FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2080965265> ?p ?o ?g. }

• W2080965265 endingPage "438" @default.
• W2080965265 startingPage "431" @default.
• W2080965265 abstract "The purpose of this study was to investigate the effects of rabbit antihuman thymocyte globulin (R-ATG) and Jurkat cell-reactive anti-T lymphocyte globulin (ATG-F) in the treatment of childhood aplastic anemia (AA) and compare their efficacy and side effects. A total of 53 children with AA were analyzed in the present study, including 32 cases of severe AA, 10 cases of very severe AA and 11 cases of transfusion-dependent nonsevere AA. While receiving immunosuppressive therapy (IST), 29 and 24 patients, all of whom received long-term oral supplement with cyclosporin A (CSA), androgen, and traditional Chinese medicines, were treated with R-ATG and ATG-F, respectively. If necessary, the patients were also given supportive care such as component transfusion and/or infection control. Absolute counts of peripheral blood lymphocyte at various time points were dynamically measured after ATG therapy. According to the International AA Treatment and Effect standards, we found that there were no statistically significant differences in the response rate (70.83% vs. 68.97%, p > 0.05) and the overall survive rate (83.33% vs. 82.76%, p > 0.05) between the ATG-F and R-ATG groups. In addition, no obvious differences were observed between these two groups in the response time, efficacy in severe AA and very severe AA, or the incidence rates of ATG-related adverse reactions. After ATG treatment, the extent of peripheral blood lymphocyte reduction and duration in peripheral blood were similar between the ATG-F and R-ATG groups. The results of this study showed that ATG-F and R-ATG had similar efficacy and adverse reactions in the first-line treatment of childhood AA, despite being derived from different immunogens. The purpose of this study was to investigate the effects of rabbit antihuman thymocyte globulin (R-ATG) and Jurkat cell-reactive anti-T lymphocyte globulin (ATG-F) in the treatment of childhood aplastic anemia (AA) and compare their efficacy and side effects. A total of 53 children with AA were analyzed in the present study, including 32 cases of severe AA, 10 cases of very severe AA and 11 cases of transfusion-dependent nonsevere AA. While receiving immunosuppressive therapy (IST), 29 and 24 patients, all of whom received long-term oral supplement with cyclosporin A (CSA), androgen, and traditional Chinese medicines, were treated with R-ATG and ATG-F, respectively. If necessary, the patients were also given supportive care such as component transfusion and/or infection control. Absolute counts of peripheral blood lymphocyte at various time points were dynamically measured after ATG therapy. According to the International AA Treatment and Effect standards, we found that there were no statistically significant differences in the response rate (70.83% vs. 68.97%, p > 0.05) and the overall survive rate (83.33% vs. 82.76%, p > 0.05) between the ATG-F and R-ATG groups. In addition, no obvious differences were observed between these two groups in the response time, efficacy in severe AA and very severe AA, or the incidence rates of ATG-related adverse reactions. After ATG treatment, the extent of peripheral blood lymphocyte reduction and duration in peripheral blood were similar between the ATG-F and R-ATG groups. The results of this study showed that ATG-F and R-ATG had similar efficacy and adverse reactions in the first-line treatment of childhood AA, despite being derived from different immunogens. Aplastic anemia (AA) is a life-threatening disease characterized by peripheral pancytopenia and bone marrow failure. It was previously documented that childhood AA was rare, with an annual incidence of around 2–6 per million population in the North America and Europe. The incidence is about twofold to threefold higher in Asian countries such as India and Japan, resulting from differences in population immunogenetic and environmental factors [1Young N.S. Scheinberg P. Calado R.T. Aplastic anemia.Curr Opin Hematol. 2008; 15: 162-168Crossref PubMed Scopus (209) Google Scholar, 2Jeong D.C. Chung M.G. Kang H.J. et al.epidemiology and clinical long-term outcome of childhood aplastic anemia in Korea for 15 years: retrospective study of the Korean Society of Pediatric Hematology Oncology (KSPHO).Pediatr Hematol Oncol. 