HASHIMOTO THYROIDITIS.

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Running Head: HASHIMOTO THYROIDITIS
HASHIMOTO THYROIDITIS
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1HASHIMOTO THYROIDITIS
Hashimoto’s Thyroiditis (HT) is an autoimmune inflammatory disease. The antibodies that
are produced in this disease are in response to the thyroid antigens that ultimately results in
the elimination of thyroid gland. Thus, it also destroys the necessary precursors for the
production of thyroid hormone. Hypothyroidism is mainly caused due to HT. However, for a
patient suffering from HT, the symptoms can suggest the possibility of fluctuation between
that of hyperthyroidism or hypothyroidism as well (Trbojevic & Djurica, 2005; Xue et al.
2015). The most common symptoms of hypothyroidism include excessive weight gain,
feeling fatigued, drying up of skin, loss of hair and increased intolerance to cold, brain fog,
muscle and joint pain as well as depression. Constipation can also be a common symptom
suggesting hypothyroidism (Crowley 2004; Kumar & Clark, 2009). Studies has shown that
HT is also associated with a large amount of other autoimmune diseases such as pernicious
anemia, vitiligo, lupus, primary adrenal autoimmune disease, celiac disease, myasthenia
gravis, rheumatoid arthritis and type 1 diabetes (Trbojevic & Djurica, 2005). The diagnosis of
the disease is done on the basis of elevated levels of TSH or Thyroid Stimulating Hormone
along with lower levels of T3 and T4. According to Gruner (2017) the treatment of thyroid
includes replacement of thyroid hormone and the prescription of certain precursors, cofactors
and stimulants that will lead to the synthesis of thyroid hormones.
The major causes of HT is not very clearly known but it is assumed to be a
multifactorial facet that involves a large number of variables. HT is thought to be caused by a
combination of factors involving genetic, environmental, immune and hormonal factors
(Hechtman, 2012). According to Cusick, Libbey & Fujinami (2013) the prolonged
proinflammatory responses to infections by both virus and bacteria have been associated with
the initiation as well as the exacerbation of Hoshimoto’s Thyroiditis’ auto immune condition.
Studies have shown that stress plays an integral role in the deregulation and
obstruction with the synthesis of hormone by triggering the release of corticotrophin-

2HASHIMOTO THYROIDITIS
releasing hormone, noradrenaline and cortisol. The roles played by these hormones are
inhibitory in nature as they hinder the secretion of TSH. Thus, it becomes a contributing
factor in the suppression of thyroid functioning (Tsigo & Chrousous, 2002). The digestive
system also plays a critical role in the homeostasis, because of its linkage to the immune
system via the GALT or Gut- Associated Lymphoid Tissue. Thus, the disbalance between the
microbes present in the gut micro-biota and the disturbances in GIT causes the infection of
the GIT and increases the permeability thereby causing impairing of the immune system
(Shuichi et al, 1999).