Hashimoto’s Thyroiditis

  |  Autoimmune Diseases  |  Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis belongs to the Thyroid Diseases.

It usually appears as Hypothyroidism.

Hashimoto’s thyroiditis now belongs to the Autoimmune Diseases, due to the growth of Auto-antibodies against the thyroid gland.

 

Diagnosis of Real Causes & Treatment of Hashimoto’s Thyroiditis

  • Gradual restoration of cellular function
  • Personalized therapeutic protocols, without chemical residues and excipients
  • Treating the real causes
  • Therapeutic formulas that work alone or in combination with any other medication
  • Adopting a Molecular / Therapeutic Nutrition Plan

 

Hashimoto’s Thyroiditis – Symptoms

The main symptom in Hashimoto’s thyroiditis is swelling of the thyroid gland. This bronchoculus (swelling), is developing slowly. Thyroid nodules may also appear. The bronchoculus is medium sized, has an uneven surface and a lusty and semi-hard composition.
The patient, could not get aware of the bronchoculus, if it doesn’t get too big. The same applies to the thyroid nodules. The thyroid gland is usually homogeneously inflated, but there may be an asymmetric swelling, in the form of a large nodule or hump, due to the superiority of pathological and anatomical processes, to a particular area of the thyroid.

Hashimoto’s thyroiditis, also shows symptoms of Hypothyroidism such as fatigue, drowsiness, memory impairment, dry skin, weight gain, etc.

The pathology of Hashimoto’s Thyroiditis involves intense lymphocyte infiltration, which completely destroys the physiological Thyroid architecture. Lymphoid follicles and germinal centers may form.

Follicular epithelial cells are often inflated and contain a basophilic cytoplasm.

 

Gland destruction causes the reduction of T3 and T4 thyroid hormones in the patient’s serum (blood) and the rise of TSH.

Initially, TSH can maintain a satisfactory hormonal synthesis, through the development of thyroid swelling or bronchoculus that it causes to the thyroid, impelling it to produce thyroid hormones. Often, however, the thyroid gland subfunctions and eventually Hypothyroidism follows, with or without a bronchoculus.

 

Hashimoto’s Thyroiditis – Treatment

The generalized view that there is no definitive treatment for Thyroid gland disorders, as for Hashimoto’s Thyroiditis (Disease), is wrong.

The usual administration of pharmaceutical preparations, has as a main purpose, to provide the body with the hormones it lacks, which it can no longer produce. This is achieved by administering synthetic thyroid hormones for decades now. In clinical practice, however, the patient is constantly deregulated. The change in the dosage of its hormones, is constantly required to treat his/her symptoms.

In addition, this cycle is infinite, with unfavorable results in everyday life, resulting to the burden of health and psychology of patients, who do not see their health levels being restored.

The key to a successful therapeutic approach is to find the causes.

Patients do not change their everyday life. Instead, they gradually see it getting improved, along with their overall physical health.

By blood sampling, tests are carried out by specialised Molecular Biopathological Laboratories. In this way, we can detect the factors that caused the disease (Hashimoto’s Thyroiditis) at a cellular level.

The total duration of the first visit is about one and a half hour and includes a specialized multi-page Personal Medical History, for all the body’s systems – Head to Toe, as well as patient’s nutritional habits and preferences.

After the neccessary biochemical hormonal or specialized metabolic tests, any malfunctions are detected and all possible deficiencies are found.

The combination of regimens to regulate the Thyroid gland’s function at its ideal levels may include:

Micro-Macronutrients Treatments

Molecular Nutrition

Hormonal Replacement Therapy with Bioidentical Hormones.

Therapies are personalized, determined by algorithms in relation to laboratory findings, thorough individual history, lesions, and the existence of additional Chronic or other Diseases.

These specific therapies have been used in clinical practice since 1997, starting from the United States of America. They do not contradict with any parallel pharmaceutical or homeopathic treatment.

The appropriate treatment and nutrition is the one that ultimately results in the greatest benefit, according to the clinical results and the relevant test scores.

 

References:

