Wednesday, July 27, 2016

Most Common Diseases of 50 Plus: Thyroid disease: Silent thyroiditis – The Causes and Risk factors

Kyle J. Norton(Scholar and Master of Nutrients, all right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
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Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.


                         Thyroid disease


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.


                   Silent thyroiditis


Silent thyroiditis is the inflammation of the thyroid gland. Patients with silent thyroiditis are experience back and forth between hypothyroidism and hyperthyroidism. The disease classically present with a triphasic course: a brief period of thyrotoxicosis due to release of preformed thyroid hormone that lasts for 1 to 3 months, followed by a more prolonged hypothyroid phase lasting up to 6 months, and eventual return to a euthyroid state. However, the types and degree of thyroid dysfunction are variable in these disorders, and individual patients may present with mild or more severe cases of thyrotoxicosis alone, hypothyroidism alone, or both types of thyroid dysfunction(a).

                           The Causes and Risk factors


A. Causes
Although the cause of silent thyroiditis is known. The autoimmune thyroiditis processus progressively and slowly tends to the necrosis/apoptosis of thyroid cells and their functional impairment. Other forms of autoimmune thyroiditis, postpartum thyroiditis and silent thyroiditis(11). There is a suggestion that silent thyroiditis is an autoimmune disease characterized by lymphocytic infiltration of the thyroid and by transient hyperthyroidism, followed occasionally by transient hypothyroidism and eventual recovery(12).
Other indicated that clinically important autoimmune thyroid disease might thus be present both in individuals with normal and with raised thyrotropin concentrations. Rises in thyrotropin concentration might also occur for several reasons other than autoimmune thyroiditis(13).

B. Risk factors
1. Gentic and environment factors
Genetic and/or environmental factors are important in the development of this familial type of silent thyroiditis, according to the study by the Gifu Red Cross Hospital(14). Other study indicated that antecedent infection or exposure to antigen may cause the development of silent thyroiditis(15).

2. Adrenalectomy
There is a report of a case of silent thyroiditis after unilateral adrenalectomy for treatment of Cushing’s syndrome as the left adrenocortical adenoma was resected, according to the Gifu University School of Medicine(16).

3. Lithium therapy
While hypothyroidism secondary to treatments by lithium are well known, cases of hyperthyroidism are less common. A 48 years old patient under lithium carbonate from about 10 years ago presents hyperthyroidism without any auto-immunity biological markers, associated with a very low thyroid tracer uptake on scintigraphy(17).

4. Alpha-interferon therapy
There is a report of a a 30-year-old woman with chronic active hepatitis C develops silent thyroiditis developed during alpha-interferon therapy(18). Other study report the development of a episode of silent thyroiditis in a patient with chronic thyroiditis and papillary adenocarcinoma following alpha interferon treatment for hepatitis C(19).

5. Thyroid-stimulation-blocking antibodies (TSBAb)
There is a report of a 24-year-old man showed thyrotoxic symptoms with hypokalemic periodic paralysis. Serum thyroid hormone levels were high and thyrotropin (TSH) was undetectable. 123I-thyroidal uptake was suppressed. TSH-binding inhibitor immunoglobulin (TBII) was positive(20).

6. Infections
Viral infection such as rubella could cause the development of silent thyroiditis. There is a report of A 40-year-old housewife was referred to our hospital for evaluation of a thyrotoxic state. A month after rubella infection, she developed heat intolerance(21).

7. Gender
If you are women, you are associated to increased risk of silent thyroiditis.

8. Low level of selenium
Se levels were significantly decreased in cases of sub-acute and silent thyroiditis. according to WOMED(22).

9. Postpartum period
Silent or painless thyroiditis is a frequent cause of transient hyperthyroidism, which is characterized by recent onset of symptoms in a patient with a normal to modestly enlarged and firm thyroid gland. No pathogenetic factors are known, but the disease may conceivably have an autoimmune basis, particularly in the postpartum patient(22a).

10. Autoimmune type 1 diabetes mellitus
Patients with autoimmune type 1 diabetes mellitus have often, besides immune diabetes markers, also other organ-specific antibodies, particularly thyroid autoantibodies (antithyreoglobulin antibodies – ATG and/or thyroid peroxidase antibodies – TPO)(22b).

11. Thyroid peroxidase autoantibodies
Thyroid peroxidase (TPO) is a key enzyme in the formation of thyroid hormones and a major autoantigen in autoimmune thyroid diseases. Titers of TPO antibodies also correlate with the degree of lymphocytic infiltration in euthyroid subjects, and they are frequently present in euthyroid subjects (prevalence 12-26%)(22c).

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Sources
(13) http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2801%2905358-2/fulltext#bib5
(14) http://www.ncbi.nlm.nih.gov/pubmed/16284442.
(15) http://www.ncbi.nlm.nih.gov/pubmed/1752238
(16) http://www.ncbi.nlm.nih.gov/pubmed/8484389
(17) http://www.ncbi.nlm.nih.gov/pubmed/17166635
(18) http://www.ncbi.nlm.nih.gov/pubmed/8128980
(19) http://www.ncbi.nlm.nih.gov/pubmed/7920883
(20) http://www.ncbi.nlm.nih.gov/pubmed/1983199
(21) http://www.ncbi.nlm.nih.gov/pubmed/2384053
(22) http://www.ncbi.nlm.nih.gov/pubmed/18221503
(22a) http://www.ncbi.nlm.nih.gov/pubmed/21278944
(22b) http://www.ncbi.nlm.nih.gov/pubmed/23599721
(23c) http://www.ncbi.nlm.nih.gov/pubmed/15826919                  






                          

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