Jan Gösta Waldenström and rheumatology

On 2 September 1943, Jan Waldenstrom (1906–1996) successfully submitted a paper to Acta Medica Scandinavica describing two patients with a new disease. The discovery was to make him world famous.1 This year marks the 75th anniversary of macroglobulinaemia and it coincided with the 10th biennial international workshop of Waldensm’s macroglobulinaemia, discussing advances in the genetic basis, pathogenesis and treatments of the disease.2 Jan Waldenstrom (JW) would have enjoyed this workshop immensely, sharing the information that over 95% of the patients had somatic mutations affecting the MYD88 gene on the second chromosome as well as the impressive advances in treatment. Attending this excellent meeting brought back memories of my time as Waldenstrom’s PhD student and triggers me to compose this vignette, focusing on connexions between the interests of my mentor and rheumatology. For a more comprehensive account of Jan Waldenstrom’s legacy, I recommend Robert Kyle’s superb obituary, published in Blood , a journal JW was attached to from its start.3 After the successful defence of his landmark PhD thesis on acute intermittent porphyria,4 Waldenstrom’s interest focused on haematology. He worked in Uppsala, a university where the study of proteins had prominence. There, The Svedberg had developed the ultracentrifuge and Arne Tiselius the free electrophoresis and Robin Fahreus the elevated sedimentation rate (ESR). Conditions with ESR caught JW’s special attention. An early witness is a paper from 1937, analysing five cases diagnosed with uveoparotitis, a rare condition most prevalent in women and then considered by many to be a form of tuberculosis. He noticed several multiorgan manifestations, the similarities with von Mikulicz disease and Boeck’s sarcoid, the presence of high ESR, unspecific Wassermann reaction, absence of proof of tuberculosis, presence of …