Immune thrombocytopenia is an acquired autoimmune disorder characterized by isolated thrombocytopenia due to antibody-mediated platelet destruction and impaired platelet production. Thrombocytopenia in pregnancy is common, but severe thrombocytopenia requires prompt evaluation to distinguish benign gestational thrombocytopenia from immune thrombocytopenia, hypertensive disorders of pregnancy, hemolysis, elevated liver enzymes, low platelet count syndrome, and thrombotic microangiopathies. We present the case of a 19-year-old gravida 1 para 0 patient with sickle cell trait and iron deficiency anemia who was initially diagnosed with pregnancy-associated immune thrombocytopenia in the first trimester after presenting with severe thrombocytopenia, with a platelet count of 9 × 10[3]/µL. She initially responded to intravenous immunoglobulin and corticosteroids, with platelet recovery to 107 × 10[3]/µL during hospitalization and 264 × 10[3]/µL shortly after discharge. However, despite outpatient hematology follow-up and prednisone therapy, her platelet count progressively declined. She was readmitted at 22 weeks and 5 days of gestation after routine obstetric laboratory testing showed relapsing severe thrombocytopenia with platelets of 15 × 10[3]/µL. The patient was otherwise asymptomatic, aside from intermittent blood-tinged nasal discharge and mild vaginal spotting a few days before presentation that resolved spontaneously. She was normotensive and had no evidence of hemolysis, renal dysfunction, significant hepatic dysfunction, or coagulopathy. Hematology and maternal-fetal medicine were consulted, and she was treated with intravenous immunoglobulin with post-treatment platelet improvement to 53 × 10[3]/µL. She was discharged on a prednisone taper with plans for scheduled outpatient intravenous immunoglobulin and close follow-up in a combined hematology and maternal-fetal medicine clinic. This case highlights the importance of a structured, multidisciplinary approach to severe thrombocytopenia in pregnancy and the need to exclude pregnancy-specific and life-threatening alternative etiologies before confirming immune thrombocytopenia.

CD47-centered signaling, involving the functionally distinct CD47-SIRPα and TSP-1-CD47 axes, has been increasingly implicated in the regulation of vascular inflammation, cellular clearance, and atherosclerotic plaque remodeling. This review examines these signaling pathways within two interrelated pathological dimensions: plaque formation and plaque vulnerability. During plaque formation, TSP-1-CD47 signaling may contribute to endothelial dysfunction, leukocyte recruitment, vascular smooth muscle cell phenotypic modulation, and macrophage foam cell formation. In particular, atherosclerosis-specific experimental evidence supports a TSP-1-CD47-Nox1-dependent mechanism that promotes receptor-independent native low-density lipoprotein uptake through macrophage macropinocytosis. During plaque progression, the CD47-SIRPα axis functions primarily as an inhibitory phagocytic checkpoint. Engagement of macrophage SIRPα recruits SHP-1/2-dependent inhibitory signaling, suppresses cytoskeletal rearrangement, and impairs efferocytosis of apoptotic cells and lipid-rich cellular remnants, thereby contributing to secondary necrosis, necrotic core expansion, and persistent inflammation. In contrast, proposed effects of CD47-centered signaling on macrophage polarization, autophagy, and angiogenic responses are more context-dependent and are supported largely by indirect evidence derived from oncology, ischemic injury, wound-healing, metabolic disease, or in vitro models. To clarify these mechanistic boundaries, we classify the available evidence according to its source and directness, distinguishing atherosclerosis-specific findings from related vascular evidence and hypothesis-generating observations. Finally, we review current CD47-targeted therapeutic strategies and their translational limitations, including anemia, thrombocytopenia, off-target phagocytosis, uncertain effects on vascular repair, and the lack of cardiovascular clinical evidence. Although plaque-targeted delivery and cell-selective modulation may improve therapeutic specificity, the efficacy and long-term safety of CD47-targeted interventions in human atherosclerotic cardiovascular disease remain unproven. Finally, we address key translational bottlenecks-including systemic hematological toxicities like anemia-and discuss how plaque-specific biomimetic nano-delivery systems represent the mandatory path forward to safely realize the therapeutic potential of CD47-targeted interventions in clinical cardiology.

