Journal articles: 'Thrombopenic purpura'

1

Majsky, A., and J. Fortynova. "HLA and Idiopathic Thrombopenic Purpura (ITP)." Tissue Antigens 15, no. 2 (December 11, 2008): 222–23. http://dx.doi.org/10.1111/j.1399-0039.1980.tb00909.x.

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Briantais, Antoine, Jean Baptiste Dalmas, Laure Swiader, Pascale Poullin, and Jean-Marc Durand. "Recurrent hypothyroidism and thrombopenic thrombotic purpura." Annales d'Endocrinologie 81, no. 5 (October 2020): 518–19. http://dx.doi.org/10.1016/j.ando.2020.07.1111.

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&NA;. "Vincristine resolves a case of thrombopenic purpura." Inpharma Weekly &NA;, no. 775 (February 1991): 17. http://dx.doi.org/10.2165/00128413-199107750-00046.

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Gregersen, N. F. "ON THROMBOPENIC PURPURA AND ITS OPERATIVE TREATMENT." Acta Medica Scandinavica 135, S234 (April 24, 2009): 136–40. http://dx.doi.org/10.1111/j.0954-6820.1949.tb05606.x.

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&NA;. "Thrombotic thrombopenic purpura therapy - too good to be true?" Inpharma Weekly &NA;, no. 787 (May 1991): 4. http://dx.doi.org/10.2165/00128413-199107870-00009.

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&NA;. "Megadose methylprednisolone temporarily increases platelet counts in immune thrombopenic purpura." Inpharma Weekly &NA;, no. 770 (January 1991): 12. http://dx.doi.org/10.2165/00128413-199107700-00038.

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Wang, Ying, Qiaoyun Gong, Mingqin Zhu, Chao Lu, Li Sun, Jiachun Feng, and Hongliang Zhang. "Aquaporin-4 positive neuromyelitis optica spectrum disorders secondary to thrombopenic purpura." Medicine 96, no. 2 (January 2017): e5792. http://dx.doi.org/10.1097/md.0000000000005792.

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&NA;. "Corticosteroid and plasma therapy are effective in thrombotic thrombopenic purpura-haemolytic uraemic syndrome." Inpharma Weekly &NA;, no. 801 (August 1991): 15. http://dx.doi.org/10.2165/00128413-199108010-00043.

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Benz, Kerstin, and Kerstin Amann. "Pathological aspects of membranoproliferative glomerulonephritis (MPGN) and haemolytic uraemic syndrome (HUS) / thrombocytic thrombopenic purpura (TTP)." Thrombosis and Haemostasis 101, no. 02 (2009): 265–70. http://dx.doi.org/10.1160/th07-12-0761.

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SummaryIn this paper, epidemiology, pathogenesis and typical morphological aspects of all three types of membranoproliferative glomerulonephritis (MPGN), of the haemolytic uraemic syndrome (HUS) as well as of thrombotic thrombopenic purpura (TTP) will be reviewed on the light microscopical, immunohistological or immunofluorescence and electron microscopical level. In particular, differences in the pathogenesis of these diseases are discussed. Important recent molecular and genetic insights into the pathogenesis of the three types of MPGN, of typical and atypical HUS and of TTP, i.e. dysregulation of the complement system, distinct molecular defects in C3 and factor H, the major regulatory protein of the alternative pathway of complement activation, and deficiency of a von Willebrand factor (VWF) -cleaving protease, i.e. ADAMTS13, are highlighted. Finally, particular emphasis will be put on differences in glomerular and vascular morphology in the three types of MPGN and in thrombotic microangiopathy (TMA), which is the characteristic morphological alteration of the kidney in HUS and TTP, respectively.

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IWAMATSU, HIROSHI. "A case of chronic renal insufficiency contracted with thrombotic thrombopenic purpura by the miliary tuberculosis." Nihon Naika Gakkai Zasshi 87, no. 2 (1998): 335–37. http://dx.doi.org/10.2169/naika.87.335.

