He observed that goiter was absent in areas where drinking water was rich in iodine and frequent when water was iodine depleted. He also noted that people who settled in an iodine-poor area would develop goiter which disappeared when traveling to an iodine rich region.
He advocated the use of iodinated salt [ 33 ]. His paper, published in , is very impressive, based on traveling in a vast area including modern Columbia and Venezuela—making stringent observations within chemistry, geology, and medicine. The French chemist Adolphe Chatin — was the first to propose that goiter might be caused by iodine deficiency. The administration of iodine yielded promising results.
Even at an early time, the clinical presentation of myxedema was well known. In the UK alone, a fair number of papers dealt with myxedema in the s and s—some have been reviewed by Doyle [ 19 ]. Many of these case reports still make fascinating reading. Before treatment became routine, hypothyroidism frequently ran a fatal course—10 years being the typical length of time from diagnosis to demise. It is apparent that the hypothyroid patient seen by physicians often would appear quite different from the one seen today.
Many patients were not diagnosed until late in the course when severe intellectual, neurological, and psychiatric deficiency had left the patient in an extreme calamitous situation with dementia, debilitating neuropathy including speaking and hearing deficits and hypothermia—symptoms seen only exceptionally rarely today. In one patient in whom hypothyroidism apparently had precipitated psychosis with religious delusions, body temperature had fallen to In , Fulop [ 36 ] called attention to what he considered an often overlooked finding in one of his hypothyroid patients: enlarged salivary glands.
He referred to an old Czechoslovakian paper which he thought was the first study to mention this phenomenon. However, several early publications, the first one seems to be Horsley's lecture in [ 28 ], pointed out that enlarged salivary glands are or at least at that time were a characteristic and not infrequent finding in myxedema.
So, at the end of the 19th century it was generally assumed that hypothyroidism was brought about by hyposecretion in the thyroid of one or more substances. He found a substance thyroiodine rich in iodine in thyroid tissue in both animals and man, effective in treating myxedema. This finding suggested that iodine somehow was crucial for thyroid function.
This made it easy to understand why iodine deficiency might lead to hypothyroidism. In , a completely novel concept was introduced: struma lymphomatosa, a thyroiditis, which for years mainly was an anatomical designation, based on the presence of lymphocytic infiltrates in the thyroid gland [ 38 ].
Within the following years, German investigators published accounts on this disorder [ 39 ] but it attracted slight interest. About the same time, it was suggested that thyroid antibodies might also be involved in the development of hypothyroidism [ 41 , 42 ]. While many details of the immunological response remain to be sorted out, there is convincing evidence that to a large extent it is controlled by genetic factors [ 43 ].
The role of exogenous issues—for example, iodine intake [ 44 ] and smoking [ 45 , 46 ]—has not been settled and appears complex. Presence of lymphocytic infiltrates correlates with the amount of circulating thyroid antibodies [ 47 ]. At present, the term thyroiditis has been used for a century and the pertinent literature is exorbitant. Nevertheless, there is still confusion how it should be defined and subdivided.
For example many use the term autoimmune thyroiditis to cover both primary myxedema without goiter and Hashimoto's goiter while others suggest they are distinct diseases. It is known that some antibodies are cytotoxic and some block the effect of thyrotropin, but exactly how these antibodies precipitate hypothyroidism has not been settled.
Davies and Amino recently proposed a simple classification: type 1 and type 2 to cover the different presentations of what many call Hashimoto's thyroiditis while type 3 includes Graves-Basedow's disease [ 48 ]. Subtypes indicate whether hyper-, hypo- or euthyroidism is present. Until recently hypothyroidism was worldwide most often caused by iodine deficiency [ 49 ].
Considering the many programs initiated where food supplies are fortified with iodine, today autoimmune thyroid disease might and certainly ought to be the most frequent cause of hypothyroidism. Recent reviews have summarized the various causes of congenital and acquired hypothyroidism [ 50 , 51 ]. Mixed or intermediate forms are encountered. The distribution of the forms varies according to the endemic area.
Obviously, iodine deficiency is a key factor in both types. Whereas the myxedematous type as the name implies is clinically associated with hypothyroidism including stunted growth and sexual immaturity , patients with the neurological type are often euthyroid though frequently with goiter. Iodine given before or early in the pregnancy will prevent the development of neurological cretinism [ 53 ].
