Abnormal red blood cell morphological changes in thalassaemia associated with iron overload and oxidative stress
AimsIron overload is a major factor contributing to the overall pathology of thalassaemia, which is primarily mediated by ineffective erythropoiesis and shorter mature red blood cell (RBC) survival. Iron accumulation in RBCs generates reactive oxygen species (ROS) that cause cellular damage such as...
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creator | Chaichompoo, Pornthip Qillah, Ariz Sirankapracha, Pornpan Kaewchuchuen, Jirada Rimthong, Poramate Paiboonsukwong, Kittiphong Fucharoen, Suthat Svasti, Saovaros Worawichawong, Suchin |
description | AimsIron overload is a major factor contributing to the overall pathology of thalassaemia, which is primarily mediated by ineffective erythropoiesis and shorter mature red blood cell (RBC) survival. Iron accumulation in RBCs generates reactive oxygen species (ROS) that cause cellular damage such as lipid peroxidation and RBC membrane deformation. Abnormal RBCs in patients with thalassaemia are commonly known as microcytic hypochromic anaemia with poikilocytosis. However, iron and ROS accumulation in RBCs as related to RBC morphological changes in patients with thalassaemia has not been reported.MethodsTwenty-one patients with thalassaemia, including HbH, HbH with Hb Constant Spring and β-thalassaemia/HbE (splenectomy and non-splenectomy) genotypes, and five normal subjects were recruited. RBC morphology was analysed by light and scanning electron microscopy. Systemic and RBC iron status and oxidative stress were examined.ResultsDecreased normocytes were observed in the samples of patients with thalassaemia, with RBC morphological abnormality being related to the type of disease (α-thalassaemia or β-thalassaemia) and splenic status. Target cells and crenated cells were mainly found in splenectomised patients with β-thalassaemia/HbE, while target cells and teardrop cells were found in non-splenectomised patients. Patients with thalassaemia had high levels of serum ferritin, red cell ferritin and ROS in RBCs compared with normal subjects (p |
doi_str_mv | 10.1136/jclinpath-2019-205775 |
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Iron accumulation in RBCs generates reactive oxygen species (ROS) that cause cellular damage such as lipid peroxidation and RBC membrane deformation. Abnormal RBCs in patients with thalassaemia are commonly known as microcytic hypochromic anaemia with poikilocytosis. However, iron and ROS accumulation in RBCs as related to RBC morphological changes in patients with thalassaemia has not been reported.MethodsTwenty-one patients with thalassaemia, including HbH, HbH with Hb Constant Spring and β-thalassaemia/HbE (splenectomy and non-splenectomy) genotypes, and five normal subjects were recruited. RBC morphology was analysed by light and scanning electron microscopy. Systemic and RBC iron status and oxidative stress were examined.ResultsDecreased normocytes were observed in the samples of patients with thalassaemia, with RBC morphological abnormality being related to the type of disease (α-thalassaemia or β-thalassaemia) and splenic status. Target cells and crenated cells were mainly found in splenectomised patients with β-thalassaemia/HbE, while target cells and teardrop cells were found in non-splenectomised patients. Patients with thalassaemia had high levels of serum ferritin, red cell ferritin and ROS in RBCs compared with normal subjects (p<0.05). Negative correlations between the amount of normocytes and serum ferritin (rs=−0.518, p=0.011), red cell ferritin (rs=−0.467, p=0.025) or ROS in RBCs (rs=−0.672, p<0.001) were observed.ConclusionsIron overload and its consequent intracellular oxidative stress in RBCs were associated with reduce normocytes in patients with thalassaemia.