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Comparison of atrophic and goitrous auto-immune thyroiditis in children: clinical, laboratory and TSH-receptor antibody studies
We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of pat...
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Published in: | European journal of pediatrics 1990-05, Vol.149 (8), p.529-533 |
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container_title | European journal of pediatrics |
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creator | Matsuura, N Konishi, J Yuri, K Harada, S Fujieda, K Nohara, Y Mikami, Y Kasagi, K Iida, Y Hosoda, A |
description | We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24 h 123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated. |
doi_str_mv | 10.1007/bf01957685 |
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The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24 h 123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated.</description><identifier>ISSN: 0340-6199</identifier><identifier>EISSN: 1432-1076</identifier><identifier>DOI: 10.1007/bf01957685</identifier><identifier>PMID: 2347350</identifier><language>eng</language><publisher>Germany</publisher><subject>Adult ; Age Factors ; Antibodies - analysis ; Atrophy ; Autoimmune Diseases - blood ; Autoimmune Diseases - complications ; Body Weight ; Carrier Proteins - blood ; Child ; Drug Evaluation ; Female ; Follow-Up Studies ; Goiter - blood ; Goiter - complications ; Humans ; Male ; Membrane Proteins - blood ; Receptors, Thyrotropin - immunology ; Sex Factors ; Thyroglobulin - immunology ; Thyroid Function Tests ; Thyroid Hormone-Binding Proteins ; Thyroid Hormones ; Thyroiditis - blood ; Thyroiditis - complications ; Thyroiditis - drug therapy ; Thyroiditis - etiology ; Thyroiditis - immunology ; Thyroiditis - pathology ; Thyroxine - therapeutic use</subject><ispartof>European journal of pediatrics, 1990-05, Vol.149 (8), p.529-533</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c263t-b9b029e8a29fd89ca86440157b30a5a2f001de8bb9438854261341a379a95b533</citedby><cites>FETCH-LOGICAL-c263t-b9b029e8a29fd89ca86440157b30a5a2f001de8bb9438854261341a379a95b533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2347350$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsuura, N</creatorcontrib><creatorcontrib>Konishi, J</creatorcontrib><creatorcontrib>Yuri, K</creatorcontrib><creatorcontrib>Harada, S</creatorcontrib><creatorcontrib>Fujieda, K</creatorcontrib><creatorcontrib>Nohara, Y</creatorcontrib><creatorcontrib>Mikami, Y</creatorcontrib><creatorcontrib>Kasagi, K</creatorcontrib><creatorcontrib>Iida, Y</creatorcontrib><creatorcontrib>Hosoda, A</creatorcontrib><title>Comparison of atrophic and goitrous auto-immune thyroiditis in children: clinical, laboratory and TSH-receptor antibody studies</title><title>European journal of pediatrics</title><addtitle>Eur J Pediatr</addtitle><description>We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24 h 123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated.</description><subject>Adult</subject><subject>Age Factors</subject><subject>Antibodies - analysis</subject><subject>Atrophy</subject><subject>Autoimmune Diseases - blood</subject><subject>Autoimmune Diseases - complications</subject><subject>Body Weight</subject><subject>Carrier Proteins - blood</subject><subject>Child</subject><subject>Drug Evaluation</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Goiter - blood</subject><subject>Goiter - complications</subject><subject>Humans</subject><subject>Male</subject><subject>Membrane Proteins - blood</subject><subject>Receptors, Thyrotropin - immunology</subject><subject>Sex Factors</subject><subject>Thyroglobulin - immunology</subject><subject>Thyroid Function Tests</subject><subject>Thyroid Hormone-Binding Proteins</subject><subject>Thyroid Hormones</subject><subject>Thyroiditis - blood</subject><subject>Thyroiditis - complications</subject><subject>Thyroiditis - drug therapy</subject><subject>Thyroiditis - etiology</subject><subject>Thyroiditis - immunology</subject><subject>Thyroiditis - pathology</subject><subject>Thyroxine - therapeutic