Neurofibromatosis type 1 (NF1) is a genetic disorder associated with an elevated risk of both benign and malignant tumors. In rare cases, it involves the lungs in a condition known as neurofibromatosis-associated diffuse lung disease (NF-DLD), marked by cystic and emphysematous changes even in nonsmokers. We report a case of a 53-year-old female with NF1 who presented with progressive chest pain and dyspnea. Imaging revealed a 6.0 × 3.1 cm left posterior chest wall mass with osseous erosion and emphysematous lung changes consistent with NF-DLD. Multidisciplinary management, including surgical resection of the chest wall mass, led to symptom relief and an uneventful recovery. This case underscores the importance of recognizing NF-DLD in NF1 patients with respiratory symptoms and the need for ongoing surveillance for malignancies to ensure early diagnosis and appropriate intervention.

Background: Iron deficiency anemia (IDA) is the most common nutritional deficiency in children and a rare, but important risk factor for cerebral venous sinus thrombosis (CVST). The association is attributed to iron deficiency–induced thrombocytosis and hypercoagulability; however, pediatric cases remain infrequently reported. Case presentation: We report a 2-year-old Estonian boy with excessive cow’s milk intake who presented with severe headaches and vomiting. Examination revealed marked pallor and a systolic murmur, while neuroimaging demonstrated thrombosis of the superior sagittal and left transverse sinuses, extending into the internal jugular vein. Laboratory investigations confirmed severe IDA with a normal thrombophilia screen. The patient was treated with low-molecular-weight heparin and intravenous iron, followed by transition to oral iron supplementation. Follow-up venography at three months demonstrated complete thrombus resolution and full clinical recovery. Conclusion: CVST is a rare, but serious complication of severe IDA in children. Early recognition and timely management with anticoagulation and iron supplementation are crucial for favorable outcomes.

Purpose: Chemotherapy-induced neutropenia (CIN) is a common complication that increases the risk of infection, hospitalization, and treatment delays. While granulocyte colony-stimulating factors (G-CSFs) like filgrastim and pegfilgrastim are used to reduce these risks, limitations in dosing schedules and variability remain. Efbemalenograstim alfa (F-627), a novel long-acting recombinant G-CSF, has emerged as a potential alternative. This systematic review and meta-analysis aimed to evaluate its comparative safety and efficacy against standard G-CSFs in patients undergoing chemotherapy for non-myeloid malignancies. Methods: A comprehensive literature search was conducted across six databases for randomised controlled trials (RCTs) comparing F-627 to standard G-CSFs. Data from three active-controlled trials were pooled using Review Manager (RevMan) 5.4.1, with results expressed as risk ratios (RR) for dichotomous outcomes and mean differences (MD) for continuous outcomes. Heterogeneity was assessed using the I² statistic. Narrative synthesis was performed for the data in the placebo-controlled trial and outcomes with insufficient data for meta-analysis. Risk of bias and evidence quality were evaluated using the Cochrane RoB 2.0 tool and GRADE guidelines, respectively. Results: Four RCTs comprising 973 patients were included, with 533 receiving F-627. F-627 showed comparable efficacy to standard G-CSFs in reducing duration of Grade 4 neutropenia in cycle 1 (MD = 0.04 days; 95% CI: − 0.04 to 0.13; I² = 0%). Incidence of severe neutropenia and febrile neutropenia were also similar (RR = 1.02; 95% CI: 0.97–1.07 and RR = 1.33; 95% CI: 0.41–4.30, respectively). However, a placebo-controlled trial showed a significant reduction in neutropenia and febrile neutropenia incidence with F-627. Secondary outcomes and adverse event profiles were broadly comparable across treatment arms. Conclusion Efbemalenograstim alfa offers a comparable safety and efficacy profile to standard G-CSFs for the prevention of CIN, supporting its role as a viable therapeutic option in non-myeloid cancers.