In an important study [ 54 ] from Congo, Vanderpas and coworkers showed that in the myxedematous type of cretinism treatment with iodine will normalize thyroid function—provided treatment is begun early in the postnatal period. If not, the prognosis remains dismal. It has puzzled researches how iodide deficiency of similar magnitude may lead to such clinical diversity. In a careful and well-argued analysis of published data and their own recent findings, Boyages and Halpern have suggested that two events are involved in endemic cretinism [ 55 ].
One is a transient thyroxine deficit transmitted from mother to fetus around the time of the midtrimester with neurological and intellectual consequences. This event occurs in all cretins whereas the second postnatal period of thyroid hormone deficit takes place in a subgroup only.
It is the length and severity of this second event that will decide the extent of clinical hypothyroid symptoms present.
Though the exact cause of myxedematous cretinism is still unclear, a wealth of skillful research has demonstrated the importance of iodine. Zimmermann has recently published a superb review of the early iodine prophylaxis [ 56 ]. In a detailed report pages delivered in by a committee set up by the Clinical Society in London on the relationship between cretinism, myxedema, and struma thyropriva, the clinical symptoms are described in detail but treatment is hardly mentioned [ 57 ].
However, a few other investigators were toiling with the possibility of therapy and clarifying thyroid function. Thus, the eminent German physician and physiologist Moritz Schiff — while working in Berne performed important experiments.
Similar grafting was performed by von Eiselberg who at the same time transplanted thyroid and parathyroid tissue and thus became the first to perform parathyroid grafting [ 59 ], though obviously he was unaware of the function of parathyroid glands. They were discovered in [ 5 ], but it would last almost until the end of the century before their function was recognized [ 60 ]. Thyroid transplantation in man was soon taken up by Bettencourt and Serrano in Lisbon [ 61 ].
The effect was remarkably swift and—in fact, so swift that the authors wisely suggested that it might be due to the absorption of the juice from healthy thyroid gland by the tissues of the patient. In a letter in June [ 62 ], Horsley informed George Redmayne Murray — about the progress made in various European countries as to finding treatment for hypothyroidism. Murray at that time was a pathologist at the Hospital for Sick Children in Newcastle.
A few months later, Murray published the first account of a human patient with hypothyroidism given substitution with thyroid extract injected subcutaneously [ 63 ]. Clinically, the effect was beyond doubt. The patient lived almost 30 years on thyroid substitution—eventually to die of cardiac failure in [ 64 ].
Within months, it was discovered that oral administration of thyroid extract was effective [ 65 — 67 ]. Fenwick [ 68 ] noted a marked increase in diuresis after commencement of thyroid substitution therapy.
Naturally, the central question as far as thyroid extract was concerned, was which substance was responsible. Magnus-Levy demonstrated the important fact that desiccated thyroid and iodothyrin increase oxygen consumption and output of carbon dioxide [ 70 ].
A vivid description has been given of what a physician might encounter at that time [ 71 ]. Around , an Irish general practitioner was asked to see a lady who obviously was dying, her family being aware no treatment was possible. The diagnosis was clinically obvious. The GP had just read in the British Medical Journal about the proposed treatment of myxedema and straight away got hold of thyroid glands from sheep.
Following the instructions in the papers, he prepared a substance which was administered to the patient who stunned everybody by a swift and complete, almost biblical, recovery. Incidentally, the physician later gained further fame by operating on an old and destitute woman on his kitchen table, curing her cataract.
In , Murray—not without a little pride—summed up the present state of treatment of hypothyroidism [ 72 ]. In the idiopathic form it is a symptom of chronic interstitial thyroiditis, just as anasarca may be a symptom of renal disease or ascites of hepatic disease.
Thus the myxedema can be cured, although the chronic interstitial thyroiditis still remains. In on Christmas day, at the Mayo Clinic, Edward Calvin Kendall — crystallized a substance—later to be named thyroxine—containing When he repeated the procedure, he failed to isolate any crystals.
It would take 15 frustrating months finally to get the procedure right. This allowed studies on its physiological properties. Perhaps because of the war, thyroxine was not chemically identified until [ 75 ]. About 25 years later, Gross and Pitt-Rivers [ 76 ] detected the second thyroid hormone—triiodothyronine, which at the same time also was demonstrated by French investigators [ 77 , 78 ]. Almost as if they were introducing a completely new drug, Hart and Maclagan in [ 79 ] reviewed the use of thyroxine and particularly L-thyroxine.
