Hashimoto’s disease (chronic autoimmune thyroiditis) occurs when the immune system attacks the thyroid gland, leading to insufficient production of thyroid hormones and resulting in hypothyroidism. Addison’s disease is a similar autoimmune process, but it targets the adrenal glands, causing inadequate production of the steroid hormones cortisol and aldosterone. Hashimoto’s disease does not directly cause Addison’s disease, but their co-occurrence is a strong medical association rooted in shared autoimmunity. This link means that an individual diagnosed with one condition has a significantly increased likelihood of developing the other.
The Shared Foundation of Autoimmunity
Both Hashimoto’s disease and Addison’s disease are classified as organ-specific autoimmune disorders, meaning the body’s defense system targets specific tissues in the endocrine system. In autoimmunity, the immune system fails to distinguish between foreign cells and its own healthy cells, leading to a destructive attack on self-tissue.
The propensity to develop autoimmune conditions is often linked to genetic factors. Specific variants of human leukocyte antigen (HLA) genes, such as HLA-DR3 and HLA-DR4 haplotypes, are frequently observed in individuals with these conditions. These genes regulate the immune response, and their variants can predispose a person to multiple autoimmune diseases. This genetic blueprint increases the risk of the immune system targeting another endocrine gland. Approximately one-quarter of patients with one autoimmune disease will eventually develop a second one.
Understanding Polyglandular Autoimmune Syndromes
The medical connection between Hashimoto’s disease and Addison’s disease is formally recognized under the umbrella of Polyglandular Autoimmune Syndromes (PAS). Their co-occurrence is the most common presentation of Polyglandular Autoimmune Syndrome Type 2 (PAS Type 2), which is also known as Schmidt’s Syndrome. PAS Type 2 is defined by the mandatory presence of autoimmune Addison’s disease along with at least one other specific autoimmune endocrine condition, most frequently Hashimoto’s disease or Type 1 Diabetes Mellitus.
This syndrome highlights that the two diseases develop independently but from a common genetic vulnerability. The prevalence of Addison’s disease is markedly higher in individuals with Hashimoto’s disease compared to the general population, occurring in about 5.3% of patients. PAS Type 2 typically manifests in adulthood, usually between the third and fourth decades of life, and is observed more frequently in women. Since the diseases may present years apart, a person with a long history of Hashimoto’s must remain vigilant for signs of adrenal insufficiency.
Recognizing and Diagnosing Addison’s Disease
For a person managing Hashimoto’s disease, recognizing the signs of Addison’s disease (primary adrenal insufficiency) is crucial because symptoms can be subtle and non-specific. Common warning signs include persistent fatigue, unexplained weight loss, and generalized muscle weakness. Other distinct symptoms include low blood pressure (hypotension) and a noticeable craving for salty foods due to aldosterone loss.
A hallmark physical sign, often present only in primary adrenal insufficiency, is hyperpigmentation, which appears as a bronzing or darkening of the skin, especially in areas like scars, joints, and gums. When Addison’s disease is suspected, diagnosis is confirmed through blood tests and the adrenocorticotropic hormone (ACTH) stimulation test. This test measures cortisol levels before and after an injection of synthetic ACTH; in Addison’s disease, the damaged adrenal glands fail to produce an adequate response. The autoimmune nature of the condition is often confirmed by detecting the presence of 21-hydroxylase antibodies in the blood.
Comprehensive Treatment for Co-occurring Conditions
Managing co-occurring Hashimoto’s and Addison’s diseases requires two distinct types of hormone replacement therapy. For the thyroid condition, patients take levothyroxine, a synthetic thyroid hormone, to restore normal metabolic function. For Addison’s disease, replacement therapy involves taking glucocorticoids, such as hydrocortisone or prednisone, to substitute for the missing cortisol.
In many cases, a mineralocorticoid medication like fludrocortisone is also necessary to replace the lost aldosterone, which regulates salt and water balance and blood pressure. A critical protocol is treating the adrenal insufficiency before starting or increasing thyroid hormone replacement. Starting levothyroxine in an individual with untreated Addison’s disease can dangerously increase the body’s metabolic rate, precipitating a life-threatening adrenal crisis. Patients must also learn “stress dosing,” which means temporarily increasing their glucocorticoid dosage during times of physical stress (illness, injury, or surgery) to mimic the body’s natural response.