Thyroid Disease : Hashimoto's thyroiditis (chronic lymphocytic thyroiditis) - The Causes

Home of Kyle J. Norton for The Better of Living & Living Health Thyroid is one of the largest endocrine glands found in the neck, below the Adam’s Apple with the function of regulating the body use of energy, make of proteins by producing its hormones as a result of the stimulation of thyroid-stimulating hormone (TSH) produced by the anterior pituitary.
Thyroid disease is defined as a condition of malfunction of thyroid. Hyperthyroidism is a condition in which the thyroid gland is over active and produces too much thyroid hormones. Hypothyroidism is a condition in which the thyroid gland is under active and produces very little thyroid hormones. Thyroid cancer is defined as condition in which the cells in the thyroid gland have become cancerous.
Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis)
Hashimoto’s thyroiditis is an autoimmune disease in which the immune system attacks the thyroid gland of that mostly often leads an underactive thyroid gland (hypothyroidism). According to the study by the University of Pisa, Women with Hashimoto’s thyroiditis (HT)  suffer from a high symptom load independently from hypothyroidism, which results just a contributing factor to the development of the clinical syndrome. In agreement with these results, we recently reported on the presence of symptoms and signs consistent with fibromyalgia (FM) in patients with HT regardless thyroid dysfunction, focusing to the weight of anti-thyroid autoimmunity in the HT-associated clinical syndrome(a).
B.1 Causes
1. Autoimmune disorder
In the study to summarize the current knowledge on Hashimoto’s thyroiditis and its pathogenesis and to introduce the readers to the basic concept of autoimmune thyroid disease, found that Hashimoto’s thyroiditis and Graves’ disease are different expressions of a basically similar autoimmune process, and the clinical appearance reflects the spectrum of the immune response in a particular patient. During this response, cytotoxic autoantibodies, stimulatory autoantibodies, blocking autoantibodies, or cell-mediated autoimmunity may be observed. Persons with classic Hashimoto’s thyroiditis have serum antibodies reacting with thyroglobulin and thyroid peroxidase. These antibodies (particularly antibodies against thyroid peroxidase) are complement-fixing immunoglobulins and may be cytotoxic. In addition, many patients have cell-mediated immunity directed against thyroid antigens. Cell mediated-immunity is also a feature of experimental thyroiditis induced in animals by injection of thyroid antigen with adjuvants. Hashimoto’s thyroiditis is predominantly the clinical expression of cell-mediated immunity leading to destruction of thyroid cells, which in its severest form causes thyroid failure(3a).
 
1. Primary hyperparathyroidism (PHPT)
In the study to investigate and determine the prevalence of patients having both HT and PHPT, and the possible relation between these two diseases including 45,231 patients, which were referred by their general practitioner or endocrinologist, under suspicion of having thyroid and/or parathyroid disease., indicated that all 2,267 patients had normal or slightly elevated TSH levels. In conclusion, although the reported rate of prevalence of PHPT in the general population is about 0.3%, our results indicated a 1.89% occurrence of PHPT in 2267 patients with HT in central Serbia. This may be due to the autoimmune inflammatory process in HT supporting PHPT to PTH or calcium supporting HT or to common genetical predisposition of both entities(3).

2. Cerebellar ataxia
Both hypothyroidism and Hashimoto’s thyroiditis (HT) can rarely be associated with cerebellar ataxia.
There is a report of a  report a 74-year-old male with hypothyroidism and a 20-year history of ET who developed cerebellar ataxia after bilateral thalamic DBS. Extensive workup revealed elevated thyroid stimulating hormone and thyroperoxidase antibody titers confirming the diagnosis of HT(4). 
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Sources
(a) http://www.ncbi.nlm.nih.gov/pubmed/22147633
(3a) http://www.ncbi.nlm.nih.gov/pubmed/19667753
(3) http://www.ncbi.nlm.nih.gov/pubmed/23865082
(4) http://www.ncbi.nlm.nih.gov/pubmed/23439792 http://medicaladvisorjournals.blogspot.com