Actually, it had been available since the s but had not gained wide acceptance maybe because of its high cost —despite its obvious advantages. Desiccated thyroid was much used for many years and as late as leading British endocrinologists felt compelled to warn against its use [ 80 ].
It is still being marketed and hence probably used in some countries—for example, USA. He had advocated the use of extracts from ovaries and testes—many of his theses were based on excellent results in experiments he had performed on himself [ 82 , 83 ]. In some respects, his theories would lead medicine into an abyss of eeriness and utter bewilderment, but in other instances it would precipitate important progress in endocrine therapy.
There can be little doubt that the benefit of thyroid substitution was a major support for the soundness of organotherapy. A veritable industry grew up and extracts from a variety of organs including brain and spinal cord were marketed and widely used Figures 3 a — 3 c.
Organotherapy could claim some other successes. Acute illness reduces the specificity of second-generation sTSH tests for thyroid disease. The positive likelihood ratio associated with an abnormal sTSH test result in ill inpatients is about 10 compared with about in outpatients. Conclusion In unselected general medical, geriatric, or psychiatric inpatient populations, sTSH testing provides a low yield of true-positive and many false-positive results.
Recommendations on the use of the sTSH assay in patients with NTI range from limiting use of the test to patients with high clinical suspicion 3 - 6 to generalized screening. Determining the optimal strategy for the use of any diagnostic test requires elucidating 3 variables: 1 the underlying risk of the target disease in the population of interest, 2 clinical variables that may raise or lower this risk, and 3 characteristics of the test in the population of interest.
The first 2 variables lead to a pretest likelihood of disease and the third leads to a posttest likelihood of disease. We applied this 3-fold framework to the diagnosis of thyroid disease in acutely ill, hospitalized patients with NTI. We conducted a systematic review that addressed the following 3 questions: 1 What is the prevalence of unrecognized thyroid disease?
In acute illness, all thyroid indices have been shown to yield false-positive results. We recognize that the new third-generation sTSH assay has greatly increased the sensitivity of diagnosis, mostly of hyperthyroidism, in an outpatient setting.
Throughout, we sought studies reported in the English language that enrolled more than 50 patients. To address the prevalence of unrecognized thyroid disease in acutely ill, hospitalized patients, we used the following MEDLINE search strategy: explode thyroid diseases and prevalence text word and 1 of the following: hospitalized or medical or inpatient all text words or atrial fibrillation or explode mental disorder or explode dementia medical subject heading [MeSH] terms or geriatrics both MeSH and text word.
We retrieved and included in the analysis all articles in which the study population was acutely ill or hospitalized with an NTI and those in which the reference standard included biochemical markers with or without clinical features and follow-up after resolution of the NTI. For this section, therefore, our main reference standard was long-term follow-up, and we did not limit ourselves to the sTSH assay as a diagnostic test.
To address the usefulness of clinical signs and symptoms in predicting thyroid disease in hospitalized patients, we used the following search strategy: explode thyroid diseases and explode cohort studies and either signs or symptoms text words.
We retrieved the articles in which the authors described clinical signs and symptoms in sufficient detail to calculate likelihood ratios LRs. Because we found no articles addressing the usefulness of clinical signs and symptoms in the diagnosis of thyroid disease among inpatients, we included studies of outpatients only in this section. To address the sensitivity and specificity of the sTSH assay in the diagnosis of thyroid disease in hospitalized patients, we combined thyrotropin MeSH and 1 of the following: hospitalized or medical or inpatient text words and either sensitivity or specificity text words.
We retrieved articles in which the study population was acutely ill or hospitalized with an NTI and the reference standard included second- or third-generation sTSH assays ie, functional lower limit of 0. We also searched the bibliographies of relevant articles and review articles for additional studies.
Two of us J. We resolved discrepancies by consensus. In abstracting the data, we excluded postpartum patients and those with previously diagnosed thyroid disease, as well as subclinical hypothyroidism or hyperthyroidism.
Subclinical thyroid disease was defined as abnormalities in 1 thyroid index ie, sTSH , while other indices ie, free thyroxine were normal in a patient without overt symptoms of thyroid disease.
