Non-Hodgkin B-cell lymphomas (B-NHLs) are a highly heterogeneous group of mature B-cell malignancies. Their classification thus requires skillful evaluation by expert hematopathologists, but the risk of error remains higher in these tumors than in many other areas of pathology. To facilitate diagnosis, we have thus developed a gene expression assay able to discriminate the seven most frequent B-cell NHL categories. This assay relies on the combination of ligation-dependent RT-PCR and next-generation sequencing, and addresses the expression of more than 130 genetic markers. It was designed to retrieve the main gene expression signatures of B-NHL cells and their microenvironment. The classification is handled by a random forest algorithm which we trained and validated on a large cohort of more than 400 annotated cases of different histology. Its clinical relevance was verified through its capacity to prevent important misclassification in low grade lymphomas and to retrieve clinically important characteristics in high grade lymphomas including the cell-of-origin signatures and the MYC and BCL2 expression levels. This accurate pan-B-NHL predictor, which allows a systematic evaluation of numerous diagnostic and prognostic markers, could thus be proposed as a complement to conventional histology to guide the management of patients and facilitate their stratification into clinical trials.

Background: Peanut allergy is one of the most severe food allergies in children. The diagnostic gold standard is the oral food challenge (OFC). However, OFC has inherent risks and is time consuming. The measurement of specific immunoglobulin E (sIgE) to peanut components in blood detects peanut sensitization, but the decision point predicting allergy is still unclear. The aim of this study was to determine the diagnostic value of these tests for the evaluation of child peanut allergy. Methods: In this retrospective study, 81 children were referred for peanut allergy. The diagnosis of peanut allergy was based on the clinical context and a positive OFC. Levels of sIgE against whole peanuts or peanut components (Ara h 2 and Ara h 8) were determined by immunoassay. Results: The Ara h 2 sIgE assay has the best negative predictive value (0.93) and positive predictive value (1) at a cutoff of 0.1 kU/l. Ara h 2 sIgE titers can predict the risk of anaphylaxis (14 kU/l, high risk). The Ara h 8 sIgE assay is not able to discriminate peanut-allergic patients but can be used to evaluate possible cross-reactions to birch pollen with a low risk of anaphylaxis. The best diagnostic strategy is to first determine the Ara h 2 sIgE level and, if negative, evaluate Ara h 8 sIgE. Conclusions: We propose an algorithm for a better use of peanut component sIgE immunoassays that should improve their diagnostic value and avoid unnecessary OFC.

Infantile pyknocytosis (IP) is a rare, probably misestimated, cause of non‐immune neonatal hemolytic anemia evolving in two phases: an initial phase with severe jaundice, followed by a second phase with hemolytic anemia, which may require neonatal intensive care. The diagnosis of IP is based on the transient presence on blood smear of hyperdense, contracted, and/or spiculated red blood cells (pyknocytes), associated with the spontaneous resolution of clinico‐biological features and the exclusion of other causes. If the etiology remains undetermined, some contributing factors, such as oxidative stress, have been proposed. We report the description of 16 patients with IP aiming at clarifying the circumstances associated with the development of this acquired disorder. In the acute phase, the mean hemoglobin nadir and pyknocyte count were 7.8 g/dL and 11%, respectively, and strikingly, Heinz bodies were evident in 50% of the newborns, but in 100% after prolonged incubation (4 hours). A high proportion of Mediterranean or African ancestry was noted in newborns, as well as a significant number of peripartum events, such as respiratory distress. If the etiology of IP is certainly multifactorial, our series reinforces the role of oxidative stress, which may, at least in part, find origin in desaturation episodes in newborns.

Glucose‐6‐phosphate dehydrogenase (G6PD) deficiency is a common enzymopathy that affects red blood cells (RBCs) and renders them susceptible to oxidative stress. G6PD deficiency can cause hemolytic anemia, especially after exposure to certain drugs or infections. The diagnosis of G6PD deficiency is usually based on spectrophotometric measurement of enzyme activity, but this method has limitations in heterozygous females and in patients with other hematological disorders. In this study, we evaluated the use of flow cytometry as an alternative method for detecting G6PD deficiency in 514 samples (265 females and 249 males) from a clinical laboratory. We compared the results of flow cytometry with those of spectrophotometry and molecular analysis, and assessed the performance of flow cytometry in different subgroups of patients. We found that flow cytometry was able to identify G6PD deficiency in most cases, with high sensitivity and specificity. Flow cytometry also allowed the quantification of the percentage of G6PD‐deficient RBCs, which varied among heterozygous females due to X‐chromosome inactivation. Moreover, flow cytometry detected several cases of G6PD deficiency that were missed by spectrophotometry, especially in heterozygous females with normal or subnormal enzyme activity. However, flow cytometry also showed some false negative results, mainly in patients with sickle cell disease. Therefore, flow cytometry is a reliable and efficient tool for screening G6PD deficiency, but some precautions should be taken in interpreting the results in patients with other hematological conditions.