![]() Archives and past articles from the Philadelphia Inquirer, Philadelphia Daily News, and Philly.com. 9789583016936 9583016934 Francis Bacon - Retrato de Una Pesadilla 4995879236796 Starlight Lounge (Import), Brigette 9780300115062 0300115067 The Invisible Museum. BlumbergExcelsior, Inc. 2017 Litigation Supplies Catalog FREE SHIPPING to the contiguous 48 states, except orders under $50.00, $9.95 blumberg.com. The full-blown expression of hypothyroidism is known as myxedema. Adult myxedema escaped serious attention until Gull described it in 1874 1.![]() ![]() Adult Hypothyroidism - Thyroid Disease Manager. Thyroid Disease Manager. HISTORICALThe full- blown expression of hypothyroidism is known as myxedema. Adult myxedema escaped serious attention until Gull described it in 1. That it was a state resembling the familiar endemic cretinism, but coming on in adult life, was what chiefly impressed Gull. Ord 2 invented the term myxedema in 1. The disorder arising from surgical removal of the thyroid gland (cachexia strumipriva) was described in 1. Reverdin 3 of Geneva and in 1. Kocher of Berne 4 . After Gull’s description, myxedma aroused enormous interest, and in 1. Clinical Society of London appointed a committee to study the disease and report its findings 5 . The committee’s report, published in 1. It is referred to in the following discussion as the Report on Myxedema. The final conclusions of the 2. They are as follows: 1. That myxedema is a well- defined disease. That the disease affects women much more frequently than men, and that the subjects are for the most part of middle age. That clinical and pathological observations, respectively, indicate in a decisive way that the one condition common to all cases is destructive change of the thyroid gland. That the most common form of destructive change of the thyroid gland consists in the substitution of a delicate fibrous tissue for the proper glandular structure. That the interstitial development of fibrous tissue is also observed very frequently in the skin, and, with much less frequency, in the viscera, the appearances presented by this tissue being suggestive of an irritative or inflammatory process. That pathological observation, while showing cause for the changes in the skin observed during life, for the falling off the hair, and the loss of the teeth, for the increased bulk of body, as due to the excess of subcutaneous fat, affords no explanation of the affections of speech, movement, sensation, consciousness, and intellect, which form a large part of the symptoms of the disease. That chemical examination of the comparatively few available cases fails to show the general existence of an excess of mucin in the tissues adequately corresponding to the amount recorded in the first observation, but that this discrepancy may be, in part, attributed to the fact that tumefaction of the integuments, although generally characteristic of myxedema, varies considerably throughout the course of the disease, and often disappears shortly before death. That in experiments made upon animals, particularly on monkeys, symptoms resembling in a very close and remarkable way those of myxedema have followed complete removal of the thyroid gland, performed under antiseptic precautions, and with, as far as could be ascertained, no injury to the adjacent nerves or to the trachea. That in such experimental cases a large excess of mucin has been found to be present in the skin, fibrous tissues, blood, and salivary glands; in particular the parotid gland, normally containing no mucin, has presented that substance in quantities corresponding to what would be ordinarily found in the submaxillary gland. That following removal of the thyroid gland in man in an important proportion of the cases, symptoms exactly corresponding with those of myxedema subsequently develop. That in a considerable number of cases the operation has not been known to have been followed by such symptoms, the apparent immunity being in many cases probably due to the presence and subsequent development of accessory thyroid glands, or to accidentally incomplete removal, or to insufficiently long observation of the patients after operation. That, whereas injury to the trachea, atrophy of the trachea, injury of the recurrent laryngeal nerves, injury of the cervical sympathetic, and endemic influences, have been by various observers supposed to be the true cases of experimental or of operative myxedema (cachexia strumipriva), there is, in the first place, no evidence to show that, of the numerous and various surgical operations performed on the neck and throat, involving various organs and tissues, any, save those in which the thyroid gland has been removed, have been followed by the symptoms under consideration; that in many of the operations on man, and in most, if not all, of the experimental operations made by Professor Horsley on monkeys and other animals, this procedure avoided all injury of surrounding parts, and was perfectly antiseptic; that myxedema has followed removal of the thyroid gland in persons neither living in nor having lived in localities the seat of endemic cretinism; that, therefore, the positive evidence on this point vastly outweighs the negative; and that it appears strongly proved that myxedema is