Protein Abnormalities in the Cold Haemagglutinin Syndrome

Harboe, Morten; Torsvik, Harald

doi:10.1111/j.1600-0609.1969.tb01836.x

Cited by 25 publications

(3 citation statements)

References 21 publications

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“…Fudenberg and Kunkel showed that these antibodies usually have a high (19 S or 1000 kDa) molecular weight [ 36 ]. Later, Harboe and co-authors further characterized the CA in CAD as monoclonal IgMκ [ 37 – 39 ].In a recent study of sera from 172 patients with monoclonal IgM associated with a variety of clinical disorders, CA were identified in 10 sera (8.5%) [ 40 ]. Both, pentameric and significant levels of hexameric IgM have been detected in samples of purified CA from CAD patients [ 41 ].…”

Section: Immune Biologymentioning

confidence: 99%

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Primary chronic cold agglutinin disease: An update on pathogenesis, clinical features and therapy

2007

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Chronic cold agglutinin disease (CAD) is asubgroup of autoimmune hemolytic anemia. PrimaryCAD has traditionally been defined by the absence of anyunderlying or associated disease. The results of therapy with corticosteroids, alkylating agents and interferon-a haveb een poor. Cold reactive immunoglobulins against erythrocyte surface antigens are essential to pathogenesis of CAD.These cold agglutinins are monoclonal, usually IgMk autoantibodies with heavychain variable regions encoded by the V H 4-34 gene segment. By flowcytometric and immunohistochemical assessments, am onoclonal CD20 þ k þ B-lymphocyte population hasb eend emonstrated in the bone marrow of 90% of thep atients, and lymphoplasmacytic lymphoma is af requent finding. Novel attempts at treatment for primaryC AD havem ostly been directed against the clonal B-lymphocytes. Phase 2s tudies haves hown that therapy with the chimeric anti-CD20 antibody rituximab produced partial response rates of more than 50% and occasional complete responses. Median response duration, however, was only 11 months. In this review,wediscuss the clinical and pathogenetic features of primaryCAD,emphasizing the more recent data on its close association with clonal lymphoproliferative bone marrow disorders and implications for therapy.W ea lso review the management and outline some perspectives on new therapy modalities.

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Section: Immune Biologymentioning

confidence: 99%

“…Pathogenic B-lymphocyte clones in CAD have been suspected or postulated for decades, based on the findings of monoclonal IgMκ CA in most, if not all patients [ 3 , 10 , 31 , 37 – 39 ]. More recently, it has been possible to verify such cell clones directly.…”

Section: Clonal B-lymphocytes In Primary Cadmentioning

confidence: 99%

Primary chronic cold agglutinin disease: An update on pathogenesis, clinical features and therapy

2007

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“…Coomassie blue was used to visualize proteins. g/l), IgA (1-4.1 g/l), IgM (0.5-2.5 g/l), C3 (0.83-Absorption and elution of CA Red cell stromata were prepared from washed 0 RhD positive erythrocytes that had been haemolysed in distilled water (11). The stromata were centrifuged for 20 rnin at 20,000 rpm at 0°C and washed 3 times with distilled water to remove residual haemoglobin.…”

Section: Serological Analysismentioning

confidence: 99%

Paradoxical haemolysis in a patient with cold agglutinin disease

Ulvestad

1998

European J of Haematology

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A patient with classical cold agglutinin disease initially experienced haemolytic episodes during cold exposure. However, with advancing disease cold‐induced haemolysis ceased and was substituted with a haemolytic disposition at elevated body temperatures. To investigate this paradoxical development of disease manifestations, we performed a clinical and immunological study. Our results indicate that the patient's complement system became exhausted during the later phase of his disease, probably due to continual consumption of complement components. Initially, the patient had slightly decreased C4 concentrations and moderately reduced total haemolytic activity (CH50). Later C4 fell to undetectable levels and CH50 declined to zero. The increased haemolytic activity experienced during febrile episodes is probably due to a cold agglutinin with a high thermal amplitude, combined with enhanced synthesis of complement molecules during the acute phase response. Although C4 concentrations never increased to detectable levels during infections or inflammations an acute phase reaction was determined each time, as evidenced by increased concentrations of CRP. By reconstituting the patient's serum with active complement from donor serum or plasma, increased haemolytic activity was observed. These results indicate that some patients with cold agglutinin disease may experience deleterious haemolytic consequences if transfused with plasma‐containing blood products.

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Cold agglutinin autoimmune hemolytic anemia in nonhematologic malignancies

1979

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Four patients with nonhematologic malignancies had the simultaneous finding of hemolytic anemia due to high-titer cold agglutinins. In each patient, the cold agglutinin had "anti-I" specificity and was of the IgM kappa immunoglobulin class. Although patients with hematologic malignancies not uncommonly have cold agglutinins, the association between these antibodies and nonhematologic malignancies is unusual.

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Protein Abnormalities in the Cold Haemagglutinin Syndrome

Cited by 25 publications

References 21 publications

Primary chronic cold agglutinin disease: An update on pathogenesis, clinical features and therapy

Primary chronic cold agglutinin disease: An update on pathogenesis, clinical features and therapy

Paradoxical haemolysis in a patient with cold agglutinin disease

Cold agglutinin autoimmune hemolytic anemia in nonhematologic malignancies

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