IMMUNOLOGIC MECHANISMS IN IDIOPATHIC AND NEONATAL THROMBOCYTOPENIC PURPURA

Abstract

Article1 March 1953IMMUNOLOGIC MECHANISMS IN IDIOPATHIC AND NEONATAL THROMBOCYTOPENIC PURPURAWILLIAM J. HARRINGTON, M.D., CHARLES C. SPRAGUE, M.D., VIRGINIA MINNICH, M.S., CARL V. MOORE, M.D., F.A.C.P., ROBERT C. AULVIN, B.S., REUBENIA DUBACH, Ph.D.WILLIAM J. HARRINGTON, M.D., CHARLES C. SPRAGUE, M.D., VIRGINIA MINNICH, M.S., CARL V. MOORE, M.D., F.A.C.P., ROBERT C. AULVIN, B.S., REUBENIA DUBACH, Ph.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-38-3-433 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe mechanisms responsible for the low platelet count in idiopathic thrombocytopenic purpura are not well understood despite the careful studies by many competent investigators. The thrombocytopenia has been attributed to:1. A decrease in the rate of platelet formation from megakaryocytes1, 2 because of splenic inhibition of these cells;3, 4, 5, 62. An increase in the rate of platelet destruction by the spleen,7, 8, 9, 10, 11, 12 and3. A combination of damage to both megakaryocytes and circulating platelets.13, 14Evidence to support the latter concept has been presented recently. A thrombocytopenic factor which damages circulating platelets and...Bibliography1. Frank E: Die essentielle Thrombopenie. (Konstitionelle Purpura Pseudo-Hämophilie) I. Klinisches Bild., Berl. klin. Wchnschr. 52: 454, 1915. II. Pathogenese, Ibid. 52: 490, 1915. Google Scholar2. Frank E: Die hämorrhagischen Diathesen, in Schittenhelm, A.: Handbuch der Krankheiten des Blutes und der Blutbildenden Organe, 1925, Julius Springer, Berlin, vol. 2, p. 289. CrossrefGoogle Scholar3. Seeliger S: Über Organbefunde und ihre Bedeutung für die Pathogenese bei essentieller Thrombopenie und Aleukie, Klin. Wchnschr. 3: 731, 1924. CrossrefGoogle Scholar4. 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CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Presented (in part) at the Thirty-third Annual Session of the American College of Physicians, Cleveland, Ohio, April 23, 1952.From the Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri.This work was supported by Grant No. H-22 C (6) from the National Heart Council of the U. S. Public Health Service, Bethesda, Maryland.†On assignment from the National Institute of Arthritis and Metabolic Diseases, U. S. Public Health Service. 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