Hyperthyroidism: Management

University of the East
Ramon Magsaysay Memorial Medical Center, Inc.
GRADUATE SCHOOL
Aurora Boulevard, Quezon City

There is no single effective formula in dealing with hyperthyroidism. The choice of medical management for hyperthyroidism would heavily depend on its etiology, age of patient, medical status of the patient and the severity of the condition. The preference of the patient himself/herself over the treatment is also weighed in.

The goals of treatment of Graves’ disease are to control symptoms efficiently and restore euthyroidism (Ginsberg, 2003) with the fewest side effects and the lowest incidence of hypothyroidism (Reid & Wheeler, 2005). Those can be done with the 3 modalities of treatment: antithyroid drugs, radioactive iodine therapy, and thyroidectomy (Pearce, 2006).


Antithyroid drugs or thionamides

These drugs are used to decrease the amount of hormone the thyroid produce but may not cure the condition (Cooper, McDermott, & Wartofsky, 2006).

The most noted are methimazole and propylthiouracil (PTU) which blocks the thyroid gland’s ability to make new thyroid hormone.

Prolonged remission of the disease was seen in about 20% to 30% of patients with Graves’ disease who took the drugs for a period of 12 to 18 months, but causing to 5% occurrence of allergic reaction (red skin rashes, hives, and occasionally fever and joint pains) (American Thyroid Association. (n.d.). According to Siraj (2008), there is a 20% to 30% chance in attaining a permanent remission within 1 to 2 years, slightly similar to the previously mentioned case. While Ginsberg (2003) states that the remission rate is 30%-40% but a 13% occurrence of minor side effects. But according to Topliss and Eastman (2004), the risk of relapse is greater than 50%. Relapse more likely happens to patients who smoked, had large goiters, or had elevated thyroid-stimulating antibody levels at the end of therapy (Reid & Wheeler, 2005).

In rare instances, agranulocytosis and hepatitis might occur (Baskin et al., 2008). Agranulocytosis occurs in approximately 0.5% of patients treated with thionamides (Pearce, 2006). Topliss and Eastman (2004) instruct to suspend therapy while obtaining a white cell count if fever, sore throat, or other sepsis develops.

Propylthiouracil is the drug of choice for hyperthyroidism during pregnancy and lactation because the transfer of propylthiouracil to a nursing infant via breast milk seems to be less than the transfer of methimazole. Methimazole is associated with congenital abnormalities. It should be noted though that there is no hard evidence that either propylthiouracil or methimazole pose a serious risk to nursing infants. Methimazole doses of up to 20 mg/d did not cause hypothyroidism in nursing infants. But until more studies are available, monitoring of thyroid function of nursing infants is a must if the mother receives a high dose of methimazole during lactation. It is important for a pregnant woman to continue methimazole, if necessary, because uncontrolled hyperthyroidism increases the risk of complications such as preterm labour and low birth weight. (Inoue, Arata, Koren, & Ito, 2009)

For childhood Graves’ disease, antithyroid drug therapy is preferred by endocrinologists (Baskin et al., 2008). Bhadada, Bhansali, Velayutham, & Masoodi (2006) used carbimazole as the first line therapy in all juvenile patients in their studies. Carbimazole is effective, cheap, easily available and rarely associated with serious side effects. Remission with their drug treatment is 47.6% which is within the range (33-64%) of previous studies.


Radioactive iodine therapy (RAI)

RAI treats hyperthyroidism by damaging or destroying the thyroid cells that make thyroid hormone. The radioactive iodine, which is usually packaged as a capsule, is taken once orally. The radioiodine enters the blood stream and promptly taken up by the overactive thyroid cells. The radioiodine that is not taken up by the thyroid cells disappears from the body within days via urine elimination or convertion into a nonradioactive state by radioactive decay. Cells that have taken up the radioactive iodine are damaged in a span of weeks to months. Up to 70% of adults with hyperthyroidism in the US are treated with this. (American Thyroid Association, n.d.)

RAI is indicated for patients “with Graves’ hyperthyroidism who relapse after long-term antithyroid drug therapy, for patients with severe thyrocardiac disease, for most patients with toxic multinodular or uninodular goiter, and for patients with a major adverse reaction to antithyroid drugs.“ (Woeber, 2000)

Using RAI for patients with hyperthyroidism due to Graves’ disease or toxic nodular goiter is very effective. Euthyroid state can be achieved within 8 weeks for 80%-90% of patients with just a single dose. It can also reduce the goiter size by 40%. (Pearce, 2006)

The American Thyroid Association and the American Association of Clinical Endocrinologists do not consider young patients to be contraindicated for radioactive iodine therapy. But noted exceptions are young patients with single toxic adenomas as there may be the theoretical risk of developing additional thyroid nodules. (Medical Research and Practice Updates, n.d.)

Bhadada, Bhansali, Velayutham, & Masoodi (2006) consider RAI as a second line of treatment for juvenile hyperthyroidism. They deem it to be safe and effective, perhaps basing on literature, but their experience with it is limited.

Pearce (2006) have a different take on children and RAI. Because of the lack of data about the long term risks associated with radiation, RAI is considered contraindicated in children and adolescents.

Pearce (2006) adds that RAI is absolutely contraindicated during pregnancy and lactation. Even conception should be postponed for at least 6 months after treatment (Woeber, 2000). Congenital hypothyroidism can occur if RAI is used after 10–12 weeks’ gestation (Ginsberg, 2003). Baskin et al. (2008) advise against breastfeeding as well because it would be present in the breastmilk.

