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Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study
Identifying people at higher risk of developing tuberculosis with human immunodeficiency virus (HIV) infection may improve clinical management of co-infections. Iron influences tuberculosis (TB) pathogenesis, but understanding the exact mechanisms of how and timing of when iron is involved remains c...
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Published in: | BMC infectious diseases 2013-01, Vol.13 (1), p.48-48, Article 48 |
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description | Identifying people at higher risk of developing tuberculosis with human immunodeficiency virus (HIV) infection may improve clinical management of co-infections. Iron influences tuberculosis (TB) pathogenesis, but understanding the exact mechanisms of how and timing of when iron is involved remains challenging since biological samples are rarely available from the disease susceptibility period due to the difficulty in predicting in who and when, if ever, TB will develop. The objective of this research was to determine how host iron status measured at HIV diagnosis and genotypes related to host iron metabolism were associated with incident TB.
Archived clinical data, plasma and DNA were analyzed from 1139 adult participants in a large HIV-1, HIV-2 and dual seroprevalent cohort based at the Medical Research Council Laboratories in The Gambia. Incident pulmonary and/or extrapulmonary TB diagnoses a minimum of 28 days after HIV diagnosis were independently re-confirmed using available evidence (n=152). Multiple host iron status biomarkers, Haptoglobin and solute carrier family 11, member 1 (SLC11A1) genotypes were modeled to characterize how indicators of host iron metabolism were associated with TB susceptibility.
Hemoglobin (incidence rate ratio, IRR=0.88, 95% CI=0.79-0.98), plasma transferrin (IRR=0.53, 0.33-0.84) and ferritin (IRR=1.26, 1.05-1.51) were significantly associated with TB after adjusting for TB susceptibility factors. While genotype associations were not statistically significant, SLC11A1 associations replicated similar directions as reported in HIV-seronegative meta-analyses.
Evidence of host iron redistribution at HIV diagnosis was associated with incident TB, and genetic influences on iron homeostasis may be involved. Low hemoglobin was associated with subsequent diagnosis of TB, but when considered in combination with additional iron status biomarkers, the collective findings point to a mechanism whereby anemia and iron redistribution are likely due to viral and/or bacteria-driven processes and the host immune response to infection. As a result, iron supplementation may not be efficacious or safe under these circumstances. Clinical and nutritional management of HIV and Mycobacterium tuberculosis co-infected individuals, especially in regions where food insecurity and malnutrition co-exist, may be further improved when the iron-related TB risk factors identified here are better understood and managed to favor host rather than pathogen outcom |
doi_str_mv | 10.1186/1471-2334-13-48 |
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Archived clinical data, plasma and DNA were analyzed from 1139 adult participants in a large HIV-1, HIV-2 and dual seroprevalent cohort based at the Medical Research Council Laboratories in The Gambia. Incident pulmonary and/or extrapulmonary TB diagnoses a minimum of 28 days after HIV diagnosis were independently re-confirmed using available evidence (n=152). Multiple host iron status biomarkers, Haptoglobin and solute carrier family 11, member 1 (SLC11A1) genotypes were modeled to characterize how indicators of host iron metabolism were associated with TB susceptibility.
Hemoglobin (incidence rate ratio, IRR=0.88, 95% CI=0.79-0.98), plasma transferrin (IRR=0.53, 0.33-0.84) and ferritin (IRR=1.26, 1.05-1.51) were significantly associated with TB after adjusting for TB susceptibility factors. While genotype associations were not statistically significant, SLC11A1 associations replicated similar directions as reported in HIV-seronegative meta-analyses.
