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      Hypothyroidism and Thyroid Substitution: Historical Aspects

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      Journal of Thyroid Research

      SAGE-Hindawi Access to Research

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          Abstract

          The last part of the 19th century was a period of great achievements in medicine and endocrinology. The thyroid gland evolved from being considered a rudimentary structure to an organ related to specific diseases. The singular importance of iodine became acknowledged. Graves-Basedow's disease was described. Surgical treatment evolved with extraordinary speed. Theodor Kocher observed that the clinical picture in patients after total thyroidectomy was similar to the one seen in cretinism. In 1850, the first case of hypothyroidism or myxedema was described. Less than 50 years later, effective treatment was introduced. Another 50 years later, autoimmune thyroiditis was ascertained as the most frequent cause of hypothyroidism (in areas with no iodine deficiency). This paper gives a short survey of the history of hypothyroidism and its treatment.

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          Most cited references 108

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          Hypothyroidism.

          Hypothyroidism is common, potentially serious, often clinically overlooked, readily diagnosed by laboratory testing, and eminently treatable. The condition is particularly prevalent in older women, in whom autoimmune thyroiditis is common. Other important causes include congenital thyroid disorders, previous thyroid surgery and irradiation, drugs such as lithium carbonate and amiodarone, and pituitary and hypothalamic disorders. Worldwide, dietary iodine deficiency remains an important cause. Hypothyroidism can present with nonspecific constitutional and neuropsychiatric complaints, or with hypercholesterolaemia, hyponatraemia, hyperprolactinaemia, or hyperhomocysteinaemia. Severe untreated hypothyroidism can lead to heart failure, psychosis, and coma. Although these manifestations are neither specific nor sensitive, the diagnosis is confirmed or excluded by measurements of serum thyrotropin and free thyroxine. Thyroxine replacement therapy is highly effective and safe, but suboptimal dosing is common in clinical practice. Patient noncompliance, drug interactions, and pregnancy can lead to inadequate treatment. Iatrogenic thyrotoxicosis can cause symptoms, and, even when mild, provoke atrial fibrillation and osteoporosis. We summarise present understanding of the history, epidemiology, pathophysiology, and clinical diagnosis and management of hypothyroidism.
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            The mechanism of pancreatic secretion.

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              Congenital hypothyroidism: etiologies, diagnosis, and management.

               S LaFranchi (1999)
              Congenital hypothyroidism is a common preventable cause of mental retardation. The overall incidence is approximately 1:4000; females are affected about twice as often as males. Approximately 85% of cases are sporadic, while 15% are hereditary. The most common sporadic etiology is thyroid dysgenesis, with ectopic glands more common than aplasia or hypoplasia. While the pathogenesis of dysgenesis is largely unknown, some cases are now discovered to be the result of mutations in the transcription factors PAX-8 and TTF-2. Loss of function mutations in the thyrotropin (TSH) receptor have been demonstrated to cause some familial forms of athyreosis. The most common hereditary etiology is the inborn errors of thyroxine (T4) synthesis. Recent mutations have been described in the genes coding for the sodium/iodide symporter, thyroid peroxidase (TPO), and thyroglobulin. Transplacental passage of a maternal thyrotropin receptor blocking antibody (TRB-Ab) causes a transient form of familial congenital hypothyroidism. The vast majority of infants are now diagnosed after detection through newborn screening programs using a primary T4-backup TSH or primary TSH test. Screening test results must be confirmed by serum thyroid function tests. Thyroid scintigraphy, using 99mTc or 123I, is the most accurate diagnostic test to detect thyroid dysgenesis or one of the inborn errors of T4 synthesis. Thyroid sonography is nearly as accurate, but it may miss some cases of ectopic glands. If maternal antibody-mediated hypothyroidism is suspected, measurement of maternal and/or neonatal TRB-Ab will confirm the diagnosis. The goals of treatment are to raise the serum T4 as rapidly as possible into the normal range, adjust the levothyroxine dose with growth to keep the serum T4 (or free T4) in the upper half of the normal range and the TSH normal, and maintain normal growth and development while avoiding overtreatment. An initial starting dose of 10-15 microg/kg per day is recommended; this dose will decrease on a weight basis over time. Serum T4 (or free T4) and TSH should be monitored every 1-2 months in the first year of life and every 2-3 months in the second and third years.
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                Author and article information

                Journal
                J Thyroid Res
                JTR
                Journal of Thyroid Research
                SAGE-Hindawi Access to Research
                2042-0072
                2011
                8 June 2011
                : 2011
                Affiliations
                Department of Endocrinology, Aarhus University Hospital, 9000 Aalborg, Denmark
                Author notes

                Academic Editor: Marian Ludgate

                Article
                10.4061/2011/809341
                3134382
                21760981
                Copyright © 2011 J. Lindholm and P. Laurberg.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Review Article

                Endocrinology & Diabetes

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