Hypothyroidism (hahy-poh-thahy-roi-diz-uhm) hypo- - Greek prefix for "under" or "below normal" thyroid - The thyroid, or thyroid gland, is an endocrine gland in vertebrates -ism - Suffix. Indicates a specific condition or state.
In 1912, Hakaru Hashimoto discovered an autoimmune disorder that affects the thyroid gland, called the Hashimoto's disease. In the early 1890s, desiccated thyroid became the preferred treatment for hypothyroidism. These natural thyroid products (thyroid extract, desiccated thyroid, or thyroglobulin) gained popularity due to their ability to replicate a normal serum protein-bound iodine (PBI) level. By 1965, around 80% of thyroid hormone prescriptions in the United States were for desiccated thyroid preparations. However, concerns arose regarding inconsistencies in the potency of these tablets, as some contained varying levels of metabolic activity. The shelf-life of desiccated tablets was also limited, leading to issues with product efficacy. The reputation of natural thyroid products was further tarnished by reports of patients not responding to treatment due to inactive thyroid hormone in their tablets. It wasn't until 1985 that the revision of the U.S. Pharmacopeia standard improved stability, but by then, natural thyroid products had lost their favor. In the 1970s, two significant developments revolutionized the treatment of hypothyroidism. Firstly, the serum thyroid-stimulating hormone (TSH) radioimmunoassay allowed for the discovery that many patients were being overtreated, leading to a significant reduction in thyroid hormone replacement dosages. Secondly, the identification of peripheral deiodinase-mediated conversion of thyroxine (T4) to triiodothyronine (T3) provided a physiological basis for l-thyroxine monotherapy. This discovery justified the use of l-thyroxine alone and addressed concerns about inconsistencies associated with desiccated thyroid. As a result, l-thyroxine monotherapy at doses to normalize serum TSH levels became the standard of care. In the 1970s, following the transition to l-thyroxine monotherapy, a subgroup of patients treated with thyroid hormone exhibited residual symptoms of hypothyroidism despite having normalized serum TSH levels. Initially, these symptoms were dismissed as unrelated to the thyroid condition or attributed to other factors such as menopause, depression, or chronic fatigue syndrome. It was challenging to determine whether these patients had been misdiagnosed, especially considering the prevalent use of thyroid hormone for nonthyroid disorders. Residual symptoms were even attributed to nonadherence to medication. To further understand the persistence of symptoms, studies examined the relationship between well-being and thyroid hormone dosage. Unblinded studies indicated that the highest well-being was achieved at supraoptimal doses, leading to suppressed TSH levels. However, a subsequent blinded trial did not replicate these findings. Patient experiences played a crucial role in highlighting the prevalence of residual hypothyroid symptoms, with numerous individuals reporting that they did not feel well despite normal serum markers of thyroid function. In 1995, the American Thyroid Association (ATA) guidelines discouraged the use of thyroid hormone preparations containing both T4 and T3 due to concerns about fluctuating and elevated serum T3 concentrations. The ATA continued to recommend l-thyroxine monotherapy in 2012, stating that synthetic combination therapies and desiccated thyroid hormone should not be used for hypothyroidism treatment. However, in 2014, the ATA revised its recommendations to acknowledge that not all l-thyroxine-treated hypothyroid patients achieve normalized serum T3 levels, and some patients experience persistent symptoms despite receiving l-thyroxine monotherapy. The guidelines now suggest titrating l-thyroxine dosage to achieve normal TSH concentrations as the primary approach, but combination therapy trials can be considered. While superiority data are lacking, some patients have reported a clinical response to desiccated thyroid preparations or combination therapy with l-thyroxine plus l-triiodothyronine. The European Thyroid Association has similar recommendations.
Hypothyroidism is a condition where the thyroid gland, located in the neck, doesn't produce enough thyroid hormones. These hormones help regulate the body's metabolism, which is how the body converts food into energy. There are many possible causes of hypothyroidism, including autoimmune disease (in which the body attacks the thyroid gland), radiation therapy, and certain medications. Symptoms of hypothyroidism can be mild or severe, and can vary from person to person. Some common symptoms include fatigue, weight gain, feeling cold, constipation, dry skin, and hair loss. In more severe cases, hypothyroidism can lead to swelling of the face, hands, and feet, as well as a hoarse voice and slowed speech. Diagnosis of hypothyroidism is typically done through blood tests, which measure levels of thyroid hormones and thyroid-stimulating hormone (TSH) in the body. Treatment for hypothyroidism involves taking a daily dose of thyroid hormone replacement medication, typically in the form of a pill. It's important to get proper treatment for hypothyroidism, as untreated hypothyroidism can lead to serious complications, including heart problems, nerve damage, and infertility. However, with proper treatment, most people with hypothyroidism can lead normal, healthy lives.
