
    • Patients with a family history of hypothyroidism or hyperthyroidism
    • Patients with Down's syndrome or Turner's syndrome

Complications

  • Complications of overreplacement with levothyroxine sodium
    • Accelerated bone loss, reduction in bone mineral density, and osteoporosis
    • Increased heart rate, increased cardiac wall thickness, and increased contractility - These problems increase the risk of cardiac arrhythmias (especially atrial fibrillation), particularly in the elderly population.
  • Myxedema coma is a state of extreme hypothyroidism with a very high mortality rate (approaching 60%). Patients with this condition usually present with an acute precipitating condition and usually in the following settings:
    • Long-standing, undiagnosed hypothyroidism
    • Discontinuation of T4 replacement therapy
    • Failure to institute T4 replacement after radioactive iodine ablation of the thyroid in Graves disease or after total thyroidectomy
  • Myxedema coma typically manifests in winter (or during extremely cold weather) in an elderly woman who has long-standing hypothyroidism. Hospitalized patients may have a history of sedating medication use. Typical clinical findings include hypothermia, obtundation or coma, hypoventilation, bradycardia, hyponatremia, hypoglycemia, and hypotension. Besides having an elevated TSH level, these patients may have undetectable free T4 levels.
    • The usual precipitating causes include infection, cardiovascular accident, pulmonary infection, congestive cardiac failure, and drugs, such as narcotics, sedatives, anesthetic agents, antidepressants, and tranquilizers (all of which depress the respiratory drive).
    • Therapy should be conducted in an acute care unit, where the patients may require the following:
      • Ventilatory support for hypoventilation and carbon dioxide retention
      • Electrocardiographic monitoring and a Swan-Ganz catheter for hemodynamic monitoring
      • Judicious rewarming to avoid excessive vasodilatation, which would increase oxygen consumption and could lead to worsening of hypotension and vascular collapse
      • Steroids, preferably hydrocortisone in stress doses
      • Levothyroxine, administered intravenously in a loading dose of 4 mcg/kg of lean body weight - This is about 300-600 mcg, which should be administered by rapid intravenous injection. The daily maintenance dose is 50-100 mcg per day, administered intravenously until the patient can take it orally.
      • Treatment of infection or any other precipitating causes
      • Fluid restriction with or without hypertonic saline and Lasix to promote water diuresis

Prognosis

  • With early diagnosis, timely institution of levothyroxine replacement therapy, informed patient follow-up care, and attention to other attendant complications, the prognosis is excellent and patients lead a normal life.
  • Untreated myxedema coma has a poor prognosis and a high mortality rate.

Patient Education

  • Patients should know that thyroid replacement therapy in Hashimoto's thyroiditis is, except in very rare cases, lifelong.
  • Patients must be informed about the importance of compliance with their replacement therapy and must be instructed to report any symptoms suggestive of hyperthyroidism caused by overreplacement.
  • Patients must be instructed to separate—by at least 4 hours—ingestion of levothyroxine from ingestion of cholestyramine, ferrous sulfate, sucralfate, calcium carbonate, aluminum hydroxide (and other antacids), and iron-containing multivitamins, all of which impair the absorption of levothyroxine.
  • For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education article Thyroid Problems.

Miscellaneous

Medicolegal Pitfalls

  • Failure to recognize, diagnose, and properly treat Hashimoto's thyroiditis or hypothyroidism from any other cause
  • Failure to provide proper follow-up care
  • Failure to educate patients about their condition

