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A Randomized, Placebo-Controlled, Pilot Clinical Trial of Dipyridamole to Decrease Human Immunodeficiency Virus–Associated Chronic Inflammation
Abstract Background Adenosine is a potent immunoregulatory nucleoside produced during inflammatory states to limit tissue damage. We hypothesized that dipyridamole, which inhibits cellular adenosine uptake, could raise the extracellular adenosine concentration and dampen chronic inflammation associa...
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| Published in: | The Journal of infectious diseases 2020-04, Vol.221 (10), p.1598-1606 |
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| container_title | The Journal of infectious diseases |
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| creator | Macatangay, Bernard J C Jackson, Edwin K Abebe, Kaleab Z Comer, Diane Cyktor, Joshua Klamar-Blain, Cynthia Borowski, Luann Gillespie, Delbert G Mellors, John W Rinaldo, Charles R Riddler, Sharon A |
| description | Abstract
Background
Adenosine is a potent immunoregulatory nucleoside produced during inflammatory states to limit tissue damage. We hypothesized that dipyridamole, which inhibits cellular adenosine uptake, could raise the extracellular adenosine concentration and dampen chronic inflammation associated with human immunodeficiency virus (HIV) type 1.
Methods
Virally suppressed participants receiving antiretroviral therapy were randomized 1:1 for 12 weeks of dipyridamole (100 mg 4 times a day) versus placebo capsules. All participants took open-label dipyridamole during weeks 12–24. Study end points included changes in markers of systemic inflammation (soluble CD163 and CD14, and interleukin 6) and levels of T-cell immune activation (HLA-DR+CD38+).
Results
Of 40 participants who were randomized, 17 dipyridamole and 18 placebo recipients had baseline and week 12 data available for analyses. There were no significant changes in soluble markers, apart from a trend toward decreased levels of soluble CD163 levels (P = .09). There was a modest decrease in CD8+ T-cell activation (−17.53% change for dipyridamole vs +13.31% for placebo; P = .03), but the significance was lost in the pooled analyses (P = .058). Dipyridamole also reduced CD4+ T-cell activation (−11.11% change; P = .006) in the pooled analyses. In post hoc analysis, detectable plasma dipyridamole levels were associated with higher levels of inosine, an adenosine surrogate, and of cyclic adenosine monophosphate.
Conclusion
Dipyridamole increased extracellular adenosine levels and decreased T-cell activation significantly among persons with HIV-1 infection receiving virally suppressive therapy.
Dipyridamole, which inhibits cellular adenosine uptake and increases extracellular adenosine concentration, did not decrease levels of soluble markers of inflammation but modestly decreased levels of CD8+ T-cell activation in virally suppressed persons with human immunodeficiency virus receiving antiretroviral therapy. |
| doi_str_mv | 10.1093/infdis/jiz344 |
| format | article |
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Background
Adenosine is a potent immunoregulatory nucleoside produced during inflammatory states to limit tissue damage. We hypothesized that dipyridamole, which inhibits cellular adenosine uptake, could raise the extracellular adenosine concentration and dampen chronic inflammation associated with human immunodeficiency virus (HIV) type 1.
Methods
Virally suppressed participants receiving antiretroviral therapy were randomized 1:1 for 12 weeks of dipyridamole (100 mg 4 times a day) versus placebo capsules. All participants took open-label dipyridamole during weeks 12–24. Study end points included changes in markers of systemic inflammation (soluble CD163 and CD14, and interleukin 6) and levels of T-cell immune activation (HLA-DR+CD38+).
Results
Of 40 participants who were randomized, 17 dipyridamole and 18 placebo recipients had baseline and week 12 data available for analyses. There were no significant changes in soluble markers, apart from a trend toward decreased levels of soluble CD163 levels (P = .09). There was a modest decrease in CD8+ T-cell activation (−17.53% change for dipyridamole vs +13.31% for placebo; P = .03), but the significance was lost in the pooled analyses (P = .058). Dipyridamole also reduced CD4+ T-cell activation (−11.11% change; P = .006) in the pooled analyses. In post hoc analysis, detectable plasma dipyridamole levels were associated with higher levels of inosine, an adenosine surrogate, and of cyclic adenosine monophosphate.
Conclusion
Dipyridamole increased extracellular adenosine levels and decreased T-cell activation significantly among persons with HIV-1 infection receiving virally suppressive therapy.
