S8C11P1-Vasculitic Patterns

S8C11P1-1: The definition of a vasculitis often emphasizes the character of the infiltrate; priority is placed on the presence, in the vascular domain, of both infiltrates of neutrophils and fragments of nuclear debris (leukocytoclasia). In addition, necrosis is often mentioned in definitions, but not rigidly required in practice. The vessel in the center of the field satisfies somewhat different criteria for the recognition of a vasculitis; it shows a central thrombus (the lumen is occluded). Fibrinoid material is present in the wall of the vessel and in its adventitia (acidophilic fibrils form a mesh [a deposit] in the adventitia of the vessel, to the right and below the center of the field). If we then require the presence of an infiltrate of inflammatory cells - and are not too demanding - the migratory histiocytes in the adventitia of the vessels would qualify the process as a necrotizing histiocytic vasculitis. It would be difficult to identify a single cell in the infiltrate as a neutrophil. There are fragments of nuclear debris; some observers would extrapolate from this evidence to conclude that all the neutrophils in the infiltrate have disintegrated. A more reasonable approach would be to cite the population of histiocytes as the source of the nuclear debris (thrombotic thrombocytopenic purpura).

S8C11P1-2: In this field, neutrophils have been caught in the act; they have infiltrated the wall of a vessel at the interface between the papillary dermis and the reticular dermis. A few neutrophils have extended beyond the adventitia of the vessel into the neighboring dermis. The papillary dermis is edematous, a sign of abnormal vascular permeability. In the proper clinical setting, this pattern is easily assigned to the category of vasculitis. On the other hand, there is no evidence of necrosis of the wall of the vessel and very little evidence of leukocytoclasia. This is a neutrophilic angiitis, but it is uncertain that, with time, the lesion would assume the qualities of classic leukocytoclastic angiitis. This could be an early manifestation of an infectious process, or of a neutrophilic dermatitis of insufficient severity to be characterized as Sweet’s syndrome; neutrophilic changes of this type have even been described in some examples of “urticaria.” There are a few fragments of nuclear debris at the dermal-epidermal interface. In the same area, there are vacuolar changes at the dermal-epidermal interface.

S8C11P1-3: An area of necrosis, as evidence of ischemia, is saucer-shaped from left to right (with the area on the right being one extremity of the zone of necrosis). The viable epithelium has regenerated along the basement membrane zone. The extremity of the regenerating epithelium is moving in a direction from right to left (the extremity is marked by red arrows). In this example, a large vessel was occluded; the dermis is relatively free of inflammatory cells. The nuclei of cells in the dermis are pyknotic; The dermis also is necrotic.

S8C11P1-4: Vasculitic disorders may be associated with edema of the papillary dermis and the epidermis, as in this field. The edema of the epidermis is not the pattern of classic spongiotic vesiculation, as seen in delayed hypersensitivity. It is prominent in the epidermis in the absence of significant infiltrates of lymphocytes and histiocytes. Having identified the changes as being in keeping with a manifestation of a vasculitis, it should then be noted that the perivascular infiltrates are not neutrophilic, but are composed of lymphocytes and histiocytes.

S8C11P1-5: Papillary dermal edema, as seen in this field, is a common feature of lesions in the category of the vasculitides. With a reticulum stain, delicate, argyrophilic reticulum fibers (many very lightly stained) are vertically oriented, few in number, and widely spaced. With progression of the edema, these fibers will break; fluid-filled defects will form in the fibrous framework of the papillary dermis. With coalescence, the defects will then form a “dermolytic” sub-spidermal vesicle.

S8C11P1-6: With this PAS stain, the fibrous framework of the papillary dermis has been blown apart; the less involved reticulum is compressed along the floor of a small, “sub-epidermal” defect. Epidermis forms the roof of this micro-vesicle; basement membrane remains attached along the roof of the vesicle. The mesh in the defect probably represents proteinaceous material, but could also represent fibrin.

S8C11P1-7: This is an example of small vessel angiitis of the kidney in the setting of polyarteritis nodosa. It is an example of classic necrotizing angiitis with fibrinoid necrosis of a portion of the wall of the involved vessel. In addition, the affected vessel in the area of necrosis shows an eccentric, aneurysmal bulge that extends close to the top of the field. The perivascular infiltrates are mixed, containing neutrophils, lymphocytes, and histiocytes (Masson’s trichrome stain). Fibrinoid is bright red.

S8C11P1-8: In this field, the perivascular infiltrates are lymphohistiocytic. The interstitial infiltrates, below the center of the field and extending to the right, contain a high-component of histiocytes. There are acidophilic, interstitial deposits (small, uniform acidophilic droplets). The character of the immune complexes (i.e., size and solubility) may influence the character of the inflammatory response.

 

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