Hashimoto’s thyroiditis is a widespread autoimmune disorder where the body’s immune system mistakenly attacks the thyroid gland, leading to chronic inflammation and often hypothyroidism. Given the thyroid gland’s location in the neck, many people with this condition wonder if the autoimmune attack extends to the nearby parathyroid glands. These four pea-sized glands are anatomically neighbors to the thyroid, but they perform a completely different function. The relationship between Hashimoto’s and parathyroid dysfunction is not one of direct cause and effect, but rather one of shared vulnerability within the broader immune system.
Distinct Functions of the Thyroid and Parathyroid Glands
While located in the same area of the neck, the thyroid and parathyroid glands have separate and specialized roles in the endocrine system. The butterfly-shaped thyroid gland is the body’s primary regulator of metabolism, growth, and energy. It produces the hormones triiodothyronine (T3) and thyroxine (T4) that influence nearly every cell and organ in the body.
The four parathyroid glands, typically situated on the back surface of the thyroid, are responsible for maintaining calcium balance in the blood and bones. They secrete Parathyroid Hormone (PTH), which acts rapidly to raise calcium levels when they drop too low. PTH achieves this by stimulating the release of calcium from bones, enhancing its absorption in the intestines, and promoting its reabsorption in the kidneys. This specific regulation of calcium is entirely independent of the thyroid hormones produced by the larger gland.
Addressing the Direct Link to Hashimoto’s
The autoimmune process specific to Hashimoto’s thyroiditis does not directly cause an autoimmune attack on the parathyroid glands. In the vast majority of cases, a diagnosis of Hashimoto’s is not linked to a subsequent diagnosis of primary hypoparathyroidism, a condition of parathyroid failure. This is because the cells and proteins targeted by the immune system are unique to the thyroid gland.
When parathyroid gland function is impaired in a patient with a thyroid disorder, the cause is most often related to a surgical complication rather than the autoimmune disease itself. Patients with long-standing Hashimoto’s or a large goiter may require a total thyroidectomy. The parathyroid glands are microscopically small and tightly adhered to the thyroid, making them susceptible to accidental removal or damage to their blood supply during the procedure.
This damage results in postoperative hypoparathyroidism, leading to low calcium levels. Though transient hypoparathyroidism is common immediately following surgery, permanent damage occurs in a small percentage of patients, necessitating lifelong hormone replacement therapy. This complication arises from the intervention needed to treat the thyroid disease, not from the autoimmune nature of Hashimoto’s itself.
Shared Autoimmunity and Specific Syndromes
While Hashimoto’s does not typically spread to the parathyroids, both glands can be affected simultaneously in rare systemic conditions known as Autoimmune Polyendocrine Syndromes (APS). These syndromes are characterized by the immune system attacking multiple endocrine glands due to a shared genetic predisposition. The co-occurrence of hypoparathyroidism and Hashimoto’s can signal the presence of one of these broader syndromes.
Autoimmune Polyendocrine Syndrome Type 1 (APS-1) is a rare genetic disorder where primary hypoparathyroidism is a defining feature, often appearing alongside chronic mucocutaneous candidiasis and adrenal insufficiency. Autoimmune thyroid disease, including Hashimoto’s, can also be a component of APS-1, although it is not one of the three primary diagnostic features.
Autoimmune Polyendocrine Syndrome Type 2 (APS-2) is more common and frequently involves the co-occurrence of Hashimoto’s thyroiditis, Type 1 diabetes, and Addison’s disease (adrenal insufficiency). Hypoparathyroidism is sometimes seen in APS-2, though less commonly than in APS-1. The presence of Hashimoto’s alongside autoimmune hypoparathyroidism is rare but suggests a shared underlying immune dysfunction that warrants evaluation for these syndromes.
Recognizing Signs of Parathyroid Dysfunction
Parathyroid dysfunction, specifically hypoparathyroidism, results in a low level of calcium in the blood, which can have immediate and noticeable effects on the nervous and muscular systems. The earliest and most common sign is paresthesia, a tingling or burning sensation often felt around the mouth, in the fingertips, or in the toes. This sensation is a direct result of increased nerve excitability caused by the low calcium concentration.
As blood calcium levels drop further, muscle involvement can become more pronounced, leading to muscle cramps, aches, and spasms. Severe hypocalcemia can cause tetany, characterized by involuntary, sustained muscle contractions, which can sometimes affect the voice box and make breathing difficult. Patients may also experience generalized fatigue, weakness, and headaches.
A definitive diagnosis of parathyroid dysfunction requires specific blood tests to measure the levels of Parathyroid Hormone (PTH) and serum calcium. A low calcium level combined with an inappropriately low or undetectable PTH level confirms a diagnosis of hypoparathyroidism. Anyone with Hashimoto’s who experiences these neurological or muscular symptoms should seek prompt medical evaluation to test their calcium status.