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MIMORI, AKIO. "Intractable complication of collagen disease. Advances in diagnosis and treatment. IV. Hemopathy. 2. Thrombotic thrombopenic purpura." Nihon Naika Gakkai Zasshi 90, no. 8 (2001): 1427–33. http://dx.doi.org/10.2169/naika.90.1427.

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MOTOMURA, TAKASHI. "A case of thrombotic thrombopenic purpura (TTP) treated effectively plasma exchange therapy and immunoglobulin high dose therapy." Nihon Naika Gakkai Zasshi 83, no. 2 (1994): 305–7. http://dx.doi.org/10.2169/naika.83.305.

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Borgi, Aida. "Congenital Thrombotic Thrombocytopenic Purpura: Atypical Presentation And First ADAMTS 13 Mutation In A Tunisian Child." Mediterranean Journal of Hematology and Infectious Diseases 5, no. 1 (June 3, 2013): e2013041. http://dx.doi.org/10.4084/mjhid.2013.041.

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Background: Congenital deficiency of ADAMTS13 is characterized by systemic platelet clumping, hemolytic anemia and multiorgan failure. Although, more than 100 mutations have been reported, atypical clinical presentation may be involved in diagnostic difficulties. Case report: A 2 year old Tunisian child presented with chronic thrombopenic purpura which failed to respond to corticosteroids. Hemolytic anemia with schizocytes, occurred ten months later, with no previous history of diarrhea or any neurological abnormality. Renal function, coagulation screening tests and complement assay were normal. The count of platelet improved after fresh frozen infusion (FFP). Extensive investigations revealed a severe deficiency of ADAMTS 13 activity (level< 5%). Gene sequencing identified mutation in exon 18 of ADAMTS 13 gene. Prophylactic regimen with regular infusions of FFP was associated to favorable outcome. Conclusion: Early ADAMTS 13 activity testing and gene sequencing associated to precocious plasmatherapy are crucial to reduce morbidity and mortality of congenital TTP.

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KISSMEYER-NIELSEN, FLEMMING. "A Study of the Thrombopoiesis before and after Spontaneous Remission in a Case of Acute Idiopathic Thrombopenic Purpura." Acta Medica Scandinavica 137, no. 5 (April 24, 2009): 367–73. http://dx.doi.org/10.1111/j.0954-6820.1950.tb12127.x.

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Plastira, C., E. Zafeiropoulou, E. Kontogeorgi, and D. Karakalos. "Immune thrombopenic purpura (ITP) elicited by childhood vaccination and antiphospholipid syndrome (APS) manifested as cerebral venous thrombosis: Coincidence or no?" Journal of the Neurological Sciences 333 (October 2013): e267. http://dx.doi.org/10.1016/j.jns.2013.07.1023.

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SUEHIRO, AKIRA. "Thrombosis. Thrombosis : Advances on diagnosis and treatment. Disease state and diagnosis of thrombotic diseases. Multiple small vein thrombosis. Thrombotic thrombopenic purpura (TTP)." Nihon Naika Gakkai Zasshi 86, no. 6 (1997): 923–28. http://dx.doi.org/10.2169/naika.86.923.

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Rodrı́guez-Calvillo, Mercedes, Izaskun Gabari, Marina Duarte, Guillermo Mazzolini, José Rifón, Eduardo Rocha, Jesús Prieto, and Ignacio Melero. "Thrombopenic purpura induced by a monoclonal antibody directed to a 35-kilodalton surface protein (p35) expressed on murine platelets and endothelial cells." Experimental Hematology 29, no. 5 (May 2001): 589–95. http://dx.doi.org/10.1016/s0301-472x(01)00630-0.

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Grall, Maximilien, Ygal Benhamou, Elie Azoulay, Eric Mariotte, Lionel Galicier, Steven Grange, Virginie Barbay, Dominique Bordessoule, Agnes Veyradier, and Paul Coppo. "Thrombotic Thrombocytopenic Purpura Misdiagnosed As Autoimmune Cytopenia: Causes of Diagnostic Errors and Consequence on Outcome. Experience of the French Thrombotic Microangiopathies Reference Centre." Blood 128, no. 22 (December 2, 2016): 3730. http://dx.doi.org/10.1182/blood.v128.22.3730.3730.

