eMedicine Specialties > Endocrinology > Thyroid

Hyperthyroidism: 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): Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Contributor Information and Disclosures

Updated: Jun 8, 2009

Follow-up

Further Outpatient Care

  • Patients with normalization of thyroid functions after surgery require routine follow-up because they may develop hypothyroidism (from their chronic thyroiditis), recurrent hyperthyroidism, or thyroid eye disease sometime in the future.
  • Care after initiation of antithyroid medications includes the following:
    • After 4-6 weeks, antithyroid medications usually must be reduced; otherwise, the patient becomes hypothyroid. Hypothyroidism causes the usual symptoms of fatigue and weight gain, but in patients with Graves disease, it has been anecdotally associated with worsening of thyroid ophthalmopathy.
    • Initially, the patient should have thyroid function tests performed every 4-6 weeks until thyroid levels are stabilized on a low dose of antithyroid medication. Perform follow-up tests of thyroid function at least every 3 months for the first year. After 12-18 months, stop antithyroid medication or decrease it in patients with Graves hyperthyroidism to determine if the patient has gone into remission.
    • Non–Graves hyperthyroidism rarely has remissions. Once a patient with Graves hyperthyroidism becomes euthyroid on oral antithyroid medication, consider other definitive treatment, such as radioactive iodine therapy. A significant fraction of patients with Graves disease go into remission, and most eventually, over many years, become hypothyroid from autoimmune destruction of the gland.
  • Care after radioactive iodine ablation includes the following:
    • Ablation of the gland occurs over several (4-5) months after the therapy. Most patients become hypothyroid. Checking thyroid functions every 4-6 weeks until they stabilize is recommended.
    • Once the thyroid hormone levels start falling into the low-normal range, stopping antithyroid medications and considering starting a low dose of thyroid hormone replacement before the patient becomes hypothyroid is reasonable; however, some prefer to document persistently elevated TSH values off antithyroid medication before starting thyroid hormone replacement. Starting with partial or low-dose thyroid hormone replacement is recommended (25-50 mcg/d and adjusted every 6-8 wk to normalize the TSH level). Starting with full replacement doses when TSH first becomes elevated after131 I therapy leads to a higher incidence of hyperthyroidism due to overreplacement.
    • After131 I therapy, patients can in rare cases become thyrotoxic due to vigorous thyroid destruction and release of preformed hormone. Also, radioablation can cause the release of thyroid antigens and exacerbate the autoimmune thyroid disease process. When the former happens, it often is accompanied by a painful, radiation-induced thyroiditis that can be treated with nonsteroidal anti-inflammatory medication or glucocorticoids.
  • Care after subthyroidectomy or other thyroid surgery includes the following:
    • Most patients remain euthyroid after a lobectomy or lobectomy plus isthmusectomy. Obtain thyroid function tests 3-4 weeks postoperatively after a lobectomy to ensure normal thyroid function.
    • After subtotal thyroidectomy for hyperthyroidism and cessation of antithyroid therapy, most patients become hypothyroid, depending on how much functional tissue is left by the surgeon.
    • After a subtotal thyroidectomy, partial replacement (T 4 , 50-75 mcg/d) is recommended, to begin shortly after surgery. Monitor thyroid function tests 4-8 weeks postoperatively, and adjust the T4 dose to maintain a normal TSH level.

Complications

  • Graves ophthalmopathy
    • Graves ophthalmopathy is more common in women than in men.
    • Although 50% of patients with Graves disease have clinical evidence of thyroid eye disease, only 5% develop severe ophthalmopathy, eg, diplopia, visual-field deficits, blurred vision, tearing, and photophobia. The less serious symptoms (photophobia, irritation, tearing) are treated with tight-fitting sunglasses that should be worn at all times when the patient is outside and saline eye drops that are taken as necessary for comfort.
    • The pathogenesis of Graves ophthalmopathy lies in the deposition of glycosaminoglycans (GAG) in the extraocular muscles and adipose and connective tissue of the retro-orbit, leading to T-cell activation. The TSH receptor antigen is thought to be a key mediator in the process of T-cell activation.
    • Patients should be monitored by an ophthalmologist if exposure keratitis is suspected. Exposure keratitis usually occurs when eyelid closure is incomplete and the cornea is exposed at night, when the patient does not blink. Characteristically, the patient complains of irritation and tearing upon awakening. This is treated with saline gel or drops and by taping eyelids closed with paper tape prior to sleep. Some ophthalmologists are concerned about corneal abrasion from the tape and instead recommend that patients wear goggles at night to maintain a moist eye.
    • A medical emergency occurs when sufficient orbital edema exists to cause optic nerve compression with early loss of color vision and orbital pain. Without treatment, continued pressure of the optical nerve may cause permanent vision loss. High-dose glucocorticoids are administered with consideration for decompressive surgery and radiation therapy. (See image below and Image 6.)


Severe proptosis and eyelid retraction from thyro...

Severe proptosis and eyelid retraction from thyroid-related orbitopathy. This patient also had optic nerve dysfunction from thyroid related orbitopathy.

Severe proptosis and eyelid retraction from thyro...

Severe proptosis and eyelid retraction from thyroid-related orbitopathy. This patient also had optic nerve dysfunction from thyroid related orbitopathy.

