Purpose of Review. Studies have been published in the field of autoimmune thyroid diseases since January 2005. The review is organized into areas of etiology, autoimmune features, autoantibodies, mechanism of thyroid cell injury, B-cell responses, and T-cell responses. Also it reviews the diagnosis and the relationship between autoimmune thyroid disease, neoplasm, and kidney disorders. Recent Findings. Autoimmune thyroid diseases have been reported in people living in different parts of the world including North America, Europe, Baalkans, Asia, Middle East, South America, and Africa though the reported figures do not fully reflect the number of people infected per year. Cases are unrecognized due to inaccurate diagnosis and hence are treated as other diseases. However, the most recent studies have shown that the human autoimmune thyroid diseases (AITDs) affect up to 5% of the general population and are seen mostly in women between 30 and 50 years. Summary. Autoimmune thyroid disease is the result of a complex interaction between genetic and environmental factors. Overall, this review has expanded our understanding of the mechanism involved in pathogenesis of AITD and the relationship between autoimmune thyroid disease, neoplasm, and kidney disease. It has opened new lines of investigations that will ultimately result in a better clinical practice. 1. Introduction The principal diseases of the human thyroid gland are goiter (diffuse or nodular), hyperthyroidism, hypothyroidism, autoimmune thyroiditis, and neoplasm [1]. The thyroiditis types cause inflammation of thyroid tissue and can release preformed hormone from the colloid space, causing thyrotoxicosis, which is transient and followed by recovery or development of hypothyroidism. In acute and subacute thyroiditis, thyroid tenderness and neck pain are often present. On the other hand, silent thyroiditis is devoid of the local symptoms [2]. In the USA and Canada, the extrapolated prevalences are 5,873,108 and 650,157, respectively. In Austria and Belgium, the prevalences are 163,495 and 206,965, respectively. In Bosnia and Macedonia, the prevalences are 8,152 and 40,801, respectively. For China and India, the prevalences are 25,976,952 and 21,301,412, respectively, while in Egypt and Iran they are 1,522,348 and 1,350,064, respectively. South Africa has a prevalence of 888,969 [3]. The annual incidence of Hashimoto’s thyroiditis worldwide is estimated to be 0.3–1.5 cases per 1000 persons, whereas Graves’ disease is estimated at about 5 per 10,000 people [4]. The human AITDs broadly include Graves’
References
[1]
V. Kumar, “24: The endocrine system,” in Robbins and Cotran Pathologic Mechanisms of Disease, p. 1113, Elsevier, Philidelphia, Pa, USA, 8th edition, 2010.
[2]
N. Dorairajan and K. Akshaya, “Total versus subotal thyroidectomy in grave’s disease: a retrospective analysis,” Indian Journal of Surgery, vol. 64, no. 6, pp. 506–510, 2002.
M. P. J. Vanderpump, W. M. G. Tunbridge, J. M. French et al., “The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey,” Clinical Endocrinology, vol. 43, no. 1, pp. 55–68, 1995.
[5]
H. Hadj-Kacem, S. Rebuffat, M. Mnif-Féki, S. Belguith-Maalej, H. Ayadi, and S. Péraldi-Roux, “Autoimmune thyroid diseases: genetic susceptibility of thyroid-specific genes and thyroid autoantigens contributions,” International Journal of Immunogenetics, vol. 36, no. 2, pp. 85–96, 2009.
[6]
A. P. Weetman and A. M. McGregor, “Autoimmune thyroid disease: further developments in our understanding,” Endocrine Reviews, vol. 15, no. 6, pp. 788–830, 1994.
[7]
K. Eguchi, N. Matsuoka, and S. Nagataki, “Cellular immunity in autoimmune thyroid disease,” Bailliere's Clinical Endocrinology and Metabolism, vol. 9, no. 1, pp. 71–94, 1995.
[8]
A. Huber, F. Menconi, S. Corathers, E. M. Jacobson, and Y. Tomer, “Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis: from epidemiology to mechanisms,” Endocrine Reviews, vol. 29, no. 6, pp. 697–725, 2008.
[9]
Y. Tomer and A. Huber, “The etiology of autoimmune thyroid disease: a story of genes and environment,” Journal of Autoimmunity, vol. 32, no. 3-4, pp. 231–239, 2009.
[10]
H. Hashimoto, “Zyr Kenntniss der lymphomatosen veranderung der schilddruse (strauma lymphomatosa),” Archiv für klinische Chirurgie, vol. 97, pp. 219–248, 1912.