Evidence of host iron redistribution at HIV diagnosis was associated with incident TB, and genetic influences on iron homeostasis may be involved. Low hemoglobin was associated with subsequent diagnosis of TB, but when considered in combination with additional iron status biomarkers, the collective findings point to a mechanism whereby anemia and iron redistribution are likely due to viral and/or bacteria-driven processes and the host immune response to infection. As a result, iron supplementation may not be efficacious or safe under these circumstances. Clinical and nutritional management of HIV and Mycobacterium tuberculosis co-infected individuals, especially in regions where food insecurity and malnutrition co-exist, may be further improved when the iron-related TB risk factors identified here are better understood and managed to favor host rather than pathogen outcomes.</description><identifier>ISSN: 1471-2334</identifier><identifier>EISSN: 1471-2334</identifier><identifier>DOI: 10.1186/1471-2334-13-48</identifier><identifier>PMID: 23360117</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adult ; Alleles ; Analysis ; Biomarkers ; CD4 Lymphocyte Count ; Coinfection ; Development and progression ; Disease susceptibility ; Evidence-based medicine ; Female ; Ferritin ; Genetic aspects ; Genetic Predisposition to Disease ; Genotype ; Haptoglobin ; Health aspects ; Hemoglobin ; HIV ; HIV (Viruses) ; HIV infection ; HIV Infections - complications ; HIV Infections - genetics ; HIV Infections - metabolism ; Human immunodeficiency virus ; Human immunodeficiency virus 1 ; Human immunodeficiency virus 2 ; Humans ; Iron ; Iron - metabolism ; Iron deficiency anemia ; Iron in the body ; Male ; Measurement ; Medical research ; Medicine, Experimental ; Middle Aged ; Mycobacterium ; Mycobacterium tuberculosis ; Physiological aspects ; Retrospective Studies ; Risk Factors ; Tuberculosis ; Tuberculosis - diagnosis ; Tuberculosis - etiology ; Young Adult</subject><ispartof>BMC infectious diseases, 2013-01, Vol.13 (1), p.48-48, Article 48</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 McDermid et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright ©2013 McDermid et al.; licensee BioMed Central Ltd. 2013 McDermid et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c655t-35a6e40350eff47cee76e3ba9cdb7d1ec952b126fd972087cc82b51e3ab38e7c3</citedby><cites>FETCH-LOGICAL-c655t-35a6e40350eff47cee76e3ba9cdb7d1ec952b126fd972087cc82b51e3ab38e7c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3568026/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1285184643?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23360117$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McDermid, Joann M</creatorcontrib><creatorcontrib>Hennig, Branwen J</creatorcontrib><creatorcontrib>van der Sande, Marianne</creatorcontrib><creatorcontrib>Hill, Adrian V S</creatorcontrib><creatorcontrib>Whittle, Hilton C</creatorcontrib><creatorcontrib>Jaye, Assan</creatorcontrib><creatorcontrib>Prentice, Andrew M</creatorcontrib><title>Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study</title><title>BMC infectious diseases</title><addtitle>BMC Infect Dis</addtitle><description>Identifying people at higher risk of developing tuberculosis with human immunodeficiency virus (HIV) infection may improve clinical management of co-infections. Iron influences tuberculosis (TB) pathogenesis, but understanding the exact mechanisms of how and timing of when iron is involved remains challenging since biological samples are rarely available from the disease susceptibility period due to the difficulty in predicting in who and when, if ever, TB will develop. The objective of this research was to determine how host iron status measured at HIV diagnosis and genotypes related to host iron metabolism were associated with incident TB.
Archived clinical data, plasma and DNA were analyzed from 1139 adult participants in a large HIV-1, HIV-2 and dual seroprevalent cohort based at the Medical Research Council Laboratories in The Gambia. Incident pulmonary and/or extrapulmonary TB diagnoses a minimum of 28 days after HIV diagnosis were independently re-confirmed using available evidence (n=152). Multiple host iron status biomarkers, Haptoglobin and solute carrier family 11, member 1 (SLC11A1) genotypes were modeled to characterize how indicators of host iron metabolism were associated with TB susceptibility.
Hemoglobin (incidence rate ratio, IRR=0.88, 95% CI=0.79-0.98), plasma transferrin (IRR=0.53, 0.33-0.84) and ferritin (IRR=1.26, 1.05-1.51) were significantly associated with TB after adjusting for TB susceptibility factors. While genotype associations were not statistically significant, SLC11A1 associations replicated similar directions as reported in HIV-seronegative meta-analyses.
