Primary Hypothyroidism Vs Secondary

[Orencio Suhag]

DrMarina Basina is an ABMS board certified endocrinologist specializing in diabetes mellitus type 1 and 2, diabetes technology, thyroid nodules, and thyroid cancer. She is currently a clinical associate professor at Stanford University School of Medicine and is a medical director of inpatient diabetes at Stanford Hospital.

Caitlin Geng lives in Johannesburg, South Africa, with her husband and three dogs. Her work, which has appeared in print and digital publications, mainly deals with health, mental well-being, parenting, and beauty. When she is not writing, Caitlin is usually curled up on the couch with her dogs, reading comics or a good book.

Doctors broadly categorize hyperthyroidism as primary or secondary. In primary hyperthyroidism, the problem originates within the thyroid gland itself. Conversely, secondary hyperthyroidism results from excessive stimulation of the thyroid gland by the pituitary gland.

Secondary hyperthyroidism is less common. It occurs when the pituitary gland, a small gland at the base of the brain, sends out excessive thyroid stimulating hormone (TSH). TSH tells the thyroid how much thyroid hormone to make. If TSH levels are high, the thyroid produces surplus thyroid hormone.

When diagnosing primary or secondary hyperthyroidism, healthcare professionals rely on specific blood tests to evaluate the levels of thyroid hormones, including triiodothyronine (T3), thyroxine (T4), and TSH.

In primary hyperthyroidism, TSH levels are usually low because the pituitary gland reduces TSH production in response to high thyroid hormone levels. In contrast, free levels of T4 or T3 are high. This inverse relationship between thyroid hormones and TSH is a key indicator of primary hyperthyroidism.

Conversely, in secondary hyperthyroidism, excessive pituitary gland production elevates the TSH levels. The elevated TSH drives the thyroid gland to produce more T3 and T4, meaning free T4 and T3 levels may be high or at the upper end of their typical ranges.

If a pituitary adenoma is causing secondary hyperthyroidism, treatments may include surgical removal of the tumor, radiation therapy, or medication to shrink or control tumor growth. Doctors may also reduce medications to reduce TSH production.

A person could also have excessive thyroid hormone levels due to taking too much thyroid medication for an underactive thyroid. Alternatively, if a person has thyroiditis, the thyroid can release stored hormones, resulting in high levels in the blood.

The outlook for both primary and secondary hyperthyroidism is generally good with appropriate treatment. Managing hyperthyroidism effectively involves regular monitoring and adjustments to treatment based on thyroid function tests.

In primary hyperthyroidism, a problem with the thyroid itself causes an overproduction of the hormones. In secondary hyperthyroidism, it is a problem with the pituitary gland that raises the thyroid stimulating hormone (TSH) levels, which then stimulates the thyroid.

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Hypothyroidism is associated with an increased risk of coronary artery disease. This observation may in part be related to the lipid abnormalities in patients with this condition. The lipid profiles of 268 patients with primary hypothyroidism and 27 with secondary hypothyroidism, who were examined in the Thyroid Clinic at the Mayo Clinic during a 1-year period, were reviewed. Hyperlipidemia was commonly associated with both primary and secondary hypothyroidism. The lipid values decreased with treatment of hypothyroidism. Type IIa hyperlipidemia was the most common lipid abnormality in patients with primary hypothyroidism, whereas type IIb was the most common in those with secondary hypothyroidism. Total/high-density lipoprotein cholesterol and low-density lipoprotein/high-density lipoprotein cholesterol ratios were increased in both male and female patients with primary and secondary hypothyroidism, and they decreased with restitution of the euthyroid state, although this decrease achieved statistical significance only in female patients. Significant associations with total thyroxine were noted for total cholesterol and triglycerides and with thyroid-stimulating hormone (thyrotropin) for total cholesterol and low-density lipoprotein cholesterol. Thus, both primary and secondary hypothyroidism are commonly associated with an atherogenic lipid profile, which improves with replacement of thyroid hormone. Even after restitution of the euthyroid state, however, the lipid profile remains atherogenic in male patients. In comparison with primary hypothyroidism, the lipid profile is more atherogenic in secondary hypothyroidism because of the lower high-density lipoprotein cholesterol levels associated with this condition.

