Few studies included ancillary laboratory procedures such as direct immunofluorescence and electron microscopy on biopsy specimens taken from patients diagnosed by them with LV.

Schroeter et al performed direct immunofluorescence investigations and found that IgM and complement components were present often whereas IgG and IgA were found inconsistently.[19] Shornick et al observed that early lesions showed fibrin deposited as a fine rim around the lumen of vessels, whereas late lesions were typified by a band of IgM, IgG, and C3 around the vessel walls accompanied by fibrin within the vessels.[22] Lih-Jen Yang et al confirmed immunofluorescence to be positive for IgM and complement, [41] Hoogenberg et al stated that C3, IgM and fibrin were present in the vessel wall as well as intraluminally,[29] and Baccard et al found IgA and C3 deposits in the small vessels of the superficial dermis.[28] In contrast, McCalmont et alwrote that immunofluorescence studies did not indicate a disease mediated by immune complexes.[16] Tsutsui et al observed deposits of C3 and fibrinogen in the mid-dermal vessel walls and IgM in half of his cases, but no deposits of IgG or IgA.[33] Calamia et al noted deposition of IgG, IgM, C3, and fibrinogen,[39] and Hairston et al saw deposition of IgG, IgM, and C3 along with fibrin around vessels.[40]

Electron microscopic studies by Shornick et al revealed lesions to be characterized by fibrin deposits which occluded the lumina of superficial dermal blood vessels.[22] McCalmont et al observed that small dermal blood vessels had a thickened and reduplicated basement membrane and that some thrombi had formed within lumina of vessels.[16]