Background The COVID‐19 vaccine from AstraZeneca (AZD1222) is one of several vaccines introduced to provide immunity against SARS‐CoV‐2. Recently, more than 50 cases have been reported presenting a combination of thrombosis, thrombocytopenia, and remarkably high levels of anti‐platelet factor 4 (PF4)/polyanion antibodies post‐AZD1222 vaccination. Now linked to the vaccine, the condition is referred to as vaccine‐induced immune thrombotic thrombocytopenia. The European Medicines Agency still recommends vaccination with AZD1222, but several European countries have temporally paused and/or restricted its use because of the perceived risk of this severe side effect. Because there is no description of PF4/polyanion antibody testing in the clinical trials, knowledge about the prevalence of such antibodies in a vaccinated cohort is needed. Objectives To investigate prevalence of thrombocytopenia and anti‐PF4/polyanion antibodies in a population recently vaccinated with AZD1222. Patients/Methods Four hundred and ninety‐two health care workers recently vaccinated with the first dose of AZD1222 were recruited from two hospitals in Norway. Study individuals were screened for thrombocytopenia and the presence of anti‐PF4/polyanion antibodies with a PF4/PVS immunoassay. Side effects after vaccination were registered. Results The majority of study participants had normal platelet counts and negative immunoassay. Anti‐PF4/polyanion antibodies without platelet activating properties were only detected in six individuals (optical density ≥0.4, range 0.58–1.16), all with normal platelet counts. No subjects had severe thrombocytopenia. Conclusions We found low prevalence of both thrombocytopenia and antibodies to PF4/polyanion‐complexes among Norwegian health care workers after vaccination with AZD1222.

Human papillomavirus (HPV) is associated with cervical intraepithelial neoplasia and cervical cancer. Vaccination against major oncogenic types of HPV has proven benefit in preventing these conditions. 1 HPV vaccines have been used for more than a decade, and their use is increasing worldwide. 2 Recently, a syndrome of thrombosis and thrombocytopenia occurring 5-24 days after vaccination with ChAdOx1 nCoV-19 (AstraZeneca) and Ad26.COV2.S (Johnson & Johnson), both recombinant adenoviral vector vaccines encoding the spike protein antigen of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was described. [3][4][5][6] This syndrome has been named vaccine-induced immune thrombotic thrombocytopenia (VITT) or

We recently reported on a 25-year-old female without a history of heparin exposure, presenting with thrombocytopenia, thrombosis, and elevated D-dimer levels 10 days after nine-valent human papillomavirus (HPV) vaccination (Gardasil, Merck and Co). 1 The patient's samples activated platelet factor 4 (PF4)-treated platelets and recognized PF4-polyanion complexes in heparin-induced thrombocytopenia (HIT) ELISA (PF4-polyanion enzyme-linked immunosorbent assay).As previously noted, 1 thrombosis sites included the right internal iliac vein and bilateral pulmonary emboli. When it was recognized that the AUTHOR CONTRIBUTIONS Adam Kanack performed the research studies. Adam Kanack, Ingvild

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BackgroundA feature of myeloproliferative neoplasia is transforming to more aggressive and malignant myeloid neoplasia, including acute myeloid leukemia. Different pathogenesis mechanisms participate in transformation, including transformation of existing potential preleukemic clones, since JAK2-mutant myeloproliferative neoplasms often transform to JAK2 wild-type acute myeloid leukemia.Case presentationHere, we present an 80 year old man with a JAK2-V617F mutant primary myelofibrosis. After 10 months the disease transform into a Philadelphia chromosome positive acute myeloid leukemia, detecting the cytogenetic aberration; t(9;22)(q34;q22) encoding the rare BCR-ABL1 fusion gene; e6a2. The patient had treatment response to tyrosine kinases, illustrating the potential benefits of such approach in treating these patients subset.ConclusionThe case illustrates the potential of leukemic transformation to Philadelphia chromosome positive myeloid malignancies from potential existing preleukemic clones, and the awareness of such an evolution among patients with myeloproliferative neoplasms. Tyrosine kinases have potential effect also in patients presenting without chronic myeloid leukemia and with rare BCR-ABL1 fusion transcripts, and should probably be a part of the treatment approach.