PATHOPHYSIOLOGY OF THALASSEMIA

The clinical manifestations in homozygous thalassemia may be attributed to the defect in hemoglobin synthesis (Figure 16). It is best typified by beta thalassemia, where excess alpha chains accumulate to form intracytoplasmic erythrocytic inclusions. This leads to anemia, bone marrow hyperplasia, os...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Annals of the New York Academy of Sciences 1980-05, Vol.344 (1), p.284-304
1. Verfasser:	Zaino, Edward C.
Format:	Artikel
Sprache:	eng
Schlagworte:	Bone Marrow - pathology Erythrocyte Aging Erythrocytes - metabolism Erythrocytes - ultrastructure Erythropoiesis Hemoglobins - biosynthesis Hemosiderosis - etiology Hemosiderosis - pathology Humans Hyperplasia Inclusion Bodies - ultrastructure Osteoporosis - etiology Osteoporosis - pathology Peptide Fragments Thalassemia - blood Thalassemia - complications Thalassemia - physiopathology
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

container_end_page	304
container_issue	1
container_start_page	284
container_title	Annals of the New York Academy of Sciences
container_volume	344
creator	Zaino, Edward C.
description	The clinical manifestations in homozygous thalassemia may be attributed to the defect in hemoglobin synthesis (Figure 16). It is best typified by beta thalassemia, where excess alpha chains accumulate to form intracytoplasmic erythrocytic inclusions. This leads to anemia, bone marrow hyperplasia, osteoporosis, hemosiderosis, and organ failure.
doi_str_mv	10.1111/j.1749-6632.1980.tb33669.x
format	Article
fullrecord	<record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_75181594</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>75181594</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3234-75daa28e587d8f8ff8b38d04c9d0a4db67315925354591a9489c74aa40e4ccd23</originalsourceid><addsrcrecordid>eNqVkM1OwkAURidGg4g-gsa4cNc6v50ZN6YhQDFAMcUQVpNpO03AItiBCG_vkDbsvZu7-L57bnIAeELQR25eVj7iVHpBQLCPpID-LiUkCKR_uADtc3QJ2hBy7gmJyTW4sXYFIcKC8hZoBZhKxFEbPEzDWRRPo0UyjEfxYPEY9x9nUTgKk6Q3Hoa34KrQpTV3ze6Az35v1o081x12w5GXEUyox1muNRaGCZ6LQhSFSInIIc1kDjXN04ATxCRmhFEmkZZUyIxTrSk0NMtyTDrgueZuq83P3tidWi9tZspSf5vN3irOkHAE6oqvdTGrNtZWplDbarnW1VEhqE5y1EqdDKiTAXWSoxo56uCO75sv-3Rt8vNpY8Plb3X-uyzN8R9kNVmEiVPrCF5NWNqdOZwJuvpSzgFnaj4ZKPzB3sdwPlVj8gfx2H9C</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>75181594</pqid></control><display><type>article</type><title>PATHOPHYSIOLOGY OF THALASSEMIA</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Zaino, Edward C.</creator><creatorcontrib>Zaino, Edward C.</creatorcontrib><description>The clinical manifestations in homozygous thalassemia may be attributed to the defect in hemoglobin synthesis (Figure 16). It is best typified by beta thalassemia, where excess alpha chains accumulate to form intracytoplasmic erythrocytic inclusions. This leads to anemia, bone marrow hyperplasia, osteoporosis, hemosiderosis, and organ failure.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/j.1749-6632.1980.tb33669.x</identifier><identifier>PMID: 6249171</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Bone Marrow - pathology ; Erythrocyte Aging ; Erythrocytes - metabolism ; Erythrocytes - ultrastructure ; Erythropoiesis ; Hemoglobins - biosynthesis ; Hemosiderosis - etiology ; Hemosiderosis - pathology ; Humans ; Hyperplasia ; Inclusion Bodies - ultrastructure ; Osteoporosis - etiology ; Osteoporosis - pathology ; Peptide Fragments ; Thalassemia - blood ; Thalassemia - complications ; Thalassemia - physiopathology</subject><ispartof>Annals of the New York Academy of Sciences, 1980-05, Vol.344 (1), p.284-304</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3234-75daa28e587d8f8ff8b38d04c9d0a4db67315925354591a9489c74aa40e4ccd23</citedby><cites>FETCH-LOGICAL-c3234-75daa28e587d8f8ff8b38d04c9d0a4db67315925354591a9489c74aa40e4ccd23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1749-6632.1980.tb33669.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1749-6632.1980.tb33669.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6249171$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zaino, Edward C.</creatorcontrib><title>PATHOPHYSIOLOGY OF THALASSEMIA</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>The clinical manifestations in homozygous thalassemia may be attributed to the defect in hemoglobin synthesis (Figure 16). It is best typified by beta thalassemia, where excess alpha chains accumulate to form intracytoplasmic erythrocytic inclusions. This leads to anemia, bone marrow hyperplasia, osteoporosis, hemosiderosis, and organ failure.