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PubMed2001

Patients with systemic vasculitis have increased levels of autoantibodies against oxidized LDL.

Oxidation of low density lipoprotein (LDL) is considered to play an important role in the development of atherosclerosis and increased levels of autoantibodies against oxidized LDL have been found in patients with various manifestations of atherosclerosis. Patients with vasculitis are prone to the development of atherosclerosis. Since production of radical oxygen species in these patients may result in increased production of oxidized LDL (Ox-LDL), we hypothesized that antibodies against Ox-LDL are elevated during lesion development in vasculitis. Therefore we measured anti Ox-LDL antibodies in 25 patients with ANCA-associated vasculitis and in 42 healthy controls using an ezyme-linked immunosorbent assay (ELISA) in which malondialdehyde modified LDL (MDA-LDL) was coated on microtitre plates. Anti Ox-LDL antibodies were significantly higher in patients as compared to controls (P = 0.0001). Anti Ox-LDL levels were also measured in 11 patients during active disease and in these same patients during complete remission. Anti Ox-LDL levels were significantly higher in patients during active disease than during full remission (P = 0.001). Our results suggest that patients with ANCA-associated vasculitis are more susceptible to oxidation of LDL, which may contribute to accelerated atherosclerosis development.

Adult↗
PubMed2002

Hypogalactosylation of serum IgG in patients with ANCA-associated systemic vasculitis.

The triad of small vessel vasculitides (SVV) comprise Wegener's granulomatosis (WG), microscopic polyangiitis (MPA) and Churg-Strauss syndrome (CS). All three are associated with presence of circulating IgG antineutrophil cytoplasm antibodies (ANCA) which target autoantigens contained, primarily, within neutrophil azurophilic granules. The widely accepted model of pathogenesis suggests that ANCA activate cytokine-primed neutrophils within the microvasculature, leading to by-stander damage to endothelial cells, and rapid escalation of inflammation with recruitment of mononuclear cells. Activation may be initiated, in vitro, by the coligation of the PR3 or MPO antigen, translocated to the cell surface, and FcgammaRIIa/FcgammaRIIIb receptors. This suggests that the IgG subclass profile of ANCA and, possibly, its glycosylation status could influence the inflammatory mechanisms activated. The glycosylation status of total IgG isolated from the sera of patients with WG (13), MPA (6) and CSS (1) was determined by analysis of the released oligosaccharides. A deficit in IgG galactosylation is demonstrated for all patient samples, compared to controls. The mean percentage values for the agalactosylated (G0) oligosaccharides were 57% (SD +/- 9.71), 47% (SD +/- 4.25) and 28% (SD +/- 4.09) for WG, MPO and control samples, respectively. The G0 levels for polyclonal IgG isolated from the sera of both WG and MPA patients were significantly increased compared to controls (P < 0.0001). The major glycoform present therefore is agalactosylated (G0) IgG. In previous studies the G0 glycoform of IgG has been shown to bind and activate mannan binding lectin, and hence to activate the complement cascade, and to facilitate mannose receptor binding and the uptake of IgG complexes by macrophages and dendritic cells. Both of these activities could impact on the processing and presentation of self-antigens in autoimmune disease.

Adolescent↗
PubMed2000

Therapy: Hyperbaric Oxygen as the Only Effective Treatment in Mutilating and Resistant Systemic Vasculitis.

A forty year old man was seen in 1984 with a four year history of a painful vasculitis that responded transiently to plasma exchange. Diagnosis was revised to atypical pyoderma gangrenosum with further temporary benefit from lamprene and continuing maximally tolerated corticosteroids. The course fluctuated over the next ten years with gradual and increasing soft-tissue damage coupled with superimposed skin infections. A variety of organisms were isolated from the ulcerated areas, with each episode successfully managed on the basis of local debridement and appropriate antibiotic administration. In 1995, with extending skin devascularization, infectious bacterial episodes became more frequent and deep non-healing ulcers led to constant pain with virtual incapacity. In response to protocol hyperbaric oxygen therapy there was immediate reversal of the cutaneous damage, granulation tissue formed and new skin grew to cover the previous extensive deficits. As the lesions in his hands and feet improved so did his quality of life, with the patient again becoming ambulant and returning to work. Vascular access had become a major problem, and venography showed extensive occlusion with collateral circulation. A standard Hickman catheter was placed through the femoral vein into the inferior vena cava and functioned well over the next five years. At the end of 1996 the patient was admitted with an acute chest pain that was complicated by a major pulmonary embolus, from which he could not be resuscitated. This anecdotal experience demonstrates the important but underutilised benefits of hyperbaric oxygen in managing refractory, painful and penetrating skin ulcers. The cost of obtaining wound healing with reduction in pain by this form of treatment was approximately one-fifth of expenditure on previously ineffective management.

Journal Article↗