Hyperthyroidism and Pregnancy

Hyperthyroidism and Pregnancy

- Hyperthyroidism refers to the signs and symptoms which are due to the production of too much thyroid hormone. An overactive thyroid gland (hyperthyroidism) often has its onset in younger women. Because a woman may think that feeling warm, having a hard or fast heartbeats, nervousness, trouble sleeping, or nausea with weight loss are just parts of being pregnant, the symptoms and signs of this condition may be overlooked during pregnancy.

- In women who are not pregnant, hyperthyroidism can affect menstrual periods, making them irregular, lighter, or disappear altogether. It may be harder for hyperthyroid women to become pregnant, and they are more likely to have miscarriages. If a woman with infertility or repeated miscarriages has symptoms of hyperthyroidism, it is important to rule out this condition with thyroid blood tests. It is very important that hyperthyroidism be controlled in pregnant women since the risks of miscarriage or birth defects are much higher without therapy. Fortunately, there are effective treatments available. Antithyroid medications cut down the thyroid gland's overproduction of hormones and are reviewed on another page on this site. When taken faithfully, they control hyperthyroidism within a few weeks. In pregnant women thyroid experts consider propylthiouracil (PTU) the safest drug. Because PTU can also affect the baby's thyroid gland, it is very important that pregnant women be monitored closely with examinations and blood tests so that the PTU dose can be adjusted. In rare cases when a pregnant woman cannot take PTU for some reason (allergy or other side effects), surgery to remove the thyroid gland is the only alternative and should be undertaken prior to or even during the pregnancy if necessary. Although radioactive iodine is a very effective treatment for other patients with hyperthyroidism, it should never be given during pregnancy because the baby's thyroid gland could be damaged.

- Because treating hyperthyroidism during pregnancy can be a bit tricky, it is usually best for women who plan to have children in the near future to have their thyroid condition permanently cured. Antithyroid medications alone may not be the best approach in these cases because hyperthyroidism often returns when medications is stopped. Radioactive iodine is the most widely recommended permanent treatment with surgical removal being the second (but widely used) choice. It is concentrated by thyroid cells and damages them with little radiation to the rest of the body. This is why it cannot be given to a pregnant woman, since the radioactive iodine could cross the placenta and destroy normal thyroid cells in the baby. The only common side effect of radioactive iodine treatment is underactivity of the thyroid gland, which occurs because too many thyroid cells were destroyed. This can be easily and safely treated with levothyroxine. There is no evidence that radioactive iodine treatment of hyperthyroidism interferes with a woman's future chances of becoming pregnant and delivering a healthy baby.

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Hypothyroidism: Prognosis and Future Perspectives

Hypothyroidism - Prognosis and Future Perspectives

Differential Diagnosis.
The differential diagnosis of hypothyroidism includes nonthyroidal illness (i.e., decreased T3 or T4 , or both, without clinical hypothyroidism), euthyroid hypothyroxinemia (decreased T4 caused by decreased thyroid-binding globulin), and drugs that inhibit T4 binding (salicylates, phenytoin, and phenobarbital). Once hypothyroidism has been diagnosed, the most important clinical distinction is between primary and secondary hypothyroidism. The clinical and laboratory similarities between myxedema coma and other life-threatening causes of the comatose state may make its diagnosis extremely difficult. Regarding hypothyroid myopathy, the muscular appearance, stiffness, and exacerbation by cold may suggest a mild form of myotonia congenita, which can present in adulthood. Although the stiffness noted in patients with pyramidal and extrapyramidal diseases may appear similar to that of hypothyroid myopathy, the characteristic history, appearance, and laboratory studies usually permit the diagnosis of hypothyroidism.

Evaluation.
The combination of a low T4 level and an elevated thyroid-stimulating hormone (TSH) level is virtually diagnostic of primary hypothyroidism, because TSH elevation does not occur in central hypothyroidism. Further delineation between primary and secondary hypothyroidism is dependent on history, examination, and other laboratory studies. In addition to TFTs, other laboratory abnormalities have been described, including anemia (normocytic-normochromic, microcytic-hypochromic, or macrocytic) and hyponatremia (factitious due to hyperlipidemia or secondary to impaired free water excretion), as well as elevated serum creatine kinase, myoglobin, and prolactin. Because of the possibility of concomitant adrenal insufficiency, a serum cortisol level should also be obtained. The EEG may show slowing of the posterior dominant rhythm and a generalized voltage decrease, as well as triphasic waves that disappear with replacement therapy. CSF analysis may reveal an elevated protein content which may exceed 100 mg/dl.

Management.
The treatment of hypothyroidism, regardless of cause, consists of thyroid hormone replacement. Even in the setting of hypothyroid-induced seizures, achievement of the euthyroid state facilitates control. Precipitants of myxedema coma (e.g., infection, cold exposure, certain drugs phenothiazines, narcotics, and sedative-hypnotics, phenytoin, rifampin , and other stressors surgery, trauma ) require correction.