[11]
M. A. Iddah, B. N. Macharia, A. G. Ng’wena, A. Keter, and A. V. O. Ofulla, “Thryroid hormones and hematological indices levels in thyroid disorders patients at Moi teaching and referral hospital, Western Kenya,” ISRN Endocrinology, vol. 2013, Article ID 385940, 6 pages, 2013.
[12]
G. J. Canaris, N. R. Manowitz, G. Mayor, and E. C. Ridgway, “The Colorado thyroid disease prevalence study,” Archives of Internal Medicine, vol. 160, no. 4, pp. 526–534, 2000.
[13]
L. Chiovato, P. Bassi, F. Santini et al., “Antibodies producing complement-mediated thyroid cytotoxicity in patients with atrophic or goitrous autoimmune thyroiditis,” Journal of Clinical Endocrinology and Metabolism, vol. 77, no. 6, pp. 1700–1705, 1993.
[14]
T. H. Brix, K. O. Kyvik, K. Christensen, and L. Hegedüs, “Evidence for a major role of heredity in Graves' disease: a population-based study of two Danish twin cohorts,” Journal of Clinical Endocrinology and Metabolism, vol. 86, no. 2, pp. 930–934, 2001.
[15]
Y. Ban, D. A. Greenberg, E. Concepcion, L. Skrabanek, R. Villanueva, and Y. Tomer, “Amino acid substitutions in the thyroglobulin gene are associated with susceptibility to human and murine autoimmune thyroid disease,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 25, pp. 15119–15124, 2003.
[16]
D. S. Cooper, “Antithyroid drugs,” The New England Journal of Medicine, vol. 352, no. 9, pp. 905–917, 2005.
[17]
T. Hanafusa, R. Pujol-Borrell, and L. Chiovato, “Aberrant expression of HLA-DR antigen on thyrocytes in Graves' disease: relevance for autoimmunity,” Lancet, vol. 2, no. 8359, pp. 1111–1115, 1983.
[18]
R. S. Cotran, V. Kumar, and S. I. Robins, “The thyroid,” in Pathological Bases of Disease, S. I. Robins, Ed., WB Saunders, Philadelphia, Pa, USA, 5th edition, 1994.
[19]
G. F. Bottazzo, R. P. Borrell, T. Hanafusa, and M. Feldmann, “Role of aberrant HLA-DR expression and antigen presentation in induction of endocrine autoimmunity,” The Lancet, vol. 2, no. 8359, pp. 1115–1118, 1983.
[20]
P.-W. Wang, R.-T. Liu, S.-H. Juo et al., “Cytotoxic T lymphocyte-associated molecule-4 polymorphism and relapse of Graves’ hyperthyroidism after antithyroid withdrawal,” Journal of Clinical Endocrinology and Metabolism, vol. 8, no. 1, pp. 169–173, 2004.
[21]
D. S. Neufeld, M. Platzer, and T. F. Davies, “Reovirus induction of MHC class II antigen in rat thyroid cells,” Endocrinology, vol. 124, no. 1, pp. 543–545, 1989.
[22]
E. L. Khoury, L. Pereira, and F. S. Greenspan, “Induction of HLA-DR expression on thyroid follicular cells by cytomegalovirus infection in vitro: evidence for a dual mechanism of induction,” The American Journal of Pathology, vol. 138, no. 5, pp. 1209–1223, 1991.
[23]
H. Kimura and T. F. Davies, “Thyroid-specific T cells in the normal Wistar rat. II. T cell clones interact with cloned Wistar rat thyroid cells and provide direct evidence for autoantigen presentation by thyroid epithelial cells,” Clinical Immunology and Immunopathology, vol. 58, no. 2, pp. 195–206, 1991.
[24]
M. Londei, J. R. Lamb, G. F. Bottazzo, and M. Feldmann, “Epithelial cells expressing aberrant MHC class II determinants can present antigen to cloned human T cells,” Nature, vol. 312, no. 5995, pp. 639–641, 1984.
[25]
N. Shimojo, Y. Kohno, K. Yamaguchi et al., “Induction of Graves-like disease in mice by immunization with fibroblasts transfected with the thyrotropin receptor and a class II molecule,” Proceedings of the National Academy of Sciences of the United States of America, vol. 93, no. 20, pp. 11074–11079, 1996.
