The aim of the study is to evaluate the association between platelet (PLT) parameters and the need for treatment of retinopathy of prematurity (ROP) in preterm infants. This single-center, retrospective cohort study was conducted at the Neonatal Intensive Care Unit of Fukushima Medical University Hospital between January 1, 2011, and December 31, 2023. The present study included preterm infants born before 30 weeks of gestation. Medical records were reviewed for 1,836 infants, of whom 187 met the inclusion criteria. Data on PLT parameters and ROP treatment were extracted from the medical records. Receiver operating characteristic analysis was used to determine cutoff values for PLT parameters associated with the need for ROP treatment. Multiple logistic regression analyses were performed to assess the association between ROP treatment and PLT parameters at birth and on day of life 28. Among the 187 infants included, 42.8% required treatment for ROP. After adjusting for confounders, an association was found between ROP treatment and plateletcrit (PCT) values < 0.23% (odds ratio [OR]: 3.44; 95% confidence interval [CI]: 1.37-8.63) and platelet mass index (PMI) values < 2,303.0 fL/nL (OR: 4.50; 95% CI: 1.77-11.41) at birth. Infants born before 30 weeks of gestation with PCT values < 0.23% and PMI values < 2,303.0 fL/nL at birth had an increased risk of developing ROP warranting treatment. · ROP is a leading cause of preventable blindness in preterm infants.. · There are no reliable early postnatal biomarkers that can predict ROP outcomes.. · We evaluated the association between PLT parameters and the ROP treatment in preterm infants.. · PCT < 0.23% and PMI < 2,303 fL/nL at birth were associated with a risk of requiring ROP treatment.. · PLT parameters may be useful in determining the ROP screening schedule and treatment for ROP..

Cancer-associated thrombosis (CAT) remains a leading cause of morbidity and mortality in oncology, reflecting the convergence of tumor-driven hypercoagulability, endothelial dysfunction, and venous stasis. While current models of CAT pathogenesis emphasize tumor-derived procoagulant factors, platelets, and leukocytes, the contribution of red blood cell (RBC) biomechanics has received comparatively limited attention. Emerging evidence indicates that both malignancy and cancer-related therapies impair RBC deformability and increase RBC aggregation; alterations that are known to influence blood viscosity, platelet margination, microvascular flow, and clot contraction. Hence, these alterations have been hypothesized to promote thrombosis, supported by evidence of increased thrombosis risk in diseases that primarily affect RBC biomechanics. While cancer-induced alterations in RBC biomechanics and their role in thrombosis are well-described in non-cancerous conditions, the relationship between altered RBC biomechanics and thrombosis in the setting of cancer has not been thoroughly investigated. Accordingly, this review synthesizes the mechanistic and clinical data linking altered RBC biomechanics to thrombus initiation, propagation, and stability, with particular emphasis on their relationship with established cancer-related prothrombotic pathways such as extracellular vesicle release, neutrophil extracellular trap formation, stasis, and oxidative stress. Finally, we critically assess current CAT risk assessment models (RAMs) and discuss the potential role of RBC biomechanical parameters as dynamic, integrative biomarkers to improve thrombosis risk stratification in cancer patients. Advances in automated and standardized rheological technologies may facilitate the clinical translation of RBC biomechanics, offering new opportunities to refine risk prediction and deepen mechanistic understanding of CAT.

The Total Thrombus-formation Analysis System 01 (T-TAS 01) is an advanced microchip-based device that enables quantitative assessment of blood thrombogenicity. However, broader clinical implementation remains limited by the lack of well-established reference intervals (RIs) in healthy, antithrombotic drug-naïve individuals. This study aimed to define RIs and identify clinical determinants of blood thrombogenicity in antithrombotic drug-naïve adults using T-TAS 01. Blood thrombogenicity was measured using T-TAS 01 in 319 adults without antithrombotic therapy who underwent health checkups at the Miyakonojo Health Service Center. The T-TAS 01 parameters, PL18-AUC10 and AR10-AUC30, were calculated as the areas under the flow-pressure curves of the PL-chip (type I collagen-coated) and the AR-chip (type I collagen and tissue factor-coated), respectively. Their associations with clinical parameters were assessed using multivariate regression analysis. The median age was 46.0 years; 64.3% of participants were female, and 82.1% had no hypertension, dyslipidemia, or diabetes. The median platelet count was 247 × 109/L. The median PL18-AUC10 and AR10-AUC30 values were 392.3 and 1335.9, with RIs of 236.3 to 468.1 and 1010.0 to 1496.2, respectively. PL18-AUC10 was independently associated with white blood cell count (coefficient, 5.15; 95% CI, 0.88-9.41) and platelet count (0.36; 95% CI, 0.25-0.47), whereas AR10-AUC30 was independently associated with body mass index (4.06; 95% CI, 0.06-8.06), platelet count (0.79; 95% CI, 0.52-1.06), and γ-glutamyl transpeptidase (-0.54; 95% CI, -0.90 to -0.18). Our findings provide foundational reference data for the clinical application of T-TAS 01 and support its potential as a point-of-care tool for individualized assessment of thrombogenicity.

