The Pathophysiology of Hashimoto’s Disease

NB: We do not resell your papers. Upon ordering, we do an original paper exclusively for you.

NB: All your data is kept safe from the public.

Table of Contents

Introduction
Pathophysiology
Diagnosis
Signs and symptoms
Treatment and management
Conclusions
Reference List

Introduction

Hashimoto’s disease, which is sometimes referred to as Hashimoto’s thyroiditis and Chronic thyroiditis, is known as the main cause of hypothyroidism (Rapoport 1991). It normally involves the destruction of the thyroid gland rendering them incapable of producing adequate thyroid hormone, the condition which is referred to as hypothyroidism. These hormones, however, are very critical in metabolism.

Thus, with Hashimoto’s disease, one’s immune system attacks the thyroid gland resulting in an irritated and swollen gland. This prevents the normal production of thyroid hormones. This autoimmune disease was initially described by Hakaru Hashimoto in 1912 after examination of various cases (Rapoport 1991; Odeke & Lee 2009). This paper is a discussion of the pathophysiology of Hashimoto’s disease, why the signs and symptoms of these diseases occur as they are seen, the clinical tests applied in diagnosis, and the treatment options available.

Pathophysiology

Hashimoto’s disease involves the destruction of cells in the thyroid gland by “various cell- and antibody-mediated immune processes” (Odeke & Lee 2009). It is not yet understood how this process begins (Dayan and Daniels 1996; Duntas 2008; Tomer & Huber 2009; Hadj-Kacem, Rebuffat & Mnif-Feki 2009). However, Pearce, Farwell, and Braverman (2003) indicate that the “antithyroid immune response” in Hashimoto’s disease starts when T-cells, which are thyroid antigen-specific helpers, become activated.

In another theory, it is shown that this activation is caused by a virus infection whose protein is identical to that of the thyroid, although there is a lack of clear evidence on this viral cause (Dayan and Daniels (1996; Kuhr, Hala, Dietrich, Herold & Wick 1994). Elsewhere, it is indicated that epithelial cells of the thyroid introduce their “own intracellular proteins to T-cells” (Pearce, Farwell, and Braverman 2003). Imaizumi, Pritsker, Unger, and Davies (2002) assert that the build-up of fetal cells within the “maternal thyroid gland” may induce autoimmune thyroiditis in women during their pregnancy.

When one has Hashimoto’s thyroiditis, the thyroid gland is usually goitrous, although it may remain at normal size or rather atrophic. The antibodies that bind and block the thyroid-stimulating hormone receptor are a potential cause of the impairment of the functionality of the thyroid gland (Odeke & Lee 2009). This results in inadequate production of the thyroid hormone and its secretion; nonetheless, preformed triiodothyronine and thyroxine go into circulation when cells are damaged (Pearce, Farwell & Braverman 2003).

Hashimoto’s disease patients “ have antibodies to various thyroid antigens”, with antithyroglobulin and anti-thyroid peroxidase being frequently diagnosed, whereas “TSH receptor-blocking antibodies” are detected to a lesser extent (Odeke & Lee 2009). The thyroid-stimulating antibody and cytotoxic antibody may also be found in Hashimoto’s thyroiditis (Dayan & Daniels 1996; Pearce, Farwell & Braverman 2003). Besides Hashimoto’s thyroiditis, atrophic thyroiditis, juvenile thyroiditis (Fava, Oliverio & Giuliano 2009), postpartum thyroiditis, silent thyroiditis, and focal thyroiditis, constitute the variants of autoimmune thyroid diseases (Odeke & Lee 2009; Pearce, Farwell & Braverman 2003).

Diagnosis

Diagnosis of Hashimoto’s thyroiditis is normally established through medical examinations that show the following: swollen thyroid, high amounts of “antibodies against thyroglobulin and thyroid peroxidase”- which is determined by a blood test, “fine needle aspiration” or biopsy of the thyroid, – which indicates the presence of both macrophages and lymphocytes, “diffuse uptake in enlarged thyroid gland” – determined through radioactive scanning, and swollen thyroid as shown by ultrasound (Shomon 2009).

