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HypothyroidismEdit

Hypothyroidism is a common endocrine disorder characterized by insufficient production of thyroid hormones by the gland, most often the thyroid follicular cells. When the body does not receive enough of these hormones, metabolic processes slow down, leading to fatigue, weight gain, cold intolerance, and a range of physical and mental changes. In adults, the condition usually arises from disease of the thyroid itself, most notably autoimmune thyroiditis such as Hashimoto's thyroiditis, or as a consequence of treatment for other thyroid conditions. It can also result from iodine deficiency in some regions, or from surgical removal or destruction of the gland. The condition is typically lifelong and requires ongoing monitoring and treatment with hormone replacement.

From a practical, patient-centered perspective, the core aim is to restore normal thyroid hormone levels in a reliable, predictable way while minimizing side effects and unnecessary medicalization. The standard therapy is inexpensive, well-studied, and effective for the vast majority of patients when properly dosed and monitored. A pragmatic approach emphasizes patient autonomy, the clinician’s judgment, and cost-conscious care, with attention to safety in special populations such as older adults and pregnant people. This article outlines the causes, diagnosis, treatment options, and the principal debates surrounding hypothyroidism, including issues of subclinical disease and management in pregnancy.

Overview

Hypothyroidism reflects a deficiency of circulating thyroid hormones, most commonly due to damage, inflammation, or loss of functional thyroid tissue. The main hormones involved are thyroxine (T4) and triiodothyronine (T3); the pituitary gland senses hormone levels via the thyroid-stimulating hormone (TSH) and responds by adjusting production. In primary hypothyroidism, the problem lies in the thyroid gland itself, whereas secondary or central hypothyroidism involves the pituitary or hypothalamus. Autoimmune destruction, surgical removal, and radioiodine therapy are among the leading causes of primary hypothyroidism, while central hypothyroidism is rarer but clinically important to recognize because it requires different diagnostic and treatment considerations.

Key points include: - The most common cause in many populations is autoimmune thyroiditis, especially in middle age and older women, with autoimmune activity detectable by antibodies such as thyroid peroxidase antibodies. See Hashimoto's thyroiditis. - Long-standing hypothyroidism can affect cardiovascular health, lipid metabolism, bone density, mood, and cognitive function, among other systems. - Diagnosis relies on laboratory testing and clinical assessment, with TSH as the primary screening test and free T4 (and sometimes free T3) to guide interpretation. See Thyroid-stimulating hormone and Free thyroxine.

Causes and pathophysiology

  • Primary hypothyroidism: The thyroid gland itself fails to produce adequate hormones. Hashimoto's disease is the leading autoimmune cause in many populations. Other causes include surgical thyroidectomy, radioactive iodine treatment for hyperthyroidism, congenital defects, and certain medications.
  • Central hypothyroidism: A pituitary or hypothalamic disorder leads to inadequate stimulation of the thyroid, often with accompanying abnormalities in other pituitary axes.
  • Iodine status: Iodine deficiency remains a major global cause of hypothyroidism in areas without iodized salt or adequate dietary iodine, though in many developed countries iodine deficiency is well controlled.
  • Drugs and other factors: Some medicines (for example, lithium or certain antiarrhythmics) can impair thyroid function or hormone metabolism; radiation exposure to the neck can also contribute.

Diagnosis

  • Screening and baseline assessment: TSH is the primary screening test because it is sensitive to small changes in thyroid hormone levels. In primary hypothyroidism, TSH is elevated and free T4 is typically low or low-normal. In central hypothyroidism, TSH may be normal or low, with a low free T4.
  • Autoimmune markers: The presence of antibodies such as thyroid peroxidase antibodies supports an autoimmune etiology in many patients. See TPO antibodies.
  • Additional testing: Free T4 and, when appropriate, free T3 help refine the diagnosis and monitor treatment. Imaging, such as thyroid ultrasound, is typically reserved for evaluating nodules or structural concerns rather than for diagnosing classic hypothyroidism.
  • Special populations: Pregnancy alters thyroid physiology and requires trimester-specific interpretation of TSH and free T4, as well as dose adjustments for replacement therapy. See Hypothyroidism in pregnancy.

