Overview of Hyperthyroidism
Hyperthyroidism arises when the body is subjected to excessive quantities of thyroid hormone. This endocrine disorder affects nearly one percent of the total American population, with women experiencing it five to 10 times more frequently than men. In its mildest manifestation, hyperthyroidism may not present discernible symptoms; however, in many cases, the symptoms can be uncomfortable, disabling, or even potentially fatal.
Causes of Hyperthyroidism
Graves’ disease (attributed to Irish physician Robert Graves) is an autoimmune disorder often leading to thyroid enlargement and hyperthyroidism. Some individuals afflicted with this condition may experience swelling of muscles and other tissues surrounding the eyes, resulting in eye prominence, discomfort, or diplopia. As with other autoimmune diseases, Graves’ disease tends to impact multiple family members and is more prevalent among women than men; it typically surfaces in younger patients.
Between five and 10 percent of women develop mild to moderate hyperthyroidism within a few months following childbirth. Usually lasting for approximately one to two months in these cases, hyperthyroidism is often succeeded by several months of hypothyroidism; nonetheless, most women ultimately regain normal thyroid function. Occasionally though, the thyroid gland fails to heal—rendering hypothyroidism permanent and necessitating lifelong thyroid hormone replacement—and this condition might recur with subsequent pregnancies.
Transient (temporary) hyperthyroidism can result from silent thyroiditis: a condition seemingly identical to postpartum thyroiditis but unrelated to pregnancy and unaccompanied by a painful thyroid gland.
Subacute thyroiditis might emerge after a viral infection, characterized by the painful enlargement and inflammation of the thyroid gland. Consequently, large amounts of thyroid hormones are released into the bloodstream. Fortunately, this condition usually resolves itself spontaneously over several months—though not before a temporary period of hypothyroidism transpires.
Toxic Multinodular Goiter
Toxic multinodular goiter involves multiple nodules within the thyroid generating excessive thyroid hormone and thus causing hyperthyroidism. Typically diagnosed in patients over 50 years old, this disorder is more likely to influence heart rhythm; frequently, patients experiencing goiters for many years only become overactive later on.
A solitary nodule or lump in the thyroid might also produce an excess of thyroid hormone and consequently induce hyperthyroidism. This disorder does not exhibit familial patterns.
Excessive Iodine Ingestion
Occasionally, high concentrations of iodine from various sources—including kelp tablets, some expectorants, amiodarone (Cordarone, Pacerone – medications utilized for treating certain heart rhythm issues), and x-ray dyes—may trigger hyperthyroidism in susceptible individuals.
Overmedication with Thyroid Hormone
Patients receiving excessive thyroxine replacement therapy may develop hyperthyroidism as well. They should undergo evaluations by a physician at least once per year to determine their appropriate thyroid hormone dosage and must refrain from taking “extra” doses under any circumstances.
What are the signs and symptoms of hyperthyroidism?
When hyperthyroidism develops, a goiter (enlargement of the thyroid) is usually present and may be associated with some or many of the following features:
- Fast heart rate, often more than 100 beats per minute
- Becoming anxious, irritable, argumentative
- Trembling hands
- Weight loss, despite eating the same amount or even more than usual
- Intolerance of warm temperatures and increased likelihood to perspire
- Loss of scalp hair
- Tendency of fingernails to separate from the nail bed
- Muscle weakness, especially of the upper arms and thighs
- Loose and frequent bowel movements
- Smooth skin
- Change in menstrual pattern
- Increased likelihood for miscarriage
- Prominent “stare” of the eyes
- Protrusion of the eyes, with or without double vision (in patients with Graves’ disease)
- Irregular heart rhythm, especially in patients older than 60 years of age
- Accelerated loss of calcium from bones, which increases the risk of osteoporosis and fractures
While a general practitioner may sometimes recognize and treat the underlying cause of hyperthyroidism, input from an endocrinologist – a specialist in managing thyroid disorders – is often required. A skilled physician can identify characteristic symptoms and physical manifestations of the condition, while various diagnostic tests can help confirm the diagnosis and ascertain its etiology.
- TSH (Thyrotropin or Thyroid-Stimulating Hormone): Decreased TSH levels in blood are considered to be the most precise indicator of hyperthyroidism. When there is even a slight overproduction of thyroid hormones, the body inhibits TSH secretion. It is crucial to assess thyroid hormone concentrations along with TSH levels for an accurate hyperthyroidism diagnosis.
- Measurements of Free Thyroxine (FT4) and Free Triiodothyronine (FT3): In cases of hyperthyroidism, FT4 and FT3 values tend to elevate beyond their previous individual-specific levels (though they might remain within the standard range for the general populace). These hormone concentrations are often considerably augmented.
- TSI (Thyroid-Stimulating Immunoglobulin): A substance typically detected in blood when Graves’ disease triggers hyperthyroidism.
- RADIOACTIVE IODINE UPTAKE (RAIU) Test: The RAIU test evaluates iodine uptake by the thyroid gland, while a thyroid scan reveals its distribution throughout this gland.