frequently produced by the removal, as well as by the pathological destruction, of the thyroid gland. That whereas, according to Clause 2, in myxedema women are much more numerously affected than men, in the operative form of myxedema no important numerical difference is observed. That a general review of symptoms and pathology leads to the belief that the disease described under the name of myxedema, as observed in adults, is practically the same disease as that named sporadic cretinism when affecting children; that myxedema is probably identical with cachexia strumipriva; and that a very close affinity exists between myxedema and endemic cretinism. That while these several conditions appear, in the main, to depend on, or to be associated with, destruction or loss of the function of the thyroid gland, the ultimate cause of such destruction or loss is at present not evident. DEFINITION AND EPIDEMIOLOGY OF HYPOTHYROIDISMHypothyroidism is traditionally defined as deficient thyroidal production of thyroid hormone. The term primary hypothyroidism indicates decreased thyroidal secretion of thyroid hormone by factors affecting the thyroid gland itself; the fall in serum concentrations of thyroid hormone causes an increased secretion of TSH resulting in elevated serum TSH concentrations. Decreased thyroidal secretion of thyroid hormone can also be caused by insufficient stimulation of the thyroid gland by TSH, due to factors directly interfering with pituitary TSH release (secondary hypothyroidism) or indirectly by diminishing hypothalamic TRH release (tertiary hypothyroidism); in clinical practice it is not always possible to discriminate between secondary and tertiary hypothyroidism, which are consequently often referred to as central hypothyroidism. In rare cases, symptoms and signs of thyroid hormone deficiency are caused by the inability of tissues to respond to thyroid hormone by mutations in the nuclear thyroid hormone receptor TR. Mutations in other genes involved with extrathyroidal metabolism and action of thyroid hormones in target tissues may also cause a hypothyroid state. Such cases could be labelled as peripheral (extrathyroidal) hypothyroidism. It thus seems more appropriate to define hypothyroidism as thyroid hormone deficiency in target tissues, irrespective of its cause. GRADES OF HYPOTHYROIDISMHypothyroidism is a graded phenomenon, ranging from very mild cases in which biochemical abnormalities are present but the individual hardly notices symptoms and signs of thyroid hormone deficiency, to very severe cases in which the danger exists to slide down into a life- threatening myxedema coma. In the development of primary hypothyroidism, the transition from the euthyroid to the hypothyroid state is first detected by a slightly elevated serum TSH, caused by a minor decrease in thyroidal secretion of T4 which doesn’t give rise to subnormal serum T4 concentrations. The reason for maintaining T4 values within the reference range is the exquisite sensitivity of the pituitary thyrotroph for even very small decreases of serum T4, as exemplified by the log- linear relationship between serum TSH and serum FT4 1 . A further decline in T4 secretion results in serum T4 values below the lower normal limit and even higher TSH values, but serum T3 concentrations remain within the reference range. It is only in the last stage that subnormal serum T3 concentrations are found, when serum T4 has fallen to really very low values associated with markedly elevated serum TSH concentrations ( Figure 9- 1 ). Hypothyroidism is thus a graded phenomenon, in which the first stage of subclinical hypothyroidism may progress via mild hypothyroidism towards overt hypothyroidism ( Table 9- 1 ) 3 . Figure 9- 1. Individual and median values of thyroid function tests in patients with various grades of hypothyroidism. Grades of hypothyroidism. Grade 1. Subclinical hypothyroidism. TSH +FT4 NT3 N(+)Grade 2. Mild hypothyroidism. TSH +FT4 –T3 NGrade 3. Overt hypothyroidism. TSH +FT4 –T3 –+, above upper normal limit; N, within normal reference range; - , below lower normal limit. Maintenance of a normal serum T3 concentration until a relatively late stage in the development of hypothyroidism obviously serves as an appropriate mechanism of the body to counteract the impact of diminishing production of T4. It is accomplished by a preferential thyroidal secretion of T3: the increased secretion of TSH enhances the synthesis of T3 more than that of T4 and stimulates thyroidal 5. It explains why sometimes a slightly elevated serum T3 is found in the early stage of development of hypothyroidism. About 8. 0% of the daily production rate of T3 is generated in extrathyroidal tissues via the conversion of T4 into T3. The peripheral tissues also have a defense mechanism against developing hypothyroidism by increasing the overall fractional conversion rate of T4 into T3 6 . EPIDEMIOLOGY OF HYPOTHYROIDISMThyroid hormone resistance syndromes are seldom the cause of hypothyroidism; the number of registered patients approximates one thousand (see Ch. Central hypothyroidism is also rare; its precise prevalence is unknown, but has been estimated as 0. Primary hypothyroidism, in contrast, is a very prevalent disease worldwide.
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