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Hemoglobinopathy

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is endemic. Malaria parasites live inside red blood cells, but subtly disturb normal cellular function. In patients predisposed for rapid clearance of red blood cells, this may lead to early destruction of cells infected with the parasite and increased chance of survival for the carrier of the trait.
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Hb structural variants are qualitative defects that cause a change in the structure (primary, secondary, tertiary, and/or quaternary) of the Hb molecule. The majority of Hb variants do not cause disease and are most commonly discovered either incidentally or through newborn screening. A subset of Hb
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Nabarrete, J. M.; Pereira, A. Z.; GarĂłfolo, A.; Seber, A.; Venancio, A. M.; Grecco, C. E.; Bonfim, C. M.; Nakamura, C. H.; Fernandes, D.; Campos, D. J.; Oliveira, F. L.; Cousseiro, F. K.; Rossi, F. F.; Gurmini, J.; Viani, K. H.; Guterres, L. F.; Mantovani, L. F.; Darrigo Lg, Junior; Albuquerque, M.
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Fetal Hb (HbF) is produced from approximately eight weeks of gestation through birth and constitutes approximately 80 percent of Hb in the full-term neonate. It declines during the first few months of life and, in the normal state, constitutes <1 percent of total Hb by early childhood. HbF is
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Change in oxygen affinity: High or low oxygen affinity Hb molecules are more likely than normal to adopt the relaxed (R, oxy) state or the tense (T, deoxy) state, respectively. High oxygen affinity variants (R state) cause polycythemia (e.g., Hb Chesapeake, Hb Montefiore). Low oxygen affinity
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Thalassemias: Thalassemias are quantitative defects that lead to reduced levels of one type of globin chain, creating an imbalance in the ratio of alpha-like chains to beta-like chains. As noted above, this ratio is normally tightly regulated to prevent excess globin chains of one type from
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accumulating. The excess chains that fail to incorporate into Hb form non-functional aggregates that precipitate within the RBC. This can lead to premature RBC destruction in the bone marrow (beta thalassemia) and/or in the peripheral blood (alpha thalassemia). Types:
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This is how abnormal hemoglobin variants are isolated and identified using these two methods. For example, a Hgb G-Philadelphia would migrate with S on alkaline electrophoresis and would migrate with A on acid electrophoresis, respectively
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Natarajan K, Townes TM, Kutlar A. Disorders of hemoglobin structure: sickle cell anemia and related abnormalities. In: Williams Hematology, 8th ed, Kaushansky K, Lichtman MA, Beutler E, et al. (Eds), McGraw-Hill, 2010.
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to the tissues: This is due to the peculiar cooperation of the globin chains that allows the molecule to take in more oxygen where there is increased oxygen and to release oxygen in low concentration of
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Methemoglobinemia: The iron in the heme portion of hemoglobin is easily oxidised and this reduces the ability of hemoglobin to bind oxygen. More deoxygenated hemoglobin are formed and the blood becomes
211:(HbA) is the predominant Hb in children by six months of age and onward; it constitutes 96-97% of total Hb in individuals without a hemoglobinopathy. It is composed of two α globins and two β globins (α 1099:
Monga I, Kaur K, Dhanda S (March 2022). "Revisiting hematopoiesis: applications of the bulk and single-cell transcriptomics dissecting transcriptional heterogeneity in hematopoietic stem cells".
103:, which are caused by an underproduction of otherwise normal hemoglobin molecules. The main structural hemoglobin variants are HbS, HbE and HbC. The main types of thalassemia are 386:
Copy number variation (e.g., deletion, duplication, insertion) is also a common genetic cause of Hb disorders, and complex rearrangements and globin gene fusions can also occur.
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Huisman TH. The structure and function of normal and abnormal haemoglobins. In: Baillière's Clinical Haematology, Higgs DR, Weatherall DJ (Eds), W.B. Saunders, London 1993. p.1.
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Forman SJ, Negrin RS, Antin JH, Appelbaum FR. Thomas' hematopoietic cell transplantation: stem cell transplantation. 5th ed. Vol. 2. New Jersey: Wiley-Blackwell; 2016. p.1416.
