No abstract

Background: The oral aspirin (ASA) provocation test is considered to be the gold standard in the diagnosis of ASA sensitivity. However, since it may be associated with severe adverse reactions, safer alternatives would be highly desirable. The basophil activation test has been proposed as such an alternative, but there is limited information about its usefulness. Our aim was to evaluate the clinical usefulness of flow cytometric basophil activation in the diagnosis of ASA sensitivity. Methods: Patients with ASA sensitivity (n = 18), patients with ASA tolerance (n = 12) and healthy volunteers (n = 12) were included in the study. A 2-day single-blind placebo-controlled oral ASA provocation test was performed on all patients. Basophil activation after lysine-ASA and diclofenac stimulation was measured by Flow-CAST^TM (Bühlmann Laboratories) for CD63 and an allergenicity kit (Beckman Coulter) for CD203c. The results of CD63 and CD203c were compared within groups, and sensitivity and specificity of the assay were measured against oral ASA provocation. Results: The highest sensitivity and specificity of CD63 were 33.3 and 79.2%, respectively, and of CD203c were 16.7 and 100%, respectively, for ASA. The highest sensitivity and specificity of CD63 were 16.7 and 91.7%, respectively, and of CD203c were 22.2 and 100%, respectively, fordiclofenac. Neither the addition of CD203c to CD63 nor the addition of diclofenac improves the overall sensitivity and specificity of CD63 to ASA. Conclusion: At present, basophil activation using CD63 and CD203c does not seem to be optimally sensitive for the diagnosis of ASA sensitivity.

No abstract

The CD203c basophil activation test seems to be a reliable tool in the diagnosis of grass pollen allergy. It could be used when conventional diagnostic tests fail or can not be performed.

Purine nucleoside phosphorylase (PNP) deficiency is a rare combined immunodeficiency disorder presenting with clinically recurrent infections, failure to thrive, various neurological disorders, malignancies, and autoimmune diseases. Here, we report two sisters with a fatal course of PNP deficiency due to delay in diagnosis. The first patient developed a liver abscess by Aspergillus fumigatus and the second patient developed Mycobacterium tuberculosis complex lymphadenitis and probable pulmonary tuberculosis due to disseminated BCG infection. The patients also suffered from sclerosing cholangitis. Mutation analysis of the PNP gene from both sisters revealed a homozygous mutation for a G>A at nucleotide 349 (349 G>A transition), which changes alanine 117 to theronine in exon 4 (A117T). An increased awareness of early signs, symptoms, and abnormal laboratory findings of PNP deficiency will establish the early prognosis and treatment.

Background: An aluminum hydroxide-adsorbed depot allergoid preparation of six-grass pollen allergens has been developed for short-term preseasonal immunotherapy in pollinosis. However, only limited knowledge exists about its immunological and clinical effects. The aim of this study was to evaluate the basophil response, which can explain early clinical findings of short-term preseasonal allergoid immunotherapy in allergic rhinitis. Methods: In a double-blind, placebo-controlled study, 31 patients allergic to grass pollens received one course of short-term preseasonal allergoid immunotherapy or placebo. Immunogenicity was assessed by the levels of specific IgG4, IgE antibodies and an allergen-induced CD203c basophil activation test. The primary clinical end point was the combined symptom and medication score/average combined score (ACS). Results: There was a 52.9% difference in ACS between the treatment and placebo groups in favor of immunotherapy (p = 0.01). Active treatment induced Phleum pratense-specific IgG4 and IgE antibodies (p < 0.05). A decrease in allergen-induced basophil activation at submaximal allergen concentrations was demonstrated at the end of immunotherapy and at the peak of the grass pollen season after immunotherapy. Conclusions: This study shows that grass pollen-allergic patients treated with one course of short-term preseasonal allergoid immunotherapy exhibit a decrease in allergen-induced basophil activation, an increase in allergen-specific IgG4 antibodies and early clinical improvement.

This study suggests that mode of delivery affects cord blood Treg cells. Higher CD4+CD25+FOXP3+ Treg cells of newborns and their mothers in vaginal delivery group and their relationship with serum cortisol levels suggest a stress phenomenon related to vaginal delivery.

Vascular endothelial growth factor (VEGF) seems to play a central role in angiogenesis-lymphangiogenesis in hematological malignancies. There are limited data related to childhood hematologic malignancies. The aim of the study was to evaluate soluble VEGF (sVEGF) levels in children with acute leukemia and malignant lymphoma (ML) at diagnosis and in remission. The levels of serum sVEGF were measured by enzyme-linked immunosorbent assay (ELISA) in 20 children with acute leukemia, 33 children with different histopathological subtypes of ML, and 20 healthy controls. The levels of sVEGF at diagnosis (range 2 -1040 pg/mL; median 52 pg/mL) was significantly lower than in remission (range 136 -1960 pg/mL; median 630 pg/mL) in acute myeloid leukemia (AML) group (P = .018). The sVEGF levels at diagnosis (range: 2 -640 pg/mL; median 89 pg/mL) was significantly lower compared to remission values (range: 116 -1960 pg/mL; median 136 pg/mL) in patients with acute lymphoblastic leukemia (ALL) (P = .002). In ML group, including Burkitt's lymphoma (BL), T-cell non-Hodgkin's lymphoma (NHL), and Hodgkin's lymphoma (HL), sVEGF levels at diagnosis were higher than remission levels, but there was no statistically significant difference (P >.05). On the other hand, there were significant difference between levels in active disease and control group, ie, BL versus control, T-cell NHL versus control, and HL versus control (P = .008, P = .043, P = .007, respectively). The authors noticed that sVEGF levels showed distinct behavioral pattern in different childhood malignancies at diagnosis and in remission. In acute leukemia and ML patients, VEGF acts through different pathophysiological mechanisms, in both bone marrow (BM) angiogenesis and lymphoid tissue lymphangiogenesis.