Type 1 (Insulin-Dependent) Diabetic Patient with Remarkable Infiltration of Lymphocytes to the Islets
We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5μg/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was susp...
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| Veröffentlicht in: | Endocrine Journal 1993, Vol.40(6), pp.633-639 |
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| container_title | Endocrine Journal |
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| creator | OHASHI, TSUTOMU MORI, YUTAKA NARIMIYA, MANABU YOKOYAMA, JUNICHI IKEDA, YOSHIO ISOGAI, YUKIHIDE |
| description | We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5μg/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus. |
| doi_str_mv | 10.1507/endocrj.40.633 |
| format | Article |
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Her urinary C-peptide was 3.5μg/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus.</description><identifier>ISSN: 0918-8959</identifier><identifier>EISSN: 1348-4540</identifier><identifier>DOI: 10.1507/endocrj.40.633</identifier><identifier>PMID: 7951531</identifier><language>eng</language><publisher>Tokyo: The Japan Endocrine Society</publisher><subject>Adenoma - complications ; Adenoma - pathology ; Associated diseases and complications ; Autoantibodies - blood ; Biological and medical sciences ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - pathology ; Diabetes. Impaired glucose tolerance ; Diabetic Ketoacidosis - etiology ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Female ; HLA-DR Antigens - analysis ; HLA-DR Serological Subtypes ; Humans ; IDDM ; Immunophenotyping ; Inflammation ; Insulitis ; Islet ; Islets of Langerhans - immunology ; Islets of Langerhans - pathology ; Lymphocyte ; Lymphocyte Subsets - pathology ; Medical sciences ; Middle Aged ; Pancreatic Neoplasms - complications ; Pancreatic Neoplasms - pathology ; Pathology ; Receptors, Interleukin-2 - analysis</subject><ispartof>Endocrine Journal, 1993, Vol.40(6), pp.633-639</ispartof><rights>The Japan Endocrine Society</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-8c73ac703d4a4d35042aee7fc61433d66be5af1bd4ef2558cefa230651dc6d323</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4032364$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7951531$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OHASHI, TSUTOMU</creatorcontrib><creatorcontrib>MORI, YUTAKA</creatorcontrib><creatorcontrib>NARIMIYA, MANABU</creatorcontrib><creatorcontrib>YOKOYAMA, JUNICHI</creatorcontrib><creatorcontrib>IKEDA, YOSHIO</creatorcontrib><creatorcontrib>ISOGAI, YUKIHIDE</creatorcontrib><title>Type 1 (Insulin-Dependent) Diabetic Patient with Remarkable Infiltration of Lymphocytes to the Islets</title><title>Endocrine Journal</title><addtitle>Endocr J</addtitle><description>We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5μg/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus.</description><subject>Adenoma - complications</subject><subject>Adenoma - pathology</subject><subject>Associated diseases and complications</subject><subject>Autoantibodies - blood</subject><subject>Biological and medical sciences</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Ketoacidosis - etiology</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>HLA-DR Antigens - analysis</subject><subject>HLA-DR Serological Subtypes</subject><subject>Humans</subject><subject>IDDM</subject><subject>Immunophenotyping</subject><subject>Inflammation</subject><subject>Insulitis</subject><subject>Islet</subject><subject>Islets of Langerhans - immunology</subject><subject>Islets of Langerhans - pathology</subject><subject>Lymphocyte</subject><subject>Lymphocyte Subsets - pathology</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pancreatic Neoplasms - complications</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pathology</subject><subject>Receptors, Interleukin-2 - analysis</subject><issn>0918-8959</issn><issn>1348-4540</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM1vEzEQxS0EKmnLlRuSDwiVwwY7Y-_HEbVQIkWiqtrzatY7Jg7O7mI7QvnvMWTJxSP5_ebNzGPsrRRLqUX1iYZ-NGG3VGJZArxgCwmqLpRW4iVbiEbWRd3o5jW7jHEnBIBWcMEuqkZLDXLB6Ok4EZf8Zj3Eg3dDcUdTtqQhfeR3DjtKzvAHTC7_8N8ubfkj7TH8xM4TXw_W-RSyOg58tHxz3E_b0RwTRZ5GnrYZiZ5SvGavLPpIb-Z6xZ6_fnm6_VZsvt-vbz9vCqPqJhW1qQBNJaBXqHrQQq2QqLKmlAqgL8uONFrZ9YrsSuvakMUViFLL3pQ9rOCKfTj5TmH8daCY2r2LhrzHgcZDbKsSBFRVk8HlCTRhjDGQbafg8l3HVor2b67tnGurRJtzzQ3vZudDt6f-jM9BZv39rGM06G3Awbh4xpTI25UqY_cnbBcT_qCzjiHn7On_VNk08G_y6ckLnAmzxZAx-AMswJwV</recordid><startdate>1993</startdate><enddate>1993</enddate><creator>OHASHI, TSUTOMU</creator><creator>MORI, YUTAKA</creator><creator>NARIMIYA, MANABU</creator><creator>YOKOYAMA, JUNICHI</creator><creator>IKEDA, YOSHIO</creator><creator>ISOGAI, YUKIHIDE</creator><general>The