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is a minor adult Hb that normally accounts for approximately 2.5–3.5% of total Hb from six months of age onward. It is composed of two α globins and two δ (delta) globins (α
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The two conditions may overlap because some conditions which cause abnormalities in hemoglobin proteins also affect their production. Some hemoglobin variants do not cause
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Haemoglobin variant are not necessarily pathological. For example, haemoglobin Valletta and haemoglobin Marseille are two haemoglobin variants which are non-pathological
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Joseph Bonavetura and Austin Riggs, March 1968, "Hemoglobin Kansas, A Human Hemoglobin with a Neutral Amino Acid Substitution and an Abnormal Oxygen Equilibrium",
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composed of two pairs of globin chains, each of which contains one α (alpha) chain and one β (beta) chain. Each globin chain is associated with an iron-containing
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is a form of Hb that contains the ferric form of iron. The affinity for oxygen of ferric iron is impaired. The binding of oxygen to methaemoglobin results in an
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residues, can produce M-hemoglobin, in which the iron atom in heme is oxidized from the ferrous (Fe) state to the ferric (Fe) state, with resultant
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In general a sickling test is performed on abnormal hemoglobins migrating in the S location to see if the hemoglobin precipitates in solution of
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In general on alkaline electrophoresis in order of increasing mobility are hemoglobins A2, E=O=C, G=D=S=Lepore, F, A, K, J, Bart's, N, I, and H.
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state in combination with another structural variant or a thalassemia mutation. When clinical consequences occur, they may include anemia due to
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Percy, M. J.; Butt, N. N.; Crotty, G. M.; Drummond, M. W.; Harrison, C.; Jones, G. L.; Turner, M.; Wallis, J.; McMullin, M. F. (2009).
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due to alterations in the oxygen affinity of the abnormal Hb. Common examples of hemoglobin variants associated with hemolysis include
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Oxidation of heme iron: Mutations of the heme binding site, particularly those affecting the conserved proximal or distal
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Change in physical properties (solubility): Common beta globin mutations can alter the solubility of the Hb molecule: HbS
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methods; however, DNA-based methods may be required for variants with ambiguous or unusual results from protein analysis.
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There are two main groups: abnormal structural hemoglobin variants caused by mutations in the hemoglobin genes, and the
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affinity for oxygen in the remaining heme sites that are in ferrous state within the same tetrameric haemoglobin unit.
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to produce water and carbon dioxide. The carbon dioxide is mopped up by hemoglobin to favor this reversible reaction.
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In general on acid electrophoresis in order of increasing mobility are hemoglobins F, A=D=G=E=O=Lepore, S, and C.
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Felfly H, Haddad GG (2014). "Hematopoietic stem cells: potential new applications for translational medicine".
885:"Severe hemolytic anemia associated with the homozygous state for an unstable hemoglobin variant (Hb Bushwick)" 1763: 1671: 1836: 1788: 582:. This assists in the regulation of vascular reaction in times of stress as experienced during inflammation. 1693: 607:
Unstable hemoglobins: Red blood cells are easily destroyed under stress and hemolysis occurs with possible
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Greene DN, Vaughn CP, Crews BO, Agarwal AM (January 2015). "Advances in detection of hemoglobinopathies".
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Reduced protein stability (instability): Unstable Hb variants are mutations that cause the Hb molecule to
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due to reduced life span of the red cells of reduced production of the cells, e.g., HbS, HbC and HbE.
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I.; Brumatti, M.; Neves, M. A.; Duran, N.; Villela, N. C.; Zecchin, V. G.; Fernandes, J. F. (2021).
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Pathology and organic structural abnormalities may lead to any of the following disease processes:
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The specific α and β chains that are incorporated into Hb are highly regulated during development:
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Wilcox I, Boettger K, Greene L, Malek A, Davis L, Steinberg MH, Luo HY, Chui DH (January 2009).
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Increased oxygen affinity: The red blood cells do not release their oxygen content readily in
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from the tissues to the lungs: The end product of tissue metabolism is acidic which increases
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Srivastava, P.; Kaeda, J. S.; Roper, D.; Vulliamy, T. J.; Buckley, M.; Luzzatto, L. (1995).
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Weatherall DJ. The New Genetics and Clinical Practice, Oxford University Press, Oxford 1991.
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The major functional consequences of Hb structural variants can be classified as follows:
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Category:Hereditary hemolytic anemias Category:Disorders of globin and globulin proteins
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Eaton, William A.; Hofrichter, James (1990). "Sickle Cell Hemoglobin Polymerization".
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blood to replicate inside a patient and to produce normal blood cells. It may be
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Hb Gower-1, composed of two ζ (zeta) globins and two ε (epsilon) globins, i.e., ζ
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therefore needs to produce more red blood cells and there is polycythemia.
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and disappear around the eighth week of gestation as they are replaced by
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a condition caused by elevated levels of methemoglobin in the blood.
