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Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice

BACKGROUND: Erythrocytes require an ability to deform and withstand shear stress while negotiating microcirculation. These properties are largely due to their excess surface area per volume and the characteristics of the membrane’s protein. Deficiencies of these proteins are associated with chronic...

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Autores principales: Dosunmu, Adedoyin, Uche, Ebele, Osikomaiya, Bodunrin, Ismail, Ayobami, Akinbami, Akinsegun, Akanmu, Alani
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Babol University of Medical Sciences 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7442468/
https://www.ncbi.nlm.nih.gov/pubmed/32874435
http://dx.doi.org/10.22088/cjim.11.3.283
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author Dosunmu, Adedoyin
Uche, Ebele
Osikomaiya, Bodunrin
Ismail, Ayobami
Akinbami, Akinsegun
Akanmu, Alani
author_facet Dosunmu, Adedoyin
Uche, Ebele
Osikomaiya, Bodunrin
Ismail, Ayobami
Akinbami, Akinsegun
Akanmu, Alani
author_sort Dosunmu, Adedoyin
collection PubMed
description BACKGROUND: Erythrocytes require an ability to deform and withstand shear stress while negotiating microcirculation. These properties are largely due to their excess surface area per volume and the characteristics of the membrane’s protein. Deficiencies of these proteins are associated with chronic hemolysis. METHODS: This was a cross-sectional study aimed at determining the prevalence of red cell membrane protein abnormalities as determined by sodium dodecyl sulphate polyacrilamide gel electrophoresis (SDS-PAGE) among patients with anemia attending the outpatient clinics of the hospital. RESULTS: A total of 823 participants were recruited into the study with a mean age of 34±14 years. There were 410 (49.8%) participants with hematocrit ≥ 36% and 413 with hematocrit ≤ 35.9% of which 192 participants (23.3%) had abnormal red cell indices. Following SDS-PAGE, 21 (10.9%) of the 192 participants had deficient PAGE tracing. Abnormal spectrin band was observed in 17 (81%) of the 21 participants. The hematocrit was significantly lower while the reticulocyte count and red cell distribution width were higher in participants with red cell membrane abnormalities. CONCLUSION: One in ten patients with mild anemia and abnormal red cell indices in clinical practice may be having hereditary red cell membrane protein defect. Presence of raised reticulocyte count, family history of mild anemia, increased red cell distribution width and red cell morphology may be used to screen for membrane deficiency.
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spelling pubmed-74424682020-08-31 Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice Dosunmu, Adedoyin Uche, Ebele Osikomaiya, Bodunrin Ismail, Ayobami Akinbami, Akinsegun Akanmu, Alani Caspian J Intern Med Original Article BACKGROUND: Erythrocytes require an ability to deform and withstand shear stress while negotiating microcirculation. These properties are largely due to their excess surface area per volume and the characteristics of the membrane’s protein. Deficiencies of these proteins are associated with chronic hemolysis. METHODS: This was a cross-sectional study aimed at determining the prevalence of red cell membrane protein abnormalities as determined by sodium dodecyl sulphate polyacrilamide gel electrophoresis (SDS-PAGE) among patients with anemia attending the outpatient clinics of the hospital. RESULTS: A total of 823 participants were recruited into the study with a mean age of 34±14 years. There were 410 (49.8%) participants with hematocrit ≥ 36% and 413 with hematocrit ≤ 35.9% of which 192 participants (23.3%) had abnormal red cell indices. Following SDS-PAGE, 21 (10.9%) of the 192 participants had deficient PAGE tracing. Abnormal spectrin band was observed in 17 (81%) of the 21 participants. The hematocrit was significantly lower while the reticulocyte count and red cell distribution width were higher in participants with red cell membrane abnormalities. CONCLUSION: One in ten patients with mild anemia and abnormal red cell indices in clinical practice may be having hereditary red cell membrane protein defect. Presence of raised reticulocyte count, family history of mild anemia, increased red cell distribution width and red cell morphology may be used to screen for membrane deficiency. Babol University of Medical Sciences 2020-05 /pmc/articles/PMC7442468/ /pubmed/32874435 http://dx.doi.org/10.22088/cjim.11.3.283 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Dosunmu, Adedoyin
Uche, Ebele
Osikomaiya, Bodunrin
Ismail, Ayobami
Akinbami, Akinsegun
Akanmu, Alani
Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice
title Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice
title_full Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice
title_fullStr Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice
title_full_unstemmed Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice
title_short Red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a West African region hospital practice
title_sort red cell membrane protein abnormalities as defined by sds-page among patients with anemia in a west african region hospital practice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7442468/
https://www.ncbi.nlm.nih.gov/pubmed/32874435
http://dx.doi.org/10.22088/cjim.11.3.283
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