Laboratory tests such as the Free T4 test, Serum TSH test, and T3 test as well as a test on antithyroid peroxidase antibody and antithyroglobulin antibody are done to determine the functionality of the thyroid (Holt 2008). The Free T4 test measures the amount of thyroxine (T4) available in the blood, while the T3 test shows the level of triiodothyronine (T3), both of which are thyroid hormones. The expectation is that T4 hormones are low, while T3 hormones are low or normal (Holt 2008). Serum TSH test determines the level of thyroid-stimulating hormone in the blood, with the expectation of high levels (Holt 2008; Rapoport 1991).

Signs and symptoms

The signs and symptoms of Hashimoto’s thyroiditis can vary among individual patients. In some patients, there are no verifiable symptoms of the disease (Ladenson & Kim 2007; Milobratovic, et. al 2005). Holt and Zieve (2008) agree that the disease may take quite some time before it can be detected. However, several patients with Hashimoto’s disease experience enlargement of the thyroid and subsequent swelling of the neck (Abdel, et. al 2001). Note that the swelling of the thyroid is known as goiter. This goiter can be characterized by a slight swelling without other symptoms, or even a considerable increase in the size of the thyroid (Odeke & Lee 2009).

The swelling of the neck or presence of goiter may cause discomfort in areas around the neck (Abdel, et. al 2001; Pearce, Farwell, and Braverman 2003). One may feel like the neck is sore or uncomfortably swollen. Moreover, the throat and/or neck may become tender or sore. Though uncommon, Hashimoto’s disease patients can experience difficulties while swallowing and sometimes while breathing when goiter blocks the esophagus or the windpipe (Milobratovic, et. al 2005; Rapoport 1991).

The onset of this disease, as well as an increase in the levels of the antibodies, will, in several cases, be associated with various symptoms such as anxiety, fatigue, difficulty in finding sleep, weight changes, loss of hair, depression, fertility problems, and joint and muscle pains and aches (Pearce, Farwell & Braverman 2003; Ladenson & Kim 2007; Odeke & Lee 2009; Rapoport 1991). Odeke and Lee (2009) further states that “fatigue, constipation, dry skin, and weight gain are nonspecific”, noting that weight gain caused by hypothyroidism is often less than “10% of the baseline euthyroid weight.” The weight gain is mostly accredited to the accumulation of fluid in the interstitial tissues (Pearce, Farwell & Braverman 2003).

Sometimes, Hashimoto’s thyroiditis’ patient may develop thyroiditis attack, which is often characterized by inflammation and pain in the thyroid (Langer & Scheer 2000). Langer and Scheer (2000) further affirm that the symptoms of anxiety, swelling of the area around the thyroid, sleeping problems, heart palpitation, and panic attacks during thyroiditis attack. Other symptoms that may be associated with Hashimoto’s disease include dry skin, constipation, thinking or concentration difficulties, irregular and heavy periods in women, “intolerance to cold”, stiff joints, or “swelling of the face” (Holt 2008). Holt (2008) also notes that cold intolerance may be a result of problems in metabolism.

Although Hashimoto’s disease involves mainly hypothyroidism, there are episodes where the thyroid springs back to efficient production of the thyroid hormone and sometimes causes momentary hyperthyroidism (Rapoport 1991). Pearce, Farwell, and Braverman (2003) affirm that this intermittent occurrence of hypothyroidism and hyperthyroidism is typical of Hashimoto’s thyroiditis, probably because of the “intermittent presence of thyroid-stimulating and thyroid-blocking antibodies”. Therefore, for instance, it is normal for someone suffering from Hashimoto’s disease to experience episodes of fatigue, depression, constipation, and weight gain that precede episodes of insomnia, anxiety, diarrhea, and weight loss.

