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Hypothyroidism

HYPOTHYROIDISM

Hypothyroidism is characterized by a hypoactive thyroid gland, which fails to produce and secrete sufficient thyroid hormones to meet the body’s needs. There are decreased levels of free thyroxine (fT4) and free triiodothyronine (fT3) and elevated levels of thyroid-stimulating hormone (TSH). It predominantly affects women as compared to men. Subclinical hypothyroidism is a term used when TSH levels are raised, but free T4 and free T3 levels remain within normal range. The term myxoedema is not synonymous with hypothyroidism and refers to the accumulation of glycosaminoglycans in the dermis occurring in severe hypothyroidism. The term hypothyroxinaemia refers to low serum fT4 concentrations in the presence of normal levels of TSH.

Types of Hypothyroidism:

  1. Primary hypothyroidism. It occurs due to a disturbance within the thyroid gland itself. It is spontaneous and is due to loss of the thyroid after total or subtotal resection without subsequent hormonal replacement, congenital hypoplasia or aplasia, ectopic thyroid in children, or disordered synthesis of thyroid hormone.
  2. Secondary or central hypothyroidism. It occurs due to a disturbance within the hypothalamic–pituitary–thyroid axis. It is caused by absent TSH stimulation from the anterior pituitary. It accounts for less than 1% of all cases of hypothyroidism. The most common cause is the hypothalamic or pituitary tumour and the surgery or radiotherapy used to treat them. It should be distinguished from primary hypothyroidism by a normal or low-serum TSH concentration.

Causes:

  1. Autoimmune thyroiditis (Hashimoto’s thyroiditis): This is the most common cause of hypothyroidism and is more commonly observed in females. Hashimoto disease is an autoimmune disorder. This condition is. In Hashimoto’s disease, antibodies develop against thyroglobulin and the thyroid peroxidase enzyme. This immune response leads to hypothyroidism, characterized by insufficient production of thyroid hormones, and a consequent increase in thyroid-stimulating hormone (TSH) levels. The thyroid parenchyma is typically diffusely infiltrated with lymphocytes, and fibrotic septae extend into the parenchyma. The size of the thyroid gland in Hashimoto’s disease can vary. It may be normal, enlarged, or small. Additionally, multiple or single regenerative nodules may form within the gland. Diagnosis of Hashimoto disease is primarily achieved by measuring the levels of antibodies against thyroglobulin and the thyroid peroxidase enzyme. Nodules that develop in Hashimoto’s disease have the potential to evolve into a lymphoma or, in some cases, papillary cell carcinoma. Treatment of Hashimoto disease is thyroxine therapy.
  2. Iatrogenic causes: It is seen as a consequence of thyroid surgery (total or subtotal thyroidectomy), treatment with radioactive iodine for Grave’s disease or external beam radiotherapy for head and neck malignancies. It can also result from overtreatment of hyperthyroidism with antithyroid medication. Hypothyroidism is seen in patients undergone total or subtotal thyroidectomy not on thyroid hormone replacement therapy in the postoperative phase. Majority of patients treated with radioiodine will develop hypothyroidism which may be transient, resulting from radiation thyroiditis some 4–6 weeks after treatment, or permanent. Radiotherapy for the neck may result in both hypothyroidism and an increased risk of thyroid malignancy.
  3. Congenital hypothyroidism. Neonatal hypothyroidism or cretinism can arise from inadequate iodine in the mother’s diet, or the mother is having Hashimoto thyroiditis, administration of antithyroid drugs or radioactive iodine to the mother to treat her thyrotoxicosis or agenesis of thyroid in the infant. It is therefore essential for all pregnant mothers to maintain a euthyroid state to ensure both maternal and foetal health. Untreated congenital hypothyroidism can result in cretinism. Hypothyroidism can also occur in neonates (1:5000) and thus there is a need to test them after birth. Cretinism manifests after several months of extrauterine life. It causes lethargy, stunted growth, mental retardation and hearing loss.
  4. Iodine deficiency. Insufficient intake of iodine, an essential mineral required for thyroid hormone synthesis.
  5. Medications. Certain medications, such as amiodarone, lithium, iodides, phenylbutazone or antithyroid drugs or goitrogenic substances in diet, can interfere with thyroid hormone production.
  6. Secondary or central hypothyroidism.
Symptoms: The symptoms of hypothyroidism can vary widely among individuals and may develop gradually over time. Common signs and symptoms include:
  1. Fatigue and weakness: Feeling tired and sluggish despite getting enough sleep.
  2. Muscle weakness and joint pain: Weakness, aches, and pains, particularly in the muscles and joints, are often reported.
  3. Weight gain with poor appetite: Despite maintaining a healthy diet and exercise regimen.
  4. Constipation: Sluggish bowel movements and constipation are common complaints.
  5. Cold intolerance: Feeling unusually cold, particularly in the extremities, and having cold hands and feet.
  6. Poor memory and lack of concentration.
  7. Depression with mood changes and irritability.
  8. Menstrual irregularities: Excessive menstrual bleeding followed later by oligomenorrhoea or amenorrhea.
  9. Hearing loss.

