· BackgroundThe use of levothyroxine to treat subclinical hypothyroidism is controversial. We aimed to determine whether levothyroxine provided clinical benefits in older persons with this condition. MethodsWe conducted a. · Patients with goitre may be asymptomatic, or may present with compressive symptoms such as cough or dysphagia. Goitre may also present with symptoms due to associated hypothyroidism or hyperthyroidism. Thyroid stimulating hormone is the appropriate first test for all patients with goitre; if this. 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 . ![]() 2013 ETA Guideline: Management of Subclinical Hypothyroidism Eur Thyroid J 2013;2:215–228 DOI: 10.1159/000356507 217 generally classified in two categories according to serum TSH level: mildly increased TSH.
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. Show more Information If you select "Keep me signed in on this computer", you can stay signed in to WebMD.com on this computer for up to 2 weeks or until you sign out. Answers Wanted When you come to WebMD Answers with questions, you also bring. · The family physician's holistic approach to patients forms the basis of good health care for adults with Down syndrome. Patients with Down syndrome are likely to have a variety of illnesses, including thyroid. · Hypothyroidism is a clinical disorder commonly encountered by the primary care physician. Untreated hypothyroidism can contribute to hypertension, dyslipidemia, infertility, cognitive impairment, and neuromuscular dysfunction. Data derived from the National Health. 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 TRß; this condition, known as thyroid hormone resistance (see Ch. 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. Discontinuous horizontal lines represent upper limit (TSH) and lower limit (FT4,T3) of the normal reference ranges. Reproduced with permission) (2)Table 9- 1. 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′- monodeiodination of T4 into T3 4,5 . 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 . RACGP - Goitre - Causes, investigation and management. Kiernan Hughes Creswell Eastman Background. Goitre refers to an enlarged thyroid. Common causes of goitre. Objective/s. This article outlines the causes, investigation and. Australian general practice. Discussion. Patients with goitre may be asymptomatic, or may present. Goitre may also present with symptoms due to associated. Thyroid stimulating. Thyroid. ultrasound has become an extension of physical examination. Ultrasound. can determine what nodules should be biopsied. Treatment. options for goitre depend on the cause and the clinical. Goitre refers to an enlarged thyroid gland. Causes of goitre include autoimmune disease, the formation of one or more thyroid nodules and iodine deficiency (Table 1). Goitre occurs when there is reduced thyroid hormone synthesis secondary to biosynthetic defects and/or iodine deficiency, leading to increased thyroid stimulating hormone (TSH). This stimulates thyroid growth as a compensatory mechanism to overcome the decreased hormone synthesis. Elevated TSH is also thought to contribute to an enlarged thyroid in the goitrous form of Hashimoto thyroiditis, in combination with fibrosis secondary to the autoimmune process in this condition. In Graves disease, the goitre results mainly from stimulation by the TSH receptor antibody (Figure 1). Table 1. Common causes of goitre. Hashimoto thyroiditis. Graves disease. Familial or sporadic multinodular goitre. Iodine deficiency. Follicular adenoma. Colloid nodule or cyst. Thyroid cancer. Figure 1. Macroscopic appearance of a thyroid gland removed from a patient with diffuse goitre secondary to Graves disease. When diffuse enlargement of the thyroid occurs in the absence of nodules and hyperthyroidism, it is referred to as a diffuse nontoxic goitre. This is sometimes called 'simple goitre' because of the absence of nodules, or 'colloid goitre' because of the presence of uniform follicles that are filled with colloid. Worldwide, diffuse goitre is most commonly caused by iodine deficiency and is termed 'endemic goitre' when it affects > 5% of the population in a given geographic area (Figure 2). The prevalence of goitre, diffuse and nodular, is dependent on the status of iodine intake of the population. In general, in iodine sufficient countries the prevalence of clinically palpable goitre is less than 4%. In countries with a previous deficiency corrected by universal salt iodination, elderly subjects may have a prevalence of approximately 1. This can be attributed to lack of nutritional iodine in early adult life, as longstanding endemic goitres usually do not regress with iodine supplementation. Smoking is also known to be goitrogenic, with cigarette smoke containing goitrogens including thiocyanates. Smoking may also exacerbate autoimmune thyroid disease (and possibly autoimmunity in general). The goitrogenic effect of smoking is most pronounced in people with intercurrent iodine or selenium deficiency. Certain raw foods, such as soybeans, cassava and cruciferous vegetables, are lightly goitrogenic but their typical impact is only modest. Figure 2. Woman from Northern Thailand with endemic goitre secondary to iodine deficiency. Iodine deficiency. Iodine deficiency has re- emerged in Australia over recent decades. Urinary iodine concentration (UIC) is an excellent proxy marker for current iodine intake and is a useful screening tool for iodine deficiency at a population level. However, day- to- day variations in UIC preclude the use of UIC as a diagnostic tool to assess the iodine nutritional status of an individual, unless multiple samples are collected over a period of weeks to derive an average level. As this is neither practical nor a prudent use of resources, the public health response has instead focused on supplementation. Since October 2. 