[26]
M. Kita, L. Ahmad, R. C. Marians et al., “Regulation and transfer of a murine model of thyrotropin receptor antibody mediated Graves' disease,” Endocrinology, vol. 140, no. 3, pp. 1392–1398, 1999.
[27]
A. K. Abbas, K. M. Murphy, and A. Sher, “Functional diversity of helper T lymphocytes,” Nature, vol. 383, no. 6603, pp. 787–793, 1996.
[28]
T. Nanba, M. Watanabe, N. Inoue, and Y. Iwatani, “Increases of the Th1/Th2 cell ratio in severe Hashimoto's disease and in the proportion of Th17 cells in intractable Graves' disease,” Thyroid, vol. 19, no. 5, pp. 495–501, 2009.
[29]
A. Martin, G. Barbesino, and T. F. Davies, “T-cell receptors and autoimmune thyroid disease—signposts for T-cell-antigen driven diseases,” International Reviews of Immunology, vol. 18, no. 1-2, pp. 111–140, 1999.
[30]
M. S. Horwitz, L. M. Bradley, J. Harbertson, T. Krahl, J. Lee, and N. Sarvetnick, “Diabetes induced by Coxsackie virus: initiation by bystander damage and not molecular mimicry,” Nature Medicine, vol. 4, no. 7, pp. 781–785, 1998.
[31]
N. Arata, T. Ando, P. Unger, and T. F. Davies, “By-stander activation in autoimmune thyroiditis: studies on experimental autoimmune thyroiditis in the GFP+ fluorescent mouse,” Clinical Immunology, vol. 121, no. 1, pp. 108–117, 2006.
[32]
Y. Nagayama, “Graves' animal models of Graves' hyperthyroidism,” Thyroid, vol. 17, no. 10, pp. 981–988, 2007.
[33]
S. Fountoulakis, G. Vartholomatos, N. Kolaitis, S. Frillingos, G. Philippou, and A. Tsatsoulis, “HLA-DR expressing peripheral T regulatory cells in newly diagnosed patients with different forms of autoimmune thyroid disease,” Thyroid, vol. 18, no. 11, pp. 1195–1200, 2008.
[34]
Y. Tomer, Y. Ban, E. Conception et al., “Common and unique susceptibility loci in graves and hashimoto diseases: results of whole-genome screening in a data set of 102 multiplex families,” The American Journal of Human Genetics, vol. 73, no. 4, pp. 736–747, 2003.
[35]
R. Villanueva, D. A. Greenberg, T. F. Davies, and Y. Tomer, “Sibling recurrence risk in autoimmune thyroid disease,” Thyroid, vol. 13, no. 8, pp. 761–764, 2003.
[36]
Y. Tomer and T. F. Davies, “Searching for the autoimmune thyroid disease susceptibility genes: from gene mapping to gene function,” Endocrine Reviews, vol. 24, no. 5, pp. 694–717, 2003.
[37]
Q. Y. Chen, W. Huang, and J. X. She, “HLA-DRB108, DRB103/DRB30101, and DRB30202 are susceptibility genes for Graves' disease in North American Caucasians, whereas DRB107 is protective,” Journal of Clinical Endocrinology and Metabolism, vol. 84, no. 9, pp. 3182–3186, 1999.
[38]
B. Vaidya, P. Kendall-Taylor, and S. H. S. Pearce, “The genetics of autoimmune thyroid disease,” Journal of Clinical Endocrinology and Metabolism, vol. 87, no. 12, pp. 5385–5397, 2002.
[39]
M. Humphrey, J. Mosca, J. R. Baker Jr. et al., “Absence of retroviral sequences in Graves' disease,” The Lancet, vol. 337, no. 8732, pp. 17–18, 1991.
[40]
D. Neumann-Haefelin, U. Fleps, R. Renne, and M. Schweizer, “Foamy viruses,” Intervirology, vol. 35, no. 1–4, pp. 196–207, 1993.
[41]
Y. Tomer and T. F. Davies, “Infection, thyroid disease, and autoimmunity,” Endocrine Reviews, vol. 14, no. 1, pp. 107–120, 1993.
[42]
N. Sonino, M. E. Girelli, M. Boscaro, F. Fallo, B. Busnardo, and G. A. Fava, “Life events in the pathogenesis of Graves' disease. A controlled study,” Acta Endocrinologica, vol. 128, no. 4, pp. 293–296, 1993.
[43]
A. W. C. Kung, “Life events, daily stresses and coping in patients with Graves' disease,” Clinical Endocrinology, vol. 42, no. 3, pp. 303–308, 1995.
