Endovascular resolution of complete common iliac vein stenosis in a case of May-Thurner syndrome with underlying malignancy.

INTRODUCTION AND IMPORTANCE: May-Thurner Syndrome (MTS) is an uncommon etiology of left common iliac vein thrombosis due to arterial compression. In this report, we describe a case of MTS with severe occlusion of the left common iliac vein in the context of a previously undiagnosed pancreatic cancer. We detail the endovascular resolution of the iliac vein compression and show long-term patency. CASE PRESENTATION: A 33-year-old woman on oral contraceptive pills presented with extensive thrombosis of the left common iliac vein extending cephalad into the lower IVC and inferiorly to the femoral vein. The thrombus was refractory to therapeutic heparin. Mechanical thrombectomy removed the occluding thrombus. Intravenous ultrasound identified severe compression of the left common iliac vein by the right common iliac artery. Angioplasty and stenting provided complete resolution of the lesion. Imaging and hematologic workup revealed a pancreatic malignancy and concomitant hypercoagulable state that likely precipitated the patient's presentation. CLINICAL DISCUSSION: Endovascular intervention provided complete resolution of severe iliac vein compression. Patency was maintained at 6-month follow-up. Research suggests that the anatomical lesion predisposing individuals to MTS is relatively common despite infrequent occurrence of the syndrome. This case highlights the importance of a high clinical suspicion for associated hypercoagulable states when MTS is discovered. CONCLUSION: There is limited research exploring the relationship between severity of iliac vein compression and endovascular treatment outcome. This case documents endovascular resolution of a severe lesion with maintained patency.

Longitudinal profiling of respiratory and systemic immune responses reveals myeloid cell-driven lung inflammation in severe COVID-19.

Immune response dynamics in coronavirus disease 2019 (COVID-19) and their severe manifestations have largely been studied in circulation. Here, we examined the relationship between immune processes in the respiratory tract and circulation through longitudinal phenotypic, transcriptomic, and cytokine profiling of paired airway and blood samples from patients with severe COVID-19 relative to heathy controls. In COVID-19 airways, T cells exhibited activated, tissue-resident, and protective profiles; higher T cell frequencies correlated with survival and younger age. Myeloid cells in COVID-19 airways featured hyperinflammatory signatures, and higher frequencies of these cells correlated with mortality and older age. In COVID-19 blood, aberrant CD163+ monocytes predominated over conventional monocytes, and were found in corresponding airway samples and in damaged alveoli. High levels of myeloid chemoattractants in airways suggest recruitment of these cells through a CCL2-CCR2 chemokine axis. Our findings provide insights into immune processes driving COVID-19 lung pathology with therapeutic implications for targeting inflammation in the respiratory tract.

Impact and Clinical Implications of Prematurity on Adaptive Immune Development.

PURPOSE OF REVIEW: Detail normal adaptive immune maturation during fetal and neonatal life and review the clinical implications of arrested immune development. RECENT FINDINGS: Advancements in the field of immunology have enabled investigations of the adaptive immunity starting during fetal life. New insights have drawn important distinctions between the neonatal and adult immune systems. The presence of diverse immunologic responses in the perinatal period suggests the importance of in utero immune development. Disruption of immune maturation due to premature birth may have significant implications for clinical pathology. SUMMARY: Establishing protective adaptive immunity during the perinatal period is critical for effective immune responses later in life. Preterm infants are susceptible to aberrant immune system maturation and inflammatory immune responses have been associated with the development of necrotizing enterocolitis (NEC) and bronchopulmonary dysplasia (BPD). Improving our understanding of how immune responses contribute to the pathogenesis of NEC and BPD may offer new opportunities for future treatment and prevention of these diseases.