A 37‐Year‐Old Man With Primary Antiphospholipid Syndrome Presenting With Respiratory Distress and Worsening Toe Ischemia

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137728/1/acr23168.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137728/2/acr23168_am.pd

A case of acute generalized exanthematous pustulosis associated with polyarteritis nodosa, responding to systemic steroids

A patient with a known biopsy of polyarteritis nodosa diagnosis presented with cyclic fevers, acute kidney injury, and progression of rash from macular to pustular, worsening despite being on antibiotics, without evidence of infection on multiple cultures. The patient had a pathological diagnosis from a skin biopsy of acute generalized exanthematous pustulosis syndrome, with a total resolution of rash, fevers, and acute kidney injury on treatment with pulse steroids

Heterotypic intercellular interactions as regulators of NETosis

Neutrophil extracellular traps (NETs) are chromatin-derived webs extruded from neutrophils in response to either infection or sterile stimulation with chemicals, cytokines, or microbial products. The vast majority of studies have characterized NET release (also called NETosis) in pure neutrophil cultures in vitro. The situation is surely more complex in vivo as neutrophils constantly sample not only pathogens and soluble mediators, but also signals from cellular partners including platelets and endothelial cells. This complexity is beginning to be explored by studies utilizing in vitro co-culture, as well as animal models of sepsis, infective endocarditis, lung injury, and thrombosis. Indeed, various selectins, integrins, and surface glycoproteins have been implicated in platelet-neutrophil interactions that promote NETosis, albeit with disparate results across studies. NETosis can also clearly be regulated by soluble mediators derived from platelets such as eicosanoids, chemokines, and alarmins. Beyond platelets, the role of the endothelium in modulating NETosis is being increasingly revealed, with adhesive interactions likely priming neutrophils toward NETosis. The fact that the same selectins and surface glycoproteins may be expressed by both platelets and endothelial cells complicates the interpretation of in vivo data. In summary, we suggest in this review that the engagement of neutrophils with activated cellular partners provides an important in vivo signal or hit toward NETosis. Studies should therefore increasingly consider the triumvirate of neutrophils, platelets, and the endothelium when exploring NETosis, especially in disease states