Primary And Secondary Hypothyroidism

[Hildegard Mccauley]

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-stimulating hormone, also known as TSH, is a glycoprotein hormone produced by the anterior pituitary. It is the primary stimulus for thyroid hormone production by the thyroid gland. It also exerts growth effects on thyroid follicular cells leading to enlargement of the thyroid. The hypothalamic-pituitary axis regulates TSH release. Specifically, neurons in the hypothalamus release TRH, or thyroid-releasing hormone, which stimulates thyrotrophs of the anterior pituitary to secrete TSH. TSH, in turn, stimulates thyroid follicular cells to release thyroid hormones in the form of T3 or T4. Triiodothyronine, or T3, is the active form of thyroid hormone. Though it represents only 20% of the released hormone, the majority of T3 comes from the peripheral conversion of T4 to T3. Tetraiodothyronine, also known as thyroxine or T4, constitutes more than 80% of the secreted hormone. When released into the circulation, it forms T3 through the process of de-iodination. T4 and T3 can then exert negative feedback on the anterior pituitary with high levels of T3/T4 decreasing TSH secretion and low levels of T3/T4 increasing TSH release. In this review, we discuss the physiology, biochemistry, and clinical relevance of TSH.[1]

Primary thyroid disease refers to problems arising from the thyroid gland itself. In contrast, secondary thyroid disease refers to central problems arising from the anterior pituitary that indirectly affects thyroid function. A thyroid problem can exist in the form of hyperthyroidism or hypothyroidism. Hyperthyroidism occurs when there is excessive thyroid hormone synthesis or release. Hypothyroidism, on the other hand, happens due to inadequate thyroid hormone production.

In primary hyperthyroidism, the thyroid produces large amounts of T3 and T4, which, through negative feedback inhibition, suppress TSH secretion from the anterior pituitary. In primary hypothyroidism, the thyroid produces insufficient amounts of T3 and T4, which leads to loss of negative feedback inhibition, and increased production of TSH from the anterior pituitary. In secondary hyperthyroidism, the anterior pituitary produces large amounts of TSH, which, in turn, stimulate the thyroid follicular cells to secrete thyroid hormones in excessive amounts. On the other hand, if the anterior pituitary were to produce low levels of TSH, lack of stimulation of thyroid follicular cells causes T3 and T4 levels to go down, thus secondary hypothyroidism.

TSH is the first-line screening test for the majority of patients with a suspected thyroid problem. Together, with T3 and T4, it helps assess whether thyroid disease is primary or secondary. Thyroid function tests measure the levels of T3, T4, and TSH in the blood. They are critical not only for diagnosing thyroid problems but also in differentiating between a primary and a secondary cause of thyroid disease. A change in TSH that parallels T3 and T4 changes indicates a secondary problem originating in the anterior pituitary. In contrast, a TSH change that follows the opposite direction of T3 and T4 suggests a problem in the thyroid gland itself.[2][3][4]

TSH is a peptide hormone produced by the anterior pituitary. It consists of two chains: an alpha chain and a beta chain. It has a molecular mass of approximately 28,000 Da. The composition is very similar to other glycoprotein hormones made by the anterior pituitary. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and human chorionic gonadotropin (HCG) very much resemble TSH. Specifically, they all have the same alpha subunit as TSH, but different beta chains that confer biological specificity. Since TSH, LH, FSH, and HCG share the same alpha subunit, they all function through the same cyclic adenine monophosphate (cAMP) second messenger system. The cAMP second messenger system entails adenine monophosphate (AMP) conversion to cAMP. In addition to cAMP, TSH also activates the IP3 signaling cascade. The IP3 second messenger system involves calcium release from the sarcoplasmic reticulum. Both cAMP and IP3/Ca2+ cascades lead to downstream physiological effects that enhance thyroid hormone synthesis and thyroid gland growth.

The primary target of TSH is the thyroid gland. Specifically, TSH modulates the release of T3 and T4 from thyroid follicular cells. Around 80% of the thyroid hormone is released as T4. T4 is de-iodinated to T3, which is a more potent thyroid hormone. Even though only about 20% of T3 originates from the thyroid gland, 80% comes from peripheral conversion via a deiodinase. More than 99% of thyroid hormones bind to thyroid-binding globulin, prealbumin, and albumin, and only 1% circulates freely in the blood. Once T3 binds to its receptor in the nucleus, it activates DNA transcription, followed by mRNA translation, and new protein synthesis. These new proteins influence many organ systems, promoting growth as well as bone and central nervous system (CNS) maturation. T3 and T4 act on almost all cells in the body to increase the basal metabolic rate. Specifically, they increase the synthesis of Na?/K?-ATPase, leading to an increase in oxygen consumption and heat production. They also act on B1 receptors in the heart to increase heart rate and contractility through increasing the number of beta-1 receptors on the myocardium such that the myocardium is more sensitive to stimulation by the sympathetic nervous system. Thyroid hormones also activate metabolism, with an increase in glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, and protein synthesis and degradation (net catabolic).[5]

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