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Abstract Introduction: Thrombotic thrombocytopenic purpura (TTP) is a life threatening disease defined by the association of a hemolytic mechanical anemia, a profound thrombopenia and organ failure with a severe ADAMTS13 deficiency. A rapid diagnosis represents a major goal and sources of misdiagnosis need to be identified to avoid diagnostic wandering and delayed adapted treatment that may translate in increased morbi-mortality. The main objective of this study is to describe the characteristics of TTP initially misdiagnosed and analyse the impact of a late diagnosis on patient's outcomes. Methods: From May 2000 to May 2014, all patients with acquired TTP and severe ADAMTS13 deficiency enrolled prospectively in the French TMA Reference Centre registry were included. A misdiagnosis was retained if initial diagnosis was not TTP and if patients did not receive TPE as initial treatment. Results: Among the 423 studied patients, 84 (20%) were initially misdiagnosed and not received plasma exchange. Main diagnostic errors were attributed to an Evans syndrome and an auto-immune thrombopenic purpura in 51% and 37% of cases respectively. Median time to diagnosis was longer in the misdiagnosed group than in the accurately diagnosed (5 [IQR, 2-8] vs. 1 [IQR, 0-3] days, P=.008). At admission, compared to the accurately diagnosed patients, misdiagnosed patients had a higher rate of low or undetectable schizocytosis (57.5% vs. 32%, P=.001), higher hemoglobin level (8.4 [IQR, 6.7-9.7] g/dl vs. 7.7 [IQR, 6.5-9.1] g/dl, P=.008) and rate of positive DAT (18% vs. 4%, P=.008). Anti-nuclear antibodies (65% vs. 51%, P=.045) and an associated auto-immune disease (24% vs. 13%, P=.017) were also more frequent. In multivariate analysis, a positive DAT and hemoglobin level were retained as risk factor (OR= 8.71, 95% CI [1.759-43.181], P=.008 and OR= 1.27, 95% CI [1.002-1.602], P=.048), respectively. Platelet count recovery over time was significantly longer in the misdiagnosed group (log-rank test: P=.041) without any consequence on overall mortality, exacerbation and relapse. However, specific causes of death probably differed between groups: in the accurately diagnosed group, patients died more frequently on early stage from a fulminant form of TTP within the first week, whereas in the misdiagnosed group patients died later (13 [IQR, 3-20] vs. 6 [IQR, 2-9] days; P=.023), had less organ involvement at early diagnosis (49% vs.64%, P=.019) and received more salvage therapies (80% vs. 35%, P=.009), suggesting that prognosis could have been improved with an earlier treatment. Conclusion: TTP is frequently misdiagnosed with auto-immune cytopenias and usual biological parameters may be initially absent. In a context of hemolysis and thrombocytopenia, a low or undetectable rate of schizocytosis at admission, and a positive DAT should not rule out the diagnosis of TTP, especially when associated with organ failure. A rapid accurate diagnosis of TTP may result in a shorter time to platelet recovery and could improve prognosis. Disclosures No relevant conflicts of interest to declare.

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NARUSE, TAKUJI. "Special issue : systemic disease and renal lesion.An advance on diagnosis and treatment of a renal lesion which sets in other disease.Renal lesion which follow hemolytic uremic syndrome, thrombotic thrombopenic purpura, diseminated intravascular coagulation syndrome." Nihon Naika Gakkai Zasshi 81, no. 1 (1992): 73–76. http://dx.doi.org/10.2169/naika.81.73.

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20

Aladjidi, Nathalie, Antoine Pariente, Thierry Leblanc, Brigitte Bader Meunier, Yves Bertrand, Gerard Michel, Francoise Ledeist, et al. "Autoimmune Hemolytic Anemia (AIHA) in Children: A French Observational Study of 171 Patients for the French Society of Pediatric Hematology and Immunology (SHIP)." Blood 106, no. 11 (November 16, 2005): 1684. http://dx.doi.org/10.1182/blood.v106.11.1684.1684.