2011; 33: 172-178Crossref Scopus (21) Google Scholar]. However, in recent years, a higher incidence of childhood AA has been observed in less developed Asian areas due to a number of adverse factors, such as environmental pollution and viral infection [3Passweg J.R. Tichelli A. Immunosuppressive treatment for aplastic anemia: are we hitting the ceiling?.Haematologica. 2009; 94: 310-312Crossref PubMed Scopus (40) Google Scholar]. Precise statistical data regarding childhood AA have not been available until recently. The age distribution of this disease is biphasic, with a peak in the 10–25 age range and another peak in the older than 60 range. Therefore, the incidence of childhood AA might be higher than that of adult patients [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar]. In children with AA, severe AA (SAA) accounts for a higher proportion, and, if not promptly treated, the short-term mortality rate could reach 60% [5Howard S.C. Naidu P.E. Hu X.J. et al.Natural history of moderate aplastic anemia in children.Pediatr Blood Cancer. 2004; 43: 545-551Crossref PubMed Scopus (49) Google Scholar, 6Davies J.K. Guinan E.C. An update on the management of severe idiopathic aplastic anaemia in children.Br J Haematol. 2007; 136: 549-564Crossref PubMed Scopus (72) Google Scholar]. Effective diagnosis and management of childhood AA is currently a significant goal in China and other less developed Asian countries. A fraction of childhood AA is congenital (e.g., inherited bone marrow failure syndrome [IBMFS] such as the Fanconi anemia [FA] and congenital dyskeratosis [DC]). In Europe and the United States, IBMFS accounts for about 20% of all cases, but in Asia, the proportion of IBMFS is significantly lower at about 5% [2Jeong D.C. Chung M.G. Kang H.J. et al.epidemiology and clinical long-term outcome of childhood aplastic anemia in Korea for 15 years: retrospective study of the Korean Society of Pediatric Hematology Oncology (KSPHO).Pediatr Hematol Oncol. 2011; 33: 172-178Crossref Scopus (21) Google Scholar, 4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar]. With the exception of a few DC and IBMFS cases, most cases of AA are acquired. The exact etiology of a majority of acquired AA remains unknown, but dysfunction of T lymphocytes is considered as the main pathogenic mechanism [1Young N.S. Scheinberg P. Calado R.T. Aplastic anemia.Curr Opin Hematol. 2008; 15: 162-168Crossref PubMed Scopus (209) Google Scholar, 7Song E.Y. Kang H.J. Shin H.Y. et al.Association of human leukocyte antigen class II alleles with response to immunosuppressive therapy in Korean aplastic anemia patients.Hum Immunol. 2010; 71: 88-92Crossref PubMed Scopus (20) Google Scholar]. According to a recently issued guideline on diagnosis and management of AA, immunosuppressive therapy (IST) in combination with antithymocyte globulin (ATG) and cyclosporin A (CSA) is a preferred treatment modality for SAA patients who have no matched sibling donor (MSD) for hematopoietic stem cell transplantation (HSCT), as well as for transfusion-dependent nonsevere AA (NSAA) patients [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar]. The internationally recommended ATG preparation for first-line immune suppression therapy in AA is horse ATG (H-ATG), and rabbit ATG (R-ATG) is used mainly as second-line treatment for patients with refractory or relapsed AA [8Atta E.H. Dias D.S.P. Marra V.L.N. et al.Comparison between horse and rabbit antithymocyte globulin as first-line treatment for patients with SAA: a single-center retrospective study.Ann Hematol. 2010; 89: 851-859Crossref PubMed Scopus (74) Google Scholar, 9Young N.S. Bacigalupo A. Marsh J.C.W. Aplastic anemia: pathophysiology and treatment.Biol Blood Marrow Transplant. 2010; 16: 119-125Abstract Full Text Full Text PDF Scopus (114) Google Scholar]. However, in recent years, H-ATG supply has been deficient. Moreover, it was shown that there was no significant difference in long-term outcomes between R-ATG and H-ATG treatment, as revealed by a case-control study [10Chang M.H. Kim K.H. Kim H.S. et al.Predictors of response to immunosuppressive therapy with antithymocyte globulin and cyclosporine and prognostic factors for survival in patients with severe aplastic anemia.Eur J Haematol. 2009; 84: 154-159Crossref PubMed Scopus (45) Google Scholar]. Furthermore, it was also documented that R-ATG might be superior to H-ATG in enhancing regulatory Treg (T) cell function for immunosuppression [11Feng X. Kajigaya S. Solomou E.E. et al.Rabbit ATG but not horse ATG promotes expansion of functional CD4+CD25highFOXP3+ regulatory T cells in vitro.Blood. 