Treatment and management

There is the various treatment of Hashimoto’s disease used depending on the symptoms. The thyroid hormone substitution drugs are normally used to treat Hashimoto’s disease (Mandel, Brent & Larsen 1993). Levothyroxine sodium (Mandel, Brent & Larsen 1993), as well as the natural desiccated thyroid, can be given to patients with a large goiter to reduce its size (Pearce, Farwell & Braverman 2003), especially if it has caused breathing or swallowing difficulties. Surgery may also be done to remove some part or all of the thyroid if the replacement therapy fails (Padberg Heller, Usadel, Schumm-Draeger 2001).

If there is no presence of goiter, most traditional physicians and endocrinologists will hesitate to treat Hashimoto’s thyroiditis – is diagnosed through elevated levels of the antibodies – unless more tests on thyroid function such as TSH indicate a range that is not normal (Owen & Lazarus 2003; Rapoport 1991). Nonetheless, some health practitioners including osteopaths and endocrinologists trust that Hashimoto’s thyroiditis – as validated by the existence of thyroid antibodies – together with symptoms are sufficient to merit treatment with thyroid hormone substitution (Rapoport 1991; Padberg, Heller, Usadel and Schumm-Draeger 2001).

Dayan and Daniels (1996) claim that when Hashimoto’s disease is clinically suspected, “a test for thyroid antibodies and measurement of the serum thyrotropin concentration” is normally enough to substantiate a diagnosis of the disease. A study conducted by Padberg, Heller, Usadel, and Schumm-Draeger (2001) supports the treatment of patients with Hashimoto’s thyroiditis even when thyroid function tests indicate a normal range. They argue that using levothyroxine therapy to treat Hashimoto’s disease when TSH is within the normal range has the potential to reduce the scale and incidence of the disease advancement.

Several studies have indicated the significance of selenium in combating autoimmune thyroid thyroiditis (Padberg, Heller, Usadel and Schumm-Draeger 2001). It has been revealed that supplementation with a daily dose of about 200 micrograms of selenium can reduce elevated levels of thyroid antibody significantly, or return it to normal levels, thereby preventing progression to full autoimmune thyroid thyroiditis, which would cause hypothyroidism (Endocrine Society 2001; Journal of Clinical Endocrinology & Metabolism 2002; Rapoport 1991).

Nevertheless, the damage on the thyroid gland autoimmune reduces gradually its ability to function well, which eventually, leads to its under activity. If hypothyroidism can be gauged through blood tests then several medical practitioners or endocrinologists will eventually diagnose it and use replacement therapy with the appropriate drugs to treat it (Pearce, Farwell & Braverman 2003).

Langer & Scheer (2000) recommend the use of calcium and magnesium for patients who have developed a “thyroiditis attack” to help them sleep. Note that these minerals are sedative. Langer & Scheer (2000) further indicate that the use of these minerals may be accompanied by pain relievers such as ibuprofen and aspirin to relieve inflammation.

Conclusions

This discussion has examined Hashimoto’s disease – the main cause of hypothyroidism by exploring its pathophysiology, signs and symptoms, the clinical tests used in diagnosis, and its treatments. Though the mechanism of its initiation is not well understood, studies show that T-cells are involved and that Hashimoto’s disease is sometimes goitrous. Swelling of the neck area, tender or sore throat, breathing and swallowing difficulties, pain and inflammation, fatigue, constipation, dry skin, and weight changes, sleeping difficulties, depression, and stiff joints are some of the symptoms of the disease. It is normally treated with Levothyroxine sodium, while natural desiccated thyroid and selenium have also been useful in its treatment. Surgery can also be performed when these therapies fail.

Reference List

Abdel, A B, Ayman, A, Alaa, K, Gamal, E, Yasser, K, Rajhi, A, Nasser, G, Gamal, G, Danish, A, Alan, A, Henrik, S & Adnan, E 2001, Primary Thyroid Lymphoma: A Retrospective Analysis of Prognostic Factors and Treatment Outcome for Localized Intermediate and High-Grade Lymphoma, American Journal of Clinical Oncology, vol. 24, no. 3, pp. 299-305.

