Erik Adolf von Willebrand (1 February 1870 – 12 September 1949) was a Finnish physician who made major contributions to hematology.

During this time, he spent his summers collecting botanical, lepidopterological and ornithological specimens, and his winters exploring the Gulf of Bothnia.

[4] After graduation, Von Willebrand became assistant physician in the department of medicine at the Deaconess Hospital in Helsinki, where Ossian Schauman supervised his doctoral thesis on the changes in hemocyte count after venesection.

[4] He received his Ph.D. in 1899 from the University of Helsinki, for the thesis Zur Kenntnis der Blutveränderungen nach Aderlässen ("Blood Changes after Venesection").

[6][7] After the completion of his dissertation in 1899, Von Willebrand was appointed chief physician at a spa in Heinola, and he shifted his interest from hematology to applied physiology.

During this period, he researched thermotherapy, particularly the health effects of saunas,[8] and phototherapy, and invented an apparatus for measuring the dermal excretion of carbon dioxide and water.

[6] In 1918, nearly two decades after his last paper of the sort, Von Willebrand resumed his publishing of hematologic works, releasing studies on aplastic, hypochromic and pernicious anaemia.

[9] He also published a study regarding heart valve conditions based on data from over 10,000 autopsies performed in Helsinki from 1867 to 1916,[9] and was a pioneer in the use of insulin, describing in 1922 its use in the treatment of diabetic comas.

[6] In February 1924, he successfully brought a moribund patient out of a diabetic coma through the application of insulin, using some of the first batch of the hormone ever delivered to Finland.

[7] Hjördis was brought to Von Willebrand's laboratory in Helsinki and he did not himself visit Föglö, but with the cooperation of a local schoolteacher he mapped the family pedigree.

An analysis of the heredity involved led Von Willebrand to assume the inheritance was dominant, in contrast to hemophilia which was known to be a recessive disorder.

[7] The earlier authors attributed the condition to hemophilia (even in the cases of females) or to thrombopathy, which was discovered shortly before as the cause of what had previously been known as purpura hemorrhagica or Werlhof's disease.

[7] He recorded a normal or slightly reduced number of platelets and an undisturbed clot retraction, unlike Glanzmann's thrombasthenia.

[7] Von Willebrand published a German-language version of Hereditär pseudohemofili in 1931, which attracted international attention in the disease.

[5][13] In 1957, it was discovered that von Willebrand disease is caused by a deficiency of a protein in blood plasma that enables hemostasis.

[15] In 2011, Jan van Gijn and Joost P. Gijselhart, writing in the Nederlands Tijdschrift voor Geneeskunde, remarked that Von Willebrand was not far wrong when he named the disease "hereditary pseudohemophilia".