Emerging role of cell membrane-coated nanoparticles in targeted therapy for brain disorders.

Long-term safety, tolerance, and population-specific effects of innovatively fermented D-allulose are lacking in the Chinese population. This study aimed to address these gaps and support its application as a novel food ingredient in China. A 30-day randomized, double-blind, parallel-group design with pre-post comparison trial was conducted, enrolling 50 healthy Chinese adults (high-dose group: 36 g/day, 0.6 g/kg body weight, n = 26; low-dose group: 24 g/day, 0.4 g/kg body weight, n = 24). Gastrointestinal tolerance was monitored via daily questionnaires; systemic safety was evaluated using hematological tests, serum biochemical tests, urinalysis, fecal analysis, and body composition measurements. The incidence of gastrointestinal symptoms was 48.0%, which were mild, transient, and most frequent on Days 1-3, with no significant intergroup differences. All statistically significant changes in safety indicators remained within normal clinical reference ranges. Compared with baseline, the 30-day intervention resulted in reduced red blood cell count, hematocrit, and platelet count, as well as elevated mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration in both groups. For serum biochemical parameters, levels of alkaline phosphatase, gamma-glutamyl transferase, uric acid, total cholesterol, and high-density lipoprotein cholesterol decreased in both groups, while fasting blood glucose was reduced only in high-dose group. Notably, high-dose D-allulose intervention decreased bone mineral density T-scores in participants aged 35 years and older. All statistically significant alterations in the measured indicators remained within normal clinical ranges and were clinically insignificant. This study provides critical safety data to support the planned approval of D-allulose as a novel food ingredient in China in 2025. Its modulation of hematological and serum biochemical parameters suggests effects on hematopoiesis and glycolipid metabolism. Given the limitations of the 30-day intervention duration, relatively modest sample size, and restriction to healthy normal-BMI adults, a provisional safe intake limit of 0.4 g/kg body weight per day is proposed for Chinese adult population, requiring validation in longer-term and larger-scale studies.

HSP47 inhibitor Col003 attenuates thromboinflammation after cerebral ischemia-reperfusion by suppressing GPVI-mediated CD84 shedding in platelets.

Diabetic wounds represent an escalating clinical challenge driven by the rising global prevalence of diabetes and the lack of effective treatments. Platelets serve as natural reservoirs of diverse growth factors, holding considerable promise for promoting tissue regeneration and wound repair. However, current platelet-derived therapies are constrained by donor dependence, protocol variability, and inconsistent product quality. This study established an efficient in vitro protocol for generating functional platelets from human hematopoietic stem and progenitor cells (HSPCs). These regenerative platelets were subsequently lysed to produce induced human platelet lysate (ihPL). The contents of key growth factors in ihPL and human peripheral blood platelet lysate (hPL) were compared by enzyme-linked immunosorbent assay (ELISA). We established diabetic mice wound model to evaluate the therapeutic efficacy of ihPL on wound healing. Furthermore, in vitro experiments assessed the effects of ihPL on dermal fibroblasts proliferation, migration, and collagen synthesis. Transcriptome sequencing and Western blot (WB) were employed to elucidate the underlying signaling pathways. HSPCs differentiation into megakaryocytes exceeded 80%, with a subsequent platelet production efficiency of 38.3% ± 5.35%. ELISA revealed that the concentrations of fibroblast growth factor (140.1 ± 0.986 vs. 1.0 ± 0.008) and vascular endothelial growth factor (12.74 ± 5.280 vs. 1.0 ± 0.276) were significantly elevated in ihPL compared with hPL. In diabetic mice, ihPL (89.44% ± 9.83%), hPL (73.60% ± 12.21%), and epidermal growth factor (EGF, 59.72% ± 12.87%) significantly accelerated wound closure compared with the vehicle control group (43.53% ± 16.09%) at day 14 (P < 0.05). Notably, ihPL demonstrated superior efficacy relative to both hPL and EGF (P < 0.05). Histological analysis and Optical coherence tomography angiography confirmed enhanced extracellular matrix deposition and angiogenesis with ihPL versus vehicle control. Furthermore, ihPL significantly promoted dermal fibroblasts proliferation, migration, and collagen synthesis in vitro. Transcriptome analyses indicated activation of multiple tissue regeneration-associated signaling pathways and WB further confirmed the upregulation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway representing a potential underlying mechanism. This study establishes a standardized, donor-independent, and immunologically safer cell-based therapeutic strategy for diabetic wound management, with considerable potential for clinical translation.

