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Carcinoembryonic antigen: Transmission by blood products
The frequency and pattern of CEA development in acute hepatitis and its association with hepatitis transmission by blood products have been investigated. In a series of studies, stored aliquots of blood units were tested for CEA. Recipients of CEA positive units were prospectively followed with reci...
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Published in: | Cancer 1978-09, Vol.42 (S3), p.1568-1573 |
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description | The frequency and pattern of CEA development in acute hepatitis and its association with hepatitis transmission by blood products have been investigated. In a series of studies, stored aliquots of blood units were tested for CEA. Recipients of CEA positive units were prospectively followed with recipients of CEA negative blood units matched for race, age, sex, and transfusion volume. Plasma from patients without malignancies was obtained before and at 2‐week intervals after transfusion for 10 months. In other studies plasma samples obtained at peak SGPT levels from 19 hepatitis B and 29 non‐A non‐B hepatitis patients were tested for CEA. Among 486 hepatitis B surface antigen (HBsAg) negative blood units, 50 had CEA levels over 4.9 ng/ml. Among the 50 recipients of CEA positive blood, 23 developed hepatitis (SGPT > 5 times the upper limit of normal on 2 serial assays 7 days apart) while of the 50 recipients of CEA negative blood, only 8 developed hepatitis (p < .0005). Among all recipients of CEA positive blood who developed hepatitis and who previously lacked CEA, CEA developed before or at the same time as the first SGPT elevation, peaked with the SGPT and gradually fell off after the SGPT had returned to normal. Eight recipients of CEA positive blood became CEA positive and failed to develop hepatitis but carried CEA for the 10 months of follow‐up. Donor or recipient smoking history, transfusion volume and source of blood were factors equally distributed among the study groups. In the other study group, plasma of 5 of 19 (26%) hepatitis B patients and 18 of 29 (62%) non A non B hepatitis patients were CEA positive. In summary: 1) CEA is often an early indicator of developing hepatitis appearing earlier than the SGPT, remaining elevated during hepatitis and not returning to normal until after SGPT has become normal, 2) HBsAg negative, CEA positive blood units often transmit hepatitis or a chronic CEA carrier state (46% of CEA positive blood units transmitted hepatitis and 16% produced a chronic CEA carrier state without concomitant acute or chronic liver disease, cancer or smoking), and 3) Sera of patients with non‐A non‐B hepatitis are frequently CEA positive (62%). |
doi_str_mv | 10.1002/1097-0142(197809)42:3+<1568::AID-CNCR2820420832>3.0.CO;2-P |
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L. ; Molnar, I. G.</creator><creatorcontrib>Gitnick, G. L. ; Molnar, I. G.</creatorcontrib><description>The frequency and pattern of CEA development in acute hepatitis and its association with hepatitis transmission by blood products have been investigated. In a series of studies, stored aliquots of blood units were tested for CEA. Recipients of CEA positive units were prospectively followed with recipients of CEA negative blood units matched for race, age, sex, and transfusion volume. Plasma from patients without malignancies was obtained before and at 2‐week intervals after transfusion for 10 months. In other studies plasma samples obtained at peak SGPT levels from 19 hepatitis B and 29 non‐A non‐B hepatitis patients were tested for CEA. Among 486 hepatitis B surface antigen (HBsAg) negative blood units, 50 had CEA levels over 4.9 ng/ml. Among the 50 recipients of CEA positive blood, 23 developed hepatitis (SGPT > 5 times the upper limit of normal on 2 serial assays 7 days apart) while of the 50 recipients of CEA negative blood, only 8 developed hepatitis (p < .0005). Among all recipients of CEA positive blood who developed hepatitis and who previously lacked CEA, CEA developed before or at the same time as the first SGPT elevation, peaked with the SGPT and gradually fell off after the SGPT had returned to normal. Eight recipients of CEA positive blood became CEA positive and failed to develop hepatitis but carried CEA for the 10 months of follow‐up. Donor or recipient smoking history, transfusion volume and source of blood were factors equally distributed among the study groups. In the other study group, plasma of 5 of 19 (26%) hepatitis B patients and 18 of 29 (62%) non A non B hepatitis patients were CEA positive. In summary: 1) CEA is often an early indicator of developing hepatitis appearing earlier than the SGPT, remaining elevated during hepatitis and not returning to normal until after SGPT has become normal, 2) HBsAg negative, CEA positive blood units often transmit hepatitis or a chronic CEA carrier state (46% of CEA positive blood units transmitted hepatitis and 16% produced a chronic CEA carrier state without concomitant acute or chronic liver disease, cancer or smoking), and 3) Sera of patients with non‐A non‐B hepatitis are frequently CEA positive (62%).