[44]
A. Matos-Santos, E. L. Nobre, J. G. Costa et al., “Relationship between the number and impact of stressful life events and the onset of Graves' disease and toxic nodular goitre,” Clinical Endocrinology, vol. 55, no. 1, pp. 15–19, 2001.
[45]
X. Yin, R. Latif, Y. Tomer, and T. F. Davies, “Thyroid epigenetics: X chromosome inactivation in patients with autoimmune thyroid disease,” Annals of the New York Academy of Sciences, vol. 1110, pp. 193–200, 2007.
[46]
P. W. Kincade, K. L. Medina, G. Smithson, and D. C. Scott, “Pregnancy: a clue to normal regulation of B lymphopoiesis,” Immunology Today, vol. 15, no. 11, pp. 539–544, 1994.
[47]
J. A. P. Da Silva, “Sex hormones, glucocorticoids and autoimmunity: facts and hypotheses,” Annals of the Rheumatic Diseases, vol. 54, no. 1, pp. 6–16, 1995.
[48]
L. Bartalena, E. Martino, C. Marcocci et al., “More on smoking habits and Graves' ophthalmopathy,” Journal of Endocrinological Investigation, vol. 12, no. 10, pp. 733–737, 1989.
[49]
M. F. Prummel and W. M. Wiersinga, “Smoking and risk of Graves' disease,” The Journal of the American Medical Association, vol. 269, no. 4, pp. 479–482, 1993.
[50]
I. A. Holm, J. E. Manson, and K. B. Michels, “Smoking and other lifestyle factors and the risk of Graves' hyperthyroidism,” Archives of Internal Medicine, vol. 165, no. 14, pp. 1606–1611, 2005.
[51]
D. Glinoer, “The regulation of thyroid function during normal pregnancy: Importance of the iodine nutrition status,” Best Practice and Research: Clinical Endocrinology and Metabolism, vol. 18, no. 2, pp. 133–152, 2004.
[52]
T. Ando and T. F. Davies, “Postpartum autoimmune thyroid disease: the potential role of fetal microchimerism,” Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 7, pp. 2965–2971, 2003.
[53]
R. Jansson, P. A. Dahlberg, B. Winsa, O. Meirik, J. Safwenberg, and A. Karlsson, “The postpartum period constitutes an important risk for the development of clinical Graves' disease in young women,” Acta Endocrinologica, vol. 116, no. 3, pp. 321–325, 1987.
[54]
N. R. Rose, R. Bonita, and C. L. Burek, “Iodine: an environmental trigger of thyroiditis,” Autoimmunity Reviews, vol. 1, no. 1-2, pp. 97–103, 2002.
[55]
C. A. Benbassat, S. Mechlis-Frish, M. Cohen, and I. Blum, “Amiodarone-induced thyrotoxicosis type 2: a case report and review of the literature,” The American Journal of the Medical Sciences, vol. 320, no. 4, pp. 288–291, 2000.
[56]
J. P. Walsh, L. C. Ward, V. Burke et al., “Small changes in thyroxine dosage do not produce measurable changes in hypothyroid symptoms, well-being, or quality of life: results of a double-blind, randomized clinical trial,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 7, pp. 2624–2630, 2006.
[57]
J. Srinivasappa, C. Garzelli, T. Onodera, U. Ray, and A. L. Notkins, “Virus-induced thyroiditis,” Endocrinology, vol. 122, no. 2, pp. 563–566, 1988.
[58]
K. Bendtzen, K. Buschard, M. Diamant, T. Horn, and M. Svenson, “Possible role of IL-1, TNF-α, and IL-6 in insulin-dependent diabetes mellitus and autoimmune thyroid disease,” Lymphokine Research, vol. 8, no. 3, pp. 335–340, 1989.
[59]
T. G. Strieder and M. F. Prummel, “Risk factors for and prevalence of thyroid disorders in a cross sectional study among healthy female relatives of patients with autoimmune thyroid disorder,” Clinical Endocrinology, vol. 59, no. 3, pp. 396–401, 2003.
[60]
Y. Tomer, G. Barbesino, D. A. Greenberg, E. Concepcion, and T. F. Davies, “Mapping the major susceptibility loci for familial Graves' and Hashimoto's diseases: evidence for genetic heterogeneity and gene interactions,” Journal of Clinical Endocrinology and Metabolism, vol. 84, no. 12, pp. 4656–4664, 1999.