Signs:

  1. Puffy face. Fluid retention, particularly around the eyes and face, can give a puffy appearance.
  2. Puffiness of hands and feet
  3. Dry skin and coarse & sparse hair: Skin may become dry, rough, and pale, and hair may become brittle and thin.
  4. Cool extremities
  5. Husky voice due to oedema of vocal cords or due to compression from goitre
  6. Bradycardia and shortness of breath.

Diagnosis: It involves a combination of clinical evaluation, blood tests, and thyroid function tests. The primary blood test measures levels of thyroid-stimulating hormone (TSH) and thyroxine (T4). Elevated TSH levels along with low T4 levels are indicative of hypothyroidism. Low serum T4 with normal or suppressed TSH are seen in central hypothyroidism.

Treatment: Levothyroxine is the drug of choice for the treatment of hypothyroidism. This medication restores euthyroid state both by normal thyroid hormone levels in the body and helps alleviate symptoms. Dosage adjustments may be necessary over time to ensure optimal hormone levels. In addition to medication, adopting a healthy lifestyle with regular exercise and a balanced diet can help manage symptoms and support overall well-being.

Treatment under specific conditions: In elderly patients, thyroxine should be started from 25–50μg daily and increased every 4 weeks until stable. Overtreatment, resulting in a suppressed TSH concentration, should be avoided due to the risk of precipitating atrial fibrillation. During pregnancy, thyroxine should be increased around 40%. In patients having congenital hypothyroidism, T4 is started at a dose of 10–15 μg/kg per d, and the dose is adjusted by close monitoring of TSH levels. In patients having central hypothyroidism, first exclude hypoadrenalism before initiating thyroxine therapy else adrenal crisis may get precipitated.

Complications: Untreated or poorly managed hypothyroidism can lead to various complications, including:

  1. Cardiovascular problems: Hypothyroidism increases the risk of heart disease, including heart failure, high blood pressure, and elevated cholesterol levels.
  2. Myxoedema coma: A rare but life-threatening condition characterized by severe hypothyroidism, resulting in altered mental status, hypothermia, and organ failure.
  3. Neurological complications: Prolonged untreated hypothyroidism can lead to peripheral neuropathy, characterized by tingling, numbness, or weakness in the extremities.
  4. Mental health issues: Hypothyroidism is associated with an increased risk of depression, anxiety, and cognitive impairment if left untreated.

Management and Follow-Up: Effective management of hypothyroidism involves regular monitoring of thyroid function, adherence to medication, and lifestyle modifications to address symptoms and reduce complications. Patients should work closely with healthcare providers to optimize treatment and adjust medication dosage as needed. Periodic follow-up visits are essential to evaluate treatment response, adjust medication dosage, and address any emerging concerns or complications. With appropriate management, most individuals with hypothyroidism can lead healthy, fulfilling lives.

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Reference Textbooks.
  • Scott-Brown, Textbook of Otorhinolaryngology-Head and Neck Surgery.
  • David J. Terris, William S. Duke. Textbook of Thyroid and Parathyroid Diseases Medical and Surgical Management.
  • Cummings, Otolaryngology-Head and Neck Surgery.
  • Stell and Maran’s, Textbook of Head and Neck Surgery and Oncology.
  • Ballenger’s, Otorhinolaryngology Head And Neck Surgery
  • Susan Standring, Gray’s Anatomy.
  • Frank H. Netter, Atlas of Human Anatomy.
  • B.D. Chaurasiya, Human Anatomy.
  • P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
  • Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
  • Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck Surgery.
  • Hans Behrbohm, Textbook of Ear, Nose, and Throat Diseases With Head and Neck Surgery.
  • Logan Turner, Textbook of Diseases of The Nose, Throat and Ear Head And Neck Surgery.
  • Arnold, U. Ganzer, Textbook of  Otorhinolaryngology, Head and Neck Surgery.
  • Ganong’s Review of Medical Physiology.
Author:
Acoustic Neuroma

Dr. Rahul Bagla MBBS (MAMC, Delhi) MS ENT (UCMS, Delhi) Fellow Rhinoplasty & Facial Plastic Surgery. Renowned Teaching Faculty Mail: msrahulbagla@gmail.com India

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