Jacobson DH , Gorman CA Endocrine ophthalmopathy: current ideas concerning etiology, pathogenesis, and treatment. Endocr Rev 5 : — Acta Endocrinol Copenh : — Vestergaard P Smoking and thyroid disorders—a meta-analysis. Silman AJ Smoking and the risk of rheumatoid arthritis. J Rheumatol 20 : — Calkins BM A meta-analysis of the role of smoking in inflammatory bowel disease. Dig Dis Sci 34 : — The Thyroid Study Group.
N Engl J Med : — Clin Exp Immunol 2 Suppl : — Risch N Linkage strategies for genetically complex traits. The power of affected relative pairs. Am J Hum Genet 46 : — J Clin Endocrinol Metab 87 : — Allahabadia A , Gough SC The different approaches to the genetic analysis of autoimmune thyroid disease. J Endocrinol : 7 — Todd JA Genetic analysis of type 1 diabetes using whole genome approaches. Eur J Hum Genet 13 : — Am J Hum Genet 59 : — European Consortium on Rheumatoid Arthritis Families.
J Rheumatol 28 : — Neurology 62 : — Gut 42 : — Thyroid 13 : — Brix TH , Kyvik KO , Hegedus L Validity of self-reported hyperthyroidism and hypothyroidism: comparison of self-reported questionnaire data with medical record review. Thyroid 11 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Subjects and Methods. Manji , N. Oxford Academic. Franklyn J. Cite Cite N. Select Format Select format. Permissions Icon Permissions. Open in new tab Download slide. TABLE 1. Percentage n.
Median age, yr IQR. Median age at diagnosis is also displayed for each group. Open in new tab. TABLE 2. Hyperthyroidism n. Hypothyroidism n. Affected mother 8. TABLE 3. Affected mother 5. TABLE 4. GD females. GD males. HT females. HT males. No FH Google Scholar Crossref. Search ADS. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey.
Searching for the autoimmune thyroid disease susceptibility genes: from gene mapping to gene function. A population-based study of chronic autoimmune hypothyroidism in Danish twins. Google Scholar PubMed. Further evidence for a strong genetic influence on the development of autoimmune thyroid disease: the California twin study. Age and gender influence the severity of thyroid-associated ophthalmopathy: a study of patients attending a combined thyroid-eye clinic.
Endocrine ophthalmopathy: current ideas concerning etiology, pathogenesis, and treatment. Linkage strategies for genetically complex traits. The different approaches to the genetic analysis of autoimmune thyroid disease.
Genetic anticipation in rheumatoid arthritis in Europe. Anticipation of age at onset in multiple sclerosis: a Sardinian cohort study. Validity of self-reported hyperthyroidism and hypothyroidism: comparison of self-reported questionnaire data with medical record review. Issue Section:. Download all slides. View Metrics. Email alerts Article activity alert. He named it struma lymphomatosa and emphasized infiltration of lymphoid cells and formation of lymphoid follicles with a germinal center.
Neither of these had been reported previously. Hashimoto did thorough research for his monograph and defended his classification with numerous comparisons to existing diseases of the thyroid. It is characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes, and is sometimes associated with non-Hodgkin lymphoma. He received especially limited recognition of his discovery in Japan, because many there could not read German, the language in which he chose to publish.
By the mids this would change. Soon after, Hashimoto began to be mentioned in thyroid surgery textbooks and his name was routinely attached to the disease in America. Healio News Endocrinology Thyroid. Issue: November Read next. November 01, Receive an email when new articles are posted on.
Please provide your email address to receive an email when new articles are posted on. You've successfully added to your alerts. You will receive an email when new content is published. He was, however, aware of one substance which was infallible in treating goiter: iodine. 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.
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