Bastenie / Ermans / Alexander Thyroiditis and Thyroid Function

Clinical, Morphological, and Physiopathological Studies
1. Auflage 2013
ISBN: 978-1-4831-8684-9
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 356 Seiten

Modern Trends in Physiological Sciences, Volume 36: Thyroiditis and Thyroid Function: Clinical, Morphological, and Physiopathological Studies presents a detailed understanding of the incipient stages of hypothyroidism that have important clinical connections with atherosclerosis and obesity. This book provides an overall view of iodine metabolism and pituitary thyroid relationships. Organized into 15 chapters, this volume begins with an overview of the role of the thyroid in converting inorganic iodine into thyroid hormones. This text then discusses the concept of autoimmunity, with emphasis on the immunizing mechanisms to combat the foreign agents invading the body. Other chapters consider the possible relationship with autoimmune processes of the struma fibrosa giant-cell variant. This book discusses as well several case studies concerning chronic lymphocytic thyroiditis, Hashimoto's disease, and autoimmune thyroiditis. The final chapter deals with the pathogenic importance of each type of autoimmune thyroiditis. This book is a valuable resource for thyroid specialists, endocrinologist, and physicians.

Autoren/Hrsg.

Bastenie, P. A.

Ermans, A. M.

Alexander, P.

Bacq, Z. M.