use</subject><issn>0340-6199</issn><issn>1432-1076</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><recordid>eNo9kD1PwzAURS0EKqWwsCN5YkAE7NhxbDaoKEWqxECZI3-FGiVxsJ2hE3-dQAvT0706OtK7AJxjdIMRKm9VjbAoSsaLAzDFlOQZRiU7BFNEKMoYFuIYnMT4gUZYYD4Bk5zQkhRoCr7mvu1lcNF30NdQpuD7jdNQdga-ezfGIUI5JJ-5th06C9NmG7wzLrkIXQf1xjUm2O4O6sZ1TsvmGjZS-SCTD9tfzfp1mQWrbT82Y5Gc8mYLYxqMs_EUHNWyifZsf2fgbfG4ni-z1cvT8_x-lemckZQpoVAuLJe5qA0XWnJGKcJFqQiShcxrhLCxXClBCecFzRkmFEtSCikKVRAyA5c7bx_852BjqloXtW0a2dnxxaoUfFQwNoJXO1AHH2OwddUH18qwrTCqftauHhZ_a4_wxd46qNaaf3Q_L_kG0h97YQ</recordid><startdate>199005</startdate><enddate>199005</enddate><creator>Matsuura, N</creator><creator>Konishi, J</creator><creator>Yuri, K</creator><creator>Harada, S</creator><creator>Fujieda, K</creator><creator>Nohara, Y</creator><creator>Mikami, Y</creator><creator>Kasagi, K</creator><creator>Iida, Y</creator><creator>Hosoda, A</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199005</creationdate><title>Comparison of atrophic and goitrous auto-immune thyroiditis in children: clinical, laboratory and TSH-receptor antibody studies</title><author>Matsuura, N ; Konishi, J ; Yuri, K ; Harada, S ; Fujieda, K ; Nohara, Y ; Mikami, Y ; Kasagi, K ; Iida, Y ; Hosoda, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c263t-b9b029e8a29fd89ca86440157b30a5a2f001de8bb9438854261341a379a95b533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Adult</topic><topic>Age Factors</topic><topic>Antibodies - analysis</topic><topic>Atrophy</topic><topic>Autoimmune Diseases - blood</topic><topic>Autoimmune Diseases - complications</topic><topic>Body Weight</topic><topic>Carrier Proteins - blood</topic><topic>Child</topic><topic>Drug Evaluation</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Goiter - blood</topic><topic>Goiter - complications</topic><topic>Humans</topic><topic>Male</topic><topic>Membrane Proteins - blood</topic><topic>Receptors, Thyrotropin - immunology</topic><topic>Sex Factors</topic><topic>Thyroglobulin - immunology</topic><topic>Thyroid Function Tests</topic><topic>Thyroid Hormone-Binding Proteins</topic><topic>Thyroid Hormones</topic><topic>Thyroiditis - blood</topic><topic>Thyroiditis - complications</topic><topic>Thyroiditis - drug therapy</topic><topic>Thyroiditis - etiology</topic><topic>Thyroiditis - immunology</topic><topic>Thyroiditis - pathology</topic><topic>Thyroxine - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsuura, N</creatorcontrib><creatorcontrib>Konishi, J</creatorcontrib><creatorcontrib>Yuri, K</creatorcontrib><creatorcontrib>Harada, S</creatorcontrib><creatorcontrib>Fujieda, K</creatorcontrib><creatorcontrib>Nohara, Y</creatorcontrib><creatorcontrib>Mikami, Y</creatorcontrib><creatorcontrib>Kasagi, K</creatorcontrib><creatorcontrib>Iida, Y</creatorcontrib><creatorcontrib>Hosoda, A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pediatrics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsuura, N</au><au>Konishi, J</au><au>Yuri, K</au><au>Harada, S</au><au>Fujieda, K</au><au>Nohara, Y</au><au>Mikami, Y</au><au>Kasagi, K</au><au>Iida, Y</au><au>Hosoda, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of atrophic and goitrous auto-immune thyroiditis in children: clinical, laboratory and TSH-receptor antibody studies</atitle><jtitle>European journal of pediatrics</jtitle><addtitle>Eur J Pediatr</addtitle><date>1990-05</date><risdate>1990</risdate><volume>149</volume><issue>8</issue><spage>529</spage><epage>533</epage><pages>529-533</pages><issn>0340-6199</issn><eissn>1432-1076</eissn><abstract>We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24 h 123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated.</abstract><cop>Germany</cop><pmid>2347350</pmid><doi>10.1007/bf01957685</doi><tpages>5</tpages></addata></record> |
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ispartof | European journal of pediatrics, 1990-05, Vol.149 (8), p.529-533 |
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subjects | Adult Age Factors Antibodies - analysis Atrophy Autoimmune Diseases - blood Autoimmune Diseases - complications Body Weight Carrier Proteins - blood Child Drug Evaluation Female Follow-Up Studies Goiter - blood Goiter - complications Humans Male Membrane Proteins - blood Receptors, Thyrotropin - immunology Sex Factors Thyroglobulin - immunology Thyroid Function Tests Thyroid Hormone-Binding Proteins Thyroid Hormones Thyroiditis - blood Thyroiditis - complications Thyroiditis - drug therapy Thyroiditis - etiology Thyroiditis - immunology Thyroiditis - pathology Thyroxine - therapeutic use |
title | Comparison of atrophic and goitrous auto-immune thyroiditis in children: clinical, laboratory and TSH-receptor antibody studies |
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