Thirty-one articles addressed the inpatient population, 16 of which had the required follow-up after resolution of the NTI, allowing us to calculate the prevalence of unrecognized thyroid disease. We grouped these 16 articles according to whether they studied general medical inpatients, geriatric inpatients, inpatients with atrial fibrillation, or psychiatric inpatients.
Two studies addressing the prevalence of thyroid disease in general medical inpatients met our inclusion criteria Table 1. The first study 11 is the most methodologically sound of all those included in this review. The authors screened general medical inpatients on admission with a sTSH level and found False-positive results were attributed to acute illness and drug interactions, in particular glucocorticoids.
The second study 12 tested female medical inpatients on admission using free thyroxine and found 9. Combining the 2 studies, we found a prevalence of thyroid disease of approximately 1. Six studies addressing the prevalence of unrecognized thyroid disease in the geriatric population met the inclusion criteria Table 2.
Three studies are prospective, 3 , 4 , 13 and 3 are retrospective. Two studies describing the prevalence of thyroid disease in patients with atrial fibrillation met our criteria Table 3. The first, a longitudinal cohort study, 17 included both inpatients and outpatients. The diagnosis of thyroid disease was left to routine follow-up by the physician. The second study 18 documented a much higher rate of hyperthyroidism and did not examine hypothyroidism.
The authors used a shorter follow-up 6 weeks and an older population and relied on TSH response to thyrotropin-releasing hormone. Six studies 19 - 24 addressing the prevalence of thyroid disease in admissions for acute psychiatric illness met our criteria Table 4.
In total, patients were studied, In summary, the overall incidence of thyroid disease among inpatients was between 1. The highest incidence of hyperthyroidism was 0. No studies addressed the question of the usefulness of clinical signs and symptoms of thyroid disease in inpatients. We reviewed several studies that addressed this issue in outpatients, keeping the remaining inclusion criteria fixed. With the relaxed criteria, our MEDLINE search identified titles, 8 of which met our inclusion criteria; 6 of these addressed individual signs and symptoms, and 2 addressed the total number of signs and symptoms in the diagnosis of thyroid disease.
Table 5 presents the 6 studies that provide information on individual signs and symptoms. The first study 25 is the most comprehensive, listing 38 signs and symptoms of thyroid disease in 99 euthyroid, hypothyroid, and hyperthyroid patients from 6 specialty centers in the United States and Australia. We calculated LRs from these data and included clinical features with the highest predictive power.
These LRs are similar to those calculated from results in 2 other studies, 26 , 27 but they are probably inflated due to the fact that the clinicians were not blinded to the thyroid function test results before performing their physical examination.
Other studies found that clinical features were disappointingly poor in predicting thyroid disease. In a retrospective review of charts, Schectman et al 28 found a poor correlation between clinical features and thyroid disease. These investigators depended on the primary care physicians' records of the initial history and physical examination, and it was unclear whether specific signs and symptoms of thyroid disease were sought and not found or were not sought at all; the latter would underestimate test sensitivity.
Two other studies 29 , 30 also gave disappointing results, perhaps because they depended on patients' self-report in the form of a questionnaire. But if you have a history of postpartum thyroiditis, your risk is higher for developing permanent hypothyroidism within 5 to 10 years.
A goiter is an unusually enlarged thyroid gland. It may happen only for a short time and may go away on its own without treatment. Or it could be a symptom of another thyroid disease that requires treatment.
Usually, the only symptom of a goiter is a swelling in your neck. It may be large enough that you can see it or feel the lump with your hand. A very large goiter can also cause a tight feeling in your throat, coughing, or problems swallowing or breathing. Your doctor will do tests to see if it is caused by another thyroid disease. If you do need treatment, medicine should make the thyroid shrink back to near normal size. You may need surgery to take out part or most of the thyroid.
A thyroid nodule NAHD-yool is a swelling in one section of the thyroid gland. The nodule may be solid or filled with fluid or blood. You may have just one thyroid nodule or many. Thyroid nodules are common and affect four times as many women as men.
Most thyroid nodules do not cause symptoms and are not cancerous. Sometimes, nodules grow so big that they cause problems with swallowing or breathing. About one-third of nodules are found by the patient, another third by the doctor, and the other third through an imaging test of the neck.