00. Australia and New Zealand (with the exception of organic bread) must contain added iodine from iodised salt. Consequently, adults and children who eat bread regularly should receive sufficient quantities of iodine. However, the iodised salt in bread alone does not meet the increased daily requirements of the majority of pregnant and breastfeeding women. The National Health and Medical Research Council recommends that all women who are pregnant, breastfeeding or considering pregnancy, take an iodine supplement of 1. Women with preexisting thyroid conditions should seek advice from their medical practitioner before commencing a supplement. Clinical presentation. Nodular goitre is most often detected simply as a mass in the neck, but an enlarging gland may also produce pressure symptoms on the trachea and the oesophagus. As well as discomfort, there may be difficulty in breathing, dysphagia, cough and hoarseness. Paralysis of the recurrent laryngeal nerve may occur when the nerve is stretched taut across the surface of an expanding goitre, but this event is rare. Symptoms suggesting obstruction of the trachea may occur. These include cough, stridor and shortness of breath. Occasionally tenderness and a sudden increase in goitre size arise due to haemorrhage into a nodule. Symptoms of hyperthyroidism or hypothyroidism may be evident at presentation. Thyroid examination. The thyroid gland is located superficially and, while usually not visible, is easily palpated. A careful examination should record the size, shape and consistency of the gland. The number, dimensions and consistency of any nodules should also be recorded. Importantly, in patients with long, thin necks, a prominent but normal thyroid gland may be perceived by an examiner as abnormal and in patients with short, fat necks, nodules may be extremely difficult to detect. The accuracy of thyroid palpation depends greatly on the experience of the examiner. Substernal goitre may obstruct the thoracic inlet. Pemberton sign refers to faintness with evidence of facial congestion and cyanosis due to external jugular venous obstruction when the arms are raised above the head, a manoeuvre that draws the thyroid into the thoracic inlet. Laboratory investigations. Patients with goitre or thyroid nodules should have a serum thyroid stimulating hormone (TSH) to determine the current functional status of the thyroid. If the TSH is abnormal, a free T4 and free T3 should also be checked. Checking for antibodies against thyroperoxidase (anti- TPO) and thyroglobulin (anti- TG) is recommended as thyroid autoimmunity may coexist with goitre. If the patient is hyperthyroid, a thyroid receptor antibody (TRAb) can help to confirm Graves disease. Imaging. Due to the limitations of the physical examination, ultrasound has become an invaluable tool and an extension of clinical examination in specialist endocrinology practice. An ultrasound performed at the time of the initial clinical assessment is not only useful for diagnosis, but also as a baseline for monitoring the progress of thyroid volume or the size of nodules. Thyroid ultrasound should be performed in all patients with known or suspected thyroid nodules. A radionuclide thyroid scan is indicated in patients with a subnormal TSH to determine the functional status of any nodules within the thyroid and the underlying cause of clinical or subclinical hyperthyroidism. Since hyperfunctioning ('hot') nodules rarely harbour malignancy, if one is found that corresponds to the nodule in question no cytological evaluation is necessary. A computed tomography (CT) scan of the neck is not a routine part of the investigation of a thyroid nodule, but may be performed in patients with significant compressive symptoms, or to evaluate the degree of retrosternal extension or tracheal compression. In the presence of a nodule or goitre, CT scans should be ordered as 'noncontrast' due to risk of contrast induced hyperthyroidism or hypothyroidism in patients with nodular thyroid disease. Contrast should also be routinely avoided when imaging other regions in the presence of goitre unless essential for medical care. Thyroid nodules. The normal thyroid gland is a fairly homogenous structure, but nodules often form within its substance. These nodules may be the result of growth and fusion of localised colloid filled follicles, or discrete adenomas or cysts. Thyroid carcinoma also typically presents as a nodule. Between 4% and 7% of the general population have a palpable thyroid nodule. Around 3. 0–5. 0% of adults have a thyroid nodule visible on ultrasound. The major challenge for the clinician and patient is determining which of these nodules are clinically important; a structured diagnostic approach is required (Figure 3). Ultrasound enables characterisation of nodules and detection of other clinically significant nodules that are not palpable (Figure 4). Importantly, the risk of malignancy is the same for incidental impalpable lesions as for nodules of the same size that are palpable. Ultrasound is essential to determine those nodules, if any, which should be subjected to fine needle aspiration (FNA) cytology (Table 2). Increasingly, thyroid ultrasound is being performed by endocrinologists and endocrine surgeons at the time of their initial assessment. For patients who require a biopsy, ultrasound is useful to guide the biopsy and essential when the nodule is not readily palpable, as ultrasound increases the likelihood of obtaining a diagnostic sample. There has been a move toward greater uniformity in thyroid FNA cytology reporting to help provide more clinically useful results. Any patient who doesn't have benign cytology should be referred for specialist opinion – this includes referring patients with results of undetermined significance on histology. It is recommended that all benign thyroid nodules be followed with serial ultrasound examination 6–1. FNA to assess for interval change. If the nodule has grown significantly (> 2. FNA should be repeated.
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