Selected quotes

 
"The cause of this disease in not known, although the available data point to a vascular origin and discount an infectious basis." [8]
 
"The associated edema and increased vasodilatation during the summer may be a factor in the increased frequency of ulcerations during the summer months in certain individuals." [10]
 
"The etiology of atrophie blanche is not known but our observations indicate a high incidence of atopic reactivity, eczematous eruptions, and systemic disease." [12]
 
"Why it characteristically occurs only on the lower extremities (about the ankles) is not readily apparent but may be related to hemodynamics of the region." [13]
 
"The presence of circulating immune complexes . . . may be . . . the cause of the hyaline vascular degeneration, . . . . Such an explanation might account for the variable laboratory results, particularly the persistent absence of coagulation defects in livedoid vasculitis." [14]
 
" . . . antigen-antibody complexes and deposition of serum complement may play no causative role in atrophie blanche" [15]
 
"The association of infectious diseases and hyalinizing segmental vasculitis with deposits of immunoglobulins and complement in the vessel wall further supports the concept of an immune pathogenesis of which bacterial antigens may be an integral part." [20]
 
"The increased platelet aggregation found in our patients indicates possible abnormal functioning of coagulation. . . . It is possible that injury to small vessels leads to platelet activation, with thrombosis of small vessels and resultant superficial ischemic ulcerations. Alternatively, these patients may have a primary hyperaggregability of platelets that results in clinical disease." [22]
 
" . . . .vascular occlusion is the pivotal event in the production of atrophie blanche." [16]
 
"Either a defect in plasminogen activator or prostacyclin synthesis might serve as mechanisms by which early fibrin deposition occurs. . . . Thus we suggest that atrophie blanche represents a primary vasculopathy, related perhaps to abnormalities in endothelial cell or platelet function or metabolism, rather than an immune complex-mediated vasculitis." [23]
 
" . . . abnormal paraproteins may damage the endothelium, perhaps initiating the coagulation cascade and resulting in thrombosis." [28]
 
"These results (elevated fibrinopeptide A levels) support classification of this disorder (livedo vasculitis) as a thrombogenic vasculopathy rather than as a small vessel vasculitis." [17]
 
" . . . we suggest that a basic immunological disorder (lymphocyte activation?) and activated platelet expression of P-selectin may have an important cooperative role in inducing LV(livedo vasculopathy)." [18]
 
"The dramatic outcome of treatment with corticosteroids in this patient suggests that inflammation, even though paucicellular, rather than simple plugging of vessels, may be a critical feature in the pathogenesis . . . or, alternatively, that corticosteroids may be active in the disorder because of their fibrinolytic activity. . . . " [32]
 
" . . . we demonstrated a markedly reduced TM (thrombomodulin) expression on the endothelial cells in the involved mid-dermal vessels in livedo vasculitis, without destruction of vessel walls, and found normal levels of serum sTM, a vascular injury marker. The results suggest the reduction of TM expression is a primary, rather than a secondary event to vascular injury." [34]
 
"Four patients with livedoid vasculitis . . . had associated raised anticardiolipin antibodies but no other evidence of systemic disease. We suggest that livedoid vasculitis may be a manifestation of the antiphospholipid syndrome." [35]
 
"Perhaps an immunologic mechanism is involved in the beneficial effect of PUVA treatment in this disorder (livedo reticularis and livedoid vasculitis)." [36]
 
"The finding of the factor V Leiden mutation in our patient with livedo vasculitis supports the hypothesis that enhanced thrombosis, resulting from a number of possible causes, may be a central mechanism in the onset of this chronic occlusive vasculopathy." [40]
 
"This study demonstrates a possible association between plasma homocysteine levels and a small vessel thrombotic vasculopathy, livedoid vasculitis." [44]
 
" . . . a hypercoagulative state due to factor XII deficiency should be emphasized as a possible cause of painful ulcer and livedo, . . . ." [45]
 
"The good clinical response to immunosuppressive therapy seems to suggest that immune-mediated pathomechanisms may play a cooperating role." [46]