Homologous blood transfusion (HBT) doping, using donor red blood cells (RBCs) to enhance oxygen capacity, remains a persistent challenge for doping control laboratories, especially in specific populations. Current RBC antigen-based flow cytometric detection (double population, DP) has limited sensitivity in genetically homogeneous populations due to common phenotypic overlap. This study aimed to enhance HBT detection by optimizing population-specific RBC antigen panels and incorporating complementary platelet-derived human leukocyte antigen (HLA) markers. Based on antigen-negative frequency, M, N, and Leb antigens were evaluated as candidate markers for improved discrimination in the Japanese population. In simulated HBT samples with a 5% mixing ratio, N antigen showed a clearly separated bimodal distribution, indicating strong potential for DP detection. Although Leb antigen showed unclear DP, M antigen displayed uniformly high expression, useful for distinguishing expressing populations. In addition, platelet HLA analysis, especially targeting HLA-A24, enabled detection of donor-derived components even with identical RBC antigen phenotypes. Mixed samples containing as low as 1%-5% donor cells produced visually detectable DP signals in the platelet gate. In conclusion, integrating a race-tailored RBC antigen panel with complementary platelet HLA monitoring may provide a potentially improved framework for HBT detection, particularly in ethnically homogeneous populations like Japan. The optimal antigen panel is highly population-specific due to genetic variations, requiring adaptation for other diverse ethnic groups. Future cohort studies are warranted to validate this dual approach and refine detection sensitivity.

Mass casualty and disaster events (MCEs) and national blood donation appeals generate surges in blood donation, but how these responses differ by product type, donor demographics, and retention remains incompletely understood, particularly for apheresis platelets. We analyzed donation data from five major U.S. MCEs and five national blood donation appeals between 2000 and 2024, characterizing whole blood (WB) and platelet donations by donor age, first-time versus repeat status, and return within 1 year. WB donation demonstrated rapid, high-amplitude surges during MCEs that resolved within 1-2 weeks, driven in part by younger and first-time donors. In contrast, appeals produced smaller increases sustained through the duration of the appeal. Platelet donation followed a distinct pattern, with a smaller, yet slightly longer surge response during MCEs and more robust increases during national blood donation appeals, while both relied almost exclusively on older, repeat donors. Donor retention differed primarily by donor history. Repeat donors were substantially more likely to return than first-time donors across age groups and event types, with older repeat donors showing the highest retention. These findings highlight structural differences between WB and platelet donor systems with direct implications for disaster preparedness and long-term blood supply resilience in the United States.

Bleeding is a major complication in patients with hematologic malignancies, who frequently develop severe thrombocytopenia. The effectiveness of prophylactic tranexamic acid (TXA) in reducing clinically bleeding remains uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials to evaluate whether prophylactic TXA reduces WHO grade ≥ 2 bleeding and transfusion requirements. Studies enrolling adults receiving chemotherapy, immunotherapy, or hematopoietic stem cell transplantation, or those expected to develop severe thrombocytopenia were eligible; studies including patients with prior thromboembolism, therapeutic anticoagulation, or platelet transfusion refractoriness were excluded. MEDLINE, EMBASE, and Cochrane CENTRAL were searched through April 2025. Two reviewers independently extracted data, assessed risk of bias with the Cochrane RoB 2 tool, and synthesized results using random-effects meta-analysis. Six trials involving 1086 participants were included. TXA showed little to no reduction in WHO grade ≥ 2 bleeding compared with control (OR 0.84, 95% CI 0.64-1.12; moderate certainty). For other outcomes, TXA had minimal effects on red blood cell and platelet transfusion requirements (low certainty), and thromboembolic events were uncommon, with no clear signal of increased risk (low certainty). Prophylactic TXA likely offers limited clinical benefit for patients with hematologic malignancies but appears generally safe.