2008; 111: 3675-3683Crossref PubMed Scopus (184) Google Scholar]. Therefore, R-ATG has also been recommended as the first choice for IST [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar]. In China, in recent decades, H-ATG supply was discontinued for a short period. Currently, there are two kinds of R-ATG preparations available in China, namely rabbit antihuman thymocyte globulin (Genzyme Polyclonals S.A.S., France) and antihuman T lymphocyte globulin (ATG-F) (Fresenius Biotech GmbH, Germany), which are generated through the immunization of rabbits with human thymocytes and Jurkat cell lines, respectively. The immunogen sources are different, but both belong to human T lymphocytes, and therefore both of these ATG formulations are expected to exert effects by targeting human T cells. Recently, however, the R-ATG and ATG-F supplies in China have been unstable. As a result, sometimes only one ATG formation is available for application. Whereas R-ATG has been widely recommended as a first-line formulation in AA patients [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar], ATG-F is normally administered for transplantation [12Basara N. Baurmann H. Kolbe K. et al.Antithymocyte globulin for the prevention of graft-versus-host disease after unrelated hematopoietic stem cell transplantation for acute myeloid leukemia: results from the multicenter German cooperative study group.Bone Marrow Transplant. 2005; 35: 1011-1018Crossref PubMed Scopus (90) Google Scholar]. Zheng et al. reported that the overall response rate in adult SAA to ATG-F and H-ATG reached 65.6% and 73.3%, respectively. No significant differences between these two ATG groups were observed [13Zheng Y. Liu Y. Chu Y. Immunosuppressive therapy for acquired severe aplastic anemia (SAA): a prospective comparison of four different regimens.Exp Hematol. 2006; 34: 826-831Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar]. Li et al. also reported that R-ATG combined with cyclosporine is efficacious as a first-line immunosuppressive regimen for SAA when using an optimal rather than a standard protocol [14Li X. Shi J. Ge M. et al.Outcomes of optimized over standard protocol of rabbit antithymocyte globulin for severe aplastic anemia: a single-center experience.PLoS One. 2013; 8: e56648Crossref PubMed Scopus (22) Google Scholar]. Recently, Shat et al. reported that, in a cohort of 345 adult patients with AA, the R-ATG Fresenius was significantly inferior to the R-ATG Sangstat (Genzyme Polyclonals S.A.S.,France) in 3- and 6-month responses, as well as in the 5-year overall survival rate [15Shao Y.Q. Li X.X. Ge M.L. et al.A long-term follow up study on 345 severe aplastic anemia patients treated with antithymocyte globulin/lymphoglobulin.Zhonghua Xue Ye Xue Za Zhi. 2013; 34: 30-35PubMed Google Scholar]. However, to our knowledge, no comparison of the efficacy of R-ATG versus ATG-F in the treatment of childhood AA has been conducted. In view of the instability of the supply of R-ATG and ATG-F in China, we used these two formulations in this study to treat children with AA and compared their efficacy and safety. Fifty-three pediatric patients with AA, including 27 male and 26 female cases, were retrospectively evaluated. All were between 3 and 12 years old at diagnosis and were hospitalized in our pediatric hematology ward. All patients received IST between January, 2005, and December, 2012. In accordance with the International Diagnosis Criteria for Aplastic Anaemia [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar, 16Camitta B.M. Rappeport J.M. Parkman R. et al.Selection of patients for bone marrow transplantation in severe aplastic anemia.Blood. 