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Hb Portland, composed of two ζ globins and two γ (gamma) globins (ζ
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Clinica Chimica Acta; International Journal of Clinical Chemistry
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Hb Gower-2, composed of two α globins and two ε globins (α
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Some hemoglobinopathies (and also related diseases like
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variants can cause severe disease when inherited in the
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Red blood cells from a person with sickle cell trait
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Red blood cells from a person with beta thalassemia
1974: 125: 1463: 1098: 1045:. National Center for Biotechnology Information 837: 688: 151:are expressed as early as four to six weeks of 197:composed of two α globins and two Îł globins (α 1449: 76:is the medical term for a group of inherited 1598:Glucose-6-phosphate dehydrogenase deficiency 1195: 1057: 969: 902:10.1182/blood.V86.5.1977.bloodjournal8651977 567:in solution. The hydrogen ions combine with 523:glucose-6-phosphate dehydrogenase deficiency 1482: 783: 489: 373: 247: 1954:Hereditary persistence of fetal hemoglobin 1456: 1442: 1225: 670:Centers for Disease Control and Prevention 92:and, in most cases, they are inherited as 62: 38: 1906:Mean corpuscular hemoglobin concentration 1728:Warm antibody autoimmune hemolytic anemia 1302: 1292: 1251: 1221: 1219: 1191: 1189: 1160: 993: 952: 900: 786:"A Syllabus of Human Hemoglobin Variants" 706: 695:Bulletin of the World Health Organization 639:(the patient's own stem cells are used), 345: 16:Any of various genetic disorders of blood 689:Weatherall, D. J.; Clegg, J. B. (2001). 377: 314:Hb can attach to the inner layer of the 1226:Park B, Yoo KH, Kim C (December 2015). 922: 920: 657: 625:Hematopoietic stem cell transplantation 504: 482:Hemoglobin variants can be detected by 295:when deoxygenated and HbC crystallizes. 1975: 1216: 1186: 1127: 1092: 643:(the stem cells come from a donor) or 406: 1511: 1437: 1281:International Journal of Cell Biology 1274: 318:of the red blood cell (RBC) and form 1615:triosephosphate isomerase deficiency 1153:10.31744/einstein_journal/2021AE5254 917: 731:"Hemoglobinopathies and Thalassemia" 238:Classification of hemoglobinopathies 1770:paroxysmal nocturnal hemoglobinuria 1738:Donath–Landsteiner hemolytic anemia 1718: 1026:The Journal of Biological Chemistry 735:medicalassistantonlineprograms.org/ 663: 13: 478:Electrophoretic migration patterns 368: 330:(e.g., Hb Kansas, Hb Beth Israel). 14: 1994: 1779:Microangiopathic hemolytic anemia 1750:Mixed autoimmune hemolytic anemia 242: 1810:Hemolytic disease of the newborn 1101:Briefings in Functional Genomics 1268: 1177: 1031: 1018: 876: 792:. Pennsylvania State University 1743:Paroxysmal cold hemoglobinuria 982:American Journal of Hematology 831: 821: 812: 803: 723: 682: 1: 852:10.1016/S0065-3233(08)60287-9 840:Advances in Protein Chemistry 666:"Hemoglobinopathies Research" 650: 619: 130:Normal human hemoglobins are 126:Hemoglobin structural biology 1694:Southeast Asian ovalocytosis 1682:Minkowski–Chauffard syndrome 945:10.3324/haematol.2009.008037 516: 7: 10: 1999: 1803:Drug-induced nonautoimmune 1784:Thrombotic microangiopathy 1610:pyruvate kinase deficiency 647:(from an identical twin). 