Evidence of host iron redistribution at HIV diagnosis was associated with incident TB, and genetic influences on iron homeostasis may be involved. Low hemoglobin was associated with subsequent diagnosis of TB, but when considered in combination with additional iron status biomarkers, the collective findings point to a mechanism whereby anemia and iron redistribution are likely due to viral and/or bacteria-driven processes and the host immune response to infection. As a result, iron supplementation may not be efficacious or safe under these circumstances. Clinical and nutritional management of HIV and Mycobacterium tuberculosis co-infected individuals, especially in regions where food insecurity and malnutrition co-exist, may be further improved when the iron-related TB risk factors identified here are better understood and managed to favor host rather than pathogen outcomes.</description><subject>Adult</subject><subject>Alleles</subject><subject>Analysis</subject><subject>Biomarkers</subject><subject>CD4 Lymphocyte Count</subject><subject>Coinfection</subject><subject>Development and progression</subject><subject>Disease susceptibility</subject><subject>Evidence-based medicine</subject><subject>Female</subject><subject>Ferritin</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Haptoglobin</subject><subject>Health aspects</subject><subject>Hemoglobin</subject><subject>HIV</subject><subject>HIV (Viruses)</subject><subject>HIV infection</subject><subject>HIV Infections - complications</subject><subject>HIV Infections - genetics</subject><subject>HIV Infections - metabolism</subject><subject>Human immunodeficiency virus</subject><subject>Human immunodeficiency virus 1</subject><subject>Human immunodeficiency virus 2</subject><subject>Humans</subject><subject>Iron</subject><subject>Iron - metabolism</subject><subject>Iron deficiency anemia</subject><subject>Iron in the body</subject><subject>Male</subject><subject>Measurement</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Middle Aged</subject><subject>Mycobacterium</subject><subject>Mycobacterium tuberculosis</subject><subject>Physiological aspects</subject><subject>Retrospective Studies</subject><subject>Risk Factors</subject><subject>Tuberculosis</subject><subject>Tuberculosis - diagnosis</subject><subject>Tuberculosis - etiology</subject><subject>Young Adult</subject><issn>1471-2334</issn><issn>1471-2334</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNkt2L1DAUxYso7rr67JsEfNGH7jZJ81EfhGVRZ2BhwY99DWl6M5ux04xJujj4z5s667AVQSkl6cnvHtJ7T1E8x9UpxpKf4VrgklBal5iWtXxQHB-Uh_f2R8WTGNdVhYUkzePiKGu8wlgcFz8WPibkgh9QgM7FFFw7Jpc_dUQaBRe_IqtN8gHZ_LrBuA6GhNLYQjBj76OLWUWL5XVeLJip9g3SA8K43IEO2TYFH7fTyS0g4298SCimsds9LR5Z3Ud4dreeFF_ev_t8sSgvrz4sL84vS8MZSyVlmkNdUVaBtbUwAIIDbXVjulZ0GEzDSIsJt10jSCWFMZK0DAPVLZUgDD0plnvfzuu12ga30WGnvHbql-DDSumQnOlBNUI30oquAsJrYoUUjDSMkgY3WlNrs9fbvdd2bDfQmdyLoPuZ6fxkcDdq5W8VZVxWhGeDV3cGwX8bISa1cdFA3-sB_BgVpphxXOeh_Rslkjc1lxxn9OUf6NqPYchdnSiGZc2z5YFa6fyveVw-X9FMpuqc0ZpXOR7TDU__QuWng40zfgDrsj4reD0ryEyC72mlxxjV8tPH_2evrufs2Z41OUAxgD20GVdqir-aAq6mgOe2qVrmihf3p3Pgf-ed_gQ3yf08</recordid><startdate>20130129</startdate><enddate>20130129</enddate><creator>McDermid, Joann M</creator><creator>Hennig, Branwen J</creator><creator>van der Sande, Marianne</creator><creator>Hill, Adrian V S</creator><creator>Whittle, Hilton C</creator><creator>Jaye, Assan</creator><creator>Prentice, Andrew M</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7T2</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7U1</scope><scope>7U2</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130129</creationdate><title>Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study</title><author>McDermid, Joann M ; Hennig, Branwen J ; van der Sande, Marianne ; Hill, Adrian V S ; Whittle, Hilton C ; Jaye, Assan ; Prentice, Andrew M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c655t-35a6e40350eff47cee76e3ba9cdb7d1ec952b126fd972087cc82b51e3ab38e7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Analysis</topic><topic>Biomarkers</topic><topic>CD4 Lymphocyte Count</topic><topic>Coinfection</topic><topic>Development and progression</topic><topic>Disease susceptibility</topic><topic>Evidence-based medicine</topic><topic>Female</topic><topic>Ferritin</topic><topic>Genetic aspects</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Haptoglobin</topic><topic>Health aspects</topic><topic>Hemoglobin</topic><topic>HIV</topic><topic>HIV (Viruses)</topic><topic>HIV infection</topic><topic>HIV Infections - complications</topic><topic>HIV Infections - genetics</topic><topic>HIV Infections - metabolism</topic><topic>Human immunodeficiency virus</topic><topic>Human immunodeficiency virus 1</topic><topic>Human immunodeficiency virus 2</topic><topic>Humans</topic><topic>Iron</topic><topic>Iron - metabolism</topic><topic>Iron deficiency anemia</topic><topic>Iron in the body</topic><topic>Male</topic><topic>Measurement</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Middle