- Thyroid Scan: The data obtained via a thyroid scan can provide valuable insights into identifying the etiology of hyperthyroidism and devising an appropriate treatment plan.
Effectively managing hyperthyroidism necessitates extensive evaluation and constant attention from a seasoned physician who is familiar with treating this intricate condition.
Before the advent of modern therapeutic approaches, severe cases of hyperthyroidism recorded mortality rates up to 50 percent. Today, several potent treatments are available, reducing fatal outcomes stemming from hyperthyroidism to extremely rare occurrences. Determining the optimal intervention strategy depends on factors such as the cause of hyperthyroidism, its severity, and any concurrent medical conditions.
Pharmacological Management of Hyperthyroidism
In the United States, two primary medications are utilized in addressing hyperthyroidism: propylthiouracil (PTU) and methimazole (Tapazole). Methimazole is generally favored, except during early gestation, as PTU has the potential to induce severe hepatic complications, although infrequently. These pharmacological agents function by decelerating thyroid hormone synthesis and might necessitate several months to stabilize thyroid hormone concentrations.
Antithyroid Medications and Potential Remission for Graves’ Disease Patients
Certain patients afflicted with hyperthyroidism as a consequence of Graves’ disease could undergo spontaneous or intrinsic remission following a 12- to 18-month therapeutic course with antithyroid drugs. This may occasionally circumvent the irreversible hypothyroidism that typically arises from employing other methods of therapy for hyperthyroidism. Regrettably, this remission is often transient, leading to recurrent hyperthyroidism several months or years after discontinuing medication and necessitating further intervention; therefore, a relatively small proportion of patients rely solely on antithyroid medications in the United States.
Allergic Reactions and Adverse Effects Associated with Antithyroid Drugs
Approximately five percent of patients utilizing antithyroid medications could experience an allergic reaction during the initial six weeks of therapy. Such reactions may encompass dermal manifestations like rash or urticaria; however, symptoms typically resolve within one to two weeks upon cessation of drug use without permanent sequelae.
A less frequent but more critical side effect observed in about one per 250-500 patients during the first four to eight weeks is a precipitous decline in white blood cell count in circulation. This event can heighten susceptibility to grave infections. Presenting symptoms such as pharyngalgia, infections or fever should be reported to your physician expeditiously and necessitate an immediate leukocyte evaluation. In virtually every case, discontinuation of medication restores white blood cell count to baseline values. Antithyroid drugs may also very rarely induce hepatic dysfunction or arthropathies characterized by joint pain and/or edema. The presence of icteric skin tone (jaundice), fever, appetite loss or abdominal discomfort warrants contacting your attending physician.
Radioactive Iodine Therapy
As an indispensable element in thyroid hormone synthesis, iodine is incorporated into either four (T4) or three (T3) molecules in each thyroid hormone molecule. Due to the avidity for iodine displayed by most hyperfunctional thyroid glands demonstrated during the 1940s, researchers uncovered that the gland could be effectively “deceived” into self-destruction via administration of radioactive iodine. This radionuclide is ingested orally, typically encapsulated, with rapid gastrointestinal absorption and subsequent entry into the intravascular compartment before being integrated into thyroid cells wherein a gradual process of cellular demolition ensues. Maximal benefits are generally observed within a period of three to six months.
Dose calibration for patient-specific radioiodine treatment aims to eradicate the entirety of abnormal thyroid tissue since it is not feasible to excise only an appropriate amount without eventual damage to all cells within this endocrine organ. Consequently, most endocrinologists endeavor to entirely eliminate diseased thyroid structures in a single radioiodinated therapy session. This intentionally engenders hypothyroidism which can then be efficiently managed via lifelong daily administration of orally-ingested replacement hormones.
Although treatment success rates vary according to factors such as goiter size and dosage calculation accuracy, radioactive iodine therapy has been employed safely and effectively in thousands including distinguished figures like former U.S President George H.W Bush alongside First Lady Barbara Bush. This approach is thus deemed the optimal intervention for hyperthyroidism attributable to thyroid hormone overproduction by most American thyroid specialists.
Although infrequently adopted as a first-line treatment for hyperthyroidism at present, surgical excision of the majority of thyroid tissue might be selectively indicated in specific contexts such as gestating women experiencing uncontrolled hyperthyroid symptoms that may compromise fetal health if addressed via radioactive iodine therapy. Such procedures customarily instigate permanent hypothyroidism necessitating lifelong hormonal supplementation.
Adjuvant and Alternative Therapies
Beta-adrenergic blocking agents are prescribed on an interim basis to modulate symptomatology associated with excess thyroid hormone while awaiting alternative or supplementary therapeutic onset. These drugs might exclusively suffice in instances wherein hyperthyroidism arises from inflammatory pathologies, excessive iodine intake or inadvertent ingestion of surplus exogenous thyroid hormones. High-dose iodine drops can also be administered to ameliorate severe cases of hyperthyroidism or as a preoperative measure in patients indicated for Graves’ disease surgical management.