Acute Respiratory Failure With a Rare, Rapidly Progressing Pediatric Desmoid Tumor Anterior Mediastinal Mass.

We present an unusual case of a 6-year-old boy who presented with the sudden presence of left neck mass and acute hypoxemic respiratory failure, whose subsequent imaging demonstrated a previously undiagnosed anterior mediastinal mass (AMM) extending into the left neck. Biopsy of the mass was consistent with a desmoid tumor, which is a rare cause of AMM in children. Desmoid tumors are locally aggressive, often invading and enveloping surrounding tissues, but overall slow growing.

Rupture of an Occult Intracranial Mycotic Aneurysm after Intravenous Thrombolysis with Recombinant Tissue Plasminogen Activator for Acute Ischemic Stroke.

Background: The treatment of acute ischemic stroke with recombinant tissue plasminogen activator (rtPA) has become the mainstay of treatment, but its use carries a risk of subsequent intracranial hemorrhage (ICH). Guidelines have been developed to aid in the selection of the appropriate candidates to treat with rtPA to reduce this risk. We present a case of a stroke patient who was an appropriate candidate and was treated with rtPA who experienced a fatal subarachnoid hemorrhage due to a ruptured mycotic aneurysm (MA).

Deficient Neutrophil Extracellular Trap Formation in Patients Undergoing Bone Marrow Transplantation.

Overwhelming infection causes significant morbidity and mortality among patients treated with bone marrow transplantation (BMT) for primary immune deficiencies, syndromes of bone marrow failure, or cancer. The polymorphonuclear leukocyte (PMN; neutrophil) is the first responder to microbial invasion and acts within the innate immune system to contain and clear infections. PMNs contain, and possibly clear, infections in part by forming neutrophil extracellular traps (NETs).

Mammalian target of rapamycin regulates neutrophil extracellular trap formation via induction of hypoxia-inducible factor 1 α.

Neutrophils are highly specialized innate immune effector cells that evolved for antimicrobial host defense. In response to inflammatory stimuli and pathogens, they form neutrophil extracellular traps (NETs), which capture and kill extracellular microbes. Deficient NET formation predisposes humans to severe infection, but, paradoxically, dysregulated NET formation contributes to inflammatory vascular injury and tissue damage.