Treatment and management

  • First-line therapy: The standard treatment is lifelong replacement with levothyroxine, a synthetic form of T4 that the body converts to the active hormone T3 as needed. The goal is to normalize TSH within the reference range appropriate for age and context. The therapy is favored for its predictability, stability, affordability, and strong evidence base.
  • Dosing and titration: In adults, starting doses commonly approximate 1.6 mcg/kg/day, adjusted based on weight, age, cardiovascular status, and comorbidities. Doses are rechecked after 6–8 weeks, with TSH used to guide ongoing adjustments.
  • Monitoring: Once a stable dose is achieved, monitoring intervals lengthen, but periodic checks of TSH and free T4 are recommended to ensure continued adequacy, particularly during pregnancy, aging, or changes in weight or other medications.
  • Special considerations:
    • Cardiovascular risk: In patients with ischemic heart disease or significant risk, cautious dosing and slower titration help minimize atrial fibrillation and other adverse events.
    • Interactions: Calcium, iron, certain vitamins, and some medications can interfere with levothyroxine absorption; dosing schedules should account for such interactions.
    • Pregnancy: Increasing doses during pregnancy is often necessary to maintain maternal euthyroid status for fetal development; close monitoring and frequent dose adjustments are common. See Hypothyroidism in pregnancy.
  • Alternatives and adjuncts: Some patients seek or report benefit from natural desiccated thyroid or combination therapy with liothyronine (T3). The evidence base for these approaches is mixed, and most guidelines favor T4 monotherapy as the standard unless specific circumstances or patient preferences justify a different plan. See Natural desiccated thyroid and Liothyronine.

Subclinical hypothyroidism and controversies

Subclinical hypothyroidism is defined by an elevated TSH with a normal free T4, in the absence of overt symptoms attributable to thyroid failure. This situation raises questions about when to treat: - Thresholds for treatment: Many guidelines reserve treatment for those with TSH above roughly 10 mU/L or for those with symptoms, positive autoimmune markers, or pregnancy. Those thresholds reflect concerns about overtreatment, costs, and potential side effects. - Controversies: Critics worry about overdiagnosis and medicalization of mild or nonspecific fatigue, depression, or aging-related changes. Proponents argue that treating certain subgroups—especially pregnant people or younger patients with TSH elevations or positive antibodies—can prevent adverse outcomes and improve quality of life. - Treatment options: When treatment is pursued, levothyroxine remains the standard, with careful dosing and monitoring. In some settings, clinicians may consider more conservative observation rather than immediate replacement in low-risk cases.

From a policy and practice standpoint, the balance between broad screening and targeted testing reflects a focus on cost-effective care and avoidance of unnecessary exposure to medications. The discussion often bands around the risks of overtreatment (such as accelerated bone loss and atrial fibrillation) versus the benefits of symptom relief and prevention of long-term complications.

Hypothyroidism in pregnancy

Pregnancy imposes increased demands on thyroid hormone production, and untreated maternal hypothyroidism can affect fetal neurodevelopment and pregnancy outcomes. For pregnant patients with hypothyroidism: - Dose adjustments are common and often necessary, especially in the first trimester. - Target TSH ranges are lower in the first trimester and vary by guideline; consistent monitoring is essential to maintain euthyroid status. - Antibodies and autoimmune disease status can influence management decisions and surveillance. - Postpartum thyroiditis is a consideration in some individuals, and monitoring should continue after delivery.

See Hypothyroidism in pregnancy for a detailed discussion of guidelines, targets, and practical management.

Public health, policy, and practical considerations

  • Iodine and nutrition: Adequate iodine intake is essential for thyroid hormone synthesis. Public health measures, such as iodization of salt in many countries, have dramatically reduced iodine deficiency–related hypothyroidism where implemented. See Iodine.
  • Screening and access to care: Population-level screening for overt hypothyroidism is common in primary care, but universal adult screening remains debated because of concerns about yield, cost, and downstream management. Access to affordable, reliable replacement therapy and periodic monitoring remains a central policy issue.
  • Drug safety and cost: Levothyroxine’s long track record and broad availability help keep costs down, making therapy accessible to a wide spectrum of patients. The economic and logistical implications of alternative therapies or management strategies are frequently discussed in health policy circles.
  • Patient autonomy and the marketplace: In a system that emphasizes personal responsibility and informed consent, patients are encouraged to participate actively in decisions about testing, dosing, and preference for therapy. Clinicians weigh evidence, safety, and costs while respecting patient values and lifestyle.

See also