Goiter is a condition characterized by abnormal enlargement of the thyroid gland. Majority of the cases is caused due to iodine deficiency.
Presentation
An enlarged thyroid gland is the classical symptom of goiter. The size of the enlarged gland may either appear as a single nodule, or large lump. In rare cases, goiter may produce the following signs and symptoms [5]:
- Difficulty in breathing
- Hoarseness in voice
- Coughing
- Trouble in swallowing
- Feeling of tightness in throat
Workup
Several tests are employed for diagnosing goiter. These include:
- Physical examination: A preliminary examination of the neck of the individual is done. The individual would be asked to swallow, and swelling can be determined in the neck region.
- Blood tests: Blood tests will be done to detect the levels of T3 and T4. The levels of thyroid hormones, and TSH would indicate the underlying cause of goiter. In addition, antibody test would also be required.
- Thyroid scan: This would furnish information about the size and nature of the thyroid.
- Ultrasonography: This test provides information about the size of the thyroid gland and presence of nodules, if they had been missed out during physical examination [6].
- Biopsy: This is achieved using fine needle aspiration technique, wherein a sample is obtained for analysis of the nature of the thyroid [7].
Treatment
Treatment of goiter would depend on the nature and size of the enlarged gland, underlying disease conditions if any, and symptoms experienced by the individual. The following types of methods are employed for treating the condition:
- Medications: Hormone replacement medications are required if goiter is caused due to underactive thyroid. In addition, if inflammation is the cause, then medications to reduce the same will be administered. If hyperthyroidism is the underlying cause, then medications to normalize the levels of hormones is given.
- Surgery: Surgery is the method of choice if goiter causes uncomfortable signs and symptoms. It is also considered in patients with nodular goiter [8].
- Radioactive iodine is considered in cases, when overactive thyroid has caused goiter. The radioactive material destroys the thyroid cells, thereby reducing the size of the gland [9].
Prognosis
In certain cases, simple forms of goiter can resolve on its own, without treatment. In some other cases, the gland can eventually enlarge, as a result of which, thyroid gland can stop producing enough thyroid hormone, leading to hypothyroidism.
In yet some other cases, goiter can turn toxic, and begin producing thyroid hormones on its own, causing over production of hormones, leading hyperthyroidism.
Etiology
Iodine deficiency is the most common cause of goiter in countries that do not use iodized salt. However, goiter is also a common occurrence in those parts of the world that routinely use iodized salt. In such conditions, following are the factors that lead to goiter:
- Disease conditions: Underlying disease conditions, such as Graves disease, or Hashimoto thyroiditis, which are autoimmune disorders, cause the development of goiter.
- Development of nodules: Development of fluid filled sacs at both sides of the thyroid glands causes it to enlarge, giving rise development of multinodular goiter.
- Solitary thyroid nodules: In this, a single nodule takes shape in one part of the gland causing goiter.
- Pregnancy: In such conditions, the thyroid gland can enlarge due to hormone HCG that is produced during pregnancy.
- Thyroiditis: This condition can cause the thyroid gland to swell and enlarge [2].
Epidemiology
Iodine deficiency is the most common cause of goiter worldwide. It has been estimated that about 200 to 800 million individuals with iodine deficiency develop goiter. In the US, majority of the cases of goiter occur due to underlying autoimmune disease, such as Hashimoto thyroiditis [3]. Females are more prone to develop goiter, as compared to males, with female to male ratio been 4:1.
Pathophysiology
The functioning of the thyroid gland is regulated by the hormone TSH, which is produced by the pituitary gland. The thyroid gland produces 2 hormones, namely T3 and T4. These hormones are responsible for regulating the metabolism. Along with T3 and T4, the gland also produces the hormone known as calcitonin which regulates the calcium levels in blood. The pituitary gland along with hypothalamus, also controls and regulates the hormones that are produced.
Any form of deficiency occurring in synthesis of thyroid hormone, causes increased production of TSH. Increase in the levels of TSH causes the thyroid gland to enlarge, causing in order to normalize the levels of thyroid hormones. When such a phenomenon continues for prolonged duration, goiter develops [4].
Prevention
Taking iodized salt can prevent the development of most forms of simple goiter [10]. Other forms of goiter can seldom be prevented.
Summary
Improper functioning of the thyroid gland causes it to enlarge, which eventually paves way for development of compressive syndromes. The thyroid gland is anatomically linked to the trachea, larynx, esophagus and laryngeal nerves. As a result of this, the enlargement of the gland, also gravely affects the functioning of the neighboring regions. Goiter is a painless condition; however in some it can pose difficulty in swallowing food [1].
Patient Information
Definition
Goiter is a condition characterized by enlarged thyroid gland. Enlargement of the gland is in many cases non cancerous in nature. Such a type of condition strikes more women than men.
Cause
Iodine deficiency is the most common cause of goiter worldwide. However, in countries where iodized salt is regularly used, certain underlying disease conditions, and autoimmune diseases cause goiter.
Symptoms
In majority of the cases, goiter does not cause any symptoms. In cases when the gland enlarges to a great extent, individuals experience difficulty in breathing and swallowing. Affected individuals also experience hoarseness in voice.
Diagnosis
A preliminary physical examination is done, followed by blood tests to determine the levels of thyroid hormones. In addition, thyroid scans, ultrasonography and biopsy, are also indicated to analyze the fundamental cause of goiter.
Treatment
Simple forms of goiter do not require treatment. In many cases, a wait and watch approach is considered. When symptoms are experienced, the mode of treatment is designed, depending on nature and size of thyroid gland. Medications, surgery and radioactive iodine, are administered for treating goiter.
References
- Bardin CW. Endemic goiter. In: Current Therapy in Endocrinology and Metabolism. 6th ed. Mosby-Year Book; 1997:101-112.
- Knudsen N, Perrild H, Christiansen E, et al. Thyroid structure and size and two-year follow-up of solitary cold thyroid nodules in an unselected population with borderline iodine deficiency. Eur J Endocrinol 2000; 142:224.
- Sawin CT, Geller A, Hershman JM, Castelli W, Bacharach P. The aging thyroid. The use of thyroid hormone in older persons. JAMA. May 12 1989;261(18):2653-5.
- Elte JW, Bussemaker JK, Haak A. The natural history of euthyroid multinodular goitre. Postgrad Med J 1990; 66:186.
- Braverman LE, Utiger RD. Thyroid diseases: nontoxic diffuse and multinodular goiter. In: Werner and Ingbar, eds. The Thyroid: A Fundamental and Clinical Text. 7th ed. Lippincott-Raven; 1996:889-900.
- Hegedüs L. Thyroid ultrasound. Endocrinol Metab Clin North Am 2001; 30:339.
- Arda IS, Yildirim S, Demirhan B, Firat S. Fine needle aspiration biopsy of thyroid nodules. Arch Dis Chil. 2001;85(4):313-7.
- Romanchishen AF, Iakovlev PN. [Special surgical treatment of patients with nodular tumors of the thyroid gland against the background of diffuse toxic goiter]. Vestn Khir Im I I Grek. 2005;164(1):21-4.
- Fast S, Nielsen VE, Grupe P, et al. Prestimulation with recombinant human thyrotropin (rhTSH) improves the long-term outcome of radioiodine therapy for multinodular nontoxic goiter. J Clin Endocrinol Metab 2012; 97:2653.
- Dohán O, De la Vieja A, Paroder V, et al. The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance. Endocr Rev. Feb 2003;24(1):48-77