Dipyridamole, which inhibits cellular adenosine uptake and increases extracellular adenosine concentration, did not decrease levels of soluble markers of inflammation but modestly decreased levels of CD8+ T-cell activation in virally suppressed persons with human immunodeficiency virus receiving antiretroviral therapy.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/jiz344</identifier><identifier>PMID: 31282542</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>Adenosine ; Adolescent ; Adult ; Antiretroviral drugs ; Antiretroviral therapy ; Biomarkers - blood ; CD14 antigen ; CD163 antigen ; CD38 antigen ; CD4 antigen ; CD8 antigen ; Cell activation ; Chronic Disease ; Clinical trials ; Cyclic AMP ; Dipyridamole ; Dipyridamole - therapeutic use ; Double-Blind Method ; Editor's Choice ; Histocompatibility antigen HLA ; HIV ; HIV Infections - complications ; HIV Infections - drug therapy ; HIV-1 ; Human immunodeficiency virus ; Humans ; Immune response ; Immunoregulation ; Inflammation ; Inflammation - drug therapy ; Inflammation - etiology ; Interleukin 6 ; Lymphocytes T ; Major and Brief Reports ; Middle Aged ; Phosphodiesterase Inhibitors - therapeutic use ; Pilot Projects ; Young Adult</subject><ispartof>The Journal of infectious diseases, 2020-04, Vol.221 (10), p.1598-1606</ispartof><rights>The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com. 2019</rights><rights>The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-593fbf83169e65d2b35a9d4fa3a906d0a375cad84eb244162275b787507fbdd43</citedby><cites>FETCH-LOGICAL-c448t-593fbf83169e65d2b35a9d4fa3a906d0a375cad84eb244162275b787507fbdd43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,1591,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31282542$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Macatangay, Bernard J C</creatorcontrib><creatorcontrib>Jackson, Edwin K</creatorcontrib><creatorcontrib>Abebe, Kaleab Z</creatorcontrib><creatorcontrib>Comer, Diane</creatorcontrib><creatorcontrib>Cyktor, Joshua</creatorcontrib><creatorcontrib>Klamar-Blain, Cynthia</creatorcontrib><creatorcontrib>Borowski, Luann</creatorcontrib><creatorcontrib>Gillespie, Delbert G</creatorcontrib><creatorcontrib>Mellors, John W</creatorcontrib><creatorcontrib>Rinaldo, Charles R</creatorcontrib><creatorcontrib>Riddler, Sharon A</creatorcontrib><title>A Randomized, Placebo-Controlled, Pilot Clinical Trial of Dipyridamole to Decrease Human Immunodeficiency Virus–Associated Chronic Inflammation</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>Abstract
Background
Adenosine is a potent immunoregulatory nucleoside produced during inflammatory states to limit tissue damage. We hypothesized that dipyridamole, which inhibits cellular adenosine uptake, could raise the extracellular adenosine concentration and dampen chronic inflammation associated with human immunodeficiency virus (HIV) type 1.
Methods
Virally suppressed participants receiving antiretroviral therapy were randomized 1:1 for 12 weeks of dipyridamole (100 mg 4 times a day) versus placebo capsules. All participants took open-label dipyridamole during weeks 12–24. Study end points included changes in markers of systemic inflammation (soluble CD163 and CD14, and interleukin 6) and levels of T-cell immune activation (HLA-DR+CD38+).
Results
Of 40 participants who were randomized, 17 dipyridamole and 18 placebo recipients had baseline and week 12 data available for analyses. There were no significant changes in soluble markers, apart from a trend toward decreased levels of soluble CD163 levels (P = .09). There was a modest decrease in CD8+ T-cell activation (−17.53% change for dipyridamole vs +13.31% for placebo; P = .03), but the significance was lost in the pooled analyses (P = .058). Dipyridamole also reduced CD4+ T-cell activation (−11.11% change; P = .006) in the pooled analyses. In post hoc analysis, detectable plasma dipyridamole levels were associated with higher levels of inosine, an adenosine surrogate, and of cyclic adenosine monophosphate.
Conclusion
Dipyridamole increased extracellular adenosine levels and decreased T-cell activation significantly among persons with HIV-1 infection receiving virally suppressive therapy.