</description><identifier>ISSN: 0008-543X</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/1097-0142(197809)42:3+<1568::AID-CNCR2820420832>3.0.CO;2-P</identifier><identifier>PMID: 709526</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Blood - microbiology ; Carcinoembryonic Antigen ; Hepatitis - diagnosis ; Hepatitis - metabolism ; Hepatitis - transmission ; Hepatitis B - metabolism ; Hepatitis B - transmission ; Hepatitis B virus ; Humans ; Prospective Studies ; Transfusion Reaction</subject><ispartof>Cancer, 1978-09, Vol.42 (S3), p.1568-1573</ispartof><rights>Copyright © 1978 American Cancer Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4632-1ba8a27ffb63ae65a3761e194f87d70371bfe83ff7540dcf784f1db5886ec2063</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/709526$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gitnick, G. L.</creatorcontrib><creatorcontrib>Molnar, I. G.</creatorcontrib><title>Carcinoembryonic antigen: Transmission by blood products</title><title>Cancer</title><addtitle>Cancer</addtitle><description>The frequency and pattern of CEA development in acute hepatitis and its association with hepatitis transmission by blood products have been investigated. In a series of studies, stored aliquots of blood units were tested for CEA. Recipients of CEA positive units were prospectively followed with recipients of CEA negative blood units matched for race, age, sex, and transfusion volume. Plasma from patients without malignancies was obtained before and at 2‐week intervals after transfusion for 10 months. In other studies plasma samples obtained at peak SGPT levels from 19 hepatitis B and 29 non‐A non‐B hepatitis patients were tested for CEA. Among 486 hepatitis B surface antigen (HBsAg) negative blood units, 50 had CEA levels over 4.9 ng/ml. Among the 50 recipients of CEA positive blood, 23 developed hepatitis (SGPT > 5 times the upper limit of normal on 2 serial assays 7 days apart) while of the 50 recipients of CEA negative blood, only 8 developed hepatitis (p < .0005). Among all recipients of CEA positive blood who developed hepatitis and who previously lacked CEA, CEA developed before or at the same time as the first SGPT elevation, peaked with the SGPT and gradually fell off after the SGPT had returned to normal. Eight recipients of CEA positive blood became CEA positive and failed to develop hepatitis but carried CEA for the 10 months of follow‐up. Donor or recipient smoking history, transfusion volume and source of blood were factors equally distributed among the study groups. In the other study group, plasma of 5 of 19 (26%) hepatitis B patients and 18 of 29 (62%) non A non B hepatitis patients were CEA positive. In summary: 1) CEA is often an early indicator of developing hepatitis appearing earlier than the SGPT, remaining elevated during hepatitis and not returning to normal until after SGPT has become normal, 2) HBsAg negative, CEA positive blood units often transmit hepatitis or a chronic CEA carrier state (46% of CEA positive blood units transmitted hepatitis and 16% produced a chronic CEA carrier state without concomitant acute or chronic liver disease, cancer or smoking), and 3) Sera of patients with non‐A non‐B hepatitis are frequently CEA positive (62%).</description><subject>Blood - microbiology</subject><subject>Carcinoembryonic Antigen</subject><subject>Hepatitis - diagnosis</subject><subject>Hepatitis - metabolism</subject><subject>Hepatitis - transmission</subject><subject>Hepatitis B - metabolism</subject><subject>Hepatitis B - transmission</subject><subject>Hepatitis B virus</subject><subject>Humans</subject><subject>Prospective Studies</subject><subject>Transfusion Reaction</subject><issn>0008-543X</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1978</creationdate><recordtype>article</recordtype><recordid>eNqNkFtLw0AQhRfxVi__wIc8iSKps5dkN1UEjbdCsSIK4suwSXYlkiaabZH-e7dGBH0Qn2aGM3PO8BFyRqFPAdghhUSGQAXbo4lUkOwLNuAHxzSK1WBwOjwP05v0jikGgoHi7IT3oZ-Oj1h4u0R638fLpAcAKowEf1wnG869-FGyiK-RVQlJxOIeUalu87JuzCRr501d5oGup-WzqQfBfatrNymdK5s6yOZBVjVNEby2TTHLp26LrFhdObP9VTfJw-XFfXodjsZXw_R0FOYi5iykmVaaSWuzmGsTR5rLmBqaCKtkIYFLmlmjuLUyElDkViphaZFFSsUmZxDzTbLb-frgt5lxU_Qv5aaqdG2amUMpmFJcSr_41C3mbeNcayy-tuVEt3OkgAuquACDCzDYUUXfccQFVURPFX9S9RpgOkaGt9585-uLWTYxxbd1h9HLRSe_l5WZ_zP4M_fP2F8K_wD7YZRH</recordid><startdate>197809</startdate><enddate>197809</enddate><creator>Gitnick, G. L.