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Abstract Introduction: AIHA is a rare and potentially severe condition in children. To assess the presentation, treatment response and outcome of childhood AIHA, a national multicentric observational study has been started in 2002 in 32 French pediatric hematologic units. Patients and Methods: A descriptive analysis of 171 children under 18 years old, who are still being followed is presented. Inclusion criteria were hemoglobin <10 g/dl, positive Coombs test, and one of the three following hemolysis criteria: reticulocytes >120 000/mm3, haptoglobin <10 mg/dl, bilirubin >10 mg/dl. Etiological investigations were standardised. Treatment procedures were at the appreciation of each physician, according to the SHIP guidelines. Complete response (CR) was defined as Hb >10g/dl and absence of biological hemolysis for more than 3 months. Variables associated with survival in CR without treatment at the last follow up were assessed using a Cox model of multivariate analysis. Results: AIHA was diagnosed between January 1986 and March 2005 in 94 males and 77 females. The median follow-up is 9 months (range 0.2 to 234). Median age at diagnosis is 3,8 years (range 0.1–17.4). Familial or personal dysimmune history was respectively positive in 21 and 28 patients. A concomitant febrile episode was present in 50% of cases, and for half of the patients, the onset was sudden and severe. Median hemoglobin level at diagnosis was 5,6 g/dl (2 to 12,8) with a reticulocyte count below 100.000/mm3 in 43 patients. The direct Coombs test was positive for IgG in 37%, for IgG+C3b in 37%, for isolated C3b in 17%, for cold agglutinin +IgM in 7% and for IgA in 2% of patients. Thrombopenia and neutropenia were associated in 26% and 18% of patients respectively. Evans syndrome was diagnosed in 66/171 patients, among whom idiopathic thrombopenic purpura and AIHA occurred simultaneously in 31/66. AIHA was a component of a dysimmune clinical or biological disease in 50% of patients, of post infectious origin in 25%, associated with malformations in 5%, and isolated in 20%. All but 8 patients received steroid therapy (1 to 5 mg/kg prednisone daily). Resistance to steroids led 91/163 patients to receive a median of 3 (1 to 8) subsequent modalities of treatment, mainly ciclosporine (n=25), anti-CD20 (n=24), splenectomy (n=22), and azathioprine (n=14). Nine children died, 8 of whom had Evans syndrome. Survival in CR without treatment at 5 and 10 years from diagnosis were respectively 42% and 20%. In multivariate analysis, three variables were associated with the absence of CR without treatment at the last follow up: Coombs test of IgG/IgG+C3b class (RR 0,22, 95% IC [0,09–0,5], p = 0,0004), dysgammaglobulinemia (RR 0,28, 95% IC [0,11–0,71], p = 0,007), and age more than 4 years (RR 0,53, 95% IC [0,27–1,02], p = 0,05). Conclusion: The present French cohort is the largest reported study of AIHA in children. Heterogeneous underlying etiological subsets are confirmed. Two prognostic factors are clearly identified: direct Coombs test of IgG or IgG+C3b class, and presence of a dysgammaglobulinemia. Ongoing hemato-immunologic and therapeutic studies will allow better comprehension and treatment of this rare disease

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UND, S. WERNER, and E. ADLERCREUTZ. "EIN FALL VON IRITIS HAEMORRHAGICA GLAUCOMATOSA MIT PURPURA THROMBOPENICA." Acta Ophthalmologica 9, no. 1-4 (May 27, 2009): 329–33. http://dx.doi.org/10.1111/j.1755-3768.1931.tb08656.x.

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Murai, Kazunori, Shugo Kowata, Yasuhiko Tsukushi, Mamiko Ishiguro, Tatsuo Oyake, Takeshi Sugawara, and Yoji Ishida. "Thrombocytopoiesis Is Not Regulated by Thrombopoietin (TPO) but Proplatelet Formation (PPF) Stimulating Factor." Blood 108, no. 11 (November 16, 2006): 1112. http://dx.doi.org/10.1182/blood.v108.11.1112.1112.