Dipyridamole, which inhibits cellular adenosine uptake and increases extracellular adenosine concentration, did not decrease levels of soluble markers of inflammation but modestly decreased levels of CD8+ T-cell activation in virally suppressed persons with human immunodeficiency virus receiving antiretroviral therapy.</description><subject>Adenosine</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Antiretroviral drugs</subject><subject>Antiretroviral therapy</subject><subject>Biomarkers - blood</subject><subject>CD14 antigen</subject><subject>CD163 antigen</subject><subject>CD38 antigen</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>Cell activation</subject><subject>Chronic Disease</subject><subject>Clinical trials</subject><subject>Cyclic AMP</subject><subject>Dipyridamole</subject><subject>Dipyridamole - therapeutic use</subject><subject>Double-Blind Method</subject><subject>Editor's Choice</subject><subject>Histocompatibility antigen HLA</subject><subject>HIV</subject><subject>HIV Infections - complications</subject><subject>HIV Infections - drug therapy</subject><subject>HIV-1</subject><subject>Human immunodeficiency virus</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunoregulation</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - etiology</subject><subject>Interleukin 6</subject><subject>Lymphocytes T</subject><subject>Major and Brief Reports</subject><subject>Middle Aged</subject><subject>Phosphodiesterase Inhibitors - therapeutic use</subject><subject>Pilot Projects</subject><subject>Young Adult</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNqFkcuKFDEARYMoTju6dCsBNy4sJ89KaiM0Neo0DCgyug2pJOWkyaNNqoSelb8g_qFfYmmP42PjJoHkcLiXC8BDjJ5h1NETn0br68nWX1HGboEV5lQ0bYvpbbBCiJAGy647Avdq3SKEGG3FXXBEMZGEM7ICX9bwrU42R3_l7FP4Jmjjhtz0OU0lh_DzzYc8wT745I0O8KL45cwjPPW7ffFWxxwcnDI8daY4XR08m6NOcBPjnLJ1ozfeJbOH732Z67fPX9e1ZuP15CzsL0terHCTxqBj1JPP6T64M-pQ3YPr-xi8e_nioj9rzl-_2vTr88YwJqeGd3QcRklx27mWWzJQrjvLRk11h1qLNBXcaCuZGwhjuCVE8EFIwZEYB2sZPQbPD97dPERnjVsa66B2xUdd9iprr_7-Sf5SfciflMCSdbhbBE-uBSV_nF2dVPTVuBB0cnmuihBOJSWt5Av6-B90m-eSlnpqCSdbKSQVC9UcKFNyrcWNN2EwUj_GVoex1WHshX_0Z4Mb-te6vxPmefcf13egx7kr</recordid><startdate>20200427</startdate><enddate>20200427</enddate><creator>Macatangay, Bernard J C</creator><creator>Jackson, Edwin K</creator><creator>Abebe, Kaleab Z</creator><creator>Comer, Diane</creator><creator>Cyktor, Joshua</creator><creator>Klamar-Blain, Cynthia</creator><creator>Borowski, Luann</creator><creator>Gillespie, Delbert G</creator><creator>Mellors, John W</creator><creator>Rinaldo, Charles R</creator><creator>Riddler, Sharon A</creator><general>Oxford University Press</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200427</creationdate><title>A Randomized, Placebo-Controlled, Pilot Clinical Trial of Dipyridamole to Decrease Human Immunodeficiency Virus–Associated Chronic Inflammation</title><author>Macatangay, Bernard J C ; Jackson, Edwin K ; Abebe, Kaleab Z ; Comer, Diane ; Cyktor, Joshua ; Klamar-Blain, Cynthia ; Borowski, Luann ; Gillespie, Delbert G ; Mellors, John W ; Rinaldo, Charles R ; Riddler, Sharon A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-593fbf83169e65d2b35a9d4fa3a906d0a375cad84eb244162275b787507fbdd43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenosine</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Antiretroviral drugs</topic><topic>Antiretroviral therapy</topic><topic>Biomarkers - blood</topic><topic>CD14 antigen</topic><topic>CD163 antigen</topic><topic>CD38 antigen</topic><topic>CD4 antigen</topic><topic>CD8 antigen</topic><topic>Cell activation</topic><topic>Chronic Disease</topic><topic>Clinical trials</topic><topic>Cyclic AMP</topic><topic>Dipyridamole</topic><topic>Dipyridamole - therapeutic use</topic><topic>Double-Blind Method</topic><topic>Editor's Choice</topic><topic>Histocompatibility antigen HLA</topic><topic>HIV</topic><topic>HIV Infections - complications</topic><topic>HIV Infections - drug therapy</topic><topic>HIV-1</topic><topic>Human immunodeficiency virus</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunoregulation</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - etiology</topic><topic>Interleukin 6</topic><topic>Lymphocytes T</topic><topic>Major and Brief Reports</topic><topic>Middle Aged</topic><topic>Phosphodiesterase Inhibitors - therapeutic use</topic><topic>Pilot Projects</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Macatangay, Bernard J C</creatorcontrib><creatorcontrib>Jackson, Edwin