Prognosis and Future Perspectives.
With early recognition and treatment, as well as improved intensive supportive care, the mortality rate of myxedema coma has decreased from roughly 50 to 70 percent to around 15 to 20 percent.
Without early recognition and prompt institution of replacement therapy, the prognosis is grave.

Data from Mitehell JM: Thyroid disease in the emergeney department: Thyroid fune~tion tests and hypothyroidism and myxedema eoma Emerg Med Clin North Am 1989;7:885-902; Mazzafern EL: Adult hypothyroidism: 1. Manifestations and elinical presentation. Postgrad Med 1986;79:64 72; Myers L, Hays J: Myxedema eoma. Cnt Care Clinie 1991;7:43 56.

Clinical Features of Hypothyroidism

Hypothyroidism: Clinical Features and Associated Disorders

Clinically, the onset of hypothyroidism may range from subtle and insidious findings to florid psychosis. The general examination features of hypothyroidism are numerous:

1) Subjective: Fatigue, somnolenee, eold intoleranee, syneope, exertional dyspnea, weight gain, arthralgias, nausea, anorexia, indigestion, eonstipation, menstrual abnormalities;

2) Objective: Bradyeardia, hair changes (sparse, eoarse, dry, brittle), puffy face, loss of lateral aspeets of the eyebrows, penorbital edema, maeroglossia, voiee deepening and hoarsening, skin ehanges (sealy, thiek, doughy, eoarse, dry, earotenemia), bnttle nails, nonpitting edema, galaetorrhea, effusions

CNS features include forgetfulness, inattention, apathy, and slowing of speech, movement and mentation. These features may mimic depression. Seizures, personality changes, psychotic states, coma, and dementia may also be clinically apparent. Cerebellar ataxia is seen in 5 to 10 percent of patients, and may be the presenting sign (so-called myxedema staggers). A psychotic presentation (myxedema madness) characterized by agitation, disorientation, delusions, hallucinations, paranoia, and restlessness is observed in approximately 3 to 5 percent of patients. Myxedema coma is extremely rare, and its characteristic features include extreme hypothermia, seizures (the presenting manifestation in nearly 20 percent of patients ), respiratory depression, and areflexia. Death can occur when early recognition and prompt treatment are lacking. Dementia may develop when hypothyroidism is severe. Except for the marked increase in the number of hours these patients remain asleep or resting, the clinical features of the dementia are similar to those secondary to other causes.

Peripheral neuromuscular features include cranial and peripheral neuropathies, prolonged reflex relaxation time (up to 85 percent of hypothyroid patients), and myopathy. Visual field defects can occur when pituitary enlargement causes hypothyroidism with concomitant chiasmal compression. A facial mononeuropathy, due to nerve entrapment in the fallopian canal of the temporal bone, may rarely occur. Although sensorineural hearing loss has been reported to correlate with the degree of hypothyroidism and has a high incidence among patients with congenital

Hypothyroidism, its reported incidence among adult hypothyroid patients varies. Minor evidence of polyneuropathy, such as distal lower extremity sensory dysfunction and absent ankle jerks, is observed in approximately 10 percent of patients, and rarely, a moderately severe sensorimotor polyneuropathy has been described. Carpal tunnel syndrome (i.e., median mononeuropathy at the wrist) occurs in 15 to 30 percent of hypothyroid patients, is usually bilateral, and is the most common mononeuropathy encountered.

Myopathy can be a feature of hypothyroidism and manifests with proximal muscle weakness. Regardless of the cause of the hypothyroidism, weakness is observed in about one third of these patients. Increased muscle size and firmness, which is most obvious in the limb musculature, as well as slowed muscle contraction are important features to identify. Exertional pain, stiffness, and cramps may be noted, and myoedema may be observed. Myoedema, a mounding of the muscle in response to direct percussion, is painless and electrically silent, and occurs in one third of hypothyroid patients. Difficulty relaxing the hand grip and exacerbation by cold weather may suggest myotonia. However, unlike myotonia, hypothyroid myopathy involves a slowness of muscle relaxation and contraction, and resolves with correction of the hypothyroid state. Although sleep apnea is usually of the obstructive type, other possibilities include a central abnormality, chest muscle weakness, and blunted responses to hypoxia and hypercapnia. Reports have associated hypothyroidism with SIADH, idiopathic intracranial hypertension, and myasthenia gravis.

Hypothyroidism: Causes and Risk factors

Causes of Hypothyroidism

Your thyroid gland produces two main hormones, thyroxine (T-4) and triiodothyronine (T-3), that influence every cell in your body. They maintain the rate at which your body uses fats and carbohydrates, help control your body temperature, influence your heart rate and help regulate the production of protein. Your thyroid gland also produces calcitonin, a hormone that regulates the amount of calcium in your blood.

