Overview:

• Hypothyroidism results from low levels of thyroid hormone with varied etiology and manifestations. Untreated hypothyroidism increases morbidity and mortality. In the United States, autoimmune thyroid disease (Hashimoto thyroiditis) is the most common cause of hypothyroidism, but globally lack of iodine in the diet is the most common cause. 

• The patient's presentation can vary from asymptomatic disease to myxedema coma. Today, the diagnosis of hypothyroidism is easily made with simple blood tests and can be treated with exogenous thyroid hormone.

Etiology

• Hypothyroidism is majorly divided into two categories, primary and secondary (central) hypothyroidism. Hypothyroidism is termed primary when the thyroid gland itself is not able to produce adequate amounts of thyroid hormone. The less common, secondary, or central hypothyroidism is labeled when the thyroid gland itself is normal, and the pathology is related to the pituitary gland or hypothalamus.

• The most prevalent etiology of primary hypothyroidism is an iodine deficiency in iodine-deficient geographic areas worldwide. Autoimmune thyroid diseases are the leading causes of hypothyroidism in the United States and the iodine-sufficient regions. Hashimoto thyroiditis is the most common etiology in the United States, and it has a strong association with lymphoma. Etiology can be influenced locally by iodine fortification and the emergence of new iodine-deficient areas.

Other common causes of hypothyroidism include:

• Drugs such as amiodarone, thalidomide, oral tyrosine kinase inhibitors (sunitinib, imatinib) stavudine, interferon, bexarotene, perchlorate, rifampin, ethionamide, phenobarbital, phenytoin, carbamazepine, interleukin-2, and lithium,

• Thyroid radioactive iodine therapy. Thyroid surgery

• Radiotherapy to head or neck area

• Central hypothyroidism from neoplastic, infiltrative, inflammatory, genetic, or iatrogenic disorders of the pituitary or hypothalamus.

• A new class of cancer medications such as anti-CTLA-4 and anti-PD-L1/PD-1 therapy has been associated with both primary and/or secondary hypothyroidism.

Common Complaints:

• Tiredness, lethargy. Being sensitive to cold.

• Weight gain.Constipation. Irregular uterine bleeding.

• Depression. Slow movements and thoughts.

• Muscle aches and weakness. Sexual dysfunction

• Hair loss or dryness. Brittle nails. Irritability

• Enlarged thyroid. High cholesterol. Slow heart rate.

 Treatments if recommended:

Treatment / Management

• Hypothyroidism is mainly treated with levothyroxine monotherapy.

• Thyroid replacement treatment can exacerbate co-existing adrenal insufficiency. Patients with known or suspected adrenal insufficiency should be tested and treated for adrenal insufficiency while awaiting results.

• Adrenal insufficiency can also be associated with subclinical hypothyroidism that is reversible with the treatment of adrenal insufficiency. In patients who have confirmed adrenal insufficiency consider a reassessment of thyroid tests following an adequate treatment of adrenal insufficiency. It is important to rule out or treat adrenal insufficiency when a patient has severe hypothyroidism as in myxedema coma. 

• Replacement levothyroxine dose is 1.6 mcg/kg per day; however, in elderly and atrial fibrillation patients, it is important to reduce the dose.

• In order to help the absorption, levothyroxine should be taken 30-45 minutes before breakfast and at least 3 hours post-meal at bedtime which are the convenient times for most patients.

•  Moreover, elemental supplements such as calcium, magnesium, to name a few, do affect the absorption of levothyroxine. Commonly used medications such as proton pump inhibitors also have a negative impact on levothyroxine absorption. Maintaining a consistent formulation or brand of levothyroxine is essential.

• There can be slight variations in the dose of the generic formulations, which can have a clinical impact in a small subset of very sensitive hypothyroid patients.

Evaluation

• Serum TSH level is used to screen for primary hypothyroidism in most patients. In overt hypothyroidism, TSH levels are elevated, and free T4 levels are low. In subclinical hypothyroidism, TSH levels are elevated, and free T4 levels are normal.

• Central hypothyroidism is of pituitary or hypothalamic origin. TSH produced can be biologically inactive and can affect the levels of bioactive TSH, hence the diagnosis of central hypothyroidism should be based on free T4 rather than TSH.

• Labs should include evaluation for autoimmune thyroid diseases with levels of anti-thyroid antibodies such as the thyroid peroxidase antibodies. 

• Patients with subclinical hypothyroidism and thyroid peroxidase antibody positivity have a greater risk of developing overt hypothyroidism. The studies have shown that 50% of the patients will develop primary hypothyroidism in the course of 20 years. The decision to follow up periodically with clinical evaluation as well as lab tests is based on clinical judgment as there are no clear-cut guidelines in this regard.

• Hospitalized patients should undergo TSH testing only when thyroid dysfunction is suspected. Slight abnormalities of TSH in sick patients during their hospital stay should hint towards euthyroid sickness. However, if the values of TSH are very high, it does suggest hypothyroidism. "Reverse T3" will be elevated when the patient has euthyroid sickness; however, it is not routinely checked in clinical practice. 

• Laboratory workup may reveal hyperlipidemia, elevated serum CK, elevated hepatic enzymes, and anemia. BUN, creatinine, and uric acid levels can also be elevated.

• Imaging studies (ultrasound) of the neck are not routinely recommended for hypothyroidism.

Screening for Hypothyroidism

• While there are no universal guidelines on screening the public for thyroid disease, the American Thyroid Association recommends that screening should commence at the age of 35 and should continue every five years. Individuals at high risk for hypothyroidism include the following:

• Women over the age of 60. Pregnancy

• Patients with a prior history of head and neck irradiation

• Patients with autoimmune disorders and/or type 1 diabetes

• Positive thyroid peroxidase antibodies

• Family history

 

NOTE: MUST HAVE RECENT THYROID PANEL WITH THE TSH LAB RESULTS.

 

Retrieved from:

https://www.ncbi.nlm.nih.gov/books/NBK519536/#article-23304.s8

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267409/

 

https://www.aafp.org/pubs/afp/issues/2012/0801/p244.html