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Hypothyroidism - primary

Definition
Expectations (prognosis)
Causes, incidence, and risk factors
Complications
Symptoms
Calling your health care provider
Signs and tests
Prevention
Treatment
References


Primary and secondary hypothyroidism
Primary and secondary hypothyroidism
Thyroid gland
Thyroid gland

 Definition  

Primary hypothyroidism is a condition of decreased hormone production by the thyroid gland.

 Causes, incidence, and risk factors  

The thyroid gland is an important organ that regulates metabolism. It is located in the front of the neck just below the voice box (larynx). The thyroid gland secretes two forms of thyroid hormone – thyroxine (T4) and triiodothyronine (T3). The secretion of T3 and T4 by the thyroid is controlled by a feedback system involving the pituitary gland, a small organ at the base of the brain, and the hypothalamus, a structure in the brain.

Hypothyroidism caused by the inability of the thyroid gland to make T3 and T4 is called primary hypothyroidism. Worldwide, the most common cause of primary hypothyroidism is deficiency of the element iodine. In the US, the most common cause is destruction of the thyroid gland by the immune system, a condition called Hashimoto's thyroiditis.

Other causes of primary hypothyroidism include surgical removal of part or all of the thyroid gland, radioactive iodine used for treatment of hyperthyroidism (overactive thyroid), radiation exposure to the neck, special x-ray dyes, and certain drugs such as lithium. Approximately 5-10% of women develop hypothyroidism after pregnancy (often referred to as "postpartum thyroiditis"). Some cases of hypothyroidism may be caused by a lack of enzymes that convert T3 and T4 for use in the body. In other cases, the cause of hypothyroidism is unknown.

Since the thyroid gland is regulated by the pituitary gland and hypothalamus, disorders of these organs can cause the thyroid gland to produce too little thyroid hormone as well. This condition is called secondary hypothyroidism.

Primary hypothyroidism affects the whole body and may cause a variety of symptoms. The body's normal rate of functioning slows, causing mental and physical sluggishness. Symptoms may vary from mild to severe. The most severe form is called myxedema coma and is a medical emergency. Risk factors for hypothyroidism include age (older than age 50), female gender, obesity, thyroid surgery, and x-ray or radiation treatments to the neck.

 Symptoms  

Early symptoms:

  • Weakness
  • Fatigue
  • Cold intolerance
  • Constipation
  • Weight gain  
  • Depression
  • Muscle or joint pain
  • Thin, brittle fingernails
  • Thin, brittle hair
  • Paleness

Late symptoms:

  • Slow speech
  • Dry flaky skin
  • Thickening of the skin
  • Puffy face, hands, and feet
  • Decreased sense of taste and smell
  • Thinning of eyebrows
  • Hoarseness
  • Menstrual disorders

 Signs and tests  

Physical examination may reveal a smaller than normal gland, though sometimes the gland is normal in size or even enlarged (goiter). Other physical findings include pale, yellow, and dry skin; thin, brittle hair; loss of the edges of the eyebrows; coarse facial features; firm swelling of the arms and legs; and slow muscle relaxation when reflexes are tested. Vital signs may reveal a slow heart rate, low blood pressure, and low temperature.

A chest x-ray sometimes reveals an enlarged heart.

Laboratory tests to determine thyroid function include:

  • Free T4 test (low)
  • Total T3 or free T3 (low)
  • Serum TSH (high)

Additional laboratory abnormalities may include:

  • Increased cholesterol levels
  • Increased liver enzymes
  • Increased serum prolactin
  • Low serum sodium
  • A complete blood count (CBC) shows anemia

 Treatment  

The purpose of treatment is to replace the deficient thyroid hormone. Levothyroxine (T4) is the most commonly used medication, but a preparation of T3 is also available. Most people feel their best when TSH is brought into the 1 to 2 mcIU/mL range. People get the lowest dose that is effective in relieving symptoms and normalizing blood tests.

Life-long therapy is needed. Relapses will occur if therapy is interrupted. Medication must be continued even when symptoms go away.

After replacement therapy has begun, report any symptoms of increased thyroid activity (hyperthyroidism), such as restlessness, rapid weight loss, heat intolerance, and sweating.

Myxedema coma is treated by intravenous thyroid replacement and steroid therapy. Supportive therapy (oxygen, assisted ventilation, and fluid replacement) and intensive care nursing may be indicated.

 Expectations (prognosis)  

With early treatment, the condition can be completely controlled. However, relapses will occur if the medication is not continued. Myxedema coma can result in death.

 Complications  

Myxedema coma, the most severe form of hypothyroidism, is rare. It may be caused by an infection, illness, exposure to cold, or certain medications. Symptoms and signs of myxedema coma include:

  • Unresponsiveness
  • Decreased breathing
  • Low blood pressure
  • Low blood sugar
  • Below-normal temperature

Other complications include:

  • Heart disease
  • Increased risk of infection
  • Infertility
  • Miscarriage
  • Pituitary tumors

 Calling your health care provider  

Call your health care provider if signs or symptoms of hypothyroidism or myxedema are present

Call your health care provider if restlessness, rapid weight loss, heat intolerance, rapid heart rate, excessive sweating, or symptoms of hyperthyroidism occur after beginning thyroid replacement.

 Prevention  

Primary hypothyroidism is preventable by supplemental iodine in areas where iodine in the food supply is low. Otherwise, the condition is not preventable. Awareness of risk may allow early diagnosis and treatment. Some experts advocate screening TSH testing in certain high risk groups (e.g., women older than 50 years).

 References  

AACE Thyroid Task Force. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Evaluation and Treatment Of Hyperthyroidism and Hypothyroidism. Endocr Pract. 2002;8 (6).

Review date: 5/12/2006

Reviewed By: Robert Hurd, MD, Department of Biology, College of Arts and Sciences, Xavier University, Cincinnati, OH. Review provided by VeriMed Healthcare Network.

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