When bacteria or viruses invade the body, they may attack the thyroid and cause it to become inflamed. Thyroid gland inflammation occurs in several forms: as a long-term autoimmune inflammation, as a self-limiting subacute granulomatous inflammation, or as several miscellaneous disorders (acute suppurative, chronic infective, and chronic noninfective inflammations). A postpartum form strikes women within I year after delivery. Inflammation of the thyroid is more common in women than in men.

What Causes it?

Autoimmune inflammation of the thyroid results from the immune system’s response to thyroid antigens that occur naturally in the blood. Subacute granulomatous inflammation of the thyroid usually follows mumps, influenza, coxsackievirus, or adenovirus infection.

Miscellaneous forms may result from a variety of causes. Acute suppurative thyroiditis may be caused by bacterial invasion of the gland. Chronic injective thyroiditis may be caused by tuberculosis, syphilis, actinomycosis, or other infectious agents. Chronic noninfective thyroiditis may be caused by sarcoidosis or amyloidosis.

What are its Symptoms?

The autoimmune form usually does not produce symptoms. It commonly occurs in women, with peak incidence in middle age. It’s the most prevalent cause of spontaneous hypothyroidism.

In subacute granulomatous inflammation, moderate thyroid enlargement may follow an upper respiratory tract infection or a sore throat. The thyroid may be painful and tender, and the person may have difficulty swallowing.

Clinical effects of miscellaneous inflammation are characteristic of pus-forming infection: fever, pain, tenderness, and reddened skin over the gland.

How is it Diagnosed?

Lab tests are the key to accurate diagnosis. Test results vary according to the type of thyroid inflammation.

How is it Treated?

Appropriate treatment varies with the type of thyroid inflammation. Drug therapy includes Levoxine for accompanying hypothyroidism, pain relievers and anti-inflammatory drugs for mild, subacute granulomatous inflammation, Inderal for transient hyperthyroidism, and steroids for severe episodes of acute inflammation. Suppurative inflammation requires antibiotic therapy.

What can a Person with Inflammation of the Thyroid do?

Watch for and report symptoms of hypothyroidism (sluggishness, restlessness, sensitivity to cold, forgetfulness, dry skin).

Be aware that you’ll need lifelong thyroid hormone therapy if hypothyroidism occurs. If you’re taking this medication, watch for signs of overdose, such as nervousness and palpitations.

In hyperparathyroidism, one or more of the four parathyroid glands (pea-sized organs located behind the thyroid) are overactive, causing excessive secretion of parathyroid hormone. This results in bone loss and leads to excessive calcium and a shortage of phosphates in the blood. Consequently, the kidneys and gastrointestinal system absorb more calcium.

What Causes it?

Hyperparathyroidism may be classified as primary or secondary. In primary hyperparathyroidism, one or more of the parathyroid glands become enlarged. The most common cause is an adenoma, a type of benign tumor. Other causes include genetic disorders or multiple endocrine neoplasia (a rare disorder that causes the endocrine glands to become overactive). Primary hyperparathyroidism usually occurs between ages 30 and 50 but can also occur in children and the elderly. It affects women two to three times more often than men.

Secondary hyperparathyroidism is marked by excessive production of parathyroid hormone. This type of hyperparathyroidism results from a condition outside the parathyroid glands that decreases the level of calcium in the body. Such conditions include rickets, vitamin D deficiency, chronic kidney failure, or osteomalacia (softening of the bones).

What are its Symptoms?

Symptoms of primary hyperparathyroidism may include:

• kidney: excessive urination (one of the most common effects)

• bones and joints: chronic lower back pain and easy fracturing due to bone degeneration; bone tenderness; pain associated with calcium buildup in joints, erosion of joint surfaces, and cartilage fractures

• digestive tract: severe epigastric pain radiating to the back caused by pancreatitis; abdominal pain, appetite loss, and nausea caused by peptic ulcers

• muscles: marked muscle weakness and wasting, particularly in the legs

• nervous system: psychomotor and personality disturbances, depression, overt psychosis, stupor and, possibly, coma

• other: skin destruction, cataracts, anemia, and calcification under the skin.

In secondary hyperparathyroidism, decreased levels of calcium in the blood may produce the same features of calcium imbalance, with skeletal deformities of the long bones (rickets, for example), as well as symptoms of the underlying disease.

How is it Diagnosed?

A diagnosis of primary disease is confirmed by lab tests revealing high levels of parathyroid hormone and calcium in the blood. X-rays typically show diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles. Microscopic examination of the bone typically shows increased bone turnover. Lab tests show elevated urine and blood calcium, chloride, and alkaline phosphatase levels and decreased blood phosphorus levels.

In secondary disease, lab findings show normal or slightly decreased serum calcium levels and variable serum phosphorus levels, especially when hyperparathyroidism is due to rickets, osteomalacia, or kidney disease. The person’s history may reveal a family history of kidney disease, seizure disorders, or drug ingestion. Other lab studies and physical exam findings identify the cause of secondary hyperparathyroidism.

How is it Treated?