[61]
H. Tamai, N. Ohsako, and K. Takeno, “Changes in thyroid function in euthyroid subjects with a family history of Graves' disease: a follow-up study of 69 patients,” Journal of Clinical Endocrinology and Metabolism, vol. 51, no. 4, pp. 1123–1127, 1980.
[62]
T. H. Brix, K. O. Kyvik, and L. Hegedüs, “A population-based study of chronic autoimmune hypothyroidism in Danish twins,” Journal of Clinical Endocrinology and Metabolism, vol. 85, no. 2, pp. 536–539, 2000.
[63]
Y. Tomer and T. F. Davies, “Infection, thyroid disease and autoimmunity,” Endocrine Reviews, vol. 14, no. 1, pp. 107–120, 1993.
[64]
A. P. Weetman, R. C. Smallridge, T. B. Nutman, and K. D. Burman, “Persistent thyroid autoimmunity after subacute thyroiditis,” Journal of Clinical and Laboratory Immunology, vol. 23, no. 1, pp. 1–6, 1987.
[65]
R. Raghupathy, “Th1-type immunity is incompatible with successful pregnancy,” Immunology Today, vol. 18, no. 10, pp. 478–482, 1997.
[66]
T. H. Brix, G. P. Knudsen, M. Kristiansen, K. O. Kyvik, K. H. Orstavik, and L. Hegedüs, “High frequency of skewed X-chromosome inactivation in females with autoimmune thyroid disease: a possible explanation for the female predisposition to thyroid autoimmunity,” Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 11, pp. 5949–5953, 2005.
[67]
T. F. Davies, “The thyroid immunology of the postpartum period,” Thyroid, vol. 9, no. 7, pp. 675–684, 1999.
[68]
A. P. Weetman, “The immunology of pregnancy,” Thyroid, vol. 9, no. 7, pp. 643–646, 1999.
[69]
S. Othman, D. I. W. Phillips, A. B. Parkes et al., “A long-term follow-up of postpartum thyroiditis,” Clinical Endocrinology, vol. 32, no. 5, pp. 559–564, 1990.
[70]
A. M. Gbadebo and T. M. Oyesanya, “Assessment of iodine deficiency and goitre incidence in parts of Yewa area of Ogun state, Southwestern Nigeria,” Environmental Geochemistry and Health, vol. 27, no. 5-6, pp. 491–499, 2005.
[71]
F. Pacini, T. Vorontsova, L. Molinaro et al., “Prevalence of thyroid autoantibodies in children and adolescents from Belarus exposed to the Chernobyl radioactive fallout,” The Lancet, vol. 352, no. 9130, pp. 763–766, 1998.
[72]
G. Huber, J. Staub, C. Meier et al., “Prospective study of the spontaneous course of subclinical hypothyroidism: prognostic value of thyrotropin, thyroid reserve, and thyroid antibodies,” Journal of Clinical Endocrinology and Metabolism, vol. 87, no. 7, pp. 3221–3226, 2002.
[73]
H. V?lzke, A. Werner, H. Wallaschofski et al., “Occupational exposure to ionizing radiation is associated with autoimmune thyroid disease,” Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 8, pp. 4587–4592, 2005.
[74]
K. V. Prasad and B. S. Prabhakar, “Apoptosis and autoimmune disorders,” Autoimmunity, vol. 36, no. 6-7, pp. 323–330, 2003.
[75]
S. M. McLachlan and B. Rapoport, “The molecular biology of thyroid peroxidase: cloning, expression and role as autoantigen in autoimmune thyroid disease,” Endocrine Reviews, vol. 13, no. 2, pp. 192–206, 1992.
[76]
R. McIntosh, P. Watson, and A. Weetman, “Somatic hypermutation in autoimmune thyroid disease,” Immunological Reviews, vol. 162, pp. 219–231, 1998.
[77]
R. Njemini, I. Meyers, C. Demanet, J. Smitz, M. Sosso, and T. Mets, “The prevalence of autoantibodies in an elderly sub-Saharan African population,” Clinical and Experimental Immunology, vol. 127, no. 1, pp. 99–106, 2002.
[78]
L. M. Silva, J. Chavez, M. H. B. Canalli, and C. R. Zanetti, “Determination of IgG subclasses and avidity of antithyroid peroxidase antibodies in patients with subclinical hypothyroidism—a comparison with patients with overt hypothyroidism,” Hormone Research, vol. 59, no. 3, pp. 118–124, 2003.
