THE GOITRE CYCLE AND ITS ANATOMIC FINDINGS*

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THE GOITRE CYCLE AND ITS ANATOMIC FINDINGS* A REPORT OF 1028 SECTIONED GOITRES B. MARKOWITZ During the past thirty years vast contributions have been made to the study of the etiology of goitre.

1 THE GOITRE CYCLE AND ITS ANATOMIC FINDINGS* A REPORT OF 1028 SECTIONED GOITRES B. MARKOWITZ During the past thirty years vast contributions have been made to the study of the etiology of goitre. These contributions have done much to bring about very striking changes in the prevention of this disease. Much of this has come about through studies of the anatomic changes found in the thyroid gland in relation to iodine content, and the relation between the thyroid and other glands of internal secretion. While the iodine content and the whole of thyroid chemistry is of extreme importance in preventing goitre, the anatomic changes in the gland are a constant indicator of the course and intensity of existing thyroid disturbance. True, these anatomic changes may reflect only the imbalance present in the gland but they are the only constant findings, and are described as the "hyperplasia-involutiqn cycle." In a study of over 1,000 operated goitre patients, the correlation of the case histories and the anatomic findings of the surgically removed specimens definitely indicates the existence of such a cycle. Following iodine medication the smooth hyperplastic goitre presents areas of circumscribed colloid which are definite signs of involution. In the long-standing cases with histories of remissions and exacerbations of clinical symptoms, the presence of colloid nodules in various stages of development and degeneration testify to the hyperplasia-involution cycle. The morphological changes seen in the hyperplasia of puberty, of pregnancy, of simple goitre, in "hyperplastic goitre" and in compensatory hyperplasia following partial thyroidectomy, are all essentially the same. This is contrary to the opinion of Aschoff 1 and McCarrison 2 but is generally accepted by most workers (Jaff6, 3 Hertzler, 4 Marine 6 ). The individual thyroid follicle, as first explained by Williams and Pease, 6 and later modified by Rienhoff, 7 is the histologic unit of the thyroid gland * Received for publication, March 24th,

2 94 B. MAKKOWITZ and the cells of this follicle seem to be the essential factor in the hyperplasia-involution cycle. Whenever the thyroid secretion becomes insufficient, whether due to physiological demand or due to decreased iodine, hypertrophy and hyperplasia occur; the cells of the follicles become larger and taller, they increase in number even to the point of papillary infolding, new follicles are formed and the stainable colloid is replaced. Whatever the cause, this hyperplasia is apparently due to stimulation by the thyrotropic hormone of the anterior pituitary. Loeb, Leo and Bassett 8 injected this hormone into the guineapig and produced a similar hyperplasia. When the stimulation of this thyrotropic hormone is decreased either by increased iodine intake or decreased physiological demand or some undetermined cause, the hyperplasia recedes and involution occurs. The anatomic changes in involution are the reverse of those which occur during hyperplasia; the cells of the follicles become smaller and decrease in number, the blood supply diminishes, and colloid accumulates, filling and distending the follicles. With repetition of this hyperplasia-involution cycle the gland is capable of undergoing hyperplasia and involution many times. The literature 9 calls attention to the probable explanation that the degree of stimulation may affect the resulting hyperplasiainvolution cycle. The degree of anatomical change depends upon the degree of stimulation with resulting hyperplasia, and the degree of involution with resulting recession. These anatomical changes of the thyroid in goitre are well illustrated by the following scheme of Marine and Lenhart. 10, exhaustion atrophy- Normal thyroid hypertrophy hyperplasia * colloid or resting stage X *. * exhaustion atrophy Colloid thyroid hypertrophy hyperplasia <f * colloid or resting stage I *, exhaustion atrophy Colloid hypertrophy hyperplasia * colloid or resting stage SCHEME OF ANATOMICAL CHANGES IN GOITRE (MARINE AND LENHART)