Prostate cancer (PCa) is the second leading cause of cancer-related deaths among American men. Striking disparities persist in PCa incidence and mortality, with African American (AA) men experiencing a 1.7-fold higher incidence and more than two-fold higher mortality rate compared to European American (EA) men. Despite this disparity, the Black community remains underrepresented in PCa research and clinical trials. As PCa progresses to high-grade and metastatic castration-resistant stages, treatment options become increasingly limited and median overall survival falls below two years, underscoring the urgent need for novel therapeutic strategies. One promising yet underexplored avenue is the circulatory microenvironment, which consists of platelets (PLTs) and immune cells that interact directly with circulating tumor cells (CTCs) during intravasation. Mounting evidence supports a bidirectional relationship in which tumor cells activate platelets to promote thrombosis, and platelets in turn activate tumor cells to promote tumorigenesis. In PCa, reciprocal signaling between tumor cells and platelets is increasingly being recognized. Recent transcriptomic profiling (RNA-Seq) has identified transmembrane signaling proteins mediating these interactions, broadly categorized into four groups: (1) integrin-ligand, (2) EPH receptor-ephrin, (3) immune checkpoint receptor-ligand, and (4) miscellaneous receptor-ligand interactions. Notably, many components of these signaling axes are overexpressed in platelets and/or PCa cells from individuals of African ancestry and are associated with poorer clinical outcomes. These findings highlight platelet-mediated signaling pathways as a source of novel biomarkers and pharmacologically actionable targets, offering opportunities to address both aggressive disease biology and persistent PCa disparities.

Mild bleeding disorders (MBDs) comprise a heterogeneous group of inherited conditions characterized by clinically relevant bleeding symptoms despite largely normal or inconclusive results in routine hemostatic testing. These disorders account for a substantial proportion of referrals to specialized hemostasis clinics and include von Willebrand disease (VWD), inherited platelet function disorders, and mild coagulation factor deficiencies. Despite systematic diagnostic algorithms, many patients with MBDs remain without a definitive diagnosis and are classified as having bleeding disorder of unknown cause (BDUC), complicating clinical management and counseling. Conventional diagnostic approaches rely on structured bleeding assessment tools, detailed family history, and stepwise laboratory testing. Biological variability, assay limitations, and phenotypic overlap often result in inconclusive findings. Recent advances in genetic analysis have begun to transform this diagnostic landscape. Targeted next-generation sequencing panels, whole-exome sequencing (WES), and whole-genome sequencing (WGS) enable identification of pathogenic variants across numerous hemostasis-related genes. In MBDs, genetic testing is valuable for refining diagnoses in qualitative VWD, confirming inherited platelet disorders, and identifying rare mild coagulopathies. In contrast, its diagnostic yield in type 1 and low von Willebrand factor (VWF) is modest, reflecting complex genetic architecture, modifier effects, and incomplete penetrance. In BDUC, genetic testing has revealed monogenic causes in some patients and multifactorial contributions in others. Genetic testing should therefore be regarded as a complementary tool rather than a replacing conventional diagnostics. Integrated with clinical and laboratory findings and supported by expert variant interpretation, it can reduce diagnostic uncertainty and improve disease classification in patients with MBDs.

To describe the blood product utilization during neonatal and pediatric extracorporeal membrane oxygenation (ECMO) and to determine whether its usage correlates with clinical outcomes of bleeding, thrombosis or mortality. Prospective observational study of neonatal and pediatric ECMO patients from September 2016, until January 2022. Tertiary center for pediatric and neonatal ECMO. One hundred and ten runs of ECMO, nine patients had two runs of ECMO during the same hospital admission. All patients received at least one red blood cell (RBC) transfusion. RBCs, as well as fresh frozen plasma (FFP), platelets and cryoprecipitate transfusion, as well as total donor exposure did not predict increased mortality in ECMO patients. Increased volume of platelets was associated with patients who bled, but not those who had a thrombosis or died. This prospective cohort study failed to demonstrate that the volume of red blood cells, FFP and platelets or total donor exposure was predictive of increased mortality. Of particular importance is the lack of increased volume of red blood cells transfused to patients who experienced major bleeding events compared to those who did not, suggesting that the trigger for transfusions may not be based on the clinical status of bleeding and resultant Hb in isolation.

