Objectives: Hospital-acquired anemia (HAA) is an important clinical problem that can adversely affect outcomes, particularly in critically ill patients. This study aimed to determine the incidence of hospital-acquired anemia in adult ICU patients and to evaluate its relation with diagnostic phlebotomy procedures and other etiologic factors. Methods: Data from 1170 adult ICU admissions between 1 January and 31 December 2024 were retrospectively reviewed and 321 patients were included in the analysis. The median age of the study cohort was 72 years (range: 18–102), with 45.2% females (n = 145) and 54.8% males (n = 176). The median ICU length of stay was 6 days (range: 3–29). Results: HAA developed in 35.8% of patients, while a decrease in hemoglobin levels was observed in 80.4%. Patients who developed HAA had significantly longer ICU stays and higher ferritin, CRP, and diagnostic phlebotomy (DP) volumes, while admission hemoglobin levels were lower compared with those without HAA (all p < 0.05). In multivariate analysis, a longer ICU stay, higher ferritin levels, lower admission hemoglobin levels and greater DP volumes were independently associated with the development of HAA. Conclusions: HAA was common in critically ill patients and was associated with several clinical and laboratory factors, including inflammatory burden, baseline hemoglobin level, ICU length of stay, and diagnostic phlebotomy volume. These findings suggest that HAA is a multifactorial process, with ICU length of stay, inflammatory status, baseline hemoglobin levels, and diagnostic phlebotomy volume all potentially contributing to its development.

Objectives: Novel agents such as brentuximab vedotin and anti-PD-1 antibodies, together with PET-adapted intensified strategies, have improved outcomes in advanced-stage classical Hodgkin lymphoma (cHL). However, their applicability remains limited in many middle-income countries because of restricted drug availability, reimbursement barriers, and toxicity concerns. Therefore, real-world data on the effectiveness of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) remains essential. Methods: We conducted a retrospective two-center study including 95 patients with newly diagnosed cHL treated with first-line ABVD. Baseline characteristics, treatment response, progression-free survival (PFS), overall survival (OS), and mortality were compared between early-stage (I–II, n = 33) and advanced-stage (III–IV, n = 62) disease. Results: The median age was 38 years (range, 18–73), and 69.5% were male; 65% had advanced-stage. Complete response rates were high in both early-stage (97%) and advanced-stage (95.2%) patients. Median PFS (21 vs. 23 months; p = 0.994) and OS (23 vs. 25 months; p = 0.848) were similar. Five-year OS was 84.3% for early-stage and 98% for advanced-stage patients (p = 0.292), while five-year PFS was 55.3% and 29.6% (p = 0.526). Mortality rates were comparable. Conclusions: In this real-world cohort, first-line ABVD achieved high response rates and favorable long-term survival in advanced-stage cHL, supporting its continued use as a frontline treatment option, particularly in settings where access to novel therapies may be limited.

Introduction: May–Hegglin anomaly (MHA) is a rare autosomal dominant genetic disorder caused by mutations in the MYH9 gene, leading to the presence of Döhle‐like inclusions in neutrophils, macrothrombocytes, and thrombocytopenia. This report presents a unique case of a 33‐year‐old pregnant woman diagnosed with MHA and discusses the diagnostic challenges and management strategies. Case Presentation: A 33‐year‐old pregnant woman, 17 weeks into her pregnancy, presented with a history of persistent thrombocytopenia. She had previously been diagnosed with immune thrombocytopenia (ITP) and treated with steroids, intravenous immunoglobulin (IVIG), and thrombopoietin receptor agonists (TPO‐RA). Her platelet counts had been between 35,000 and 50,000/μL. Upon referral to the hematology clinic, her platelet count was critically low at 15,000/μL, but the mean platelet volume (MPV) remained within normal limits. Despite her low platelet count, her coagulation profile was normal, and physical examination showed no pathological findings. Diagnostic Assessment: The patient’s blood smear revealed giant platelets and Döhle‐like inclusions in the granulocytes. Genetic testing confirmed a heterozygous mutation in the MYH9 gene, leading to the diagnosis of MHA. Therapeutic Intervention: Due to the risks associated with thrombocytopenia in pregnancy, her prenatal care included routine platelet monitoring and a normal bleeding time assessment. The patient underwent a cesarean delivery under general anesthesia, which resulted in the birth of a healthy baby boy. Conclusion: The case highlights the importance of accurate diagnosis and careful monitoring in managing pregnancy in patients with MHA. A multidisciplinary approach involving obstetricians and hematologists is crucial for optimizing maternal and neonatal outcomes.