Effective high-dose intravenous gammaglobulin therapy for passive immune thrombocytopenia in the neonate

1987 ◽  
Vol 146 (1) ◽  
pp. 90-91 ◽  
Author(s):  
A. Stabile ◽  
M. A. Pesaresi ◽  
S. Miceli Sopo ◽  
G. Segni
1983 ◽  
Vol 103 (4) ◽  
pp. 654-655 ◽  
Author(s):  
Gaetano Chirico ◽  
Marzia Duse ◽  
Alberto G. Ugazio ◽  
Giorgio Rondini

2020 ◽  
pp. 1-6
Author(s):  
Masuho Saburi ◽  
Masao Ogata ◽  
Yasuhiro Soga ◽  
Takako Satou ◽  
Kazuhito Itani ◽  
...  

<b><i>Objective:</i></b> Platelet-associated immunoglobulin G (PA-IgG) refers to IgG attached to the surface of platelets, while the immature platelet fraction (IPF) reflects the state of platelet production in bone marrow. Since PA-IgG and IPF are increased in patients with immune thrombocytopenia (ITP), reflecting amounts of platelet antibodies and compensatory platelet production, respectively, we hypothesized that these laboratory findings may provide useful markers for predicting treatment response in patients with ITP. We therefore retrospectively investigated associations between levels of these markers at diagnosis and response to first-line therapy in patients with ITP. <b><i>Methods:</i></b> Forty-three patients diagnosed with ITP at Oita Kouseiren Tsurumi Hospital between May 2010 and November 2018 were included. Patients were divided into 2 groups based on response to corticosteroid as first-line therapy. Laboratory findings were compared between responders and nonresponders. <b><i>Results:</i></b> Median PA-IgG was 285 ng/10<sup>7</sup> cells (range, 45.5–18,200 ng/10<sup>7</sup> cells), and median IPF was 15.5% (range, 5.4–62.1%). Median levels were higher than the respective upper limits of normal range (PA-IgG, 0–46 ng/10<sup>7</sup> cells; IPF, 1.1–9.5%). First-line therapy was performed using standard-dose prednisolone (0.5–1.0 mg/kg/day) in 32 patients and high-dose dexamethasone (40 mg/day, 4 days) or methylprednisolone (125–1,000 mg/day, 3–4 days) in 11 patients. Twenty-four patients (55.8%) responded to first-line therapy. In univariate analysis, type of corticosteroid (<i>p</i> = 0.17) tended to differ between groups but did not differ significantly, and no difference in IPF level was apparent between responders (15.35%; range, 5.4–41.5%) and nonresponders (16.7%; range, 6.3–62.1%; <i>p</i> = 0.15). PA-IgG was significantly higher among nonresponders (430 ng/10<sup>7</sup> cells; range, 101–18,200 ng/10<sup>7</sup> cells) than among responders (254.5 ng/10<sup>7</sup> cells; range, 45.5–470 ng/10<sup>7</sup> cells; <i>p</i> = 0.004). Multivariate analysis revealed PA-IgG was independently associated with response to first-line therapy (odds ratio, 1.000; 95% confidence interval, 1.000–1.010; <i>p</i> = 0.029). <b><i>Conclusion:</i></b> Our data suggested that PA-IgG at diagnosis could offer a useful predictor of response to first-line corticosteroid therapy for ITP.


Blood ◽  
2011 ◽  
Vol 118 (24) ◽  
pp. 6403-6406 ◽  
Author(s):  
Andrew R. Crow ◽  
Sara J. Suppa ◽  
Xi Chen ◽  
Patrick J. Mott ◽  
Alan H. Lazarus

Abstract To definitively determine whether the neonatal Fc receptor (FcRn) is required for the acute amelioration of immune thrombocytopenia (ITP) by IVIg, we used FcRn-deficient mice in a murine ITP model. Mice injected with antiplatelet antibody in the presence or absence of IVIg displayed no difference in platelet-associated IgG between FcRn deficient versus C57BL/6 mice. FcRn-deficient mice treated with high-dose (2 g/kg) IVIg or a low–dose (2 mg/kg) of an IVIg-mimetic CD44 antibody were, however, protected from thrombocytopenia to an equivalent extent as wild-type mice. To verify and substantiate the results found with FcRn-deficient mice, we used β2-microglobulin–deficient mice (which do not express functional FcRn) and found that IVIg or CD44 antibody also protected them from thrombocytopenia. These data suggest that for both high-dose IVIg as well as low-dose CD44 antibody treatment in an acute ITP model, FcRn expression is neither necessary nor required.


