About Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis (HT), also called Hashimoto’s disease, chronic lymphocytic thyroiditis or autoimmune thyroiditis, is a disease where the immune system attacks the thyroid gland, causing inflammation and interfering with its ability to produce thyroid hormones. Large numbers of white blood cells called lymphocytes accumulate in the thyroid. Lymphocytes make the antibodies that start the autoimmune process. The thyroid is located in the neck and is part of the endocrine system. It produces two hormones.

Hashimoto’s thyroiditis often leads to reduced thyroid function, or hypothyroidism. Hypothyroidism is a disorder that occurs when the thyroid doesn’t make enough thyroid hormone for the body’s needs. Thyroid hormones regulate metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels. Thyroid hormones affect nearly every organ in the body. Without enough thyroid hormone, many of the body’s functions slow down. Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the United States.

Many people with Hashimoto’s thyroiditis have no symptoms at first. As the disease slowly progresses, the thyroid usually enlarges and may cause the front of the neck to look swollen. The enlarged thyroid may create a feeling of fullness in the throat, though it is usually not painful. After many years, or even decades, damage to the thyroid causes it to shrink.

Not everyone with Hashimoto’s thyroiditis develops hypothyroidism. For those who do, the hypothyroidism may be mild, especially early in its course. With progression to hypothyroidism, people may have one or more of the following symptoms:

• fatigue
• weight gain
• cold intolerance
• joint and muscle pain
• constipation, or fewer than three bowel movements a week
• dry, thinning hair
• heavy or irregular menstrual periods and problems becoming pregnant
• depression
• memory problems
• a slowed heart rate

There is no established cause or cure for Hashimoto’s thyroiditis. Treatment generally depends on whether the thyroid is damaged enough to cause hypothyroidism. Some doctors choose not to treat the disease and simply monitor their patients for disease progression. Hashimoto’s thyroiditis, with or without hypothyroidism, is treated with a man-made version of thyroxine, the hormone produced by the thyroid. Health care providers routinely test the blood of patients taking synthetic thyroid hormone and adjust the dose as necessary, typically based on the result of a TSH test. Hypothyroidism can almost always be completely controlled with synthetic thyroxine, as long as the recommended dose is taken every day as instructed. People with Hashimoto’s thyroiditis may be sensitive to harmful side effects from iodine, so taking iodine drops or eating foods containing large amounts of iodine may cause or worsen hypothyroidism.

The Possible Role of MAP in Hashimoto’s Thyroiditis

Mycobacterium avium spp paratuberculosis (MAP) has been found in a number of different human diseases. The role that MAP plays in any of these conditions is still the subject of debate, and further research is necessary. Human Para will add research studies as they are released.

Molecular identification of Mycobacterium avium subspecies paratuberculosis in an Italian patient with Hashimoto’s thyroiditis and Melkersson–Rosenthal syndrome. (January 2010)
The researchers report the case of a patient with Hashimoto’s Thyroiditis and Merlkersson-Rosenthan syndrome who tested positive for MAP DNA in her blood samples. The patient had lived on a dairy farm and consumed milk produced there since childhood. The authors concluded that “the findings are consistent with early exposure to dietary cows’ milk and underline the possibility that milk from cattle with Johne’s disease could be a potential transmission vehicle for MAP to humans.”

Recognition of Zinc Transporter 8 and MAP3865c Homologous Epitopes by Hashimoto’s Thyroiditis Subjects from Sardinia: A Common Target with Type 1 Diabetes? (May 2014)
In the first study to investigate the link between Hashimoto’s Thyroiditis (HT) and MAP, researchers tested the blood of 107 HT patients and 100 healthy controls from Sardinia for antibodies to MAP. They hypothesized that MAP is one of the environmental triggers of HT through a molecular mimicry mechanism. Antibodies produced in reaction to a MAP protein (MAP3865c) are capable of cross-reacting with the human ZnT8 protein located in the thyroid tissue. They found that MAP antibodies were present in 20- 26% of HT patients but only 4-7% of healthy controls. The authors concluded that MAP is significantly associated with HT, but further studies are needed.

Detection of serum antibodies cross-reacting with Mycobacterium avium subspecies paratuberculosis and beta-cell antigen zinc transporter 8 homologous peptides in patients with high-risk proliferative diabetic retinopathy. (September 2014)
While this study primarily looked at the presence of MAP antibodies in type 1 diabetes (T1D) patients, the researchers discovered that Hashimoto’s thyroiditis was significantly more prevalent in the group of  T1D patients who tested positive for MAP antibodies. The researchers conclude that “the significantly higher prevalence of Hashimoto’s disease among type 1 diabetes patients with positive (MAP) antibodies might suggest a possible common environmental trigger for these conditions.” Further studies are necessary to determine if T1D patients may be susceptible to Hashimoto’s thyroiditis.

Bio-load of Mycobacterium avium subspecies paratuberculosis infection in human patients suffering with thyroid disorer in Agra region of North India using Indigenous ELISA and Real Time PCR. (June 2016)
In blood samples of thyroiditis patients collected from the Agra region of India, MAP DNA was detected in 32.1-35.1%. The study highlighted the high level of MAP exposure to humans in this region and the urgent need for further studies in thyroiditis patients.