Leukocytoclastic vasculitis is a small vessel vasculitis and is also described as hypersensitivity vasculitis
Histology leukocytoclastic vasculitis
Low power view of leukocytoclastic vasculitis gives the pattern of a busy dermis with a superficial and medium aspect perivascular inflammatory pattern (Figure 1). There is a predominantly neutrophils in a perivascular and interstitial pattern in addition to those who submit extravasation of the vessels (Figure 2 and 3). Leukocytoclasis (neutrophils degeneration) forming nuclear dust is seen in addition to extravasated erythrocytes (Figures 3 and 4). Fibrinoid necrosis of the glasses with fibrin extravasation, while a pathogen requirement, may be inconspicuous or absent in many cases (Figures 3 and 4 demonstrate slight fibrinoid necrosis)
A variable number of eosinophils can be seen and when increased in number it may suggest a medication as the underlying cause.
It is important to recognize that changes vary over time in the biopsy, with a significant variation in the degree of inflammation infiltrate and vessel wall damage.
Leukocytoclastic vasculitis pathology
Figure 1
Figure 2
figure 3
Figure 4
Special stains in leukocytoclastic vasculitis
Immunofluorescence can be useful to confirm vascular damage like statement of fibrinogen, C3, IgG and IgM can be seen within the vessel walls. The biopsy of the affected skin has a higher yield.
Positive IgA is also useful as a clue to Henoch Schönlein Purple.
Differential diagnosis leukocytoclastic vasculitis
Henoch Schönlein purpura: histology is identical. IgA deposition on immunofluorescence will confirm a clinical diagnosis, but IgA positivity is not synonymous with the diagnosis, as IgA can also be seen in other settings.
Urticaria Vasculitis – While the changes can be very similar in this condition, there is usually a more prominent superficial surface dermal edema, and the density of the inflammatory infiltrate is lower. In particular, there may be a less obvious neutrophilic component with even a pure lymphocytic Some claim that vasculitis is sufficient for the diagnosis.
Septic vasculitis: here the clue is vascular occlusion by thrombus. There may be little or no leukocytoclasis.
Sweet syndrome: The presence of marked papillary dermal edema and a diffuse Neutrophilic infiltrate in sweets must be discriminating. Although it is strictly suggested that there should not be significant fibrinoid necrosis, this has been documented in a minority of cases.