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Abstract TPO is believed to be the physiological humoral hematopoietic factor in megakaryopoiesis and thrombopoiesis. Some investigators reported the inverted relationship between platelet mass and serum TPO levels, resulting in the conclusion that the platelet mass may directly play a role of regulating the circulating TPO levels. In the previous ASH meeting, we reported that serum TPO levels were not elevated in Immune thrombocytopenic purpura (ITP) patients. In this study, we measured platelet count, the serum TPO level, % reticulated platelet (%RP) and megakaryocytes mass in patients with refractory anemia in myelodysplastic syndrome (MDS-RCMD). The mean plasma TPO level in 20 healthy persons was 57.3±15.2 pg/ ml, the percentage of RPs was 1.51±0.71%. Plasma TPO levels were widely distributed (799.9±883.0 pg/ ml, n=35) in MDS-RCMD, while they were less than 131.0 pg/ml in ITP (48.5±37.0 pg/ ml, n=37). There were no significant relationship between platelet counts and plasma TPO levels in MDS-RCMD or ITP. These results indicated that plasma TPO level was not regulated by the platelet mass at least in thrombocytopenic patient with MDS-RCMD or ITP. We evaluated the thrombopoiesis in thrombocytopenic patients with MDS-RCMD or ITP. %RPs were 1.9±0.2 % in MDS-RCMD (n=34), indicating that increased thrombopoiesis was not observed in MDS-RCMD, in which serum TPO levels were increased. While %RPs were 6.6±4.9 % in ITP (n=45), indicating that thrombopoiesis was observed in ITP, in which serum TPO levels were not increased. These results indicated that thrombopoiesis was not regulated by plasma TPO levels but some thrombopoiesis stimulating factor(s). Therefore, we evaluated the thrombopoiesis stimulating activity in plasma of patients with MDS-RCMD or ITP as the indicator of PPF stimulating activity of murine megakaryocytes. PPF stimulating activity was measured as the ratio of PPF bearing megakaryocytes/ viable megakaryocytes after 48 hrs serum-free culture of murine megakaryocytes. As the plasma have some inhibitory effects of PPF activiy, the HDL fraction, isolated from plasma, was used as the methods described previously in Ishida Y et al. (Thrombosis and Haemostasis, 2001; 85:349–55). The higher PPF stimulating activity was observed in patients with ITP (n=15) or MDS-RCMD (n=15) than that with healthy donors (n=10) {healthy donors 26.1±5.4 % versus ITP 38.0± 6.0% (p<0.01), MDS-RCMD 41.9±5.3%(p<0.01)}. There was a significant correlation between the PPF activity and platelet counts (R=0.68; p<0.01) in these thrombopenic patients. These data strongly suggest that thrombopoiesis may not be regulated by TPO but some PPF stimulating factor(s).

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Völker, Linus Alexander, Franziska Grundmann, and Paul Thomas Brinkkötter. "Erworbene thrombotisch-thrombozytopenische Purpura – Patientenmanagement im Licht neuer Therapien." DMW - Deutsche Medizinische Wochenschrift 144, no. 22 (October 28, 2019): 1572–75. http://dx.doi.org/10.1055/a-0963-5675.

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Zusammenfassung Anamnese Eine 42-jährige Patientin stellte sich zunächst mit einer Pyelonephritis vor. Zwei Tage später traten Hämatome und punktuelle Einblutungen der Extremitäten auf. Diagnostik/Befunde Eine erworbene thrombotisch-thrombozytopenische Purpura wurde diagnostiziert. Der klinische Befund zeigte das Bild einer thrombotischen Mikroangiopathie mit einer Thrombopenie von 8 × 10E9/l. Es konnten eine erniedrigte ADAMTS13-Aktivität und Autoantikörper nachgewiesen werden. Therapie und Verlauf Bei positivem PLASMIC Score wurde vor Erhalt der ADAMTS13-Diagnostik eine Therapie mittels Plasmaseparation, Steroiden und Caplacizumab eingeleitet und im Verlauf um Rituximab ergänzt. Darunter kam es zu einer raschen klinischen Remission mit jedoch persistierenden ADAMTS13-Antikörpern und reduzierter -Aktivität, so dass Caplacizumab für insgesamt 58 Tage appliziert wurde. Diskussion Mit Caplacizumab steht eine wirkungsvolle neue Therapie der erworbenen thrombotisch-thrombozytopenischen Purpura zur Verfügung. Die Zeit bis zum klinischen Ansprechen und die Zahl der Rückfälle können deutlich reduziert werden. Liegt jedoch eine persistierende Autoimmunaktivität über den Therapiezeitraum hinaus vor, geht diese mit einem hohen Rückfallrisiko einher und erfordert engmaschige Kontrollen.

