Antithrombin III Concentrate for Treatment of Chronic Leg Ulcers in Sickle Cell-Beta Thalassemia: A Pilot Study
Authors: Elio Cacciola
Journal: Annals of Internal Medicine (1989)

Brief Reports15 September 1989Antithrombin III Concentrate for Treatment of Chronic Leg Ulcers in Sickle Cell-Beta Thalassemia: A Pilot StudyElio Cacciola, MD, Rosario Giustolisi, MD, Roberto Musso, MD, Angela Longo, BD, Emma Cacciola, MDElio Cacciola, MD, Rosario Giustolisi, MD, Roberto Musso, MD, Angela Longo, BD, Emma Cacciola, MDAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-111-6-534 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptChronic leg ulcers are a common distressing complication in patients with sickle cell-beta thalassemia and are difficult to heal. The pathogenic mechanism of this complication is not known although some factors have been implicated, such as severe anemia or zinc deficiency (1, 2). In this context, however, it is significant that persons with either beta-thalassemia or sickle-cell anemia are regarded as being at thrombotic risk (3, 4).In sickle-cell disease, the recurrent vasocclusive episodes occurring in several areas of the body have been reported to be related to the sickling, which in turn can trigger the activation of blood coagulation...References1. Wintrobe M. Hemoglobinopathies S,C,D,E, and O, and associated disease. In: Wintrobe MM, ed. Clinical Hematology. 7th ed. Philadelphia: Lea & Febiger; 1974:822-54. Google Scholar2. GuptaChoubey VB. RBC survival, zinc deficiency and efficacy of zinc therapy in sickle cell disease. In: Fucharoen S, Rowley PT, Paul NW, eds. Thalassemia: Pathophysiology and Management. Part A. New York: Alan R. Liss; 1987:477-83. Google Scholar3. EldorRachmilewitzKrausz AEY. Hypercoagulable state in beta thalassemia major [Abstract]. Blood. 1988(Suppl 1);72:60a. Google Scholar4. GreenScott DJ. Is sickle cell crisis a thrombotic event? Am J Hematol. 1986;23:317-21. CrossrefMedlineGoogle Scholar5. LeichtmanBrewer DG. Elevated levels of fibrinopeptide A during sickle cell anemia pain crisis—evidence for intravascular coagulation. Am J Hematol. 1978;5:183-90. CrossrefMedlineGoogle Scholar6. NosselTiKaplanSpanondisSolandButler HMKKTV. The generation of fibrinopeptide A in clinical blood samples: evidence for thrombin activity. J Clin Invest. 1976;58:1136-44. CrossrefMedlineGoogle Scholar7. Vinazzer H. Clinical use of antithrombin III concentrates. Vox Sang. 1987;53:193-8. MedlineGoogle Scholar8. CollenSchetzde CockHolmerVerstraete DJFEM. Metabolism of antithrombin III (heparin cofactor) in man: effects of venous thrombosis and of heparin administration. Eur J Clin Invest. 1977;7:27-35. CrossrefMedlineGoogle Scholar9. MarciniakGockerman EJ. Heparin-induced decrease in circulating antithrombin-III. Lancet. 1977;2:581-4. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: From the University of Catania, Catania, Italy. For current author addresses, see end of text. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byInterventions for treating leg ulcers in people with sickle cell diseaseAmerican Society of Hematology 2020 guidelines for sickle cell disease: management of acute and chronic painReview/overview of pain in sickle cell diseaseA treatment algorithm to identify therapeutic approaches for leg ulcers in patients with sickle cell diseaseCritical Reviews: How we treat sickle cell patients with leg ulcersInterventions for treating leg ulcers in people with sickle cell diseaseVasculopathy, inflammation, and blood flow in leg ulcers of patients with sickle cell anemiaInterventions for treating leg ulcers in people with sickle cell diseaseInterventions for treating leg ulcers in people with sickle cell diseaseHypercoagulability in sickle cell disease: a curious paradoxHemostatic Alterations in Sickle Cell Disease: Relationships to Disease PathophysiologyProthrombotic changes in children with sickle cell disease: relationships to cerebrovascular disease and transfusionPATHOPHYSIOLOGY OF VASO-OCCLUSIONLEG ULCERS IN SICKLE CELL DISEASESickle cell disorders and chronic intravascular haemolysis are associated with low plasma heparin cofactor IIAntithrombin III ConcentratesManagement of patients with sickle cell diseaseLarge-vessel occlusion in sickle cell disease: Pathogenesis, clinical consequences, and therapeutic implications 15 September 1989Volume 111, Issue 6Page: 534-536KeywordsAnemiaBeta-thalassemiaBlood coagulationHematology and oncologyPathogensPilot studiesThalassemiaUlcersZinc ePublished: 1 December 2008 Issue Published: 15 September 1989 PDF downloadLoading ...