Successful treatment of thrombotic thrombocytopenic purpura with high‐dose corticosteroid

Toyoshige, Michihiro; Zaitsu, Yuzuru; Okafuji, Koichiro; Inoue, Yasushi; Hiroshige, Y; Matsumoto, Noboru; Kaku, Kohei; Kaneko, Takeshi

doi:10.1002/ajh.2830410119

Cited by 17 publications

(12 citation statements)

References 6 publications

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“…Though this study did not answer the question of whether a lower dose of steroids increase the likelihood of remission compared to no steroid treatment, it does at least suggest that high-dose steroid therapy improves the management of TTP. The effectiveness of high-dose corticosteroids in TTP is also supported by other published studies that suggested that patients refractory to TPE could respond rapidly to boluses of corticosteroids [27,28]. Taken together, those results argue for a role of steroids in the management of TTP in association with TPE provided there is no obvious contra-indication, though the modalities of administration still remain controversial.…”

Section: Steroidssupporting

confidence: 61%

Current management and therapeutical perspectives in thrombotic thrombocytopenic purpura

Coppo

Veyradier

2012

La Presse Médicale

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Section: Steroidssupporting

confidence: 61%

Current management and therapeutical perspectives in thrombotic thrombocytopenic purpura

Coppo

Veyradier

2012

La Presse Médicale

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“…In the literature, there are few reports suggesting the possibility that TTP is controllable by high‐dose glucocorticoid therapy (Ozsoylu, 1988, 1990; Vianelli et al. , 1991; Toyoshige et al. , 1992).…”

Section: Discussionmentioning

confidence: 99%

Thrombotic thrombocytopenic purpura in southern Turkey: a single-center experience of 29 cases

Gürkan¹,

Başlamışlı²,

Güvenç³

et al. 2005

Clin Lab Haematol

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In this retrospective, nonrandomized study, we describe our experience in the management of 29 consecutive patients with thrombotic thrombocytopenic purpura (TTP) treated with a combined therapy of plasma exchange (PE) and steroids at a single center. We compared the effectiveness of high-dose steroids (20-25 mg/kg methyl prednisolone) as first-line treatment in combination with PE therapy with the combination of standard-dose steroids (1 mg/kg methyl prednisolone) and PE in adult patients with TTP. Clinical, laboratory data and treatment outcomes such as response rate, median time to recovery and survival were evaluated retrospectively. Overall (OR) and complete (CR) response rates were 69 and 52% respectively. Similar response rates were found in patients treated with pulse or conventional dose steroids; however, the median time to response was delayed in the high-dose methyl prednisolone (HDP) group. The median time from the initiation of symptoms to initiation of treatment was approximately 15 days (range: 0-30). Delayed treatment in our patients because of delayed referral to our center resulted in poor response to treatment. In all, four of 14 (27%) complete responders experienced relapses. The predicted relapse rate was 48% at a median of 30 months. All the relapses presented with a combination of thrombocytopenia and microangiopathic hemolytic anemia. This analysis showed that high-dose steroid treatment did not prove to be beneficial for TTP patients as firstline therapy combined with PE. Moreover, pulse steroid interventions might have resulted in delayed responses and our data suggest that initiation of treatment with PE should not be delayed.

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“…In addition to corticosteroids, immune modulating agents such as vincristine, cyclosporin, azathioprine, intravenous immunoglobulin, and staphylococcal protein A adsorption column therapy have been reported to be effective in some patients [11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Minimal evidence of platelet and endothelial cell reactive antibodies in thrombotic thrombocytopenic purpura

et al. 1999

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Thrombotic thrombocytopenic purpura (TTP) is a syndrome characterized by microvascular thrombosis with thrombocytopenia and end-organ injury. Evidence suggests that platelet or endothelial cell injury may be initial pathological events in TTP. A number of factors in patient plasma, including immunoglobulins, have been proposed to mediate cellular injury in TTP. However, systematic analyses of TTP patient plasma for the presence of platelet or endothelial cell antibodies are lacking. We, therefore, analyzed 48 TTP patient plasma samples for the presence of platelet and endothelial cell antibodies by using enzyme-linked immunosorbent assay, flow cytometry, and microlymphocytotoxicity. Twelve of 48 TTP patient samples (25%) reacted against purified platelet glycoproteins. Nine (19%) also contained antibodies that bound to allogeneic target platelets in flow-cytometric assays. Nine of 48 samples (19%) contained antibodies to human umbilical vein endothelial cells in flow-cytometric assays, and seven of 48 patient samples (15%) bound to human dermal microvascular endothelial cells. Six of 48 (13%) patient plasma samples contained antibodies that bound to human umbilical vein endothelial cells activated with gamma-interferon and tumor necrosis factor-alpha. Of twenty samples that were reactive in one or more platelet or endothelial cell assay, eight contained human leukocyte antigen antibodies reactive in microlymphocytotoxicity. These studies demonstrate that antibodies reactive against platelet or endothelial cell antigens are not prevalent in TTP, and that more than a third of antibodies detected are human leukocyte antigen alloantibodies. Our findings suggest that autoantibodies against platelets or endothelial cells are not important in the pathogenesis of this syndrome.

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Successful treatment of thrombotic thrombocytopenic purpura with high‐dose corticosteroid

Cited by 17 publications

References 6 publications

Current management and therapeutical perspectives in thrombotic thrombocytopenic purpura

Current management and therapeutical perspectives in thrombotic thrombocytopenic purpura

Thrombotic thrombocytopenic purpura in southern Turkey: a single-center experience of 29 cases

Minimal evidence of platelet and endothelial cell reactive antibodies in thrombotic thrombocytopenic purpura

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