Special Concerns

  • The following medications interfere with the absorption of levothyroxine from the gastrointestinal tract, and patients should be advised to separate ingestion of these compounds from ingestion of levothyroxine by at least 4 hours:
    • Cholestyramine
    • Ferrous sulfate
    • Sucralfate
    • Calcium carbonate
    • Aluminium hydroxide and other antacids
    • Iron-containing multivitamins
  • Medications that enhance the metabolism and clearance of levothyroxine may necessitate an increase in the replacement dose. These medications include phenytoin, carbamazepine, and rifampin.
  • Pregnancy induces a state of increased need for levothyroxine. In women with hypothyroidism and in women with inadequate thyroid reserve, this is manifested by an increase in the level of TSH and a decrease in the level of free T4.
    • The increase in the levothyroxine requirement is thought to be due to increased metabolism of thyroxine by the fetoplacental unit. The increase usually resolves and the patient returns to prepregnancy levothyroxine requirements 6-8 weeks postpartum.
    • Note that total T4 and T3 levels may actually be increased in pregnancy. This phenomenon is thought to be due to the estrogen-induced sialylation (increased sialic acid content) of the thyroxine-binding globulin (TBG). This leads to decreased clearance of the TBG by the liver and to increased levels and binding capacity of the TBG. Increased TBG synthesis is also thought to play a contributory role. The pregnancy-induced increased need for T4 occurs in the first trimester, usually within the first 8 weeks, and persists throughout pregnancy. Patients with hypothyroidism may require up to a 45-50% increase in the levothyroxine dose.
    • Patients with hypothyroidism are best followed up by monitoring the TSH and free T4 levels. Upon becoming pregnant, patients should have the TSH and free T4 levels checked within 4-8 weeks, then every 6-8 weeks while dose adjustments are being made. Patients who are adequately dosed and who are in a clinically and biochemically euthyroid state should have thyroid function tests (TSH and free T4) checked every 8 weeks. Dose adjustments should be made to keep the free T4 and TSH within reference ranges. Patients who are diagnosed with Hashimoto's thyroiditis or hypothyroidism from any cause during pregnancy should be started on a levothyroxine dose close to their replacement requirement, and the TSH level should be normalized as soon as possible. Untreated hypothyroidism carries increased maternal and fetal complications.
    • A study from Denmark found that 32% of pregnant women with type 1 diabetes had anti-TPO (compared with 8% of pregnant women who did not have diabetes).11 The presence of anti-TPO was associated with slightly higher TSH levels in these women.
  • Patients who have undergone bowel resection and have short-bowel syndrome (or malabsorption for any reason) often require increased doses of levothyroxine to maintain the euthyroid state.
  • Elderly patients and patients on androgens for various reasons usually require decreased levothyroxine replacement dosing.
  • Subclinical hypothyroidism (mild thyroid failure)
    • Up to 15% of patients aged 65 years or older may have subclinical hypothyroidism (as evidenced by an elevated TSH above 3.0 uIU/mL and normal free T4 levels) with few if any symptoms suggestive of hypothyroidism. These patients have a decreased thyroid reserve.
    • The best marker of progression to overt hypothyroidism is a combination of an elevated TSH level with presence of thyroid autoantibodies, namely anti-TPO and antithyroglobulin (anti-Tg) antibodies. The rate of progression to overt hypothyroidism is estimated to be about 5% per year.
    • Patients with positive thyroid autoantibodies but a normal TSH level should be followed up periodically to monitor for symptoms of hypothyroidism and to detect any rise in TSH level and increase in cholesterol levels. Checks can usually be performed every 6-12 months. These patients should be treated if the TSH level continues to rise, even if the level is at the upper limit of the reference range.
 


More on Hashimoto Thyroiditis

Overview: Hashimoto Thyroiditis
Differential Diagnoses & Workup: Hashimoto Thyroiditis
Treatment & Medication: Hashimoto Thyroiditis
Follow-up: Hashimoto Thyroiditis
References
Further Reading

References

  1. Hadj-Kacem H, Rebuffat S, Mnif-Feki M, et al. Autoimmune thyroid diseases: genetic susceptibility of thyroid-specific genes and thyroid autoantigens contributions. Int J Immunogenet. Apr 2009;36(2):85-96. [Medline].

  2. Duntas LH. Environmental factors and autoimmune thyroiditis. Nat Clin Pract Endocrinol Metab. Aug 2008;4(8):454-60. [Medline].

  3. Tomer Y, Huber A. The etiology of autoimmune thyroid disease: a story of genes and environment. J Autoimmun. Mar 21 2009;[Medline].

  4. Fava A, Oliverio R, Giuliano S, et al. Clinical evolution of autoimmune thyroiditis in children and adolescents. Thyroid. Feb 18 2009;[Medline].

  5. Vanderpump MP, French JM, Appleton D. The prevalence of hyperprolactinaemia and association with markers of autoimmune thyroid disease in survivors of the Whickham Survey cohort. Clin Endocrinol (Oxf). Jan 1998;48(1):39-44. [Medline].

  6. Vanderpump MP, Tunbridge WM, French JM. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clin Endocrinol (Oxf). Jul 1995;43(1):55-68. [Medline].

  7. Tomer Y, Blackard JT, Akeno N. Interferon alpha treatment and thyroid dysfunction. Endocrinol Metab Clin North Am. Dec 2007;36(4):1051-66; x-xi. [Medline][Full Text].

  8. Huber A, Menconi F, Corathers S, et al. Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis: from epidemiology to mechanisms. Endocr Rev. Oct 2008;29(6):697-725. [Medline].

  9. Baloch ZW, LiVolsi VA. Fine-needle aspiration of the thyroid: today and tomorrow. Best Pract Res Clin Endocrinol Metab. Dec 2008;22(6):929-39. [Medline].