1931: 1871: 1822: 1789:Hemolytic–uremic syndrome 1709: 1701:Hereditary stomatocytosis 1689:Hereditary elliptocytosis 1582: 1567: 1520: 1504: 1475: 1396: 1326: 1078:10.1016/j.cca.2014.10.006 159:. Embryonic Hbs include: 51: 46: 37: 29: 24: 1677:Hereditary spherocytosis 1244:10.5045/br.2015.50.4.194 490:Alkaline electrophoresis 374:Production abnormalities 302:, spontaneously or upon 248:Structural abnormalities 1882:Mean corpuscular volume 1846:Diamond–Blackfan anemia 1798:Drug-induced autoimmune 1733:Cold agglutinin disease 1539:Plummer–Vinson syndrome 1534:Iron-deficiency anemia 383: 346:Chemical abnormalities 1853:Pure red cell aplasia 1620:hexokinase deficiency 1198:Journal of Stem Cells 760:"Hemoglobin Variants" 381: 94:autosomal co-dominant 90:single-gene disorders 1858:Sideroblastic anemia 1666:Hemoglobin C disease 1552:Megaloblastic anemia 1294:10.1155/2016/6940283 1113:10.1093/bfgp/elac002 784:Huisman THJ (1996). 578:: Nitric oxide is a 538:Hemoglobin functions 505:Acid electrophoresis 1657:Sickle cell disease 484:gel electrophoresis 407:Hemoglobin variants 351:Methemoglobinemia: 326:variants can cause 132:tetrameric proteins 1944:Sulfhemoglobinemia 1397:External resources 790:Globin Gene Server 664:CDC (2019-02-08). 441:Hb Constant Spring 384: 33:Hemoglobinopathies 1966: 1965: 1962: 1961: 1949:Reticulocytopenia 1939:Methemoglobinemia 1927: 1926: 1818: 1817: 1758: 1757: 1557:Pernicious anemia 1500: 1499: 1492:Polycythemia vera 1431: 1430: 1275:Mahla RS (2016). 995:10.1002/ajh.21308 529:, in areas where 435:Hb G-Philadelphia 339:methemoglobinemia 105:alpha-thalassemia 84:, the protein of 71: 70: 19:Medical condition 1990: 1716: 1715: 1630:hemoglobinopathy 1580: 1579: 1518: 1517: 1509: 1508: 1480: 1479: 1458: 1451: 1444: 1435: 1434: 1324: 1323: 1317: 1316: 1306: 1296: 1272: 1266: 1265: 1255: 1223: 1214: 1213: 1193: 1184: 1181: 1175: 1174: 1164: 1131: 1125: 1124: 1096: 1090: 1089: 1061: 1055: 1054: 1052: 1050: 1035: 1029: 1022: 1016: 1015: 997: 973: 967: 966: 956: 939:(9): 1321–1322. 924: 915: 914: 904: 895:(5): 1977–1982. 880: 874: 873: 835: 829: 825: 819: 816: 810: 807: 801: 800: 798: 797: 781: 775: 774: 772: 771: 764:Lab Tests Online 756: 750: 749: 747: 746: 737:. Archived from 727: 721: 720: 710: 686: 680: 679: 677: 676: 661: 629:peripheral blood 600:conditions. The 499:sodium bisulfite 449:Hemoglobin Kenya 369:B) Quantitative 310:. Precipitated, 308:hemolytic anemia 304:oxidative stress 109:beta thalassemia 74:Hemoglobinopathy 67: 66: 42: 25:Hemoglobinopathy 22: 21: 1998: 1997: 1993: 1992: 1991: 1989: 1988: 1987: 1983:Blood disorders 1973: 1972: 1969: 1967: 1958: 1923: 1867: 1826: 1814: 1754: 1705: 1571: 1563: 1496: 1471: 1469:red blood cells 1462: 1432: 1427: 1426: 1392: 1391: 1335: 1321: 1320: 1273: 1269: 1224: 1217: 1194: 1187: 1182: 1178: 1132: 1128: 1097: 1093: 1062: 1058: 1048: 1046: 1037: 1036: 1032: 1023: 1019: 974: 970: 925: 918: 881: 877: 862: 836: 832: 826: 822: 817: 813: 808: 804: 795: 793: 782: 778: 769: 767: 758: 757: 753: 744: 742: 729: 728: 724: 687: 683: 674: 672: 662: 658: 653: 622: 519: 507: 492: 480: 432:HbO (Hb O-Arab) 409: 376: 371: 348: 316:plasma membrane 306:, resulting in 250: 245: 243:A) Qualitative 240: 232: 228: 218: 214: 204: 200: 190: 186: 179: 175: 169: 165: 128: 86:red blood cells 78:blood disorders 61: 20: 17: 12: 11: 5: 1996: 1986: 1985: 1964: 1963: 1960: 1959: 1957: 1956: 1951: 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1091: 1056: 1030: 1017: 968: 916: 875: 860: 830: 820: 811: 802: 776: 751: 722: 701:(8): 704–712. 