</description><subject>Bone Marrow - pathology</subject><subject>Erythrocyte Aging</subject><subject>Erythrocytes - metabolism</subject><subject>Erythrocytes - ultrastructure</subject><subject>Erythropoiesis</subject><subject>Hemoglobins - biosynthesis</subject><subject>Hemosiderosis - etiology</subject><subject>Hemosiderosis - pathology</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Inclusion Bodies - ultrastructure</subject><subject>Osteoporosis - etiology</subject><subject>Osteoporosis - pathology</subject><subject>Peptide Fragments</subject><subject>Thalassemia - blood</subject><subject>Thalassemia - complications</subject><subject>Thalassemia - physiopathology</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1980</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkM1OwkAURidGg4g-gsa4cNc6v50ZN6YhQDFAMcUQVpNpO03AItiBCG_vkDbsvZu7-L57bnIAeELQR25eVj7iVHpBQLCPpID-LiUkCKR_uADtc3QJ2hBy7gmJyTW4sXYFIcKC8hZoBZhKxFEbPEzDWRRPo0UyjEfxYPEY9x9nUTgKk6Q3Hoa34KrQpTV3ze6Az35v1o081x12w5GXEUyox1muNRaGCZ6LQhSFSInIIc1kDjXN04ATxCRmhFEmkZZUyIxTrSk0NMtyTDrgueZuq83P3tidWi9tZspSf5vN3irOkHAE6oqvdTGrNtZWplDbarnW1VEhqE5y1EqdDKiTAXWSoxo56uCO75sv-3Rt8vNpY8Plb3X-uyzN8R9kNVmEiVPrCF5NWNqdOZwJuvpSzgFnaj4ZKPzB3sdwPlVj8gfx2H9C</recordid><startdate>198005</startdate><enddate>198005</enddate><creator>Zaino, Edward C.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>198005</creationdate><title>PATHOPHYSIOLOGY OF THALASSEMIA</title><author>Zaino, Edward C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3234-75daa28e587d8f8ff8b38d04c9d0a4db67315925354591a9489c74aa40e4ccd23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1980</creationdate><topic>Bone Marrow - pathology</topic><topic>Erythrocyte Aging</topic><topic>Erythrocytes - metabolism</topic><topic>Erythrocytes - ultrastructure</topic><topic>Erythropoiesis</topic><topic>Hemoglobins - biosynthesis</topic><topic>Hemosiderosis - etiology</topic><topic>Hemosiderosis - pathology</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Inclusion Bodies - ultrastructure</topic><topic>Osteoporosis - etiology</topic><topic>Osteoporosis - pathology</topic><topic>Peptide Fragments</topic><topic>Thalassemia - blood</topic><topic>Thalassemia - complications</topic><topic>Thalassemia - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zaino, Edward C.</creatorcontrib><collection>Istex</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>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zaino, Edward C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PATHOPHYSIOLOGY OF THALASSEMIA</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>1980-05</date><risdate>1980</risdate><volume>344</volume><issue>1</issue><spage>284</spage><epage>304</epage><pages>284-304</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>The clinical manifestations in homozygous thalassemia may be attributed to the defect in hemoglobin synthesis (Figure 16). It is best typified by beta thalassemia, where excess alpha chains accumulate to form intracytoplasmic erythrocytic inclusions. This leads to anemia, bone marrow hyperplasia, osteoporosis, hemosiderosis, and organ failure.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>6249171</pmid><doi>10.1111/j.1749-6632.1980.tb33669.x</doi><tpages>21</tpages></addata></record>
fulltext	fulltext
identifier	ISSN: 0077-8923
ispartof	Annals of the New York Academy of Sciences, 1980-05, Vol.344 (1), p.284-304
issn	0077-8923 1749-6632
language	eng
recordid	cdi_proquest_miscellaneous_75181594
source	MEDLINE; Access via Wiley Online Library
subjects	Bone Marrow - pathology Erythrocyte Aging Erythrocytes - metabolism Erythrocytes - ultrastructure Erythropoiesis Hemoglobins - biosynthesis Hemosiderosis - etiology Hemosiderosis - pathology Humans Hyperplasia Inclusion Bodies - ultrastructure Osteoporosis - etiology Osteoporosis - pathology Peptide Fragments Thalassemia - blood Thalassemia - complications Thalassemia - physiopathology
title	PATHOPHYSIOLOGY OF THALASSEMIA
url	https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T21%3A18%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=PATHOPHYSIOLOGY%20OF%20THALASSEMIA&rft.jtitle=Annals%20of%20the%20New%20York%20Academy%20of%20Sciences&rft.au=Zaino,%20Edward%20C.&rft.date=1980-05&rft.volume=344&rft.issue=1&rft.spage=284&rft.epage=304&rft.pages=284-304&rft.issn=0077-8923&rft.eissn=1749-6632&rft_id=info:doi/10.1111/j.1749-6632.1980.tb33669.x&rft_dat=%3Cproquest_cross%3E75181594%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=75181594&rft_id=info:pmid/6249171&rfr_iscdi=true