</creator><creator>Molnar, I. G.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><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>197809</creationdate><title>Carcinoembryonic antigen: Transmission by blood products</title><author>Gitnick, G. L. ; Molnar, I. G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4632-1ba8a27ffb63ae65a3761e194f87d70371bfe83ff7540dcf784f1db5886ec2063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1978</creationdate><topic>Blood - microbiology</topic><topic>Carcinoembryonic Antigen</topic><topic>Hepatitis - diagnosis</topic><topic>Hepatitis - metabolism</topic><topic>Hepatitis - transmission</topic><topic>Hepatitis B - metabolism</topic><topic>Hepatitis B - transmission</topic><topic>Hepatitis B virus</topic><topic>Humans</topic><topic>Prospective Studies</topic><topic>Transfusion Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gitnick, G. L.</creatorcontrib><creatorcontrib>Molnar, I. G.</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>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gitnick, G. L.</au><au>Molnar, I. G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Carcinoembryonic antigen: Transmission by blood products</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>1978-09</date><risdate>1978</risdate><volume>42</volume><issue>S3</issue><spage>1568</spage><epage>1573</epage><pages>1568-1573</pages><issn>0008-543X</issn><eissn>1097-0142</eissn><abstract>The frequency and pattern of CEA development in acute hepatitis and its association with hepatitis transmission by blood products have been investigated. In a series of studies, stored aliquots of blood units were tested for CEA. Recipients of CEA positive units were prospectively followed with recipients of CEA negative blood units matched for race, age, sex, and transfusion volume. Plasma from patients without malignancies was obtained before and at 2‐week intervals after transfusion for 10 months. In other studies plasma samples obtained at peak SGPT levels from 19 hepatitis B and 29 non‐A non‐B hepatitis patients were tested for CEA. Among 486 hepatitis B surface antigen (HBsAg) negative blood units, 50 had CEA levels over 4.9 ng/ml. Among the 50 recipients of CEA positive blood, 23 developed hepatitis (SGPT > 5 times the upper limit of normal on 2 serial assays 7 days apart) while of the 50 recipients of CEA negative blood, only 8 developed hepatitis (p < .0005). Among all recipients of CEA positive blood who developed hepatitis and who previously lacked CEA, CEA developed before or at the same time as the first SGPT elevation, peaked with the SGPT and gradually fell off after the SGPT had returned to normal. Eight recipients of CEA positive blood became CEA positive and failed to develop hepatitis but carried CEA for the 10 months of follow‐up. Donor or recipient smoking history, transfusion volume and source of blood were factors equally distributed among the study groups. In the other study group, plasma of 5 of 19 (26%) hepatitis B patients and 18 of 29 (62%) non A non B hepatitis patients were CEA positive. In summary: 1) CEA is often an early indicator of developing hepatitis appearing earlier than the SGPT, remaining elevated during hepatitis and not returning to normal until after SGPT has become normal, 2) HBsAg negative, CEA positive blood units often transmit hepatitis or a chronic CEA carrier state (46% of CEA positive blood units transmitted hepatitis and 16% produced a chronic CEA carrier state without concomitant acute or chronic liver disease, cancer or smoking), and 3) Sera of patients with non‐A non‐B hepatitis are frequently CEA positive (62%).</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>709526</pmid><doi>10.1002/1097-0142(197809)42:3+<1568::AID-CNCR2820420832>3.0.CO;2-P</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Blood - microbiology Carcinoembryonic Antigen Hepatitis - diagnosis Hepatitis - metabolism Hepatitis - transmission Hepatitis B - metabolism Hepatitis B - transmission Hepatitis B virus Humans Prospective Studies Transfusion Reaction |
title | Carcinoembryonic antigen: Transmission by blood products |
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