You can sometimes see or feel a thyroid nodule yourself. Stand in front of a mirror and raise your chin slightly. Look for a bump on either side of your windpipe below your Adam's apple. If the bump moves up and down when you swallow, it may be a thyroid nodule. Ask your doctor to look at it. Most people with thyroid cancer have a thyroid nodule that does not cause any symptoms.
If you do have symptoms, you may have swelling or a lump in your neck. The lump may cause problems swallowing. Some people get a hoarse voice. To tell if the lump or nodule is cancerous, your doctor will order certain tests.
Most thyroid nodules are not cancerous. For more information about thyroid cancer, visit the National Cancer Institute's thyroid cancer page. About three times as many women get thyroid cancer as men. The number of women with thyroid cancer is also going up. By , the number of women with thyroid cancer is expected to double, from 34, women to more than 70, women.
The main treatment for thyroid cancer is surgery to take out the whole thyroid gland or as much of it as can be safely removed. Surgery alone can cure thyroid cancer if the cancer is small and has not yet spread to lymph nodes. Your doctor may also use radioiodine therapy after surgery. Radioiodine therapy destroys any thyroid cancer cells that were not removed during surgery or that have spread to other parts of the body. Your doctor may also talk with you about other treatments for thyroid cancer.
Learn more about thyroid cancer treatments at the National Cancer Institute. It can be hard to tell if you have a thyroid disease. The symptoms are the same as many other health problems. Your doctor may start by asking about your health history and if any of your family members has had thyroid disease.
Your doctor may also give you a physical exam and check your neck for thyroid nodules. High levels of radioiodine mean that your thyroid makes too much of the thyroid hormone.
Low levels mean that your thyroid does not make enough thyroid hormone. Ultrasound may also be helpful in finding thyroid cancer, although by itself it cannot be used to diagnose thyroid cancer. Both hyperthyroidism and hypothyroidism can make it harder for you to get pregnant. This is because problems with the thyroid hormone can upset the balance of the hormones that cause ovulation.
Hypothyroidism can also cause your body to make more prolactin, the hormone that tells your body to make breastmilk.
Too much prolactin can prevent ovulation. Thyroid problems can also affect the menstrual cycle. Your periods may be heavier or irregular, or you may not have any periods at all for several months or longer called amenorrhea. Pregnancy-related hormones raise the level of thyroid hormones in the blood. Thyroid hormones are necessary for the baby's brain development while in the womb. It can be harder to diagnose thyroid problems during pregnancy because of the change in hormone levels that normally happen during pregnancy.
But it is especially important to check for problems before getting pregnant and during pregnancy. Uncontrolled hyperthyroidism and hypothyroidism can cause problems for both mother and baby.
Hyperthyroidism that is not treated with medicine during pregnancy can cause: 4. Hypothyroidism that is not treated with medicine during pregnancy can cause: 4.
For more information about thyroid diseases, call the OWH Helpline at or contact the following organizations:. Department of Health and Human Services. ET closed on federal holidays.
Breadcrumb Home A-Z health topics Thyroid disease. Thyroid disease. Thyroid disease Your thyroid produces thyroid hormone, which controls many activities in your body, including how fast you burn calories and how fast your heart beats. What is the thyroid? How do thyroid problems affect women? Your thyroid helps control your menstrual cycle.
Too much or too little thyroid hormone can make your periods very light, heavy, or irregular. Thyroid disease also can cause your periods to stop for several months or longer, a condition called amenorrhea.
If your body's immune system causes thyroid disease, other glands, including your ovaries, may be involved. This can lead to early menopause before age Problems getting pregnant. When thyroid disease affects the menstrual cycle, it also affects ovulation. This can make it harder for you to get pregnant.
Problems during pregnancy. Thyroid problems during pregnancy can cause health problems for the mother and the baby. Are some women more at risk for thyroid disease? You may want to talk to your doctor about getting tested if you: Had a thyroid problem in the past Had surgery or radiotherapy affecting the thyroid gland Have a condition such as goiter , anemia , or type 1 diabetes Screening for thyroid disease is not recommended for most women.
What kinds of thyroid disease affect women? These thyroid diseases affect more women than men: Disorders that cause hypothyroidism Disorders that cause hyperthyroidism Thyroiditis , especially postpartum thyroiditis goiter Thyroid nodules Thyroid cancer.
0コメント