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Aurran-Schleinitz, Thérèse, Gwaenaelle Gravis, Martine Vittot, Diane Coso, Jérôme Rey, Jean-Marc Schiano, Aude Charbonnier, Emmanuelle Fougereau, Dominique Maraninchi, and Reda Bouabdallah. "“One Hour” Rituximab Infusion Is Safe and Improves Patient Care and Outpatient Unit Management." Blood 106, no. 11 (November 16, 2005): 4759. http://dx.doi.org/10.1182/blood.v106.11.4759.4759.

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Abstract Background: Administration of the monoclonal anti-CD20 antibody Rituximab has been associated with infusional toxicity, leading to strict guidelines of use, i.e., infusion times from 4 to 6 hours. Even with pretreatment acetaminophen and diphenydramine, grade 3/4 adverse events including bronchospasm and hypotension occur in ~10% of patients with the first, and in < 2% with subsequent infusions. Presence of circulating malignant CD20 bearing cells represents a risk factor for developing grade 3/4 reactions. The pathophysiogy of this infusional toxicity is thought to be a “cytokine release syndrome” occuring within the 2 first hours of infusion. In few cases, it can be related to an anaphylactic reaction, occurring in the first minutes of infusion. Based on these observations and because infusional toxicity may be lower by the concomitant use of steroids, we established new guidelines of rituximab administration based on the number of circulating CD20+ cells, cycle number of the infusion, and allowing a total one-hour infusion time. Methods: A 1 mg/kg dose of steroids + diphenydramine + acetaminophen were given 20 minutes before each rituximab infusion. Rituximab dose was 375 mg/m2 diluted in 500 ml bottle. In the absence of circulating CD20+ cells, patients received their first course of rituximab according to the standard recommendations (from 50 mg/h and increasing by levels of 50mg/h every 30 min) until the fifth level. Then the remaining dose was administered at 500ml/h, with a total infusion time of ~3 h. The subsequent infusions were given at 100 mg/h for 15 minutes then at 500 ml/h, i.e. in one hour. In case of circulating malignant CD20+ cells, the first rituximab administration was administrated over 2 days: 50mg/m2 in 4h on day 1, and 325mg/m2 on day 2 according to the instructions described above. The subsequent infusions were administered according the one-hour protocol. Results: 69 patients have been treated in our outpatient unit, according to this protocol, for a total of 115 courses including 21 first cycles. Patients characteristics are as follows: median age 61 (range 26–85); 50% male; histology: 27 DLCBL including (IPI ≤1: 17 patients, IPI ≥2: 10 patients), 22 follicular, 2 mantle cell, 3 marginal zone, 2 lymphoplasmocytic, 1 Castelman disease, 11 CLL and 1 idiopathic thrombopenic purpura; treatment: R-CHOP in 51 patients, R-fludarabine/cytoxan in 15, R-chlorambucil in 1 and Rituximab alone in 2. Among the 21 first courses treatment was R-CHOP in 13, R- fludarabine/cytoxan in 3 and Rituximab in 5. No grade 3/4 toxicity was noted neither during the first nor the subsequent cycles. During the first infusion 2 patients developed grade 2, and 3 developed grade 1 reactions. One CLL patient had a grade 1 reaction after the second cycle. Conclusions: Taking into account the presence of circulating malignant CD20+ cells, a 3h first and one-hour subsequent infusion protocol is safe and well tolerated, independently of diagnosis and chemotherapy regimen. This protocol allows a sparing of 2 to 4 hours treatment time, very convenient for patients and in outpatient unit management.