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  • Finamore A, Massimi M, Conti Devirgiliis L, et al. Zinc deficiency induces membrane barrier damage and increases neutrophil transmigration in Caco-2 cells. J Nutr 2008;138(9):1664-1670.
  • Wang J, Lv S, Chen G, et al. Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients 2015;7(4):2485-2498.
  • Kim D. Low vitamin D status is associated with hypothyroid Hashimoto’s thyroiditis. Hormones (Athens). 2016;[Epub ahead of print].
  • Arslan MS, Ekiz F, Deveci M, et al. The relationship between cytotoxin-associated gene A positive Helicobacter pylori infection and autoimmune thyroid disease. Endocr Res 2015;40(4):211-214.
  • Radić M. Role of Helicobacter pylori infection in autoimmune systemic rheumatic diseases. World J Gastroenterol 2014;20(36):12839-12846.
  • Di Crescenzo V, D’Antonio A, Tonacchera M, et al. Human herpes virus associated with Hashimoto’s thyroiditis. Infez Med 2013;21(3):224-228.
  • Draborg AH, Duus K, Houen G. Epstein-Barr virus in systemic autoimmune diseases. Clin Dev Immunol 2013;2013:535738.
  • Gaberšček S, Zaletel K, Schwetz V, et al. Mechanisms in endocrinology: thyroid and polycystic ovary syndrome. Eur J Endocrinol 2015;172(1):R9-21.
  • Arduc A, Aycicek Dogan B, Bilmez S, et al. High prevalence of Hashimoto’s thyroiditis in patients with polycystic ovary syndrome: does the imbalance between estradiol and progesterone play a role? Endocr Res 2015;40(4):204-210.
  • Jara LJ, Medina G, Saavedra MA, et al. Prolactin and autoimmunity. Clin Rev Allergy Immunol 2011;40(1):50-59.
  • Nociti V, Frisullo G, Tartaglione T, et al. Multiple sclerosis attacks triggered by hyperprolactinemia. J Neurooncol 2010;98(3):407-409.
  • Legorreta-Haquet MV, Chávez-Rueda K, Chávez-Sánchez L, et al. Function of Treg cells decreased in patients with systemic lupus erythematosus due to the effect of prolactin. Medicine (Baltimore) 2016;95(5):e2384.
  • Van Die MD, Burger HG, Teede HJ, et al. Vitex agnus-castus extracts for female reproductive disorders: a systematic review of clinical trials. Planta Med 2013;79(7):562-575.
  • Yu Q, Wang JB. Subclinical hypothyroidism in PCOS: impact on presentation, insulin resistance, and cardiovascular risk. Biomed Res Int 2016;2016:2067087.
  • Tenazzani AD, Despini G, Santagni S, et al. Effects of a combination of alpha lipoic acid and myo-inositol on insulin dynamics in overweight/obese patients with PCOS. Endocrinol Metab Synd 2014;3:3. [Full text]
  • Morgante G, Cappelli V, Di Sabatino A, et al. Polycystic ovary syndrome (PCOS) and hyperandrogenism: the role of a new natural association. Minerva Ginecol 2015;67(5):457-463.
  • Mortimer RH. Thyroid function tests. Aust Prescr 2011;34:12-15.
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  • Act for Libraries. Difference between Hashimotos thyroiditis and Graves disease. Viewed 6 September, http://www.actforlibraries.org/difference-between-hashimotos-thyroiditis…
  • Lab Tests Online. Thyroid antibodies, 2015. Viewed 6 September 2016, https://labtestsonline.org/understanding/analytes/thyroid-antibodies/tab…
  • Trbojević B, Djurica S. Diagnosis of autoimmune thyroid disease. Srp Arh Celok Lek 2005;133 Suppl 1:25-33.
  • Duntas LH. Environmental factors and autoimmune thyroiditis. Nat Clin Pract Endocrinol Metab 2008;4(8):454-460.
  • Wiersinga WM. Clinical relevance of environmental factors in the pathogenesis of autoimmune thyroid disease. Endocrinol Metab (Seoul) 2016;31(2):213-222.
  • Kawicka A, Regulska-Ilow B. Metabolic disorders and nutritional status in autoimmune thyroid diseases. Postepy Hig Med Dosw (Online) 2015;69:80-90.
  • Wang L, Wang B, Chen SR, et al. Effect of selenium supplementation on recurrent hyperthyroidism caused by Graves’ disease: a prospective pilot study. Horm Metab Res 2016;[Epub ahead of print].
  • Dharmasena A. Selenium supplementation in thyroid associated ophthalmopathy: an update. Int J Ophthalmol 2014;7(2):365-375.
  • Marcocci C, Kahaly GJ, Krassas GE, et al. Selenium and the course of mild Graves’ orbitopathy. N Engl J Med 2011;364(20):1920-1931.
  • Hwang S, Byun JW, Yoon JS, et al. Inhibitory effects of α-lipoic acid on oxidative stress-induced adipogenesis in orbital fibroblasts from patients with Graves ophthalmopathy. Medicine (Baltimore) 2016;95(2):e2497.
  • Chen K, Yan B, Wang F, et al. Type 1 5′-deiodinase activity is inhibited by oxidative stress and restored by alpha-lipoic acid in HepG2 cells. Biochem Biophys Res Commun 2016;472(3):496-501.
  • Sharma BR, Joshi AS, Varthakavi PK, et al. Celiac autoimmunity in autoimmune thyroid disease is highly prevalent with a questionable impact. Indian J Endocrinol Metab 2016;20(1):97-100.
