The Harrington–Hollingsworth experiment was an experiment that established the autoimmune nature of the blood disorder immune thrombocytopenic purpura.[1] [2] It was performed in 1950 by the academic staff of Barnes-Jewish Hospital in St. Louis, Missouri.[2] __TOC__
The experiment was undertaken in 1950 by William J. Harrington and James W. Hollingsworth, who postulated that in patients with idiopathic thrombocytopenic purpura (ITP), it was a blood factor that caused the destruction of platelets.[2] To test this hypothesis, Harrington received 500 ml of blood from a patient with ITP.[2] Within three hours, his platelets dropped to dangerously low levels and he experienced a seizure.[2] His platelet count remained extremely low for four days, finally returning to normal levels by the fifth day.[2] Bone marrow biopsy from Harrington's sternum demonstrated normal megakaryocytes, the cells necessary for platelet production.[2]
Subsequently the experiment was repeated on all suitable staff members at the Barnes-Jewish Hospital. All subjects developed low platelet counts within three hours, and all recovered after a period of several days.[2]
Schwartz notes that the Harrington–Hollingsworth experiment was a turning point in the understanding of ITP's pathophysiology:
The experiment was the first to demonstrate that infusion of an ITP patient's plasma into a normal patient caused a precipitous drop in platelet count.[2] This suggested that low platelet counts (thrombocytopenia) in patients with ITP was caused by a circulating factor found in the blood.[2] Many studies performed since then have demonstrated that this circulating factor is in fact a collection of immunoglobulins.[3] [4] Many physician-scientists believe the findings had a major influence on the field of autoimmunity, which was not universally accepted at the time as a mechanism of human disease.