Electrophoretic Studies on Sera containing High‐Titre Cold Haemagglutinins: Identification of the Antibody as the Cause of an Abnormal γ Peak

Christenson, W N; Dacie, J. V.; Croucher, Betty E. E.; Charlwood, P. A.

doi:10.1111/j.1365-2141.1957.tb05795.x

Cited by 82 publications

(24 citation statements)

References 18 publications

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“…It is of interest that this specificity may be relatively frequent because we have found 5 of 100 WM proteins tested that show a so-called anti-smooth-muscle antibody activity. This incidence is in the same order of magnitude as that of two other autoantibody activities carried by monoclonal IgM-anti-IgG or anti-blood group Ii (27,28). The significance of such a high incidence of some autoantibody activities among human monoclonal IgM molecules is not obvious.…”

supporting

confidence: 50%

Human monoclonal IgM with autoantibody activity against intermediate filaments.

Dellagi¹,

Brouet²,

Perreau³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Monoclonal IgMs from two patients with Waldenstrom macroglobulinemia were found to react with intermediate filaments. This was shown by (a) immunostaining of various tissues and cultured cells and (b) immunological characterization of the reactive antigen after blotting of polypeptides separated from total cell extracts by gel electrophoresis or purified intermediate filaments on nitrocellulose sheets. One monoclonal IgM had an activity directed only against vimentin, whereas the other reacted with four different classes of intermediate filaments-vimentin, desmin, glial fibrillary protein, and keratins.

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supporting

confidence: 50%

Human monoclonal IgM with autoantibody activity against intermediate filaments.

Dellagi¹,

Brouet²,

Perreau³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…Splenomegaly is not prominent in CAD. 11,23,37 Hemoglobinuria tends to be less severe than that seen in paroxysmal cold hemoglobinuria or warm AIHA. 3 The diagnosis of CAD is established with hemolytic anemia, reticulocytosis, hyperbilirubinemia, elevated lactate dehydrogenase, and positive Coombs testing for anti-C3 and classically negative anti-IgG.…”

mentioning

confidence: 99%

Cold agglutinin disease

Swiecicki

Hegerova

Gertz

2013

Blood

265

298

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Cold agglutinin disease is a rare and poorly understood disorder affecting 15% of patients with autoimmune hemolytic anemia. We reviewed the clinical and pathologic features, prognosis, and management in the literature and describe our institutional experience to improve strategies for accurate diagnosis and treatment. Retrospective analysis identified 89 patients from our institution with cold agglutinin disease from 1970 through 2012. Median age at symptom onset was 65 years (range, 41 to 83 years), whereas the median age at diagnosis was 72 years (range, 43 to 91 years). Median survival of all patients was 10.6 years, and 68 patients (76%) were alive 5 years after the diagnosis. The most common symptom was acrocyanosis (n = 39 [44%]), and many had symptoms triggered by cold (n = 35 [39%]) or other factors (n = 20 [22%]). An underlying hematologic disorder was detected in 69 patients (78%). Thirty-six patients (40%) received transfusions during their disease course, and 82% received drug therapy. Rituximab was associated with the longest response duration (median, 24 months) and the lowest proportion of patients needing further treatment (55%). Our institution’s experience and review of the literature confirms that early diagnostic evaluation and treatment improves outcomes in cold agglutinin disease.

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“…Cold agglutinin titers were determined by haemagglutination test according to standard methods [38]. CA IgM eluates were obtained from patient's sera with C.C.A.D, by thermal absorptionelution on OI + -RBC.…”

Section: Cold Agglutininsmentioning

confidence: 99%