Pituitary Hypothyroidism Labs

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Thethyroid gland is an important organ of the endocrine system, located in the front of the neck just below the voicebox. The thyroid secretes the hormones thyroxine (T4), triiodothyronine (T3), and calcitonin, which control body metabolism and regulate calcium balance. The secretion of T3 and T4 by the thyroid is controlled by an endocrine feedback system involving the pituitary gland and the hypothalamus (structures in the brain). Lowered levels of these thyroid hormones result in increased levels of pituitary and hypothalamic hormones. The reverse is also true -- when levels of the thyroid hormones rise, pituitary and hypothalamic hormones fall back. This helps keep levels appropriately balanced.

Since the thyroid gland is regulated by the pituitary gland and the hypothalamus, thyroid disorders may result not only from defects in the thyroid itself but also from the disruption of the control system in these other organs. Thyroid disorders caused by overproduction of thyroid hormones are called hyperthyroidism, and underproduction of these hormones is known as hypothyroidism.

The cause of secondary hypothyroidism is failure of the pituitary gland to secrete thyroid stimulating hormone (TSH). This is usually caused by a tumor in the region of the pituitary. Rarely the cause is an infiltration of the pituitary by inflammatory cells from the immune system or foreign substances (such as iron in hemochromotosis). Hypothyroidism may cause a variety of symptoms and can affect all body functions. The body's normal rate of functioning slows, causing mental and physical sluggishness. Symptoms vary from mild to severe. The most severe form is called myxedema, which is a medical emergency and can lead to coma and death.

A physical exam usually reveals a small thyroid gland. Vital signs (temperature, pulse, rate of breathing, blood pressure) reveal a slow heart rate, low blood pressure, and low temperature. A chest x-ray may reveal an enlarged heart. Laboratory tests to determine thyroid function include:

The purpose of treatment is to replace the deficient thyroid hormone. Levothyroxine is the most commonly used medication. The lowest dose effective in normalizing thyroid function is used. Life-long therapy may be necessary. Medication must be continued even when symptoms subside. After replacement therapy has begun, report any symptoms of increased thyroid activity (hyperthyroidism), such as restlessness, rapid weight loss, and sweating.

A high-fiber, low-calorie diet and moderate activity will help relieve constipation and promote weight loss if weight was gained during the time when thyroid activity was low. In individuals with accompanying hypoadrenalism, steroid replacement must be instituted before thyroid replacement is begun. In patients who have hypothyroidism caused by a pituitary tumor, surgery may be required. However, surgery may not cure the hypothyroidism, and thyroid replacement will still be needed.

Myxedema coma is treated by intravenous (IV) thyroid replacement and steroid therapy. Supportive therapy of oxygen, assisted ventilation, fluid replacement, and intensive care nursing may be indicated.

Calling your health care provider:

Call your health care provider if signs of hypothyroidism are present, or if chest pain or rapid heartbeat occur. Call your provider if restlessness, rapid weight loss, sweating, or other symptoms occur after beginning treatment for this disorder. Call your provider if headache, visual loss, or breast discharge occur.

At its most severe, undiagnosed hypothyroidism can manifest as myxedema. This life-threatening condition is characterized by swelling, slowed heart rate, low blood pressure, confusion, low body temperature, and fluid buildup around the heart. It requires hospitalization for urgent treatment.

The pituitary gland is responsible for secreting hormones that interact with the kidneys, sex glands, adrenal glands, and thyroid gland. With pituitary gland failure, symptoms include fatigue, low blood pressure, irregular or absent menstrual cycles, infertility, decreased libido, mood changes, weight changes, muscle weakness, and skin, hair, and nail changes.

In primary hypothyroidism, a problem involving the thyroid gland itself, the pituitary gland can become enlarged due to enlargement (hyperplasia) of cells that secrete thyroid stimulating hormone (TSH). This is because there is excess thyrotropin stimulating hormone, which tells the pituitary gland to secrete TSH to normalize thyroid levels.

Pituitary hypothyroidism is diagnosed using laboratory tests for thyroid hormone levels (T3 and T4) as well as thyroid stimulating hormone (TSH) levels. Low T3 and T4 levels with normal or low TSH levels indicate a problem with the brain. A brain MRI is needed for further evaluation.

Dr. Kelly Wood is an ABMS board certified endocrinologist and internal medicine physician who treats adults with diabetes, thyroid disease, osteoporosis, and other hormonal conditions. She achieved her fellowship in endocrinology from University of Wisconsin Hospital and Clinics.

Heather Hobbs (she/her) is an editor at Healthline Media and RVO Health. She has also worked in content creation, marketing, copy editing, and search engine optimization (SEO) for brands, agencies, and nonprofit organizations. A former educator, she earned her MA in teaching as well as a BA with a double major in English writing and Spanish, along with a minor in French. You can find her on LinkedIn.