The rate at which thyroxine and triiodothyronine are released is controlled by your pituitary gland and your hypothalamus — an area at the base of your brain that acts as a thermostat for your whole system. The hypothalamus signals your pituitary gland to make a hormone called thyroid-stimulating hormone (TSH). Your pituitary gland then releases TSH — the amount depends on how much thyroxine and triiodothyronine are in your blood. Finally, your thyroid gland regulates its production of hormones based on the amount of TSH it receives.

Although this process usually works well, the thyroid sometimes fails to produce enough hormones. This may be due to a number of different factors, including:

• Autoimmune disease (Hashimoto's thyroiditis). Autoimmune disorders occur when your immune system produces antibodies that attack your own tissues. Sometimes this process occurs within the thyroid gland. Scientists aren't sure why the body produces antibodies against itself. Some think a virus or bacteria might trigger the response, while others believe a genetic flaw may be involved. Most likely, autoimmune diseases result from more than one factor. But however it happens, these antibodies affect the thyroid's ability to produce hormones.
• Treatment for hyperthyroidism. People who produce too much thyroid hormone (hyperthyroidism) are often treated with radioactive iodine or anti-thyroid medications to reduce their thyroid function. However, function can be reduced too much, resulting in hypothyroidism.
• Radiation therapy. Radiation used to treat cancers of the head and neck can affect your thyroid gland and may lead to hypothyroidism.
• Thyroid surgery. Removing all or a large portion of your thyroid can diminish or halt hormone production. In that case, you'll need to take thyroid hormones for life.

• Medications. A number of medications can contribute to hypothyroidism. One such medication is lithium, which is used to treat certain psychiatric disorders. If you're taking medication, ask your doctor about its effect on your thyroid gland.
  

Less often, hypothyroidism may result from one of the following:

• Congenital disease. Approximately one in 3,000 babies in the United States is born with a defective thyroid gland or no thyroid gland at all. In most cases, the thyroid gland didn't develop normally for unknown reasons, but some children have an inherited form of the disorder. Often, infants with congenital hypothyroidism appear normal at birth. That's one reason why most states now require newborn thyroid screening.
• Pituitary disorder. A relatively rare cause of hypothyroidism is the failure of the pituitary gland to produce enough TSH — usually due to a benign tumor of the pituitary gland.
• Pregnancy. Some women develop hypothyroidism during or after pregnancy (postpartum hypothyroidism), often because they produce antibodies to their own thyroid gland. Left untreated, hypothyroidism increases the risk of miscarriage, premature delivery and preeclampsia — a condition that causes a significant rise in a woman's blood pressure during the last three months of pregnancy. It can also seriously affect the developing fetus.
• Iodine deficiency. The trace mineral iodine — found primarily in seafood, seaweed, plants grown in iodine-rich soil and iodized salt — is essential for the production of thyroid hormones. In some parts of the world, iodine deficiency is common, but the addition of iodine to table salt has virtually eliminated this problem in the United States.
  

Risk factors

Although anyone can develop hypothyroidism, it occurs mainly in women older than 50, and the risk of developing the disorder increases with age.

You also have an increased risk if you:

• Have a close relative, such as a parent or grandparent, with an autoimmune disease
• Have been treated with radioactive iodine or anti-thyroid medications
• Received radiation to your neck or upper chest
• Have had thyroid surgery (partial thyroidectomy)

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Hypothyroidism: Complications

Complications of Hypothyroidism

Untreated hypothyroidism can lead to a number of health problems:

• Goiter. Constant stimulation of your thyroid to release more hormones may cause the gland to become larger — a condition known as goiter. Hashimoto's thyroiditis is one of the most common causes of a goiter. Although generally not uncomfortable, a large goiter can affect your appearance and may interfere with swallowing or breathing.
• Heart problems. Hypothyroidism may also be associated with an increased risk of heart disease, primarily because high levels of low-density lipoprotein (LDL) cholesterol — the "bad" cholesterol — can occur in people with an underactive thyroid. Even subclinical hypothyroidism, a more benign condition than true hypothyroidism, can cause an increase in total cholesterol levels and impair the pumping ability of your heart. Hypothyroidism can also lead to an enlarged heart and heart failure.
• Mental health issues. Depression may occur early in hypothyroidism and may become more severe over time. Hypothyroidism can also cause slowed mental functioning.
• Myxedema. This rare, life-threatening condition is the result of long-term, undiagnosed hypothyroidism. Its symptoms include intense cold intolerance and drowsiness followed by profound lethargy and unconsciousness. A myxedema coma may be triggered by sedatives, infection or other stress on your body. If you have symptoms of myxedema, you need immediate emergency medical treatment.
• Birth defects. Babies born to women with untreated thyroid disease may have a higher risk of birth defects than do babies born to healthy mothers. These children are more prone to serious intellectual and developmental problems.
  

Infants with untreated hypothyroidism present at birth are also at risk of serious problems with both physical and mental development. But if the condition is diagnosed within the first few months of life, the chances of normal development are excellent.

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