Japan Endocrine Society</general><general>Japan Endocrine Society</general><scope>IQODW</scope><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>1993</creationdate><title>Type 1 (Insulin-Dependent) Diabetic Patient with Remarkable Infiltration of Lymphocytes to the Islets</title><author>OHASHI, TSUTOMU ; MORI, YUTAKA ; NARIMIYA, MANABU ; YOKOYAMA, JUNICHI ; IKEDA, YOSHIO ; ISOGAI, YUKIHIDE</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-8c73ac703d4a4d35042aee7fc61433d66be5af1bd4ef2558cefa230651dc6d323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adenoma - complications</topic><topic>Adenoma - pathology</topic><topic>Associated diseases and complications</topic><topic>Autoantibodies - blood</topic><topic>Biological and medical sciences</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Ketoacidosis - etiology</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>HLA-DR Antigens - analysis</topic><topic>HLA-DR Serological Subtypes</topic><topic>Humans</topic><topic>IDDM</topic><topic>Immunophenotyping</topic><topic>Inflammation</topic><topic>Insulitis</topic><topic>Islet</topic><topic>Islets of Langerhans - immunology</topic><topic>Islets of Langerhans - pathology</topic><topic>Lymphocyte</topic><topic>Lymphocyte Subsets - pathology</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pancreatic Neoplasms - complications</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pathology</topic><topic>Receptors, Interleukin-2 - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OHASHI, TSUTOMU</creatorcontrib><creatorcontrib>MORI, YUTAKA</creatorcontrib><creatorcontrib>NARIMIYA, MANABU</creatorcontrib><creatorcontrib>YOKOYAMA, JUNICHI</creatorcontrib><creatorcontrib>IKEDA, YOSHIO</creatorcontrib><creatorcontrib>ISOGAI, YUKIHIDE</creatorcontrib><collection>Pascal-Francis</collection><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>Endocrine Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OHASHI, TSUTOMU</au><au>MORI, YUTAKA</au><au>NARIMIYA, MANABU</au><au>YOKOYAMA, JUNICHI</au><au>IKEDA, YOSHIO</au><au>ISOGAI, YUKIHIDE</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type 1 (Insulin-Dependent) Diabetic Patient with Remarkable Infiltration of Lymphocytes to the Islets</atitle><jtitle>Endocrine Journal</jtitle><addtitle>Endocr J</addtitle><date>1993</date><risdate>1993</risdate><volume>40</volume><issue>6</issue><spage>633</spage><epage>639</epage><pages>633-639</pages><issn>0918-8959</issn><eissn>1348-4540</eissn><abstract>We report the case of a 62-year-old woman who was admitted to our hospital with diabetic ketoacidosis. Her urinary C-peptide was 3.5μg/day, HLA typing was DR9, and serum was positive for islet cell antibodies. There was no significant increase in the major viral titer. Pancreatic head tumor was suspected, and pancreaticoduodenectomy was performed. The pathology of this tumor was polycystic adenoma. We examined the surgical specimen from around the tumor histologically. The pancreatic islets had decreased in number. The immunohistochemical staining of islets for insulin, glucagon and somatostatin showed that the number of B cells had decreased remarkably, while A and D cells were preserved Marked lymphocytic infiltration was observed in the islets. The majority of lymphocytes were helper/inducer and suppressor/cytotoxic T cells, which did not express HLA-DR antigen or interleukin-2 receptor. No NK cells were present in the islets. The present case, which was examined histologically in detail, is consistent with the previously proposed hypothesis that autoimmunity might play an important role in the pathogenesis of insulin-dependent diabetes mellitus.</abstract><cop>Tokyo</cop><pub>The Japan Endocrine Society</pub><pmid>7951531</pmid><doi>10.1507/endocrj.40.633</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenoma - complications Adenoma - pathology Associated diseases and complications Autoantibodies - blood Biological and medical sciences Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - pathology Diabetes. Impaired glucose tolerance Diabetic Ketoacidosis - etiology Endocrine pancreas. Apud cells (diseases) Endocrinopathies Female HLA-DR Antigens - analysis HLA-DR Serological Subtypes Humans IDDM Immunophenotyping Inflammation Insulitis Islet Islets of Langerhans - immunology Islets of Langerhans - pathology Lymphocyte Lymphocyte Subsets - pathology Medical sciences Middle Aged Pancreatic Neoplasms - complications Pancreatic Neoplasms - pathology Pathology Receptors, Interleukin-2 - analysis |
| title | Type 1 (Insulin-Dependent) Diabetic Patient with Remarkable Infiltration of Lymphocytes to the Islets |
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