CLA plays a role in the pattern of T-cell lymphocyte migration in the skin and subcutis in both reactive and neoplastic states. An alteration in the expression of this marker, whether it is in the context of the acquisition of expression in a cell that is normally CLA negative or its loss of expression, may define a key event in determining cutaneous and extracutaneous hematopoietic cell distribution.
Parvovirus B19 is a single-stranded DNA virus exhibiting affinity for a variety of cell types including endothelial cells. The basis of the affinity is globoside expression, the receptor for B19. B19 endothelial cell parasitism accelerates endothelial cell apoptosis, potentially critical in inducing neoantigenicity and secondary antibody formation. A 38-year-old previously healthy male developed intestinal and cutaneous infarction, elevated creatinine phosphokinase (CPK) levels and progressive cytopenias. The basis of his clinical presentation was unclear until a skin biopsy suggested a potential role for virally mediated endothelial cell injury. Hematoxylin and eosin, immunohistochemical, immunofluorescent and reverse transcriptase in situ polymerase chain reaction studies were conducted on skin biopsies to assess for viral triggers. B19 viremia and localization of B19 RNA transcripts to vascular endothelium were uncovered. A diagnosis of catastrophic endothelial cell injury attributable to B19 infection was rendered. The patient showed significant improvement with intravenous immunoglobulin (IVIG). Parvovirus B19 is a ubiquitous virus that in the majority of affected patients remains asymptomatic. Nevertheless, because of its ability to infect endothelium it can cause severe multiorgan endothelial cell injury.
Angiocentric lesions of the head and neck encompass a variety of benign and malignant lesions. Not unexpectedly the sequelae of an angiocentric process independent of its benign or malignant nature is one of tissue ischemia with a potential for either breakdown or reparative fibrosis. Therefore, the clinical presentations can be very similar despite a varied pathogenesis. Among the benign reactive infiltrates that will be considered are angiocentric eosinophilic fibrosis, Wegener's granulomatosis, microscopic polyangiitis and cocaine associated mid line facial destruction. We will discuss other conditions which enter into the differential diagnosis either clinically or histologically including Erdheim Chester disease and mid line facial undermining unrelated to an angiocentric event specifically in the context of trigeminal trophic ulcer and relapsing polychondritis. The two main neoplastic conditions exhibiting angiocentricity are in the context of lymphomatoid granulomatosis and NK/T cell lymphoma; hence these two particular hematologic dyscrasias will be discussed in some detail in this review.
We propose the term acute infectious id panniculitis for cases of neutrophilic lobular panniculitis triggered by non-tuberculous infectious stimuli. This course may be self-limited. Microvascular cofactors and/or procoagulant states may be pathogenetically important. Recognizing this entity may circumvent the need for an exhaustive evaluation for other causes of neutrophilic lobular panniculitis.
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