    • Cigarette smoking is also a significant risk factor, increasing the odds of ophthalmopathy approximately 7-fold. Patients who are treated with radioactive iodine are more likely to experience worsening of their ophthalmopathy than are patients treated with antithyroid medications or surgery. 
  • Dermopathy
    • This is an infiltrative dermopathy, usually over the lower extremities, that is characterized by an accumulation of glycosaminoglycans and inflammatory cells in the dermis. The skin changes usually include a nonpitting erythematous edema of the anterior shins.
    • Dermopathy can occur at other sites of repeat trauma. The dermopathy usually only occurs in the presence of significant ophthalmopathy. No effective treatment exists. Nightly occlusive wraps of the affected site are recommended with plastic wrap after application of a high-potency topical steroid cream.

Prognosis

  • Hyperthyroidism from toxic multinodular goiter and toxic adenoma is permanent and usually occurs in adults. After normalization of thyroid functions with antithyroid medications, radioactive iodine ablation usually is recommended as the definitive therapy. Long-term, high-dose antithyroid medication is not recommended. Both conditions probably will continue to grow slowly in size during antithyroid medication therapy. The prognosis is good after radioactive iodine therapy.
    • Generally, the thyrotoxic areas are ablated, and patients may remain euthyroid. Those who become hypothyroid after radioactive iodine therapy are easily maintained on thyroid hormone replacement therapy, with T4 taken once daily.
    • Patients with Graves disease often become hypothyroid in the natural course of their disease. Whether treatment is radioactive iodine or surgery, the outcome usually is hypothyroidism. The development of an eye disease can happen at a time distant from the initial diagnosis and therapy. Generally, after the diagnosis, the ophthalmopathy slowly improves over years.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • If a physician treats enough patients who are hyperthyroid, eventually the physician will encounter a patient who develops agranulocytosis or hepatitis from the antithyroid medications. Discussing these adverse effects with patients before starting therapy is important; give the patients written instructions or document verbal instructions to stop the medication and receive a blood count with differentials for a high fever (>100.5°F) or a severe sore throat.
  • The use of radioisotopes to diagnose and treat thyroid disease exposes the practitioner to certain risks. Examples of potential problems include the administration of isotopes to patients who are pregnant or may become pregnant in the near future. The Nuclear Regulatory Commission and specific state agencies maintain specific regulations on the proper use of radioisotopes, and practitioner noncompliance may lead to fines and other disciplinary actions.
 


More on Hyperthyroidism

Overview: Hyperthyroidism
Differential Diagnoses & Workup: Hyperthyroidism
Treatment & Medication: Hyperthyroidism
Follow-up: Hyperthyroidism
Multimedia: Hyperthyroidism
References
Further Reading

References

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  2. [Best Evidence] Heeringa J, Hoogendoorn EH, van der Deure WM, et al. High-normal thyroid function and risk of atrial fibrillation: the Rotterdam study. Arch Intern Med. Nov 10 2008;168(20):2219-24. [Medline].

  3. FDA MedWatch Safety Alerts for Human Medical Products. Propylthiouracil (PTU). US Food and Drug Administration. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm164162.htm. Accessed June 3, 2009.

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  7. Porterfield JR Jr, Thompson GB, Farley DR, et al. Evidence-based management of toxic multinodular goiter (Plummer's Disease). World J Surg. Jul 2008;32(7):1278-84. [Medline].

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Keywords

hyperthyroidism, thyroid, TSH, Graves disease, hyperthyroid, thyroiditis, thyroid hormone, thyroid nodule, thyroid function, thyroid treatment, thyroid goiter, thyroid medication, thyroid medicine, thyroid problem, thyroidectomy, enlarged thyroid, thyroid-stimulating hormone, thyroid problems symptoms, thyrotoxicosis, diffuse toxic goiter, Graves' disease, Hashimoto thyroiditis, toxic multinodular goiter, toxic multi-nodular goiter, Plummer disease, Plummer's disease, subacute thyroiditis, toxic adenoma, iodide-induced thyrotoxicosis, thyrotoxicosis factitia, thyroid-stimulating hormone, thyroid carcinoma, struma ovarii with thyrotoxicosis, antithyroid medication, anti-thyroid medication, radioactive iodine therapy, iodine radiotherapy, elevated levels of free thyroxine, elevated levels of free triiodothyronine, molar hydatidiform pregnancy, choriocarcinoma, pituitary tumors, metastatic thyroid carcinoma, heat intolerance, oligomenorrhea, unexplained weight loss, lid lag, sinus tachycardia, atrial fibrillation, high output failure, fine tremor, muscle weakness, anxiety, thyroid ophthalmopathy, pernicious anemia, periorbital edema, chemosis, conjunctival edema, conjunctival injection, proptosis, myasthenia gravis, vitiligo, adrenal insufficiency, type I diabetes mellitus, apathetic hyperthyroidism, follicular thyroid adenoma, toxic thyroid adenoma, Jod-Basedow syndrome, dermoid tumors, ovarian teratomas, congestive heart failure, CHF, left ventricular thickening, dermopathy, extraocular muscle dysfunction, diplopia, swelling of the pretibial area, tachycardia, atrial arrhythmia, systolic hypertension, rheumatoid arthritis, nontoxic goiter, thyroid autonomy, granulomatous thyroiditis, HLA-DRw3, HLA-B89, Hashimoto hypothyroidism

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)

Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Frederick H Ziel, MD, Associate Professor of Medicine, David Geffen School of Medicine at UCLA; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group
Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, 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.

 
 
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