Rheumatoid hyperviscosity: analysis of a patient with intermediate complexes that block other autoantibodies and a review of the literature

Scofield, R. Hal; Tardibono, George; Ogden, Steven B.; Harley, John B.; Reichlin, Morris; Kurien, Biji T.

doi:10.1016/s0049-0172(98)80018-8

Cited by 14 publications

(8 citation statements)

References 37 publications

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“…Oxidative stress, in addition, is associated with sequential oxidation processes that generate advanced glycation end (AGE) products that are damaging to proteins (93). Other potential contributing factors of RA, are the presence of circulating IgM anti-IgG advanced glycation end (AGE) products [34,35].…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

Autoimmunity and oxidatively modified autoantigens

Kurien

Scofield

2008

Autoimmunity Reviews

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246

194

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Oxidative damage mediated by reactive oxygen species results in the generation of deleterious byproducts. The oxidation process itself and the proteins modified by these molecules are important mediators of cell toxicity and disease pathogenesis. Aldehydic products, mainly the 4-hydroxy-2-alkenals, form adducts with proteins and make them highly immunogenic. Proteins modified in this manner have been shown to induce pathogenic antibodies in a variety of diseases including systemic lupus erythematosus (SLE), alcoholic liver disease, diabetes mellitus (DM) and rheumatoid arthritis (RA). 8-oxodeoxyguanine (oxidatively modified DNA) and low density lipoproteins (LDL) occur in SLE, a disease in which premature atherosclerosis is a serious problem. In addition, immunization with 4-hydroxy-2-nonenal (HNE) modified 60 kD Ro autoantigen induces an accelerated epitope spreading in an animal model of SLE. Advanced glycation end product (AGE) pentosidine and AGE modified IgG have been shown to correlate with RA disease activity. Oxidatively modified glutamic acid decarboxylase is important in type 1 DM, while autoantibodies against oxidized LDL are prevalent in Behcet's disease. The fragmentation of scleroderma specific autoantigens occurs as a result of oxidative modification and is thought to be responsible for the production of autoantibodies through the release of cryptic epitopes. The administration of antioxidants is a viable untried alternative for preventing or ameliorating autoimmune disease, particularly on account of the overwhelming evidence for the involvement of oxidative damage in autoimmunity. However, this should be viewed in the light of disappointing results obtained with the use of antioxidants in cardiovascular disease. Keywordslupus; autoimmunity; epitopes; autoantibodies; antigens Free radicalsReactive oxygen species (ROS) are oxygen-based molecules possessing high chemical reactivity. These include free radicals (superoxide and hydroxyl radicals) and non-radical species (hydrogen peroxide) which can be produced even at basal conditions by a number of ways. Free radicals are active species containing atoms or molecules with one or more unpaired electrons occupying an outer orbital. They can arise either by the univalent pathway of oxygen

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Section: Rheumatoid Arthritismentioning

confidence: 99%

Autoimmunity and oxidatively modified autoantigens

Kurien

Scofield

2008

Autoimmunity Reviews

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246

194

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“…HVS is usually treated by plasmapheresis in acute cases, and by control of the underlying diseases for long-term management. 4,9,10 Our patient's course suggests that HVS in systemic plasmacytosis can also be treated by steroid therapy to reduce the serum immunoglobulin level.…”

Section: Reportmentioning

confidence: 86%

“…2,4,5 However, systemic plasmacytosis has never been reported to cause HVS. 4,9,10 Our patient's course suggests that HVS in systemic plasmacytosis can also be treated by steroid therapy to reduce the serum immunoglobulin level. 3,6,7 The globulin fraction has been reported to exceed 5000 mg ⁄ dL in polyclonal HVS.…”

Section: Reportmentioning

confidence: 99%

“…Polyclonal gammopathies associated with rheumatoid arthritis, systemic lupus erythematosus, polymyositis and benign lymphoproliferative diseases have also been described as the cause of the condition. 2,4,5 However, systemic plasmacytosis has never been reported to cause HVS. The clinical signs of serum hyperviscosity in monoclonal gammopathy usually develop when gammaglobulins reach levels of > 4000 mg ⁄ dL for serum IgG, 6000 mg ⁄ dL for IgA and 3000 mg ⁄ dL for IgM.…”

Section: Reportmentioning

confidence: 99%

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Hyperviscosity syndrome associated with systemic plasmacytosis

Noda

Tsunemi

Ichimura

et al. 2010

Clinical and Experimental Dermatology

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Systemic plasmacytosis is characterized by plasma cell proliferation in multiple organs including skin, and by polyclonal hypergammaglobulinaemia. Hyperviscosity-related retinopathy has never been described with this condition, to our knowledge. We report a case of systemic plasmacytosis in a 49-year-old Japanese woman, who presented with fever, multiple erythematous plaques, hypergammaglobulinaemia, renal failure and bilateral retinal haemorrhage. Reduction of immunoglobulin with oral steroid reversed the retinopathy related to hyperviscosity syndrome. When marked hypergammaglobulinaemia is found in a patient with systemic plasmacytosis, funduscopic examination should be performed to reveal early asymptomatic retinal changes, because the retinopathy is treatable by control of the underlying disease.

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“…Historically various groups have used chromatographic methods such as size exclusion or ion exchange to detect antibody complexes [10]. However, to date these have been highly insensitive, as there is no opportunity for an amplification system.…”

Section: Methodologiesmentioning

confidence: 99%

Ligand binding assays and anti-drug antibodies, analytical approaches and validation issues

Overton

2002

Chromatographia

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Rheumatoid hyperviscosity: analysis of a patient with intermediate complexes that block other autoantibodies and a review of the literature

Cited by 14 publications

References 37 publications

Autoimmunity and oxidatively modified autoantigens

Autoimmunity and oxidatively modified autoantigens

Hyperviscosity syndrome associated with systemic plasmacytosis

Ligand binding assays and anti-drug antibodies, analytical approaches and validation issues

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