Posttransfusion purpura. Case report with observation on antibody detection and therapy

Erichson, Robert B.

doi:10.1001/archinte.138.6.998

Cited by 12 publications

(11 citation statements)

References 7 publications

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“…Another frequent method of therapy is plasmapheresis or exchange transfusion [1,[9][10][11]16,23,24,40]. In the initial report by Shulman et a1 [l], one patient was treated with whole blood exchange transfusion with "prompt" rise in the platelet count.…”

Section: Discussionmentioning

confidence: 99%

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Post‐transfusion purpura: A report of five patients and a review of the pathogenesis and management

1986

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We report five cases of post-transfusion purpura. Despite having profound thrombocytopenia, their management consisted only of steroid administration if serious bleeding was present. In one patient without bleeding, no specific therapy was given. This patient recovered uneventfully. Two patients died. One of these died from complicating illnesses rather than bleeding. The other suffered brain death, the result of a ruptured cerebral aneurysm. Four patients were PLA1 negative. The fifth patient had an antibody to an unidentified platelet-specific antigen.

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Section: Discussionmentioning

confidence: 99%

“…Plasma exchange appears to be associated with fewer reactions. Some patients require multiple exchange to show improvement and others have relapsed after one or multiple exchanges [ 1,4,10,23,24,40,43]. Average recovery after exchange transfusion or plasmapheresis was 12.5 days.…”

Section: Morrison and Mollison [12]mentioning

confidence: 99%

Post‐transfusion purpura: A report of five patients and a review of the pathogenesis and management

1986

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“…The complexes then sensitize the patient's own Zw'-negative platelcts which are subsequently also destroyed. Since then, other cases of the disease have been dcscribcd (Morrison & Mollison, 1966;Svejgaard et al, 1967;Morse, 1968;Svejgaard, 1969;Nicholts et al, 1970;Dubarry et al, 1970;Cimo & Aster, 1972;Gockerman & Shulman, 1973;Abramson et al, 1974;Zeigler et al, 1975;Howard et al, 1976;Erichson et al, 1978;Laurscn et a\, 1978;Soulier et al, 1979;Mueller-Eckhardt et al, 1980).…”

Section: / G Pegels Et A1mentioning

confidence: 99%

Post‐transfusion Purpura: a Serological and Immunochemical Study

et al. 1981

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By applying the platelet suspension immunofluorescence test (PSIFT), platelet-specific alloantibodies responsible for post-transfusion purpura were detected in eight patients within a period of 2 years. All patients were female and had previously received blood or had been pregnant. The platelet-specific alloantibodies had the specificity anti-Zwa in all the patients, who were all Aw(a-). In two patients the platelets were tested in the acute phase of the disease and found to be coated with IgG. In one patient an ether eluate was prepared from the platelets that reacted strongly with Zw(a+) platelets, but weakly with platelets from Zwb-homozygous individuals. The sera of these two patients, and of two others whose platelets were not directly tested, taken in the acute phase of the purpura, reacted strongly with Zwa-positive platelets. The four sera also reacted, however weakly, with Zwa-negative platelets, with autologous platelets taken during remission and with platelets from patients with Glanzmann's disease. It is postulated that Zwa-anti-Zwa complexes, present in the eluate and the sera, caused the reaction with Zwa-negative platelets and the patients' own platelets. Immunochemical characterization of the post-transfusion purpura antibodies showed that in all patients these were IgG, in two combined with IgM antibodies. Antibodies of the sub-class IgG1 were found in all patients, sometimes together with IgG3. In the indirect immunofluorescence test with anti-complement serum, the PTP antibodies in only four sera were able to fix complement. In only two of these sera were these complement-binding antibodies detectable in the 51 Cr-lysis technique and then in a much lower titre than in the immunofluorescence technique.

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“…On the day after the second Plasmaphaeresis was first introduced for the treatment of PTP by Abramson et al [3] and has since been successfully used by three other groups [4][5][6], However, two groups have reported a lack of response [10,11], Pre viously, there had been 2 reports on resolu tion of PTP following whole-blood ex change [2,9] and more recently, there have been 2 reports on response to intravenous immunoglobulin [8,10], It has previously been assumed that plasma exchange is effec tive because of reduction in titre of anti-PlA1. Indeed, in the first reported response, the antibody titre fell to less than 10% if the pre treatment level [3], However, in this case plasmaphaeresis was used late in the disease (between days 14 and 18) and it may be that levels were in any case declining.…”

Section: Case Reportmentioning

confidence: 99%

Successful Treatment of Post-Transfusion Purpura with High Dose Immunoglobulins after Lack of Response to Plasma Exchange

Hamblin¹,

Abidi²,

Nee³

et al. 1985

Vox Sanguinis

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A 77-year-old woman with post-transfusion purpura failed to respond to two 2.5-litre plasma exchanges with albumin as a replacement fluid. However, intravenous infusion of high-dose human immunoglobulin produced a response within 4 h. It is suggested that plasma exchange and exchange transfusion are effective in this condition mainly because they have allowed large doses of immunoglobulin to be infused in the form of plasma or whole blood.

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Posttransfusion purpura. Case report with observation on antibody detection and therapy

Cited by 12 publications

References 7 publications

Post‐transfusion purpura: A report of five patients and a review of the pathogenesis and management

Post‐transfusion purpura: A report of five patients and a review of the pathogenesis and management

Post‐transfusion Purpura: a Serological and Immunochemical Study

Successful Treatment of Post-Transfusion Purpura with High Dose Immunoglobulins after Lack of Response to Plasma Exchange

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