1975; 45: 355-363PubMed Google Scholar], all patients were diagnosed on the basis of clinical history, physical examination, and results of laboratory tests, including complete blood count, reticulocyte count, blood and bone marrow smear, and bone marrow biopsy. All patients analyzed in this investigation were manifested as pancytopenia with a hypocellular bone marrow, without other pancytopenia-causing blood diseases such as hypoplastic leukemia or myelodysplastic syndrome. To diagnose AA, at least two of the three following criteria in the peripheral blood were met: (1) hemoglobulin level less than 100 g/L, (2) platelet count less than 50 × 109/L, and (3) absolute neutrophil count (ANC) less than 1.5 × 109/L. Using Camitta's criteria, SAA was defined by bone marrow cell hyperplasia of less than 25% of the normal, with at least two of the three following criteria in the peripheral blood: (1) percentage of reticulocyte (Ret) less than 1% or absolute reticulocyte count (ARC) less than 20 × 109/L, (2) ANC less than 0.5 × 109/L, (3) platelet count less than 20 × 109/L. If ANC was less than 0.2 × 109/L, very severe AA (VSAA), a diagnosis of was considered [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar, 17Bacigalupo A. Hows J.M. Gluckman E. et al.Bone marrow transplantation (BMT) versus immunosuppression for the treatment of severe aplastic anaemia (SAA): a report of the EBMT SAA Working Party.Bri J Haematol. 1988; 70: 177-182Crossref PubMed Scopus (298) Google Scholar]. Thirty-two cases of SAA, 10 cases of VSAA, and 11 cases of transfusion-dependent NSAA were included in the study. We chose R-ATG preparations based on their supply in China, according to two criteria: (1) if no other ATG preparation was available, merely one R-ATG formation was employed, (2) if both R-ATG preparations were supplied, ATG-F and R-ATG were recommended to be used interchangeably. Therefore, the childhood patients were divided into the two groups, namely the ATG-F group (24 cases) and the R-ATG group (29 cases). As outlined in Table 1, patients in these two groups were comparable with respect to general information and severity of aplastic anemia, including hemoglobin (HB), ANC, ARC, and platelet count.Table 1Baseline characteristics of patients with AA before ISTTotal (n = 53)ATG-F (n = 24)R-ATG (n = 29)p valueAverage age (years)5.566.886.290.436Gender: no. males (%)27 (50.94)13 (54.17)14 (48.28)0.661Average duration (months)11.3615.048.300.147Diagnostic category VSAA+SAA (%)42 (72.25)17 (70.83)25 (86.21)0.301 SAA (%)32 (60.38)14 (58.34)18 (62.07)0.785 VSAA (%)10 (18.87)3 (12.50)7 (24.13)0.468 NSAA (%)11 (20.75)7 (29.17)4 (13.79)0.301Peripheral blood cell count before treatment (median) RBC (× 1012/l)2.112.202.030.420 HB (g/L)64.4166.4862.690.462 ANC (× 109/L)0.750.670.810.521 ALC (× 109/L)3.132.663.520.172 Plt (× 109/L)18.8323.1715.240.070AA = aplastic anemia; ALC = actual lymphocyte count; ANC = absolute neutrophil count; ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; HB = hemoglobin; IST = immunosuppressive therapy; NSAA = nonsevere aplastic anemia; Plt = platelet; R-ATG = rabbit antithymocyte globulin; RBC = red blood cell; SAA = severe aplastic anemia; VSAA = very severe aplastic anemia. Open table in a new tab AA = aplastic anemia; ALC = actual lymphocyte count; ANC = absolute neutrophil count; ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; HB = hemoglobin; IST = immunosuppressive therapy; NSAA = nonsevere aplastic anemia; Plt = platelet; R-ATG = rabbit antithymocyte globulin; RBC = red blood cell; SAA = severe aplastic anemia; VSAA = very severe aplastic anemia. The study excluded all AA patients who (1) could receive HSCT from a human leukocyte antigen (HLA)-matched sibling donor (MSD), (2) were diagnosed with FA based on clinical manifestation and mitomycin C-induced chromosomal breakage test, (3) were clinically diagnosed with DC or other IBMFS diseases, or (4) were diagnosed with paroxysmal nocturnal hemoglobinuria (PNH) by determination of CD55 and CD59 using flow cytometry. We administered ATG-F (Fresenius) or R-ATG (Genzyme) by slow intravenous infusion at a dose of 5 mg/kg/day or 3.75 mg/kg/d for 8 hours for 5 consecutive days. Twenty-four and 29 cases were included in the ATG-F group and the R-ATG group, respectively. Before the initiation of first-day ATG treatment, allergenic tests were performed to prevent adverse reactions in IST treatment. This was done by slow intravenous infusion of 5 mg ATG-F or 2.5 mg R-ATG, which were dissolved in 100 mL normal saline. The infusion persisted for 1 hour. If no adverse reactions occurred, then ATG infusion would be initiated. To avoid allergic reactions, H1 receptor blockers were routinely administered before ATG infusion, together with methylprednisolone, 30 mg/m2/day on days 1 through 14. After day 14, the dose was tapered, eventually stopping on day 30. Oral CSA, 5 mg/kg/day daily, was added to ATG. The dosage of CSA was adjusted to maintain the plasma levels of CSA to 150–200 ng/mL. To reduce the risk of relapse, CSA