681: 655: 654: 652: 649: 633:umbilical cord 621: 618: 617: 616: 612: 605: 594: 584: 583: 572: 558:carbon dioxide 554: 518: 515: 506: 503: 491: 488: 479: 476: 475: 474: 471: 468: 467:Hb N-Baltimore 465: 462: 459: 456: 453: 450: 447: 444: 443: 442: 436: 433: 430: 425: 422: 419: 416: 408: 405: 404: 403: 402: 401: 398: 395: 375: 372: 370: 367: 366: 365: 364: 363: 356:Methaemoglobin 347: 344: 343: 342: 331: 323: 296: 249: 246: 244: 241: 239: 236: 235: 234: 230: 226: 220: 216: 212: 206: 202: 198: 194: 193: 192: 188: 184: 181: 177: 173: 170: 167: 163: 127: 124: 80:involving the 69: 68: 55: 49: 48: 44: 43: 35: 34: 31: 27: 26: 18: 15: 9: 6: 4: 3: 2: 1995: 1984: 1981: 1980: 1978: 1971: 1955: 1952: 1950: 1947: 1945: 1942: 1940: 1937: 1936: 1934: 1930: 1918: 1915: 1913: 1910: 1909: 1908: 1907: 1903: 1899: 1896: 1894: 1891: 1889: 1886: 1885: 1884: 1883: 1879: 1878: 1876: 1874: 1870: 1864: 1863:Myelophthisic 1861: 1859: 1856: 1854: 1850: 1849: 1847: 1844: 1842: 1838: 1835: 1833: 1830: 1825: 1821: 1811: 1808: 1807: 1804: 1801: 1799: 1796: 1795: 1790: 1787: 1786: 1785: 1782: 1780: 1777: 1776: 1771: 1768: 1767: 1766: 1765: 1761: 1760: 1751: 1748: 1744: 1741: 1740: 1739: 1736: 1734: 1731: 1729: 1726: 1725: 1723: 1721: 1717: 1714: 1712: 1708: 1702: 1699: 1695: 1692: 1691: 1690: 1687: 1683: 1680: 1679: 1678: 1675: 1673: 1669: 1667: 1664: 1662: 1658: 1655: 1651: 1648: 1646: 1643: 1641: 1638: 1637: 1636: 1633: 1631: 1627: 1626: 1621: 1618: 1616: 1613: 1611: 1608: 1607: 1606: 1605: 1601: 1599: 1596: 1594: 1590: 1589: 1587: 1585: 1581: 1578: 1575: 1570: 1566: 1558: 1555: 1554: 1553: 1549: 1546: 1545: 1540: 1537: 1536: 1535: 1531: 1528: 1527: 1525: 1523: 1519: 1516: 1514: 1510: 1507: 1503: 1493: 1490: 1489: 1487: 1485: 1481: 1478: 1474: 1470: 1466: 1459: 1454: 1452: 1447: 1445: 1440: 1439: 1436: 1423: 1419: 1418: 1414: 1412: 1408: 1407: 1403: 1402: 1399: 1395: 1388: 1384: 1383: 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544:Transport of 543: 542: 541: 539: 535: 532: 528: 527:heterozygotes 524: 514: 510: 502: 500: 495: 487: 485: 472: 469: 466: 463: 460: 457: 454: 451: 448: 445: 440: 439: 437: 434: 431: 429: 426: 423: 420: 417: 414: 413: 412: 399: 396: 393: 392: 389: 388: 387: 380: 361: 357: 353: 352: 350: 349: 340: 336: 332: 329: 324: 321: 317: 313: 309: 305: 301: 297: 294: 290: 289: 288: 285: 283: 279: 275: 271: 267: 263: 259: 254: 224: 221: 210: 207: 195: 182: 171: 161: 160: 158: 154: 153:embryogenesis 150: 147: 146: 145: 142: 140: 137: 133: 123: 121: 117: 112: 110: 106: 102: 97: 95: 91: 87: 83: 79: 75: 65: 59: 56: 54: 50: 45: 41: 36: 32: 28: 23: 1968: 1912:normochromic 1904: 1880: 1762: 1670: 1629: 1628: 1602: 1591: 1484:Polycythemia 1415: 1404: 1380: 1369: 1354: 1339: 1284: 1280: 1270: 1235: 1231: 1201: 1197: 1179: 1144: 1140: 1129: 1104: 1100: 1094: 1069: 1065: 1059: 1047:. 