Human herpesvirus 6 (HHV-6), the causative agent of exanthema subitum (ES), is a major viral cause of acute encephalopathy in Japan. Serum procalcitonin (PCT) is widely used as a biomarker of severe bacterial infections and has also been proposed as an early predictor of encephalopathy. However, elevated PCT levels are occasionally observed in ES without bacterial co-infection or encephalopathy, potentially complicating interpretation of PCT levels in febrile children. The association between primary HHV-6 infection and PCT elevation remains unclear. We therefore investigated clinical and laboratory factors associated with serum PCT levels in young children with primary HHV-6 infection. We conducted a retrospective cohort study of 188 febrile children aged < 60 months who underwent serum PCT measurement between April 2021 and May 2024. Thirty children with clinically diagnosed ES and laboratory-confirmed primary HHV-6 infection were compared with 53 children with other virologically confirmed febrile illnesses. In exploratory analyses, multivariable logistic regression identified factors associated with ES, and multivariable linear regression explored factors associated with serum PCT levels in the ES group. Median serum PCT levels were significantly higher in the ES group than in controls (0.28 [interquartile range (IQR) 0.10-0.61] vs. 0.10 [IQR 0.10-0.31] ng/mL; P = 0.018). The PCT/C-reactive protein ratio was also higher in ES (P = 0.018). ES patients had lower white blood cell, neutrophil, and platelet counts, and higher aspartate aminotransferase and lactate dehydrogenase levels. In exploratory multivariable analysis, younger age (odds ratio [OR] 0.92; 95% confidence interval [CI] 0.87-0.98; P = 0.006), lower platelet count (OR 0.88; 95% CI 0.82-0.94; P < 0.001), and higher PCT level (OR 1.74; 95% CI 1.02-2.95; P = 0.042) were associated with ES. Among patients with ES, lower lymphocyte count and absence of febrile seizures were associated with higher PCT levels. All ES patients had a self-limited clinical course without encephalopathy. Among febrile children undergoing clinically indicated PCT testing, primary HHV-6 infection was associated with modest PCT elevation. These elevations may reflect HHV-6-associated hematologic alterations rather than bacterial co-infection or disease severity, highlighting the need for cautious interpretation of PCT in ES.

T-cell Large Granular Lymphocyte (T-LGL) leukemia is a chronic lymphoproliferative disorder associated with cytopenias and immune dysregulation, predisposing patients to infections. However, the prevalence and hematological impact of cutaneous immunocompromised-associated infections, bacterial, and fungal infections in these patients remain insufficiently characterized. A retrospective study was conducted on 60 patients with T-LGL leukemia and 60 healthy controls. Infection screening was performed using clinical examination, direct microscopy, and microbiological culture. Hematological parameters, including total White Blood Cell (WBC), Red Blood Cell (RBC), platelet counts, and differential leukocyte counts, were analyzed. Statistical analysis was performed using SPSS version 26, with significance set at p ≤ 0.05. Parasitic infections were most prevalent (38%), followed by bacterial (32%) and fungal infections (30%). Common pathogens included Sarcoptes scabiei and Leishmania tropica (parasitic), Staphylococcus aureus (bacterial), and dermatophytes (fungal). Parasitic infections were significantly associated with eosinophilia and lymphocytosis (p < 0.05), while bacterial and fungal infections showed increased neutrophil percentages. Compared to controls, infected patients exhibited leukopenia, anemia, and thrombocytopenia. Infection burden was higher in females, and age-related peaks were observed for L. tropica (30-40 years) and dermatophyte infections (20-30 years). These findings highlight distinct infection-specific hematological alterations in T-LGL leukemia, emphasizing the role of immunocompromised-associated infections in worsening cytopenias. Limitations include the retrospective design and limited sample size. Recognition of infection patterns and their hematological impact may improve diagnostic evaluation and guide targeted infection surveillance, ultimately reducing morbidity in T-LGL leukemia patients.