K</creatorcontrib><creatorcontrib>Abebe, Kaleab Z</creatorcontrib><creatorcontrib>Comer, Diane</creatorcontrib><creatorcontrib>Cyktor, Joshua</creatorcontrib><creatorcontrib>Klamar-Blain, Cynthia</creatorcontrib><creatorcontrib>Borowski, Luann</creatorcontrib><creatorcontrib>Gillespie, Delbert G</creatorcontrib><creatorcontrib>Mellors, John W</creatorcontrib><creatorcontrib>Rinaldo, Charles R</creatorcontrib><creatorcontrib>Riddler, Sharon 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Macatangay, Bernard J C</au><au>Jackson, Edwin K</au><au>Abebe, Kaleab Z</au><au>Comer, Diane</au><au>Cyktor, Joshua</au><au>Klamar-Blain, Cynthia</au><au>Borowski, Luann</au><au>Gillespie, Delbert G</au><au>Mellors, John W</au><au>Rinaldo, Charles R</au><au>Riddler, Sharon A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Randomized, Placebo-Controlled, Pilot Clinical Trial of Dipyridamole to Decrease Human Immunodeficiency Virus–Associated Chronic Inflammation</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>2020-04-27</date><risdate>2020</risdate><volume>221</volume><issue>10</issue><spage>1598</spage><epage>1606</epage><pages>1598-1606</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-News-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><abstract>Abstract
Background
Adenosine is a potent immunoregulatory nucleoside produced during inflammatory states to limit tissue damage. We hypothesized that dipyridamole, which inhibits cellular adenosine uptake, could raise the extracellular adenosine concentration and dampen chronic inflammation associated with human immunodeficiency virus (HIV) type 1.
Methods
Virally suppressed participants receiving antiretroviral therapy were randomized 1:1 for 12 weeks of dipyridamole (100 mg 4 times a day) versus placebo capsules. All participants took open-label dipyridamole during weeks 12–24. Study end points included changes in markers of systemic inflammation (soluble CD163 and CD14, and interleukin 6) and levels of T-cell immune activation (HLA-DR+CD38+).
Results
Of 40 participants who were randomized, 17 dipyridamole and 18 placebo recipients had baseline and week 12 data available for analyses. There were no significant changes in soluble markers, apart from a trend toward decreased levels of soluble CD163 levels (P = .09). There was a modest decrease in CD8+ T-cell activation (−17.53% change for dipyridamole vs +13.31% for placebo; P = .03), but the significance was lost in the pooled analyses (P = .058). Dipyridamole also reduced CD4+ T-cell activation (−11.11% change; P = .006) in the pooled analyses. In post hoc analysis, detectable plasma dipyridamole levels were associated with higher levels of inosine, an adenosine surrogate, and of cyclic adenosine monophosphate.
Conclusion
Dipyridamole increased extracellular adenosine levels and decreased T-cell activation significantly among persons with HIV-1 infection receiving virally suppressive therapy.
Dipyridamole, which inhibits cellular adenosine uptake and increases extracellular adenosine concentration, did not decrease levels of soluble markers of inflammation but modestly decreased levels of CD8+ T-cell activation in virally suppressed persons with human immunodeficiency virus receiving antiretroviral therapy.</abstract><cop>US</cop><pub>Oxford University Press</pub><pmid>31282542</pmid><doi>10.1093/infdis/jiz344</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of infectious diseases, 2020-04, Vol.221 (10), p.1598-1606 |
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| source | Oxford Academic Journals (OUP) |
| subjects | Adenosine Adolescent Adult Antiretroviral drugs Antiretroviral therapy Biomarkers - blood CD14 antigen CD163 antigen CD38 antigen CD4 antigen CD8 antigen Cell activation Chronic Disease Clinical trials Cyclic AMP Dipyridamole Dipyridamole - therapeutic use Double-Blind Method Editor's Choice Histocompatibility antigen HLA HIV HIV Infections - complications HIV Infections - drug therapy HIV-1 Human immunodeficiency virus Humans Immune response Immunoregulation Inflammation Inflammation - drug therapy Inflammation - etiology Interleukin 6 Lymphocytes T Major and Brief Reports Middle Aged Phosphodiesterase Inhibitors - therapeutic use Pilot Projects Young Adult |
| title | A Randomized, Placebo-Controlled, Pilot Clinical Trial of Dipyridamole to Decrease Human Immunodeficiency Virus–Associated Chronic Inflammation |
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