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Perrier, Quentin, Johan Noble, Steven Grangé, Pierrick Bedouch, Rachel Tetaz, and Lionel Rostaing. "Atypical Evolution of Secondary Hemolytic Uremic Syndrome Defined as Paraneoplastic Syndrome under Eculizumab and Palbociclib Therapies." Case Reports in Oncology 14, no. 1 (April 12, 2021): 676–80. http://dx.doi.org/10.1159/000514982.

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Thrombotic microangiopathy (TMA) is most of the time caused by thrombotic thrombocytopenic purpura or hemolytic uremic syndrome. A 60-year-old female was diagnosed in 2014 with mammary breast adenocarcinoma treated by several-line therapy: mastectomy, docetaxel, cyclophosphamide, radiotherapy, doxorubicine, and capecitabine. By mid-November, the patient was admitted to the hospital with regenerative, mechanical, and hemolytic anemia, schistocytes at 3%, and thrombopenia (99 G/L), associated with high blood transfusion requirement. After 9 sessions of plasmapheresis, there was no significant improvement in the biological parameters, nor after 2 cycles of paclitaxel. The patient was then treated with eculizumab during 4 weeks, with a slight reduction in blood requirement, and simultaneously with palbociclib. Since being treated with palpociclib, she had a great reduction in blood requirement and a good clinical condition. To conclude, we reported an initial moderate improvement of paraneoplasm-related TMA syndrome under eculizumab therapy with a slight reduction in red blood cell requirement; however, palbociclib therapy achieved a very good response with a dramatic reduction in red blood cell requirement.

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CROCHETTE, R., C. Ravaiau, A. Bergelin-Besancon, J. P. Coindre, M. Giral, and G. B. Piccoli. "SUN-356 THROMBOPENIA IN A KIDNEY TRANSPLANT PATIENT: A RARE CASE OF LATE-ONSET IMMUNE THROMBOCYTOPENIC PURPURA INDUCED BY TACROLIMUS." Kidney International Reports 5, no. 3 (March 2020): S346. http://dx.doi.org/10.1016/j.ekir.2020.02.894.

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"Initial Hemato-immunological Profile on the Evolution of Immunological Thrombopenic Purpura." Case Medical Research, August 27, 2019. http://dx.doi.org/10.31525/ct1-nct04070599.

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Karaz, Mina Fayez Anes, Sarah Amr Hamam, Ibrahim Mohamed Badraia, and Adel Abd El-Haleim Hagag. "Study of Serum Vitamin D Levels in Children with Immune Thrombocytopenic Purpura." Asian Journal of Pediatric Research, July 27, 2021, 12–18. http://dx.doi.org/10.9734/ajpr/2021/v6i230191.

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Background: Immune thrombocytopenic purpura (ITP) is described by an immune responding versus the host’s own platelets, in recent years is progressively studied the non-calcemic roles of vitamin-D (VD) that controls immune and inflammation responding. Aim and objectives: The current work aimed to study VD-level in children with ITP and influence of VD supplementing upon the responding of the thrombopenia to conventional therapy of ITP. Subjects and methods: This study is a cross-sectional observational work which included 30 ITP-children who were attendants to Hematology and Oncology Unit, Pediatric Department, Tanta University Hospitals with ages from 2 to 16-yrs with mean ageing of 6.43 ± 3.75-yrs, for all patients and controls serum-levels of 25-hydroxyvitamin D (25[OH]D) were measured. Results: A significant change was found among the studied groups in regard to VD-levels with lower values among patients compared with controls, a statistically significant negative association was found among platelet counts and each of vitamin D level and serum Ca, the mean platelet count after conventional therapy was significantly increased in group one ITP patients. Conclusion: VD lack is very frequent in children with recently identified or chronic ITP form. Consequently, there are advantages of supplement VD in ITP-cases.

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Journal articles on the topic 'Thrombopenic purpura'

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