According to several long term studies, there are no evidence of “increased risk of thyroid cancer, leukaemia, other malignancies, reproductive abnormalities or congenital abnormalities in the offspring of treated patients”. (Topliss & Eastman, 2004)

Permanent hypothyroidism is the major side effect of RAI (Woeber, 2000). “Thyroid indices should be monitored every 1–2 months for the next 6 months to detect hypothyroidism and ensure that euthyroidism has been restored. Thereafter, measuring thyroid indices every 3 months for 1 year and then every 6–12 months is recommended.” (Ginsberg, 2003)

It is advised for patients to limit physical contact with other people for several days to prevent contamination of others due to secretions and radiation from the neck. (Ginsberg, 2003)


Thyroidectomy

Surgical removal of the thyroid gland is a permanent solution with 90% of cases being cured (Pearce, 2006). It is recommended for those not suitable for either antithyroid medication or radioactive iodine therapy. But this method includes risks like damaging of the parathyroid glands (which control calcium metabolism in the body) and nerves to the larynx (voice box) (Cooper, McDermott, & Wartofsky, 2006). It is deemed safe to be performed on the 2nd trimester of pregnancy (Pearce, 2006). It is considered a 2nd line treatment for juvenile hyperthyroidism (Bhadada, Bhansali, Velayutham, & Masoodi, 2006).

A subtotal thyroidectomy is more commonly done. It reduces the incidence of hypothyroidism to 25 % while preserving the some thyroid tissue. Although there is an 8% chance of recurrence. But a lot of surgeons are now recommending total thyroidectomy because of the high rate of relapse after subtotal thyroidectomy (Topliss & Eastman, 2004). Total thyroidectomy is usually done for patients with severe disease or large goiters (Reid & Wheeler, 2005).

After the surgery, particularly total thyroidectomy, the patient will likely become hypothyroid. But the thyroid hormone levels can still be restored to normal by treatment once a day with a thyroid hormone supplement. (American Thyroid Association, n.d.).

Thyroidectomy is now a less popular choice of treatment because of the advent of new methods. (Siraj, 2008)


As there are several ways to treat hyperthyroidism and several conditions of the illness to take account, it is integral for patients to coordinate with their doctors especially an endocrinologist. Before, during and after treatment, the health status of the patients should be monitored especially thyroid hormone levels. Prognosis is actually good as long as the patient receives the right treatment and stick to it.


Reference:

American Thyroid Association. (n.d.). Hyperthyroidism. Retrieved on February 15, 2010 from www.thyroid.org

Baskin, H.J., Cobin, R.H., Duick, D.S., Gharib, H., Guttler, R.B., Kaplan, M.M., Segal, R.L., and the American Association of Clinical Endocrinologists. (2008). American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract, 14(6):802-3. Retrieved on February 15, 2010 from http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf

Bhadada, S., Bhansali, A., Velayutham, P., and Masoodi, S.R. (2006). Juvenile Hyperthyroidism: An Experience. INDIAN PEDIATRICS, 43(4):301-7. Retrieved on February 15, 2010 from http://medind.nic.in/ibv/t06/i4/ibvt06i4p301.pdf

Cooper, D., McDermott, M., and Wartofsky, L. (2006). Hyperthyroidism. The Journal of Clinical Endocrinology & Metabolism, Vol. 91, No. 7 0. Retrieved on February 15, 2010 from http://jcem.endojournals.org/cgi/content/full/91/7/0

Ginsberg, J. (2003). Diagnosis and management of Graves' disease. CMAJ, 168 (5). Retrieved on February 15, 2010 from http://www.cmaj.ca/cgi/reprint/168/5/575

Inoue, M., Arata, N., Koren, G., and Ito, S. (2009). Hyperthyroidism during pregnancy. Can Fam Physician, 55(7): 701–703. Retrieved on February 15, 2010 from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2718594/pdf/0550701.pdf/?tool=pmcentrez

Medical Research and Practice Updates. (n.d.). Retrieved on February 15, 2010 from http://www.regimedia.com/pdf/JMJ_SEPT2001/JMJ_9_01_page62toEND.PDF

Pearce, E. (2006). Diagnosis and management of thyrotoxicosis. BMJ, 332:1369–73. doi: 10.1136/bmj.332.7554.1369.

Reid, J. and Wheeler, S. (2005). Hyperthyroidism: Diagnosis and Treatment. Am Fam Physician, 72:623-30, 635-6. Retrieved on February 15, 2010 from EBSCohost.

Siraj, E. (2008). Update on the Diagnosis and Treatment of Hyperthyroidism. Journal of Clinical Outcomes Management, 15 (6): 298–307. Retrieved on February 15, 2010 from http://www.turner-white.com/memberfile.php?PubCode=jcom_jun08_hyperthyroidism.pdf.

Topliss, D. and Eastman, C. (2004). Diagnosis and management of hyperthyroidism and hypothyroidism. MJA , 180 (4): 186-193. Retrieved on February 15, 2010 from http://www.mja.com.au/public/issues/180_04_160204/top10414_fm.pdf

Woeber, K. (2000). Update on the Management of Hyperthyroidism and Hypothyroidism. Arch Fam Med, 9(:743-747. Retrieved on February 15, 2010 from http://archfami.ama-assn.org/cgi/reprint/9/8/743