  10. Escobar-Morreale HF, Botella-Carretero JI, Escobar del Rey F, et al. REVIEW: Treatment of hypothyroidism with combinations of levothyroxine plus liothyronine. J Clin Endocrinol Metab. Aug 2005;90(8):4946-54. [Medline][Full Text].

  11. [Best Evidence] Vestgaard M, Nielsen LR, Rasmussen AK, et al. Thyroid peroxidase antibodies in pregnant women with type 1 diabetes: impact on thyroid function, metabolic control and pregnancy outcome. Acta Obstet Gynecol Scand. 2008;87(12):1336-42. [Medline].

  12. Arafah BM. Decreased levothyroxine requirement in women with hypothyroidism during androgen therapy for breast cancer. Ann Intern Med. Aug 15 1994;121(4):247-51. [Medline].

  13. Blackshear JL, Schultz AL, Napier JS. Thyroxine replacement requirements in hypothyroid patients receiving phenytoin. Ann Intern Med. Sep 1983;99(3):341-2. [Medline].

  14. Canaris GJ, Manowitz NR, Mayor G. The Colorado thyroid disease prevalence study. Arch Intern Med. Feb 28 2000;160(4):526-34. [Medline].

  15. Doniach D, Bottazzo GF, Russell RC. Goitrous autoimmune thyroiditis (Hashimoto's disease). Clin Endocrinol Metab. Mar 1979;8(1):63-80. [Medline].

  16. Doniach D, Hudson VR, Roitt IM. Human auto-immune thyroiditis: Clinical studies. Br Med J. 1960;365-74.

  17. Fowler PB, Swale J, Andrews H. Hypercholesterolaemia in borderline hypothyroidism. Stage of premyxoedema. Lancet. Sep 5 1970;2(7671):488-91. [Medline].

  18. Holm LE, Blomgren H, Lowhagen T. Cancer risks in patients with chronic lymphocytic thyroiditis. N Engl J Med. Mar 7 1985;312(10):601-4. [Medline].

  19. Mandel SJ, Larsen PR, Seely EW. Increased need for thyroxine during pregnancy in women with primary hypothyroidism [see comments]. N Engl J Med. Jul 12 1990;323(2):91-6. [Medline].

  20. Rosenbaum RL, Barzel US. Levothyroxine replacement dose for primary hypothyroidism decreases with age. Ann Intern Med. Jan 1982;96(1):53-5. [Medline].

  21. Singer PA, Cooper DS, Levy EG. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Standards of Care Committee, American Thyroid Association [see comments]. JAMA. Mar 8 1995;273(10):808-12. [Medline].

  22. Singh N, Singh PN, Hershman JM. Effect of calcium carbonate on the absorption of levothyroxine. JAMA. Jun 7 2000;283(21):2822-5. [Medline].

  23. Stone E, Leiter LA, Lambert JR. L-thyroxine absorption in patients with short bowel. J Clin Endocrinol Metab. Jul 1984;59(1):139-41. [Medline].

  24. Surks MI, Chopra IJ, Mariash CN. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders. JAMA. Mar 16 1990;263(11):1529-32. [Medline].

  25. Tunbridge WM. The epidemiology of hypothyroidism. Clin Endocrinol Metab. Mar 1979;DA - 19790611(1):21-7. [Medline].

  26. Tunbridge WM, Brewis M, French JM. Natural history of autoimmune thyroiditis. Br Med J (Clin Res Ed). Jan 24 1981;282(6260):258-62. [Medline][Full Text].

Keywords

Hashimoto thyroiditis, Hashimoto’s thyroiditis, thyroid, hypothyroidism, TSH, hypothyroid, levothyroxine, thyroid disease, thyroid problemsgoiter, goiters, low thyroid, thyroxine, thyroid hormone, thyroiditis, thyroid treatment, hypothyroidism symptoms, T3 thyroid, T4 thyroid, thyroid disorders, thyroid-stimulating hormone, triiodothyronine, myxedema coma, chronic lymphocytic thyroiditis, struma lymphomatosa, autoimmune thyroid diseases, AITD

Contributor Information and Disclosures

Author

Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, and Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Sylvester Odeke, MD, FACE, Clinical Assistant Professor of Medicine, Division of Endocrinology and Metabolism, The Brody School of Medicine at East Carolina University
Sylvester Odeke, MD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, and North Carolina Medical Society
Disclosure: Nothing to disclose.

Steven B Nagelberg, MD, Clinical Professor, Department of Medicine, Division of Endocrinology and Metabolism, Drexel University College of Medicine
Steven B Nagelberg, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, American Medical Association, Endocrine Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Ghassem Pourmotabbed, MD†, Former Associate Professor, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Tennessee School of Medicine and Health Science Center
Ghassem Pourmotabbed, MD† is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, and Endocrine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.