1996 ◽  
Vol 41 (4) ◽  
pp. 487-491
Author(s):  
MASATOSHI TAKAGI ◽  
ATSUSHI UNNO ◽  
TOSHIHIKO SATO ◽  
TAKESHI MARUYAMA ◽  
ATSUTO HOSAKA ◽  
...  

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 13-14
Author(s):  
Ramil Fatkhullin ◽  
Vasily Shuvaev

Increased numbers of COVID-19 infection make the study of its systemic manifestations more and more important. Despite of SARS-Cov-2 main clinical respiratory syndrome other clinical infection signs as immune thrombocytopenia without respiratory failure were identified. We have seen case series of patients with thrombocytopenia and active COVID-19 infection during present epidemic outbreak. Patient 1, female, 31 years old was admitted at our hospital with ecchymoses, epistaxis, gingival hemorrhage and metrorrhagia. There were also signs of COVID-19 infection - fever up to 40oC, short of breathes with room air. The pulmonary infiltrates about to 25% were revealed by CT scan. The CBC parameters were as follows: WBC 8.9x109/l, Hb 11,2 g/dl, PLT 3 x109/l by microscopy. The patient was treated with high-dose dexamethasone 40 mg QD for 4 days. The treatment resulted to stable complete platelet response as 189x109/l in fourteen days after start of therapy. At that time, the cancer in situ of cervix uteri there was revealed by gynecologic examination, that was successfully local treated. Patient 2, female 30 years old presented epistaxis, metrorrhagia, cutaneous and gingival hemorrhagic syndrome as previous patient. There were WBC 6.4x109/l, Hb 12,6 g/dl, PLT 3x109/l by microscopy in CBC. She had no respiratory signs and abnormality in pulmonary CT. The COVID-19 infection was identified by PCR and antibody screening. The patient also received high-dose dexamethasone 40 mg QD for 4 days and yielded of platelet elevation to 25x109/l with no hemorrhagic syndrome in five days of treatment. Patient 3, female 68 years old with chronic course of immune thrombocytopenia and resistance to glucocorticoid, after splenectomy and presence of HBsAg. All relapses of thrombocytopenia in this patient were associated with virus infection. The first episode was in 2009, patient was treated with glucocorticoid with no effect. The complete platelet response was achieved after splenectomy. The relapse occurred in 2015 and was associated with acute respiratory distress syndrome (probably H7N9 flu). There treatment with prednisone 1 mg/day resulted to complete platelet response. At present time, the COVID-19 infection on this patient manifested with 75% of pulmonary volume lesions. At the recovery (25% of pulmonary infiltrates) the relapse of immune thrombocytopenia with cutaneous bleeding occurred. In CBC there were WBC 5.9x109/l, Hb 15,1 g/dl, PLT 5x109/l by microscopy. Given that history of therapy we treated this patient with high-dose dexamethasone 40 mg QD for 4 days and romiplostime 2 mqg/kg. The complete resolution of hemorrhagic signs and platelet response (65x109/l) was reached in seven days of treatment. Discussion. The virus-associated thrombocytopenia is usual in common practice. In recent COVID-19 infection outcome meta-analysis (G. Lippi et al. Clinica Chimica Acta 506 (2020) 145-148) the platelet count was significantly lower in severe course of disease. The presence of platelet below the lower limit was associated with fivefold of risk of severe COVID-19 and was a factor of mortality. The platelet decline could be as sign of disease worsening at one hand and have an own risk of mortality by bleeding at other hand. There is a need for guideline to thrombocytopenia management in COVID-19 patients. Now we are continuing to search and include the patients with COVID-19 infection and thrombocytopenia in our study. Disclosures Shuvaev: Novartis:Honoraria, Speakers Bureau;BMS:Honoraria, Speakers Bureau;Pfizer:Honoraria, Speakers Bureau.


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