Functional analysis of germline RUNX1 variants identified in individuals with suspected familial platelet disorder.

Rapid and effective hemostasis for unknown bleeding points and irregularly shaped wounds is very important. Here, water-soluble quaternized chitin (QC2) with relatively low hemolysis ratio was synthesized homogeneously in NaOH/urea aqueous solution. Then a novel self-gelling hemostatic powder was prepared based on QC2 and sodium hyaluronate (HA) through simply mixing the QC2 aqueous solution with HA aqueous solution, freeze-drying and grinding. The obtained QC2/HA powder can quickly transform into a gel via electrostatic interaction after absorbing blood, and adhere to the wound surface, concentrating blood cells and platelets to trigger coagulation and preventing blood loss. The QC2/HA powder could adhere to wet tissue after absorbing interfacial water showing good tissue adhesion property and good coagulation effect in vitro, which are important for effective hemostatic materials. The formed QC2/HA hydrogel displayed good self-healing feature due to the reversible electrostatic interaction, and good biodegradability and biocompatibility. Moreover, in the rat tail and rat liver models, the QC22.5/HA1 self-gelling powder showed much better hemostatic effect than the blank control and the traditional hemostatic chitosan. Therefore, we believe that the QC22.5/HA1 powder has great potential as a new biodegradable hemostatic material in the future.

Current status and challenges in targeting circulating amyloid-β carriers for Alzheimer's disease therapy.

Tibetan medicine Bawei Chenxiang Wan attenuates chronic mountain sickness by targeting the AKT/FOXO3a/CAT axis to inhibit oxidative stress.

Asthma is an inflammatory airway disease originating in early life, but it is understudied whether childhood trajectories of haematological and immunoglobulin (Ig) measures associate with risk of developing asthma. We modelled trajectories of blood neutrophils, lymphocytes, eosinophils, platelets and Ig (IgE, IgA, IgM and IgG) measured at ages 4, 5, 6, 7, 12 and 18 years in the Copenhagen Prospective Studies on Asthma in Childhood 2000 birth cohort (n=411) and investigated association with asthma diagnosis, airway obstruction using spirometry (forced expiratory volume in 1 s (FEV1)) and plethysmography (specific airway resistance (sRaw)), type 2 airway inflammation (fractional exhaled nitric oxide (FeNO)) and airway hyper-responsiveness (AHR) at age 18. We employed linear regression, linear mixed model (LMM) with variable slopes and intercepts and latent class trajectory (LCT) analysis adjusting for relevant confounders. In the LMM analyses, increasing blood neutrophils through childhood (slope, adjusted OR (aOR)=1.30 per 109 cells/L, 95% CI 1.01 to 1.68, p=0.040), higher eosinophils (intercept, aOR=1.51 per 109 cells/L, 95% CI 1.17 to 1.98, p=0.002), higher total IgE and increasing total IgE (intercept, aOR=1.28 per IgE g/L, 95% CI 1.00 to 1.63, p=0.049; slope, aOR=1.37, 95% CI 1.07 to 1.77, p=0.015) were significantly associated with asthma at age 18. Further, higher eosinophils (intercept, beta estimate=3.84 ppb per 109 cells/L, 95% CI 1.53 to 6.15, p=0.001), higher total IgE and increasing total IgE (intercept, beta estimate=3.91 ppb per g/L, 95% CI 1.64 to 6.18, p=0.001; slope, beta estimate=4.84, 95% CI 2.55 to 7.14, p=4.4×10-⁵) were associated with higher FeNO, whereas higher platelet count (intercept, beta estimate=-0.07 L per 109 cells/L, 95% CI -0.12 to -0.03, p=0.002) was associated with lower FEV1 at age 18, and increasing total IgE was associated with increased AHR, that is, lower methacholine dose causing a 20% drop in FEV1 (slope, beta estimate=-0.75 per g/L, 95% CI -1.24 to -0.27, p=0.002). The LCT models confirmed that specific childhood trajectories of eosinophils and total IgE were associated with higher FeNO levels and increased AHR, and that a specific platelet count trajectory was associated with lower FEV1. There were no consistent associations with trajectories of lymphocytes, IgG, IgA or IgM and no associations with sRaw. Trajectories of haematological and Ig measures throughout childhood, particularly platelet counts, eosinophils and total IgE, were associated with airway inflammation, reduced lung function and increased AHR at age 18.