</description><identifier>ISSN: 0021-9746</identifier><identifier>EISSN: 1472-4146</identifier><identifier>DOI: 10.1136/jclinpath-2019-205775</identifier><identifier>PMID: 31010830</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Anemia ; Blood ; Blood diseases ; Disease ; Hemoglobin ; Iron ; Light ; Metabolism ; Morphology ; Oxidative stress ; Reactive oxygen species ; Scanning electron microscopy ; Software</subject><ispartof>Journal of clinical pathology, 2019-08, Vol.72 (8), p.520-524</ispartof><rights>Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2019 Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b345t-154a64bd47f452e9be79d5cb1e00c210ff5c59fd29b612d7ff5492b46dc4acd53</citedby><cites>FETCH-LOGICAL-b345t-154a64bd47f452e9be79d5cb1e00c210ff5c59fd29b612d7ff5492b46dc4acd53</cites><orcidid>0000-0001-8962-7202</orcidid></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/31010830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chaichompoo, Pornthip</creatorcontrib><creatorcontrib>Qillah, Ariz</creatorcontrib><creatorcontrib>Sirankapracha, Pornpan</creatorcontrib><creatorcontrib>Kaewchuchuen, Jirada</creatorcontrib><creatorcontrib>Rimthong, Poramate</creatorcontrib><creatorcontrib>Paiboonsukwong, Kittiphong</creatorcontrib><creatorcontrib>Fucharoen, Suthat</creatorcontrib><creatorcontrib>Svasti, Saovaros</creatorcontrib><creatorcontrib>Worawichawong, Suchin</creatorcontrib><title>Abnormal red blood cell morphological changes in thalassaemia associated with iron overload and oxidative stress</title><title>Journal of clinical pathology</title><addtitle>J Clin Pathol</addtitle><description>AimsIron overload is a major factor contributing to the overall pathology of thalassaemia, which is primarily mediated by ineffective erythropoiesis and shorter mature red blood cell (RBC) survival. Iron accumulation in RBCs generates reactive oxygen species (ROS) that cause cellular damage such as lipid peroxidation and RBC membrane deformation. Abnormal RBCs in patients with thalassaemia are commonly known as microcytic hypochromic anaemia with poikilocytosis. However, iron and ROS accumulation in RBCs as related to RBC morphological changes in patients with thalassaemia has not been reported.MethodsTwenty-one patients with thalassaemia, including HbH, HbH with Hb Constant Spring and β-thalassaemia/HbE (splenectomy and non-splenectomy) genotypes, and five normal subjects were recruited. RBC morphology was analysed by light and scanning electron microscopy. Systemic and RBC iron status and oxidative stress were examined.ResultsDecreased normocytes were observed in the samples of patients with thalassaemia, with RBC morphological abnormality being related to the type of disease (α-thalassaemia or β-thalassaemia) and splenic status. Target cells and crenated cells were mainly found in splenectomised patients with β-thalassaemia/HbE, while target cells and teardrop cells were found in non-splenectomised patients. Patients with thalassaemia had high levels of serum ferritin, red cell ferritin and ROS in RBCs compared with normal subjects (p<0.05). Negative correlations between the amount of normocytes and serum ferritin (rs=−0.518, p=0.011), red cell ferritin (rs=−0.467, p=0.025) or ROS in RBCs (rs=−0.672, p<0.001) were observed.ConclusionsIron overload and its consequent intracellular oxidative stress in RBCs were associated with reduce normocytes in patients with thalassaemia.</description><subject>Anemia</subject><subject>Blood</subject><subject>Blood diseases</subject><subject>Disease</subject><subject>Hemoglobin</subject><subject>Iron</subject><subject>Light</subject><subject>Metabolism</subject><subject>Morphology</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Scanning electron microscopy</subject><subject>Software</subject><issn>0021-9746</issn><issn>1472-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkMlOwzAURS0EoqXwCSBLrAO2Y8fNsqqYJCQ2sI48pXHkxMFOC_w9rlK6ZvMGvXvvkw4A1xjdYZwX961yth_E2GQE4TIVxjk7AXNMOckopsUpmCNEcFZyWszARYwtQjjnOD8HsxwjjJY5moNhJXsfOuFgMBpK572GyjgHOx-Gxju_sSodVSP6jYnQ9nBshBMxCtNZAdPglRVj8n7ZsYE2-B76nQnOCw1Fr6H_tlqMdmdgHIOJ8RKc1cJFc3XoC_Dx-PC-fs5e355e1qvXTOaUjRlmVBRUaspryogppeGlZkpig5AiGNU1U6ysNSllgYnmaaclkbTQigqlWb4At1PuEPzn1sSxav029OllRUixRJSxxGIB2KRSwccYTF0NwXYi_FQYVXvO1ZFztedcTZyT7-aQvpWd0UfXH9gkQJNAdu0_M38BfTONfA</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Chaichompoo, Pornthip</creator><creator>Qillah, Ariz</creator><creator>Sirankapracha, Pornpan</creator><creator>Kaewchuchuen, Jirada</creator><creator>Rimthong, Poramate</creator><creator>Paiboonsukwong, Kittiphong</creator><creator>Fucharoen, Suthat</creator><creator>Svasti, Saovaros</creator><creator>Worawichawong, Suchin</creator><general>BMJ Publishing Group LTD</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0001-8962-7202</orcidid></search><sort><creationdate>20190801</creationdate><title>Abnormal red blood cell morphological changes in thalassaemia associated with iron overload and oxidative stress</title><author>Chaichompoo, Pornthip ; Qillah, Ariz ; Sirankapracha, Pornpan ; Kaewchuchuen, Jirada ; Rimthong, Poramate ; Paiboonsukwong, Kittiphong ; Fucharoen, Suthat ; Svasti, Saovaros ; Worawichawong, Suchin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b345t-154a64bd47f452e9be79d5cb1e00c210ff5c59fd29b612d7ff5492b46dc4acd53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Anemia</topic><topic>Blood</topic><topic>Blood diseases</topic><topic>Disease</topic><topic>Hemoglobin</topic><topic>Iron</topic><topic>Light</topic><topic>Metabolism</topic><topic>Morphology</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Scanning electron microscopy</topic><topic>Software</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chaichompoo, Pornthip</creatorcontrib><creatorcontrib>Qillah, Ariz</creatorcontrib><creatorcontrib>Sirankapracha, Pornpan</creatorcontrib><creatorcontrib>Kaewchuchuen, Jirada</creatorcontrib><creatorcontrib>Rimthong, Poramate</creatorcontrib><creatorcontrib>Paiboonsukwong, Kittiphong</creatorcontrib><creatorcontrib>Fucharoen, Suthat</creatorcontrib><creatorcontrib>Svasti, Saovaros</creatorcontrib><creatorcontrib>Worawichawong, Suchin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science 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>ProQuest Central Basic</collection><jtitle>Journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chaichompoo, Pornthip</au><au>Qillah, Ariz</au><au>Sirankapracha, Pornpan</au><au>Kaewchuchuen, Jirada</au><au>Rimthong, Poramate</au><au>Paiboonsukwong, Kittiphong</au><au>Fucharoen, Suthat</au><au>Svasti, Saovaros</au><au>Worawichawong, Suchin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abnormal red blood cell morphological changes in thalassaemia associated with iron overload and oxidative stress</atitle><jtitle>Journal of clinical pathology</jtitle><addtitle>J Clin Pathol</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>72</volume><issue>8</issue><spage>520</spage><epage>524</epage><pages>520-524</pages><issn>0021-9746</issn><eissn>1472-4146</eissn><abstract>AimsIron overload is a major factor contributing to the overall pathology of thalassaemia, which is primarily mediated by ineffective erythropoiesis and shorter mature red blood cell (RBC) survival. Iron accumulation in RBCs generates reactive oxygen species (ROS) that cause cellular damage such as lipid peroxidation and RBC membrane deformation. Abnormal RBCs in patients with thalassaemia are commonly known as microcytic hypochromic anaemia with poikilocytosis. However, iron and ROS accumulation in RBCs as related to RBC morphological changes in patients with thalassaemia has not been reported.MethodsTwenty-one patients with thalassaemia, including HbH, HbH with Hb Constant Spring and β-thalassaemia/HbE (splenectomy and non-splenectomy) genotypes, and five normal subjects were recruited. RBC morphology was analysed by light and scanning electron microscopy. Systemic and RBC iron status and oxidative stress were examined.ResultsDecreased normocytes were observed in the samples of patients with thalassaemia, with RBC morphological abnormality being related to the type of disease (α-thalassaemia or β-thalassaemia) and splenic status. Target cells and crenated cells were mainly found in splenectomised patients with β-thalassaemia/HbE, while target cells and teardrop cells were found in non-splenectomised patients. Patients with thalassaemia had high levels of serum ferritin, red cell ferritin and ROS in RBCs compared with normal subjects (p<0.05). Negative correlations between the amount of normocytes and serum ferritin (rs=−0.518, p=0.011), red cell ferritin (rs=−0.467, p=0.025) or ROS in RBCs (rs=−0.672, p<0.001) were observed.ConclusionsIron overload and its consequent intracellular oxidative stress in RBCs were associated with reduce normocytes in patients with thalassaemia.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>31010830</pmid><doi>10.1136/jclinpath-2019-205775</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0001-8962-7202</orcidid></addata></record> |
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subjects | Anemia Blood Blood diseases Disease Hemoglobin Iron Light Metabolism Morphology Oxidative stress Reactive oxygen species Scanning electron microscopy Software |
title | Abnormal red blood cell morphological changes in thalassaemia associated with iron overload and oxidative stress |
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