3 THE GOITRE CYCLE 95 The process is a constant repetition of these changes, with hyperplasia involuting to colloid goitre and colloid goitre progressing to hyperplasia. These anatomical changes may change their pace at any stage, whether during hyperplasia or involution, and even proceed in the opposite direction. With this capability of under-going hyperplasia and involution many times during its life cycle, we point to the accepted thought that colloid goitre is secondary to previous hyperplasia. That colloid goitre occurs in a normal gland from increased colloid secretion, is in the light of present knowledge irrational. All available evidence indicates that goitre begins as an active hyperplastic process whether the end be exhaustion atrophy or colloid goitre. If exhaustion atrophy occurs, as is seen principally in goitrous endemic cretins, and occasionally as the end result of diffuse hyperplastic goitre, the anatomic picture is that of desquamation and disintegration replacing the very active hyperplasia. If involution to colloid goitre occurs the anatomic picture is that of increased colloid and inactive follicular cells. In a previous paper 11 we have called attention,to the two distinct processes of thyroid secretion and colloid accumulation which balance each other in the physiology of the thyroid gland. With an imbalance however there is a disproportion of these two processes with resulting nodular formation. The secondary changes that occur with the production of nodules, so-called adenomas, increase with the duration of the goitre. That is, with the continued repeated cycles these nodules increase in size and number. It is possible that the foetal rest theory of Woelfer 12 can explain the true adenoma which presents only cords of cells with no attempt at follicle formation. However the great majority of the nodules found in our series seemed very closely associated with the thyroid tissue of goitre; they are most likely formed by this hyperplasia-involution cycle which in the very beginning caused the diffuse goitre. Graham 9 speaks of them as "involuted goitres which have been oscillating between involution and hyperplasia for years." While the thyrotropic hormone of the anterior pituitary appears to be the important factor in stimulating and producing

96 B. MARKOWITZ those anatomic changes in the thyroid gland, there is evidence that the converse is also true 13 ; that the thyroid also influences the anterior pituitary especially in its production

4 96 B. MARKOWITZ those anatomic changes in the thyroid gland, there is evidence that the converse is also true 13 ; that the thyroid also influences the anterior pituitary especially in its production of the thyrotropic hormone. These two glands are evidently very closely related and balance each other. A deficiency in the thyroid stimulates the pituitary while an increase in thyroid secretion causes a reduction of pituitary activity. The anatomic changes in goitre must therefore be dependent upon the maintainance of a balance between the secretion of the thyroid and the thyrotropic hormone of the anterior pituitary. From this mechanism with its associated anatomical changes the two principle clinical diseases associated with disturbed thyroid function may be listed as: (1) Hyperplastic goitre and (2) Colloid goitre. The hyperplastic or active goitre may be considered the developmental phase while the colloid or involutional goitre may be considered the recovery phase. The secondary phases between these two principle ones are great in number depending upon the number of times the cycle recurs. This cycle is the only apparent anatomical response of which the thyroid is capable and is not a response to any specific disease. Excepting the true adenomata, the recurrence of this cycle produces the nodules found in long-standing goitre and gives rise to the terms diffuse and nodose goitres. Further changes such as hemorrhage, liquefaction, calcification and other forms of degeneration may occur which are secondary to the formation of nodes. Functional disturbances of the thyroid gland can then be grouped into diffuse or nodose hyperplastic and diffuse or nodose colloid goitres with added descriptions of the secondary changes. In the hyperplastic type where the progress is very rapid and the patient is subjected to operation early, no nodes are found. The longer the history of goitre with the recurrent cycle of hyperplasia and involution the greater the probabiuty of nodular formation. This explains why in any large group of goitres the nodose type will be found in much greater numbers in the colloid goitre, while the diffuse type will be found in much greater numbers in the hyperplastic goitre. It will be found, too, that

5 THE GOITRE CYCLE 97 the very large goitres weighing 200 to 300 grams will be among the long-standing nodose colloid goitres while the diffuse colloid goitres seldom weigh over 50 to 75 grams. In our series of 1028 goitres removed at operation there were 481 of the colloid type, only 126 of which were described as diffuse while 355 were described as nodose goitres. There were 522 of the hyperplastic type, 334 of which were described as diffuse while only 188 were described as nodose goitres. That is, the incidence of nodose goitre was twice as large in the colloid while only one-half as large in the hyperplastic goitres. Of the whole colloid group very few weighed over 75 grams among the TABLE 1 TYPE NtTMBXB DUBATION BIZH Colloid: Diffuse Nodose Hyperplastic: Diffuse Nodose Adenoma Carcinoma Thyroiditis Branchial cysts months- 5 years 3 years -25 years 3 months- 1 year 3 months-20 years grams Total 1,028 ^ diffuse while many weighed over 200 grams, (a few as high as 350 grams) among the nodose goitres. Of the whole hyperplastic group there was comparatively little difference in the size of the diffuse and nodose goitres. Very few of the diffuse weighed under 40 grams while very few of the nodose weighed over 100 grams. The case histories of these patients indicate the duration of diffuse goitres usually in the terms of months while the duration of nodose goitres is always in the terms of years (some as high as 25 and 30). That is, increased size and duration of time go hand in hand with nodular formation in the colloid type where involution occurs and recurs, but are less frequently

