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Titolo:
PATHOPHYSIOLOGY OF SICKLE-CELL-ANEMIA
Autore:
BOOKCHIN RM; LEW VL;
Indirizzi:
YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,1300 MORRIS PK AVE BRONX NY 10461 PHYSIOL LAB CAMBRIDGE ENGLAND
Titolo Testata:
Hematology/oncology clinics of North America
fascicolo: 6, volume: 10, anno: 1996,
pagine: 1241 -
SICI:
0889-8588(1996)10:6<1241:POS>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTEGRAL MEMBRANE-PROTEINS; RED-CELLS; K-TRANSPORT; ERYTHROCYTES; HEMOGLOBIN; VOLUME; DETERMINANTS; DEOXYGENATION; AUTOXIDATION; PHAGOCYTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
62
Recensione:
Indirizzi per estratti:
Citazione:
R.M. Bookchin e V.L. Lew, "PATHOPHYSIOLOGY OF SICKLE-CELL-ANEMIA", Hematology/oncology clinics of North America, 10(6), 1996, pp. 1241

Abstract

The anemia results from the markedly shortened circulatory survival of SS cells, together with a Limited erythropoietic response. Both independent properties of Hb S-polymerization of the deoxy-Hb and instability of the oxy-Hb-contribute to early red cell destruction by effects on the Hb and on the red cell membranes. The erythroid response is limited mainly by the low oxygen affinity of SS cells, caused by the polymer and increased 2,3-DPG. But the worst culprits in these processes are the dense, dehydrated SS cells (including the ISCs), most of which are formed rapidly from non-Hb F-reticulocytes by cation transport mechanisms triggered by polymerization. Since the clinical consequences of microvascular occlusion far exceed those of anemia per se, measures to lessen the anemia must also inhibit polymerization and sickling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 08:48:00