  • Roy A, Laszkowska M, Sundström J, et al. Prevalence of celiac disease in patients with autoimmune thyroid disease: a meta-analysis. Thyroid 2016;26(7):880-890.
  • Drago S, El Asmar R, Di Pierro M, et al. Gliadin, zonulin and gut permeability: effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol 2006;41(4):408-419.
  • Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol 2012;42(1):71-78.
  • Park JH, Jeong SY, Choi AJ, et al. Lipopolysaccharide directly stimulates Th17 differentiation in vitro modulating phosphorylation of RelB and NF-κB1. Immunol Lett 2015;165(1):10-19.
  • Orlando A, Linsalata M, Notarnicola M, et al. Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines. BMC Microbiol 2014;14:19.
  • Anderson RC, Cookson AL, McNabb WC, et al. Lactobacillus plantarum MB452 enhances the function of the intestinal barrier by increasing the expression levels of genes involved in tight junction formation. BMC Microbiol 2010;10:316.
  • Liu Z, Li C, Huang M, et al. Positive regulatory effects of perioperative probiotic treatments on postoperative liver complications after colorectal liver metastases surgery: a double-center and double-blind randomized clinical trial. BMC Gastroenterol 2015;15:34.
  • Skrovanek S, DiGuilio K, Bailey R, et al. Zinc and gastrointestinal disease. World J Gastrointest Pathophysiol 2014;5(4):496-513.
  • Finamore A, Massimi M, Conti Devirgiliis L, et al. Zinc deficiency induces membrane barrier damage and increases neutrophil transmigration in Caco-2 cells. J Nutr 2008;138(9):1664-1670.
  • Wang J, Lv S, Chen G, et al. Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients 2015;7(4):2485-2498.
  • Kim D. Low vitamin D status is associated with hypothyroid Hashimoto’s thyroiditis. Hormones (Athens). 2016;[Epub ahead of print].
  • Arslan MS, Ekiz F, Deveci M, et al. The relationship between cytotoxin-associated gene A positive Helicobacter pylori infection and autoimmune thyroid disease. Endocr Res 2015;40(4):211-214.
  • Radić M. Role of Helicobacter pylori infection in autoimmune systemic rheumatic diseases. World J Gastroenterol 2014;20(36):12839-12846.
  • Di Crescenzo V, D’Antonio A, Tonacchera M, et al. Human herpes virus associated with Hashimoto’s thyroiditis. Infez Med 2013;21(3):224-228.
  • Draborg AH, Duus K, Houen G. Epstein-Barr virus in systemic autoimmune diseases. Clin Dev Immunol 2013;2013:535738. [Full text]
  • Gaberšček S, Zaletel K, Schwetz V, et al. Mechanisms in endocrinology: thyroid and polycystic ovary syndrome. Eur J Endocrinol 2015;172(1):R9-21. [Abstract]
  • Arduc A, Aycicek Dogan B, Bilmez S, et al. High prevalence of Hashimoto’s thyroiditis in patients with polycystic ovary syndrome: does the imbalance between estradiol and progesterone play a role? Endocr Res 2015;40(4):204-210. [Abstract]
  • Jara LJ, Medina G, Saavedra MA, et al. Prolactin and autoimmunity. Clin Rev Allergy Immunol 2011;40(1):50-59. [Abstract]
  • Nociti V, Frisullo G, Tartaglione T, et al. Multiple sclerosis attacks triggered by hyperprolactinemia. J Neurooncol 2010;98(3):407-409.
  • Legorreta-Haquet MV, Chávez-Rueda K, Chávez-Sánchez L, et al. Function of Treg cells decreased in patients with systemic lupus erythematosus due to the effect of prolactin. Medicine (Baltimore) 2016;95(5):e2384. [Full text]
  • Van Die MD, Burger HG, Teede HJ, et al. Vitex agnus-castus extracts for female reproductive disorders: a systematic review of clinical trials. Planta Med 2013;79(7):562-575. [Abstract]
  • Yu Q, Wang JB. Subclinical hypothyroidism in PCOS: impact on presentation, insulin resistance, and cardiovascular risk. Biomed Res Int 2016;2016:2067087. [Full text]
  • Tenazzani AD, Despini G, Santagni S, et al. Effects of a combination of alpha lipoic acid and myo-inositol on insulin dynamics in overweight/obese patients with PCOS. Endocrinol Metab Synd 2014;3:3. [Full text]
  • Morgante G, Cappelli V, Di Sabatino A, et al. Polycystic ovary syndrome (PCOS) and hyperandrogenism: the role of a new natural association. Minerva Ginecol 2015;67(5):457-463. [Abstract]
  • Mortimer RH. Thyroid function tests. Aust Prescr 2011;34:12-15. [Full text]
  • The Australian Thyroid Foundation Ltd. Thyroid conditions. Viewed 6 Spetember 2016, https://www.thyroidfoundation.org.au/page/58/thyroid-conditions
  • Act for Libraries. Difference between Hashimotos thyroiditis and Graves disease. Viewed 6 September, http://www.actforlibraries.org/difference-between-hashimotos-thyroiditis…
  • Lab Tests Online. Thyroid antibodies, 2015. Viewed 6 September 2016, https://labtestsonline.org/understanding/analytes/thyroid-antibodies/tab…