6 98 B. MAEKOWITZ found in the hyperplastic type where active progression of the process continues without involution. Of the remaining 25 surgically removed specimens in this series of 1028 goitres, there were 5 carcinomata, 3 branchial cysts, 9 described as thyroiditis, and 8 described as true adenomata. Those described as true adenomata were only those in which solid cords of cells were found with no attempt at follicle formation; the term foetal adenoma has not been used at all. SUMMARY The anatomic changes found in thyroid dysfunction are the only constant morphological findings and are produced by a mechanism described as the "hyperplasia-involution cycle." The mechanism of this cycle and its associated anatomical findings gives rise to the two principle clinical diseases associated with disturbed thyroid function; hyperplastic goitre and colloid goitre. Nodules in the goitre described as "nodose" are formed in thyroid glands which have been the seat of a recurrent hyperplasia-involution cycle. In a series of 1028 surgically removed specimens there were twice as many nodose as diffuse colloid goitres and only about one-half as many nodose as diffuse hyperplastic goitres. The time element and size of these goitres seem to be in accordance with the widely accepted explanation of the thyroid cycle in goitre. In 1028 surgically removed specimens only 8 were described as true thyroid adenomata. REFERENCES (1) ASCHOFF, LTJDING: Reports of International Conference on Goitre. Bern (2) MCCABEISON, R.: Reports of International Conference on Goitre. Bern (3) JAFFE, R. H.: Cook County Hospital, Chicago, 111, Personal communication. (4) HEETZLEE, A. E.: Pathogenesis of goitre considered as one continuous disease process. Arch. Surg., 16, 61-78, 1928.

7 THE GOITRE CYCLE 99 (5) MARINE, DAVID: The pathogenesis and prevention of simple or endemc. goitre. J. A. M. A., 104, 26, June 29, (6) WILLIAMSON AND PEARSE: The structure of the thyroid organ in mian J. of Path, and Bact., 26, 459, (7) RIENHOFF, WM. F., JR.: Structure of the thyroid gland. Arch. Surg., 1006, (8) LOEB, LEO AND BASSETT: Proc. Soc. Exper. Biol. & Med., 26, 860, June, (9) MARKOWITZ, B.: Pathogenesis of goitre. Am. Jour, of Clin. Path., 1, 4, July, GRAHAM, ALLEN: Nodular goitres: their relation to neoplasia. Am. Jour. Surg., 7, , BOYD, WM.: The Pathology of Internal Diseases. Lea & Febiger, (10) MARINE, D. AND LENHART, C. H.: The pathological anatomy of the Human thyroid gland. Arch. Int. Med., 7, 506, (11) MARKOWITZ, B.: Focal cyclic growth as a factor in production of nodular goitre. Am. Jour. Clin. Path., 2, 1, (12) WOELFER, A.: Arch. F. Klin. Chir., 29, 1, (13) MARINE, D. ROSEN, S. H. AND SPARK, G.: Proc. Soc. Exper. Biol. & Med., 32, 803, Feb., 1935.

Thyroid in a Nutshell Dublin Catherine Kirkpatrick Consultant Sonographer ULHT

Thyroid in a Nutshell Dublin Catherine Kirkpatrick Consultant Sonographer ULHT Thyroid in a Nutshell Dublin 2017 Catherine Kirkpatrick Consultant Sonographer ULHT Acknowledgements Dr. Steve Colley Dr. Rhodri Evans Dr. Rhian Rhys Dr. Andrew McQueen Aims Anatomy & Physiology Incidence