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They are 30:Other names 1898:macrocytic 1893:microcytic 1888:normocytic 1851:Acquired: 1837:Hereditary 1604:glycolysis 1584:Hereditary 1382:DiseasesDB 1049:7 February 846:: 63–279. 796:2008-10-12 770:2008-10-12 745:2013-11-07 675:2019-05-05 651:References 641:allogeneic 637:autologous 620:Treatments 276:(HbS) and 258:homozygous 82:hemoglobin 58:Hematology 1569:Hemolytic 645:syngeneic 615:cyanotic. 548:from the 517:Evolution 461:Hb Kansas 455:Hb Lepore 424:Hb Bart's 360:increased 335:histidine 312:denatured 274:sickle Hb 266:hemolysis 116:pathology 53:Specialty 1977:Category 1827:(mostly 1824:Aplastic 1764:membrane 1711:Acquired 1672:membrane 1572:(mostly 1465:Diseases 1417:Orphanet 1313:27516776 1262:26770947 1210:25157450 1171:34909973 1141:Einstein 1121:35265979 1086:25314938 1072:: 50–7. 1012:29114149 1004:19006227 963:19734427 828:p.ch.48. 717:11545326 609:jaundice 562:hydrogen 328:cyanosis 209:Adult Hb 157:fetal Hb 96:traits. 1376:D006453 1304:4969512 1253:4705045 1162:8664291 954:2738729 911:7655024 870:2195851 708:2566499 598:hypoxic 553:oxygen. 531:malaria 473:Hb Pisa 470:Hb Hope 1829:normo- 1574:normo- 1548:Macro- 1530:Micro- 1513:Anemia 1411:001291 1311:  1301:  1260:  1250:  1208:  1169:  1159:  1119:  1084:  1010:  1002:  961:  951:  909:  868:  858:  715:  705:  591:Anemia 546:oxygen 139:moiety 120:anemia 60:  1932:Other 1661:trait 1650:delta 1640:alpha 1422:68364 1387:19674 1365:282.7 1350:D58.2 1043:dbSNP 1008:S2CID 889:Blood 631:, or 550:lungs 394:Alpha 282:assay 1720:AIHA 1645:beta 1371:MeSH 1360:9-CM 1309:PMID 1285:2016 1258:PMID 1206:PMID 1167:PMID 1117:PMID 1082:PMID 1051:2014 1000:PMID 959:PMID 907:PMID 866:PMID 856:ISBN 713:PMID 565:ions 438:HbH 223:HbA2 136:heme 107:and 1467:of 1356:ICD 1341:ICD 1299:PMC 1289:doi 1248:PMC 1240:doi 1157:PMC 1149:doi 1109:doi 1074:doi 1070:439 990:doi 949:PMC 941:doi 897:doi 848:doi 703:PMC 464:HbJ 458:HbM 428:HbD 421:HbE 418:HbC 415:HbS 278:HbC 268:or 118:or 1979:: 1839:: 1550:: 1532:: 1420:: 1409:: 1385:: 1374:: 1363:: 1348:: 1345:10 1307:. 1297:. 1283:. 1279:. 1256:. 1246:. 1236:50 1234:. 1230:. 1218:^ 1200:. 1188:^ 1165:. 1155:. 1145:19 1143:. 1139:. 1115:. 1105:21 1103:. 1080:. 1068:. 1041:. 1006:. 998:. 986:84 984:. 980:. 957:. 947:. 937:94 935:. 931:. 919:^ 905:. 893:86 891:. 887:. 864:. 854:. 844:40 842:. 788:. 762:. 733:. 711:. 699:79 697:. 693:. 668:. 540:: 501:. 486:. 233:). 219:). 205:). 111:. 1831:) 1674:: 1659:/ 1632:: 1595:: 1576:) 1505:↓ 1476:↑ 1457:e 1450:t 1443:v 1358:- 1343:- 1333:D 1315:. 1291:: 1264:. 1242:: 1212:. 1202:9 1173:. 1151:: 1123:. 1111:: 1088:. 1076:: 1053:. 1014:. 992:: 965:. 943:: 913:. 899:: 872:. 850:: 799:. 773:. 748:. 719:. 678:. 611:. 341:. 322:. 231:2 229:δ 227:2 217:2 215:β 213:2 203:2 201:Îł 199:2 191:) 189:2 187:Îł 185:2 180:) 178:2 176:ε 174:2 168:2 166:ε 164:2

Index


Specialty
Hematology
Edit this on Wikidata
blood disorders
hemoglobin
red blood cells
single-gene disorders
autosomal co-dominant
thalassemias
alpha-thalassemia
beta thalassemia
pathology
anemia
tetrameric proteins
heme
moiety
Embryonic Hb
embryogenesis
fetal Hb
Adult Hb
HbA2
homozygous
heterozygous
hemolysis
polycythemia
sickle Hb
HbC
assay
polymerizes

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