Dayan, C M, & Daniels, G H 1996, Chronic Autoimmune Thyroiditis, The New England Journal of Medicine, vol. 335, no. 2, pp. 99-107.

Duntas, L H 2008, Environmental factors and autoimmune thyroiditis, Nat. Clinical Practice in Endocrinology and Metabolism, vol. 4, no. 8, pp. 454-60.

Endocrine Society 2001, Findings of the 83rd Annual Meeting of the Endocrine Society, Denver, Colorado.

Fava, A, Oliverio, R, Giuliano, S 2009 Clinical evolution of autoimmune thyroiditis in children and adolescents. Thyroid.

Hadj-Kacem, H, Rebuffat, S, Mnif-Feki, M 2009, Autoimmune thyroid diseases: genetic susceptibility of thyroid-specific genes and thyroid autoantigens contributions. International Journal of Immunogenetics, vol. 36, no. 2, pp. 85-96. [Medline].

Holt, E H & Zieve, D 2008, Chronic thyroiditis – Hashimoto’s disease, Medline Plus. Web.

Imaizumi M, Pritsker A, Unger, P, Davies, T F 2002, Intrathyroidal fetal microchimerism in pregnancy and postpartum. Endocrinology, vol. 143 pp. 247-253.

Kuhr, T, Hala, K, Dietrich, H, Herold, M & Wick, G 1994, Genetically determined target organ susceptibility in the pathogenesis of spontaneous autoimmune thyroiditis: aberrant expression of MHC-class II antigens and the possible role of virus. Journal of Autoimmune; vol. 7, pp. 13-25. [Medline].

Ladenson, P & Kim, M 2007, Thyroid, 23rd edn, chap. 244, Saunders, Philadelphia.

Langer, S E, Scheer, J F 2000, Solved: the riddle of illness, 3^rd edn, McGraw-Hill Professional, New York.

Maceri, D R, Sullivan, M J, Mcclatchney, K D & Arbor, A 2009, Autoimmune thyroiditis: Pathophysiology and relationship to thyroid cancer, The Laryngoscope, vol. 96, no. 1, pp. 82 – 86.

Milobratovic, D, Djordjevic, S, Vukicevic, J, Bogdanovic, Z 2005, Idiopathic eruptive macular pigmentation associated with pregnancy and Hashimoto thyroiditis, Journal of the American Academy of Dermatology, vol. 52, no. 5, pp. 919-921.

Odeke, S & Lee, S L 2009, Hashimoto Thyroiditis, emedicine. Web.

Owen ,P J D & Lazarus, J H 2003, Subclinical hypothyroidism: the case for treatment, Trends in Endocrinology and Metabolism, vol. 14, no. 6, pp. 257-261.

2002, The Journal of Clinical Endocrinology & Metabolism, vol. 87, no. 4, pp. 1490-1498.

Padberg S, Heller K, Usadel K H, Schumm-Draeger P M 2001, One-year prophylactic treatment of euthyroid Hashimoto’s thyroiditis patients with levothyroxine: is there a benefit? Thyroid, vol. 11, no. 3, pp. 249-255.

Pearce, E N, Farwell, A P & Braverman, L E 2003, Thyroiditis, The New England Journal of Medicine, vol 348, no. 26, pp. 2646-2655.

Mandel, S J, Brent, G A & Larsen, P R 1993, Levothyroxine therapy in patients with thyroid disease, Ann Intern Med, vol. 119, no. 6, pp. 492-502.

Rapoport, B 1991, Pathophysiology of Hashimoto’s thyroiditis and hypothyroidism, Annual Review of Medicine, vol. 42, pp. 91-96.

Shomon, M 2009, Hashimoto’s vs. Hypothyroidism: What’s the Difference? A Look at Autoimmune Thyroid Disease and Underactive Thyroid Conditions. Web.

Tomer, Y, Huber, A 2009, The etiology of autoimmune thyroid disease: a story of genes and environment, Journal of Autoimmune.

Click Here To Order Now!