[79]
M. I. Hawa, A. Picardi, F. Costanza et al., “Frequency of diabetes and thyroid autoantibodies in patients with autoimmune endocrine disease from Cameroon,” Clinical Immunology, vol. 118, no. 2-3, pp. 229–232, 2006.
[80]
Y. Malthiery and S. Lissitzky, “Primary structure of human thyroglobulin deduced from the sequence of its 8448-base complementary DNA,” European Journal of Biochemistry, vol. 165, no. 3, pp. 491–498, 1987.
[81]
G. Carayanniotis and V. P. Rao, “Searching for pathogenic epitopes in thyroglobulin: parameters and caveats,” Immunology Today, vol. 18, no. 2, pp. 83–88, 1997.
[82]
K. S. Collison, J. P. Banga, P. S. Barnett, G. C. Huang, and A. M. McGregor, “Autoantibody stimulation of the human thyrotropin receptor: regulation of adenylate cyclase activity, thyroglobulin and thyroid peroxidase mRNA levels in primary cultures of Graves' thyroid tissue,” Clinical and Experimental Immunology, vol. 86, no. 1, pp. 61–65, 1991.
[83]
K. Boelaert and J. A. Franklyn, “Thyroid hormone in health and disease,” Journal of Endocrinology, vol. 187, no. 1, pp. 1–15, 2005.
[84]
B. S. Prabhakar, J. Fan, and G. S. Seetharamaiah, “Thyrotropin-receptor-mediated diseases: a paradigm for receptor autoimmunity,” Immunology Today, vol. 18, no. 9, pp. 437–442, 1997.
[85]
G. Stassi and R. de Maria, “Autoimmune thyroid disease: new models of cell death in autoimmunity,” Nature Reviews Immunology, vol. 2, no. 3, pp. 195–204, 2002.
[86]
R. C. Smallridge, “Postpartum thyroid dysfunction: a frequently undiagnosed endocrine disorder,” Endocrinologist, vol. 6, no. 1, pp. 44–50, 1996.
[87]
M. Nilsson, J. Husmark, U. Bj?rkman, and L. E. Ericson, “Cytokines and thyroid epithelial integrity: Interleukin-1α induces dissociation of the junctional complex and paracellular leakage in filter-cultured human thyrocytes,” Journal of Clinical Endocrinology and Metabolism, vol. 83, no. 3, pp. 945–952, 1998.
[88]
A. P. Weetman, “Fortnightly review. Hypothyroidism: screening and subclinical disease,” The British Medical Journal, vol. 314, no. 7088, pp. 1175–1178, 1997.
[89]
A. P. Weetman, “Endocrinology,” in Handbook of HLA and Disease, R. I. Lechler and A. Warrens, Eds., Academic Press, London, UK, 2nd edition, 2000.
[90]
P. J. Simons, F. G. A. Delemarre, and H. A. Drexhage, “Antigen-presenting dendritic cells as regulators of the growth of thyrocytes: a role of interleukin-1β and interleukin-6,” Endocrinology, vol. 139, no. 7, pp. 3148–3156, 1998.
[91]
J. R. Baker Jr. and C. K. Fosso, “Immunological aspects of cancers arising from thyroid follicular cells,” Endocrine Reviews, vol. 14, no. 6, pp. 729–746, 1993.
[92]
F. Matsuzuka, A. Miyauchi, S. Katayama et al., “Clinical aspects of primary thyroid lymphoma: diagnosis and treatment based on our experience of 119 cases,” Thyroid, vol. 3, no. 2, pp. 93–99, 1993.
[93]
C. Giani, P. Fierabracci, R. Bonacci et al., “Relationship between breast cancer and thyroid disease: relevance of autoimmune thyroid disorders in breast malignancy,” Journal of Clinical Endocrinology and Metabolism, vol. 81, no. 3, pp. 990–994, 1996.
[94]
R. Balaji, B. D. Pragna, K. A. Veerendra, and R. V. Seshadri, “Renal function markers and thyroid hormone status in undialyzed chronic kidney disease,” Al Ameen Journal of Medical Science, vol. 6, no. 1, pp. 70–74, 2013.
[95]
E. M. Kaptein, “Thyroid function in renal failure,” Contributions to Nephrology, vol. 50, pp. 64–72, 1986.
[96]
A. I. Katz and M. D. Lindheimer, “Actions of hormones on the kidney,” Annual Review of Physiology, vol. 39, pp. 97–133, 1977.