Treatment varies, depending on the cause of the disease. Treatment for primary hyperparathyroidism may include surgery to remove the adenoma or, depending on the extent of hyperplasia, all but half of one parathyroid gland (necessary to maintain normal parathyroid hormone levels). Such surgery may relieve bone pain within 3 days. However, kidney damage may be irreversible.

If surgery isn’t feasible or necessary, the following treatments can decrease calcium levels:

• forcing fluids

• limiting dietary intake of calcium

• promoting sodium and calcium excretion through forced diuresis using normal saline solution, Lasix, or Edecrin

• administering sodium, potassium phosphate, calcitonin, Mithracin, or biphosphonates.

Treatment of secondary hyperparathyroidism must correct the underlying cause. It consists of vitamin D therapy or, in the person with kidney disease, administration of an oral calcium preparation for hyperphosphatemia. In the person with kidney failure, dialysis is necessary to lower calcium levels and may have to continue for life. In the person with chronic secondary hyperparathyroidism, the enlarged glands may not revert to normal size and function even after calcium levels have been controlled.

What can a Person with Hyperparathyroidism do?

Be sure to receive periodic medical follow-up through lab tests. If your condition wasn’t corrected surgically, make sure you avoid calcium-containing antacids and thiazide diuretics (such as Diuril).

What is this Condition?

Hypothyroidism in children is a deficiency of thyroid hormone secretion during fetal development or early infancy. Untreated hypothyroidism is characterized in infants by respiratory difficulties, persistent jaundice, and hoarse crying; in older children, by stunted growth (dwarfism), bone and muscle dystrophy, and mental deficiency.

Early diagnosis and treatment offer the best prognosis; infants treated before age 3 months usually grow and develop normally. However, hypothyroid children who remain untreated beyond age 3 months and children with acquired hypothyroidism who remain un­treated beyond age 2 years suffer irreversible mental retardation; their skeletal abnormalities are reversible with treatment. Hypothyroidism occurs three times more often in girls than in boys.

What Causes it?

In infants, hypothyroidism usually results from defective embryonic development that causes congenital absence or underdevelopment of the thyroid gland. The next most common cause can be traced to an inherited enzymatic defect in the synthesis of the thyroid hormone thyroxine. Less frequently, antithyroid drugs taken during pregnancy produce hypothyroidism in infants. In children older than age 2, hypothyroidism usually results from chronic autoimmune thyroiditis.

What are its Symptoms?

At birth, the weight and length of an infant with hypothyroidism appear normal, but characteristic signs of hypothyroidism develop by age 3 to 6 months. Breast-fed infants don’t show most symptoms until they’re weaned because breast milk contains small amounts of thyroid hormone.

Symptoms in Infants

Typically, an infant with hypothyroidism sleeps excessively, cries rarely (except for occasional hoarse crying), and is generally inactive.

Because of this, the parents may describe the child as a “good baby-no trouble at all.” However, such behavior actually results from a decreased metabolism and progressive mental impairment.

The infant with hypothyroidism also has abnormal deep-tendon reflexes; hypotonic abdominal muscles; a protruding abdomen; slow, awkward movements; feeding difficulties; constipation; and jaundice.

A large, protruding tongue obstructs respiration, making breathing loud and noisy and forcing the child to breathe through an open mouth. The child may have shortness of breath on exertion, anemia, abnormal facial features, and a dull expression, resulting from mental retardation. The skin is cold and mottled because of poor circulation, and the hair is dry, brittle, and dull. Teeth erupt late and tend to decay early; body temperature is below normal; and pulse rate is slow.

Symptoms in Children

In the child who gets hypothyroidism after age 2 years, appropriate treatment will likely prevent mental retardation. However, growth retardation becomes apparent in short stature, obesity, and a head that appears abnormally large because the arms and legs are stunted. An older child may show delayed or accelerated sexual development.

How is it Diagnosed?

Lab tests help determine levels of thyroid hormones. A high serum level of thyroid-stimulating hormone, associated with low levels of thyroxine and triiodothyronine, points to hypothyroidism. Since early diagnosis and treatment can minimize the effects of hypothyroidism, many states require measurement of thyroid hormone levels at birth.

Electrocardiography shows slow heart rate and electrocardiographic changes in untreated infants. Thyroid scan and radioactive iodine uptake tests show decreased uptake levels and confirm the absence of thyroid tissue in hypothyroid children. Hip, knee, and thigh X-rays reveal delayed skeletal development that is markedly inappropriate for the child’s age.

How is it Treated?

Early detection is mandatory to prevent irreversible mental retardation and permit normal physical development.

Treatment in infants under age 1 year consists of replacement therapy with oral Levoxine, starting with moderate doses. Dosage gradually increases to levels sufficient for lifelong maintenance. (However, a rapid increase in dosage may precipitate thyrotoxicity.)

Doses are proportionately higher in children than in adults because children metabolize thyroid hormone more quickly. Older children also receive Levoxine.

What can the Parents of a Child with Hypothyroidism do?

• Be aware that your child will require lifelong treatment with thyroid supplements. Stay alert for signs of overdose: rapid pulse, irritability, insomnia, fever, sweating, and weight loss. To prevent further mental impairment, be sure to comply with your child’s treatment program .

• Focus on your child’s strengths, not weaknesses. Provide stimulating activities to help the child reach maximum potential.