Thyroid disease: Thyroid adenoma - 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.
Thyroid adenoma is a benign tumor started in the layer of cell lined the inner surface of the thyroid gland. The disease are relatively common among adults living in the United States. According to the study by the Mayo Clinic and Mayo Foundation, there is a report of 4 patients described in whom a follicular carcinoma developed following thyroidectomy for a benign follicular neoplasm. Most thyroid nodules are Thyroid adenoma.
B.1. Causes
1. Iodine deficiency and excess
Iodine, as a trace element, is a necessary and limiting substrate for thyroid gland hormone synthesis. It is an essential element that enables the thyroid gland to produce thyroid hormones thyroxine (T4) and triiodothyronine (T3). According to the study by the, Iodine deficiency can cause hypothyroidism, developmental brain disorders and goiter. Iodine deficiency is the single most common cause of preventable mental retardation and brain damage in the world. It also decreases child survival, causes goiters, and impairs growth and development. Iodine deficiency disorders in pregnant women cause miscarriages, stillbirths, and other complications. Children with iodine deficiency disorders can grow up stunted, apathetic, mentally retarded, and incapable of normal movements, speech or hearing(4). Other in the study to ivestigate the thyroid tumor-promoting effects of iodine deficiency and iodine excess  in a rodent 2-stage model to estimate an optimal iodine intake range that would not effectively promote development of thyroid neoplasia with six-week-old male F344 rats were given a single subcutaneous injection of 2,800 mg/kg body weight N-bis(2-hydroxypropyl)-nitrosamine (DHPN) or saline vehicle, maintained on Remington’s iodine-deficient diet (21 +/- 2 ng/g iodide), and supplemented with various amounts of potassium iodide up to 260 mg/liter in drinking water to generate conditions ranging from severe iodine deficiency to severe iodine excess, found that iodine deficiency produced diffuse thyroid hyperplasia, characterized by small follicles with tall epithelium and reduced colloid, together with a decrease in thyroxine (T4) and an increase in thyroid-stimulating hormone (TSH). On the other hand, iodine excess produced colloid goiter, characterized by large follicles with flat epithelium and abundant colloid admixed with normal or small-sized follicles lined by epithelium of normal height, together with normal serum T4 and slightly decreased TSH. These effects were directly proportional to the severity of iodine deficiency or extent of iodine excess and suggest that each condition has a different thyroid tumor promotion mechanism. Iodine intakes that showed the least tumor promotion were 2.6 and 9.7 micrograms/rat/day in this study(5).

2. Radiation therapy
In the stuydy to hypothesize that thyroid hormones may affect the metabolic activity of tumor cells and hence modulate the response to cytotoxic treatments by measuring the influence of thyroid status on the tumor microenvironment in experimental tumors, indicated thatthyroid status was associated with a significant change in tumor radiosensitivity since the regrowth delay was increased in hypothyroid mice compared to euthyroid mice, an effect that was abolished when temporarily clamped tumors were irradiated(6).

3. Hashimoto’s thyroiditis
Acoording to the study by the University of Crete, Hashimoto’s thyroiditis also seemed to play an important role, since benign specimens with Hashimoto’s thyroiditis had a 2.2-fold higher B-Raf expression than samples without thyroiditis (1.71 ± 0.63 vs. 0.78 ± 0.13). Statistical analysis revealed that B-Raf deregulation postponed disease onset by more than 10 years in both benign and malignant thyroid (benign: 55.6 ± 3.9 vs. 45.3 ± 3.3, p = 0.049; malignant: 52.2 ± 3.5 vs. 33.0 ± 7.9, p = 0.020)(7).
 
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Sources
(4) http://www.ncbi.nlm.nih.gov/pubmed/23297615
(5) http://www.ncbi.nlm.nih.gov/pubmed/1475583
(6) http://www.ncbi.nlm.nih.gov/pubmed/17903037
(7) http://www.ncbi.nlm.nih.gov/pubmed/23263826 http://medicaladvisorjournals.blogspot.com