Hashimoto's diseaseHashimoto's disease is the most common cause of hypothyroidism, a condition in which the thyroid gland does not produce enough hormones. Hashimoto's disease is an autoimmune disorder that causes the body's immune system to attack the thyroid gland, leading to inflammation and damage to the gland over time. As a result, the gland may not be able to produce enough thyroid hormones, which can lead to symptoms of hypothyroidism. In some cases, Hashimoto's disease may cause the thyroid gland to become enlarged, forming a goiter. Other symptoms of hypothyroidism may include fatigue, weight gain, sensitivity to cold, dry skin, and constipation. The severity of symptoms can vary depending on the extent of thyroid damage and the individual's overall health. Treatment for hypothyroidism typically involves taking synthetic thyroid hormone replacement medication, which can help regulate hormone levels and alleviate symptoms. In some cases, surgery to remove the thyroid gland may be necessary. It is important for individuals with Hashimoto's disease to work closely with their healthcare provider to manage their condition and prevent complications.
Hypothyroidism, or an underactive thyroid gland, can have several causes. These causes can be broadly categorized as primary hypothyroidism, secondary hypothyroidism, or transient hypothyroidism. Here are some common causes associated with each category: Primary Hypothyroidism (Dysfunction of the Thyroid Gland): -- Autoimmune Thyroiditis (Hashimoto's Thyroiditis): This is the most common cause of hypothyroidism in developed countries. It occurs when the body's immune system mistakenly attacks and damages the thyroid gland, leading to decreased hormone production. -- Congenital Hypothyroidism: Some infants are born with an underdeveloped or absent thyroid gland (agenesis) or with genetic defects that affect thyroid hormone synthesis. This condition is often detected through newborn screening. -- Iodine Deficiency: Inadequate intake of iodine, an essential mineral required for thyroid hormone production, can result in hypothyroidism. However, iodine deficiency-induced hypothyroidism is less common in countries with iodine-rich diets. -- Thyroidectomy or Radioactive Iodine Treatment: Surgical removal of the thyroid gland or treatment with radioactive iodine, which is sometimes used to manage hyperthyroidism, can lead to hypothyroidism if too much thyroid tissue is removed or destroyed. Secondary Hypothyroidism (Pituitary or Hypothalamic Dysfunction): -- Pituitary Gland Dysfunction: A problem with the pituitary gland, such as a tumor, radiation treatment, or certain medications, can impair the secretion of thyroid-stimulating hormone (TSH), which stimulates the thyroid gland to produce thyroid hormones. -- Hypothalamic Dysfunction: The hypothalamus produces thyrotropin-releasing hormone (TRH), which stimulates the pituitary gland to release TSH. Any dysfunction or damage to the hypothalamus can disrupt the production of TRH and subsequently affect TSH secretion. Transient Hypothyroidism: -- Postpartum Thyroiditis: Some women develop temporary hypothyroidism after giving birth, often due to an autoimmune response targeting the thyroid gland. It may resolve on its own or require treatment. -- Subacute Thyroiditis: Inflammation of the thyroid gland, usually caused by a viral infection, can initially lead to hyperthyroidism and later progress to transient hypothyroidism. -- Medications and Treatments: Certain medications, such as lithium, interferon-alpha, and amiodarone, can interfere with thyroid function and lead to hypothyroidism. -- Iodine Excess: Although iodine deficiency is a common cause of hypothyroidism, excessive iodine intake from supplements, medications, or contrast agents used in medical procedures can also impair thyroid function.
The treatment for hypothyroidism typically involves taking thyroid hormone replacement medication. This medication helps to increase the levels of thyroid hormone in your body, which can alleviate your symptoms and improve your overall health. The most common thyroid hormone replacement medication is called levothyroxine, and it is typically taken once per day in the morning on an empty stomach. Once you start taking medication, your doctor will likely monitor your thyroid hormone levels periodically to ensure that you are taking the right dose. In addition to medication, it is important to maintain a healthy lifestyle by eating a balanced diet, getting regular exercise, and reducing stress. By following these treatment options, most people with hypothyroidism can manage their symptoms effectively and live healthy, active lives.