Aged</topic><topic>Mycobacterium</topic><topic>Mycobacterium tuberculosis</topic><topic>Physiological aspects</topic><topic>Retrospective Studies</topic><topic>Risk Factors</topic><topic>Tuberculosis</topic><topic>Tuberculosis - diagnosis</topic><topic>Tuberculosis - etiology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McDermid, Joann M</creatorcontrib><creatorcontrib>Hennig, Branwen J</creatorcontrib><creatorcontrib>van der Sande, Marianne</creatorcontrib><creatorcontrib>Hill, Adrian V S</creatorcontrib><creatorcontrib>Whittle, Hilton C</creatorcontrib><creatorcontrib>Jaye, Assan</creatorcontrib><creatorcontrib>Prentice, Andrew M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints Resource Center</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>BMC infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McDermid, Joann M</au><au>Hennig, Branwen J</au><au>van der Sande, Marianne</au><au>Hill, Adrian V S</au><au>Whittle, Hilton C</au><au>Jaye, Assan</au><au>Prentice, Andrew M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study</atitle><jtitle>BMC infectious diseases</jtitle><addtitle>BMC Infect Dis</addtitle><date>2013-01-29</date><risdate>2013</risdate><volume>13</volume><issue>1</issue><spage>48</spage><epage>48</epage><pages>48-48</pages><artnum>48</artnum><issn>1471-2334</issn><eissn>1471-2334</eissn><abstract>Identifying people at higher risk of developing tuberculosis with human immunodeficiency virus (HIV) infection may improve clinical management of co-infections. Iron influences tuberculosis (TB) pathogenesis, but understanding the exact mechanisms of how and timing of when iron is involved remains challenging since biological samples are rarely available from the disease susceptibility period due to the difficulty in predicting in who and when, if ever, TB will develop. The objective of this research was to determine how host iron status measured at HIV diagnosis and genotypes related to host iron metabolism were associated with incident TB.
Archived clinical data, plasma and DNA were analyzed from 1139 adult participants in a large HIV-1, HIV-2 and dual seroprevalent cohort based at the Medical Research Council Laboratories in The Gambia. Incident pulmonary and/or extrapulmonary TB diagnoses a minimum of 28 days after HIV diagnosis were independently re-confirmed using available evidence (n=152). Multiple host iron status biomarkers, Haptoglobin and solute carrier family 11, member 1 (SLC11A1) genotypes were modeled to characterize how indicators of host iron metabolism were associated with TB susceptibility.
Hemoglobin (incidence rate ratio, IRR=0.88, 95% CI=0.79-0.98), plasma transferrin (IRR=0.53, 0.33-0.84) and ferritin (IRR=1.26, 1.05-1.51) were significantly associated with TB after adjusting for TB susceptibility factors. While genotype associations were not statistically significant, SLC11A1 associations replicated similar directions as reported in HIV-seronegative meta-analyses.
Evidence of host iron redistribution at HIV diagnosis was associated with incident TB, and genetic influences on iron homeostasis may be involved. Low hemoglobin was associated with subsequent diagnosis of TB, but when considered in combination with additional iron status biomarkers, the collective findings point to a mechanism whereby anemia and iron redistribution are likely due to viral and/or bacteria-driven processes and the host immune response to infection. As a result, iron supplementation may not be efficacious or safe under these circumstances. Clinical and nutritional management of HIV and Mycobacterium tuberculosis co-infected individuals, especially in regions where food insecurity and malnutrition co-exist, may be further improved when the iron-related TB risk factors identified here are better understood and managed to favor host rather than pathogen outcomes.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23360117</pmid><doi>10.1186/1471-2334-13-48</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Alleles Analysis Biomarkers CD4 Lymphocyte Count Coinfection Development and progression Disease susceptibility Evidence-based medicine Female Ferritin Genetic aspects Genetic Predisposition to Disease Genotype Haptoglobin Health aspects Hemoglobin HIV HIV (Viruses) HIV infection HIV Infections - complications HIV Infections - genetics HIV Infections - metabolism Human immunodeficiency virus Human immunodeficiency virus 1 Human immunodeficiency virus 2 Humans Iron Iron - metabolism Iron deficiency anemia Iron in the body Male Measurement Medical research Medicine, Experimental Middle Aged Mycobacterium Mycobacterium tuberculosis Physiological aspects Retrospective Studies Risk Factors Tuberculosis Tuberculosis - diagnosis Tuberculosis - etiology Young Adult |
title | Host iron redistribution as a risk factor for incident tuberculosis in HIV infection: an 11-year retrospective cohort study |
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