A problem with any of these three glands can lead to hypothyroidism. The vast majority of hypothyroidism diagnoses are caused by problems with the thyroid gland and are categorized as primary hypothyroidism.

To diagnose pituitary hypothyroidism, a doctor will likely start by asking about your symptoms and reviewing your personal and family medical history. They may perform a physical exam where they feel your thyroid gland for abnormal changes.

For example, some people may also have secondary adrenal insufficiency that may require glucocorticoid treatment. Secondary adrenal insufficiency is when your pituitary gland does not produce enough adrenocorticotropic hormone (ACTH), which leads to low cortisol levels.

Secondary hypothyroidism is a rare form of hypothyroidism caused by your pituitary gland underproducing TSH. It makes up less than 1% of cases of hypothyroidism and can cause symptoms like fatigue, poor cold tolerance, and weight gain.

Pituitary hyperplasia is an under-recognized manifestation that can occur fairly commonly in primary hypothyroidism. Recognition of this entity is important as the primary modality of treatment is mainly thyroid hormone replacement and not surgery. This activity reviews the evaluation and treatment of pituitary hyperplasia and highlights the role of the interprofessional team in the care of patients with this condition.

Objectives:Describe the etiology of pituitary hyperplasia secondary to primary hypothyroidism.Review the common presentation of a patient with pituitary hyperplasia secondary to primary hypothyroidism.Outline the treatment options for a patient with pituitary hyperplasia secondary to primary hypothyroidism.Summarize the importance of collaboration and communication amongst the interprofessional team to enhance care coordination for patients with pituitary hyperplasia secondary to primary hypothyroidism.Access free multiple choice questions on this topic.

Pituitary hyperplasia is an under-recognized manifestation that can occur fairly commonly in primary hypothyroidism. It occurs due to the lack of negative feedback on the pituitary and hypothalamus. The presentation and imaging can mimic a pituitary mass. Patients can present with features of hypothyroidism, hyperprolactinemia, and even visual field defects if the hyperplastic pituitary gland compresses the optic chiasm. Recognition of this entity is important as the primary modality of treatment is mainly thyroid hormone replacement and not surgery.

In patients with primary hypothyroidism, the most common cause is chronic autoimmune thyroiditis or Hashimoto's thyroiditis, which results in a combination of cell and antibody-mediated thyroid destruction.[1] As a result of thyroid destruction, the low levels of circulating thyroid hormone lead to a lack of negative feedback on the hypothalamus resulting in elevated thyrotropin-releasing hormone (TRH). The elevated TRH levels lead to thyrotroph hyperplasia in the pituitary, which, in turn, results in elevated thyroid-stimulating hormone (TSH) production. The elevated TRH can also lead to lactotroph hyperplasia, which is the cause of increased prolactin in these patients.[2]

The thyrotroph hyperplasia is what ultimately results in the enlargement of the pituitary gland.[3] Important to note is that thyrotroph cells in the anterior pituitary only comprise 5% to 10% of all cell types in the gland and yet can result in significant gland enlargement in those with primary hypothyroidism.[4] One postulated mechanism is that the number of thyrotroph cells can increase by up to 34% in patients with hypothyroidism.[5]

Certain studies have demonstrated that the incidence of pituitary hyperplasia in primary hypothyroidism can range anywhere from 25%-81%.[5] These studies were based on skull x-ray findings showing increased sella turcica volume in those with primary hypothyroidism. Additional research has shown that a correlation may exist between the presence of pituitary hyperplasia as measured by the size of the sella turcica with how high the level of TSH value is.[6] One study showed that in those patients with TSH levels above 50 IU/mL, 70% had enlargement of their pituitary.[7]

History and physical examination can help tremendously to guide further work-up. The clinician needs to think in an organized fashion with regards to end-organ deficiencies or excess and their manifestations as well as local complications of an enlarged pituitary gland.

If a patient has hypothyroidism, they may experience symptoms such as weight gain, fatigue, cold intolerance, constipation, dry skin, and irregular menses in females.[8] Children may present with delayed growth, short stature, obesity, and rarely precocious puberty.[9] Since a TSH-producing adenoma is on the differential, hyperthyroid symptoms are always asked in tandem, such as unintentional weight loss, anxiety, experiencing tremors, sweating, heat intolerance, and palpitations. As prolactin levels are fairly commonly elevated in patients with pituitary hyperplasia as a result of primary hypothyroidism, the clinician should also ask about amenorrhea and galactorrhea in females as well as any issues with fertility. For structural concerns related to the enlarged pituitary gland, the clinician should ask about the presence of headaches or changes in vision that would be concerning for the mass abutting the optic chiasm.

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