Thyroid disease affects up to 0.5 percent of the population of the United States. Its prevalence is higher in women and the elderly. The management of hypothyroidism focuses on ensuring that patients receive appropriate thyroid hormone replacement therapy and monitoring their response. Hormone replacement should be initiated in a low dosage, especially in the elderly and in patients prone to cardiac problems. The dosage should be increased gradually, and laboratory values should be monitored six to eight weeks after any dosage change. Once a stable dosage is achieved, annual monitoring of the thyroid-stimulating hormone (TSH) level is probably unnecessary, except in older patients. After full replacement of thyroxine (T4) using levothyroxine, the addition of triiodothyronine (T3) in a low dosage may be beneficial in some patients who continue to have mood or memory problems. The management of patients with subclinical hypothyroidism (a high TSH in the presence of normal free T4 and T3 levels) remains controversial. In these patients, physicians should weigh the benefits of replacement (e.g., improved cardiac function) against problems that can accompany the excessive use of levothyroxine (e.g., osteoporosis).

Hypothyroidism is second only to diabetes mellitus as the most common endocrine disorder in the United States, and its prevalence may be as high as 18 cases per 1,000 persons in the general population.1 The disorder becomes increasingly common with advancing age, affecting about 2 to 3 percent of older women.2 Because hypothyroidism is so common, family physicians need to know how to diagnose the disorder and select appropriate thyroid hormone replacement therapy.

A number of conditions can lead to hypothyroidism (Table 1).3 Of noniatrogenic causes, Hashimoto's thyroiditis, or chronic lymphocytic thyroiditis, is the most common inflammatory thyroid disorder and the most frequent cause of goiter in the United States.4 For an unknown reason, the prevalence of Hashimoto's thyroiditis has been increasing dramatically in this country over the past 50 years.5 Other common causes of hypothyroidism include irradiation of the thyroid subsequent to Graves' disease and surgical removal of the thyroid gland.

Long-term thyroid dysfunction after subacute granulomatous thyroiditis (de Quervain's thyroiditis) or subacute lymphocytic thyroiditis (silent or painless thyroiditis) is fairly rare. Full thyroid function is regained in 90 percent of patients with these conditions.6

Hypothyroidism can also develop secondary to hypothalamic and pituitary disorders. These endocrine conditions occur primarily in patients who have undergone intracranial irradiation or surgical removal of a pituitary adenoma.

The signs and symptoms of hypothyroidism are nonspecific and may be confused with those of other clinical conditions, especially in postpartum women and the elderly. Because of the variety of possible manifestations, family physicians must maintain a high index of suspicion for the disorder, especially in high-risk groups.

Patients with severe hypothyroidism generally present with a constellation of signs and symptoms that may include lethargy, weight gain, hair loss, dry skin, forgetfulness, constipation and depression. Not all of these signs and symptoms occur in every patient, and many may be blunted in patients with mild hypothyroidism. The most common manifestations of hypothyroidism are listed in Table 2.7

In older patients, hypothyroidism can be confused with Alzheimer's disease and other conditions that cause cognitive impairment. Because depression can be a manifestation of hypothyroidism, patients with this endocrine condition may be treated as depressed, and other signs and symptoms of the disorder may be overlooked. This is particularly true with hypothyroidism that develops or worsens during pregnancy, or with postpartum thyroiditis, which has many of the same symptoms as postpartum depression.

Physical findings in patients with hypothyroidism are also nonspecific. These findings can include lowered blood pressure with bradycardia, nonpitting edema, generalized hair loss (especially along the outer third of the eyebrows), dry skin and a diminished relaxation phase of reflexes.

The evaluation of patients with new-onset hypothyroidism is quite limited. In patients with primary hypothyroidism, the thyroid-stimulating hormone (TSH) level is elevated, indicating that thyroid hormone production is insufficient to meet metabolic demands, and free thyroid hormone levels are depressed. In contrast, patients with secondary hypothyroidism have a low or undetectable TSH level.

TSH results have to be interpreted in light of the patient's clinical condition. A low TSH level should not be misinterpreted as hyperthyroidism in the patient with clinical manifestations of hypothyroidism. When symptoms are nonspecific, a follow-up assessment of the free thyroxine (T4) level can help distinguish between primary and secondary hypothyroidism. A guide to the laboratory diagnosis of hypothyroidism and the interpretation of TSH, T4 and triiodothyronine (T3) levels is provided in Table 3.

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