Strategies for improved management of hypothyroidism
Management is clear-cut—yet many patients don’t reach treatment goals. To optimize quality of life, master the fine points of T4 replacement and address the impact of comorbidities.
PRACTICE RECOMMENDATIONS
› Prescribe levothyroxine (LT4) to maintain thyroid-stimulating hormone (TSH) at 4 to 7 mIU/L in select patients with primary hypothyroidism for whom that range of the serum TSH level can be considered appropriate (ie, those older than 65 years and those who have underlying coronary artery disease or another debilitating chronic disorder). A
› Counsel all women of childbearing age with primary hypothyroidism that they need to have their dosage of LT4 increased as soon as pregnancy is suspected. A
› Keep in mind that treating hypothyroidism is not always necessary in older patients who have subclinical disease and a serum TSH level < 10 mIU/L. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
The hormones thyroxine (T4) and triiodothyronine (T3), produced by the thyroid gland, are crucial for maintaining metabolism. A deficit of thyroid hormone production—hypothyroidism—is a common endocrine disorder seen in primary care.
Although the diagnosis and management of hypothyroidism are considered straightforward, many patients with hypothyroidism do not achieve optimal treatment goals or see an improvement in their quality of life. In this article, we address the questionable utility of screening; outline the diagnostic approach, including the central role of laboratory testing; and explain why treatment requires a precise approach to address the range of patient types.
Epidemiology and classification
Estimates are that almost 5% of Americans 12 years or older have hypothyroidism; older people and women are more likely to develop the condition. 1 In the US National Health and Nutrition Examination Survey (NHANES III) of 13,344 people without known thyroid disease or a family history, hypothyroidism was found in 4.6% (overt [clinical] in 0.3% and subclinical in 4.3%); 11% had a high serum thyroid peroxidase antibody level, which increases their risk of hypothyroidism, and is treated the same as hypothyroidism of other causes; and, overall, lower serum thyroid-stimulating hormone (TSH) levels were seen in Blacks, compared to Whites and Mexican Americans.1
Primary hypothyroidism accounts for > 95% of cases of hypothyroidism, representing a failure of the thyroid gland to produce sufficient hormone. It has been shown that, in iodine-replete countries such as the United States, the prevalence of spontaneous hypothyroidism is 1% to 2%, and it is 10 times more common in women.2,3
Central hypothyroidism is caused by insufficient stimulation of the thyroid gland by TSH, due to pituitary (secondary hypothyroidism) or hypothalamic (tertiary hypothyroidism) disease and is estimated to occur in 1 in every 20,000 to 80,000 people in the general population.4
How does hypothyroidism manifest?
Signs and symptoms. Manifestations of hypothyroidism range from life-threatening to minimal or no clinical signs and symptoms (TABLE W1). Signs and symptoms of low thyroid function vary by the degree of hypothyroidism at presentation.
Common signs and symptoms of low thyroid function include fatigue, weight gain, dry skin, brittle hair, hair loss, morning stiffness, muscle aches, joint pain, cold intolerance, diffuse headache, constipation, difficulty concentrating, low libido, depression, and menstrual irregularities. On physical examination, a patient might present with bradycardia, hypotension, hypothermia with slow speech or movement, coarse facial appearance, goiter, diffuse hair loss, cold hands and feet, and a prolonged Achilles tendon reflex.5 Skin findings, such as keratosis pilaris, palmoplantar keratoderma (thickening of the skin), and pityriasis rubra pilar, can be associated with autoimmune hypothyroidism.6,7
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