Background Severe dengue is a leading contributor to intensive care unit (ICU) admissions and death in tropical regions. Identifying factors associated with poor outcomes early is critical for guiding treatment and allocating resources in critically ill patients. Methods This prospective observational cohort enrolled 100 consecutive patients with WHO 2009-defined severe dengue admitted to the ICU and Emergency Department of Maharishi Markandeshwar Institute of Medical Science and Research (MMIMSR), Mullana, Haryana, between March 2025 and January 2026. Clinical, laboratory, and severity-score data (Acute Physiology and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA)) were recorded and compared between survivors and non-survivors using appropriate statistical tests, relative risks (RR) with 95% CI, and ROC analysis. Results The mean age was 47.2 ± 17.5 years; 58% were male. ICU mortality was 21.0% (21/100). Thrombocytopenia showed no mortality link (p = 0.678). Higher pulse rate, respiratory rate, body temperature, total leucocyte count, creatinine, bilirubin, and lactate, together with lower blood pressure, Glasgow Coma scale (GCS) score, arterial pH, and PaO2, were each associated with ICU mortality (all p < 0.05). Among warning signs, only hepatomegaly >2 cm was significant (50.0% vs. 17.0% mortality; RR 2.93, 95% CI 1.41-6.09; p = 0.024). Impaired consciousness (72.4% vs. 0% mortality; RR 103.20, 95% CI 6.46-1649.18; p < 0.001), acute respiratory distress syndrome (ARDS; 100% vs. 12.2%; RR 7.55, 95% CI 4.33-13.16; p < 0.001), and multiorgan dysfunction syndrome (MODS; 76.9% vs. 12.6%; RR 6.08, 95% CI 3.25-11.39; p = 0.002) showed the strongest associations (φ = 0.807, 0.647, 0.531 respectively). APACHE II (AUC 0.935) and SOFA (AUC 0.938) had the best discriminative accuracy, followed by lactate (AUC 0.835) and arterial pH (AUC 0.824). Conclusions Impaired consciousness, ARDS, and MODS strongly predicted mortality in this severe dengue cohort, forming a clinically vital cluster for early risk stratification. These single-center findings question the thrombocytopenia-centric paradigm and support closer attention to neurological status and organ dysfunction from ICU admission onward.

Type II heparin-induced thrombocytopenia (HIT) is a catastrophic immunothrombotic disorder that can be triggered by minimal heparin exposure during routine coronary angiography.

[This corrects the article DOI: 10.1016/j.rpth.2026.103381.].

Primary immune thrombocytopenia (ITP) in pregnancy presents significant therapeutic challenges, particularly when refractory to standard treatments such as corticosteroids, intravenous immunoglobulin, and immunosuppressants. Data on thrombopoietin receptor agonists (TPO-RAs) during pregnancy remain scarce. This study reports four pregnancies in three women with refractory ITP who received Romiplostim during gestation. All cases were retrospectively analyzed, with detailed documentation of treatment courses, platelet trajectories, and maternal and neonatal outcomes. Romiplostim was introduced in the second or third trimester at doses ranging from 3.1 to 6.25 µg/kg/week, following inadequate response to conventional therapy. All patients demonstrated hematologic improvement, often within one to two weeks of initiation, enabling corticosteroid tapering and preparation for delivery. Delivery outcomes were favorable, including four term vaginal deliveries without major hemorrhagic or thromboembolic complications. Neonatal outcomes were reassuring, with all infants born healthy, exhibiting platelet counts between 73,000 and 233,000/µL and no evidence of bleeding or congenital anomalies. One patient experienced transient postpartum thrombocytosis managed with low-molecular-weight heparin prophylaxis. No maternal or neonatal adverse events were attributed to Romiplostim exposure. These findings are consistent with previous limited reports suggesting that Romiplostim may be a viable rescue therapy for severe, refractory ITP in pregnancy. The favorable hematologic responses and reassuring neonatal outcomes observed in this series highlight the potential role of Romiplostim as an alternative treatment in carefully selected cases, provided that therapy is conducted under close multidisciplinary supervision.