Leseproben

Introduction
P.A. BASTENIE,     ‘Chronic thyroiditis: a potentially confusing picture’(24) THE subject of chronic thyroiditis is surrounded by many confusing concepts and denominations. The main cause of this situation is our ignorance of the aetiology of the various disorders which are included under this term. Early clinico-pathological studies ascribed all forms of chronic lymphocytic thyroiditis to some infectious process(25,28) and blamed tuberculosis, syphilis, and non-specified infections as the pathogenic agents. Other non-specified infections were thought to invade the thyroid through the remnants of the thyroglossal duct. It is doubtful whether, except in a few cases of tuberculous infection, any of these agents have ever played an important role in the genesis of lymphocytic thyroiditis. It is, however, most likely that certain viral infections are responsible for the development of acute, subacute, and possibly chronic reactions of the thyroid parenchyma. The description of all conditions of lymphocytic thyroiditis under the single heading of nonspecific chronic thyroiditis has not helped matters. Many years ago the study of a number of well-delineated nosological entities (myxoedema, Hashimoto’s struma lymphomatosa, toxic goitre) showed that these conditions have in common identical parenchymatous and inflammatory lesions, varying only in degrees.(4) Alongside these conditions of diffuse chronic lymphocytic thyroiditis, offering a definite clinical appearance, identical focal or diffuse inflammatory lesions were described in otherwise normal thyroids which had produced no clinical symptoms.(4,25) The presence of the same lesions observed in such different conditions suggested that they were part of the same pathological process superimposed on different thyroid states. No evidence of an infectious origin was found, and the lymphocytes and plasma cell infiltrates were explained as inflammatory reactions to particular metabolic cell lesions leading to cell degeneration and lysis.(4,11) At the present time, the fundamental sameness of the process, as first suggested by microscopical study, is generally admitted(10,19,22,26) This view is based on very strong evidence. Electron microscopy has confirmed the previous observations by showing identical lesions in different variants of lymphocytic thyroiditis.(18) Biochemical studies have identified the same alterations of iodine metabolism in the hypertrophic thyroiditis of Hashimoto’s disease(5) and in atrophic thyroiditis.(6,7) Finally, immunological studies have detected the same thyroid antibodies in most variants of lymphocytic thyroiditis.(10,21) The discovery of thyroid antibodies circulating in the blood of subjects affected with chronic lymphocytic thyroiditis by Roitt et al.(20) and the experimental production of autoimmune thyroiditis in the rabbit by Witebsky and Rose(30) have been of capital importance in the study of this pathology. There is no doubt that the autoimmune process corresponds to important tissue alterations, possibly leading to the development of a self-maintaining destructive process. The concept of lymphocytic thyroiditis as an autoimmune disease naturally led to the use of the general term “autoimmune thyroiditis”(9) for all the clinical entities previously described as individual variants of “non-specific chronic thyroiditis”. Thus, as Wayne(27) put it so well, “the definition of the disease is switched from histological bases to an immunological aetiology”. This attitude assumes that the autoimmune process is solely responsible for all forms of lymphocytic thyroiditis. It implies, as the essential cause of the disease, the existence of a primary inborn anomaly of the autoimmune apparatus(12,14,23) However, the basis for such an attitude is not proven. A viral or metabolic anomaly may well trigger off the inflammatory process. In many textbooks on thyroid diseases(13,17,27) or on autoimmune diseases,(3,15) the section on chronic thyroiditis is entitled “Hashimoto’s disease”, and in many papers the terms “chronic thyroiditis” and “Hashimoto’s thyroiditis” are used synonymously. But chronic thyroiditis may occur with several variants which display different clinical characteristics, follow different courses, and require different treatments. Further confusion arises from the assignment of an autoimmune origin to thyrotoxicosis by Adams(2) and by McKenzie.(16) This disease is claimed to be induced and maintained by a particular factor—the long-acting thyroid stimulator (LATS) discovered in the serum of hyperthyroid subjects(1) and displaying the characteristics of a thyroid antibody. Some authors consider that thyrotoxicosis and Hashimoto’s disease are two facets of the same pathological process.(10) Moreover, it is believed that thyrotoxicosis might originate during the course of lymphocytic thyroiditis of the Hashimoto type, and the term “Hashitoxicosis” has even been proposed. Thus autoimmune lymphocytic thyroiditis might lead in some cases to the progressive destruction of the gland, with ensuing hypothyroidism, and in others to the development of thyrotoxicosis. Lastly, it should be remembered that in certain types of chronic thyroiditis no serological signs of thyroid autoimmunity are observed. This is the case in invasive fibrous thyroiditis, described at the end of the last century by Riedel, and which has since been confused with the sclerotic variant of Hashimoto’s thyroiditis. It is therefore understandable that a paper describing such developments was entitled “Chronic thyroiditis; a potentially confusing picture”.(24) The classification of thyroid diseases recently proposed by the Committee of Nomenclature of the American Thyroid Association(29) goes a long way to combat these intricacies (Table I.1). Thyroiditis is mentioned under “Diseases primarily characterized by euthyroidism”, and atrophic thyroiditis (a variant of lymphocytic chronic thyroiditis) is also referred to under the heading of “Diseases primarily characterized by hypothyroidism”. However, chronic thyroiditis is still identified with Hashimoto’s disease, although different variants are recognized. Moreover, thyroiditis is not listed under the “Diseases primarily characterized by hyperthyroidism.” TABLE I.1 CLASSIFICATION OF THYROIDITIS (AM. THYROID Assoc. 1969)
“Diseases characterized by euthyroidism” *This condition is further mentioned under the heading “II. Diseases primarily characterized by hypothyroidism.” These preliminary remarks underline the importance of the new concepts introduced in the study of thyroid diseases. The interest of chronic thyroiditis extends far beyond the narrow limits assigned to it by the textbooks. Study of the subject must embrace the aetiology of idiopathic myxoedema, the mechanism of thyrotoxicosis, and many important problems of diagnosis and therapy in general thyroidology. The aim of the present monograph is to clarify this complex pathological picture as far as possible. Material for such an endeavour is provided by recent progress in morphological, biochemical, and serological thyroid studies, and by work currently under way in our own department of medicine and in the laboratories of Nuclear Medicine (Dr. J. E. Dumont), Radioisotopes (Dr. A. M. Ermans), and Pathological Anatomy (Prof. P. Dustin) of this University. References
1. ADAMS, D.D. The presence of an abnormal thyroid stimulating hormone in the serum of some thyrotoxic patients. J. clin. Endocr. 1958; 18:699. 2. ADAMS, D.D. Pathogenesis of the hyperthyroidism of Graves’ disease. Brit. med. J. 1965; 1:1015. 3. ANDERSON, J.R., BUCHANAN, W.W., GOUDIE, R.B.Auto-immunity: clinical and experimental. Springfield: C. C. Thomas, 1967. 4. BASTENIE, P.A. Étude anatomo-clinique et expérimentale des inflammations chroniques et des scléroses du corps thyroïde. Arch. int. Méd. exp. (Liège). 1937; 12:1. 5. BUCHANAN, W.W., KOUTRAS, D.A., ALEXANDER, W.D., CROOKS, J., RICHMOND, M.H., MCDONALD, E.M., WAYNE, E.J. Iodine metabolism in Hashimoto’s thyroiditis. J. clin. Endocr. 1961; 21:806. 6. BUCHANAN, W.W., HARDEN, R.MCG., KOUTRAS, D.A., GRAY, K.G. Abnormalities of iodine metabolism in euthyroid non-goitrous women with complement-fixing anti-microsomal thyroid antibodies. J. clin. Endocr. 1965; 25:301. 7. CAMUS, M., ERMANS, A.M., BASTENIE, P.A. Alterations of iodine metabolism in asymptomatic thyroiditis. Metabolism. 1968; 17:1064. 8. DE GROOT, L.J. Current concepts in management of thyroid disease. Med. Clin. N. Am. 1970; 54:117. 9. DONIACH, D., HUDSON, R.V., ROITT, I.M. Human auto-immune thyroiditis: clinical studies. Brit. med. J. 1960; 1:365. 10....