The Progress Test of the European Hematology Association: A New Tool for Continuous Learning.

info:eu-repo/semantics/publishedVersio

The Progress Test of the European Hematology Association: A New Tool for Continuous Learning

The European Hematology Curriculum, first launched in 2006, was created by the European Hematology Association (EHA) with the aim of harmonizing hema tology training in Europe. Its goals were to define the different areas hematologists are expected to cover during their training, and to establish the minimum recommended levels of competence that a hematology trainee should attain. EHA's education platform (EHA Campus) offers opportu nities for continuous learning for both trainees and specialists. Content is guided by the European Hematology Curriculum, which provides a structure for individual study and self-assess ment. To complete this organized learning environment, a tool for objective assessment of knowledge during and after specialist training was needed. In the spring of 2020, EHA started offering a progress test: a longitudinal test based on equivalent evalua tions given at fixed intervals, assessing developments in knowl edge. The EHA Progress Test was inspired by an earlier version developed by the Swedish Hematology Association in 2013, which has become widely used by specialist trainees and spe cialists in Sweden. Noticeable pedagogical effects, like targeted study efforts in weak knowledge areas, changes in clinical rota tions, and more have been reported in personal questionnaires

A case of legionellosis during treatment with a TNFα antagonist

We report a patient with Legionella pneumophila pneumonia after infliximab therapy for rheumatoid arthritis. Arguments are discussed for an emerging incidence of infections with intracellular microorganisms, granulomatous and non-granulomatous, in patients having received anti-TNFα therapy. These discussions consist of clinical and epidemiological data, experimental data in animals, theoretical evidence, and we provide a possible pathogenetic mechanism

An Acute Promyelocytic Leukemia Resistant to All-Trans Retinoic Acid: A Case Report of the ZBTB16::RARa Variant and Review of the Literature

Introduction: Acute promyelocytic leukemia (APL) is characterized by the PML::RARa gene fusion and treatment consists of all-trans retinoic acid (ATRA). Rarely, genetic APL variants have been described which are insensitive to ATRA treatment and are therefore associated with a worse prognosis. Rapid identification of the APL variant is essential to start the correct treatment. Case Presentation: Here, we present a case of a 66-year-old male patient with weight loss and arthralgia. Laboratory results showed an anemia and mild leukocytosis with predominantly monocytes. Bone marrow investigation unexpectedly revealed a t(11;17)(q23;q21). This raised suspicion of an ATRA-resistant APL. By demonstrating the ZBTB16::RARa gene fusion, the diagnosis was confirmed. Conclusion: This case study emphasizes the importance of integrated diagnostics and provides guidance to recognize the ZBTB16::RARa APL, which is the most prevalent ATRA-resistant APL. Furthermore, an overview of other genetic APL variants is presented and how to treat these uncommon diseases in clinical practice

Severe Secondary Polycythemia in a Female-to-Male Transgender Patient While Using Lifelong Hormonal Therapy: A Patient's Perspective

After a registered drug is available on the market and used in everyday circumstances, hitherto unknown adverse drug reactions (ADRs) may occur. Furthermore, the patient can experience a previously unknown course of a known ADR. Voluntary reports by patients play an important role in gaining knowledge about ADRs in daily practice. The Netherlands Pharmacovigilance Centre Lareb received a report from a 55-year-old female-to-male transgender patient who experiences secondary polycythemia while using lifelong testosterone therapy. The onset age of the symptoms was 38 years. The symptoms appeared gradually and after approximately 1 year it was clear that the patient's hemoglobin and hematocrit had started to increase. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient's polycythemia and use of the suspect drug. Polycythemia is a known ADR in testosterone treatment, but little attention has been paid to the possible severity and complications of these symptoms as well as the impact on the patient's well-being

18 F-fluorothymidine uptake in follicular lymphoma and error-prone DNA repair

BACKGROUND: We observed a disproportional 18 F-fluorothymidine (F-FLT) uptake in follicular lymphoma (FL) relative to its low cell proliferation. We tested the hypothesis that the 'excess' uptake of 18 F-FLT in FL is related to error-prone DNA repair and investigated whether this also contributes to 18 F-FLT uptake in diffuse large B cell lymphoma (DLBCL). METHODS: We performed immunohistochemical stainings to assess the pure DNA replication marker MIB-1 as well as markers of both DNA replication and repair like PCNA, TK-1 and RPA1 on lymph node biopsies of 27 FLs and 35 DLBCLs. In 7 FL and 15 DLBCL patients, 18 F-FLT-PET had been performed. RESULTS: 18 F-FLT uptake was lower in FL than in DLBCL (median SUVmax 5.7 vs. 8.9, p = 0,004), but the ratio of 18 F-FLT-SUVmax to percentage of MIB-1 positive cells was significantly higher in FL compared with DLBCL (p = 0.001). The median percentage of MIB-1 positive cells was 10% (range, 10% to 20%) in FL and 70% (40% to 80%) in DLBCL. In contrast, the median percentages of PCNA, TK-1 and RPA1 positive cells were 90% (range, 80 to 100), 90% (80 to 100) and 100% (80 to 100) in FL versus 90% (60 to 100), 90% (60 to 100) and 100% (80 to 100) in DLBCL, respectively. CONCLUSIONS: This is the first demonstration of a striking discordance between 18 F-FLT uptake in FL and tumour cell proliferation. High expression of DNA replication and repair markers compared with the pure proliferation marker MIB-1 in FL suggests that this discordance might be due to error-prone DNA repair. While DNA repair-related 18 F-FLT uptake considerably contributes to 18 F-FLT uptake in FL, its contribution to 18 F-FLT uptake in highly proliferative DLBCL is small. This apparently high contribution of DNA repair to the 18 F-FLT signal in FL may hamper studies where 18 F-FLT is used to assess response to cytostatic therapy or to distinguish between FL and transformed lymphoma