should be continued for an additional 12 months after achieving maximal hematologic response, followed by a very slow tapering. The dose of CSA should be decreased by 10% of the initial dose approximately once every 3 months. Oral androgen (testosterone undecanoate) and Chinese traditional medicine were administered to all of the patients as an adjuvant therapy. Platelet transfusion, if required, was performed to maintain a platelet count higher than 20 × 109/L before ATG treatment and during 5-day ATG treatment. During the follow-up observation period, red blood cells were transfused in patients with symptomatic anemia to maintain the hemoglobin level to 80g/dL. According to their tolerance to anemia, frequency of red blood cell infusion could be appropriately controlled. Platelets were transfused prophylactically in all patients with a platelet count lower than 10 × 109/L. Platelets were also transfused in patients with evidence of infection and a platelet count below 20 × 109/L. Methylprednisolone, at a dose of 40 mg/m2/day, was given to patients with ATG-induced serum sickness, accompanied with antibiotics and platelet transfusion. Granulocyte colony-stimulating factor (G-CSF) and potent broad-spectrum antibiotics were administered if clinically indicated, usually in patients with severe neutropenia and evidence of infection. During ATG treatment, ATG-induced adverse reactions, including serum sickness and anaphylactoid reactions, such as transient fever and joint pain, were observed and calculated. If clinically necessary, platelets were transfused to patients to maintain peripheral blood platelet count higher than 20 × 109/L. All of the patients were evaluated at baseline and strictly followed up once every 1 month, followed by once every 3 months, in the first 6 months after ATG treatment at our institutional hospital. At each evaluation, clinical assessments were performed and a complete blood count (CBC), absolute reticulocyte count, and platelet count were obtained. Clinical assessments included the determination of requirement for red blood cell and/or platelet transfusion, the transfusion frequency, the transfusion dependence, the infectious complications, and the overall response rates. Flow cytometry was repeatedly performed to detect CD55 and CD59 in surviving patients to monitor the development of late clonal complications (PNH) after ATG therapy. When necessary, bone marrow aspiration and biopsy were also repeatedly performed once every 6 months, especially in relapsed patients, to preclude late clonal complications including myelodysplastic syndromes (MDS). The survival rate in IST nonresponders, as well as any deaths and their causes, were also recorded. The follow-up period expired in May, 2013. In accordance with the Camitta criteria recommended by the British Guidelines for Treatment of AA (Table 2) [4Marsh J.C.W. Ball S.E. Cavenagh J. et al.Guidelines for the diagnosis and management of aplastic anaemia.Br J Haematol. 2009; 147: 43-70Crossref PubMed Scopus (397) Google Scholar, 18Camitta B.M. What is the definition of cure for aplastic anemia?.Acta Haematol. 2000; 103: 16-18Crossref PubMed Scopus (93) Google Scholar], patients were divided into complete responders, partial responders, and nonresponders. Complete response and partial response were considered to be efficacious.Table 2Criteria for response to IST in patients with AAResponse criteria for SAA NRStill severe PRTransfusion independentNo longer meeting criteria for severe disease CRHB normal for ageANC > 1.5 × 109/LPlt > 150 × 109/LResponse criteria for NSAA NRWorse or not meeting criteria below PRTransfusion independence (if previously dependent)or doubling or normalization of at least one cell lineor increase of baseline HB of > 30 g/L (if initially <60g/L)or increase of baseline ANC of > 0.5 × 109/L (if initially <0.5)or increase of baseline Plt of > 20 × 109/L (if initially <20) CRSame criteria as for severe diseaseAA = aplastic anemia; ANC = absolute neutrophil count; HB = hemoglobin; IST = immunosuppressive therapy; NSAA = nonsevere aplastic anemia; Plt = platelet; SAA = severe aplastic anemia. Open table in a new tab AA = aplastic anemia; ANC = absolute neutrophil count; HB = hemoglobin; IST = immunosuppressive therapy; NSAA = nonsevere aplastic anemia; Plt = platelet; SAA = severe aplastic anemia. To evaluate and compare the efficacy of ATG-F and R-ATG in scavenging lymphocytes, peripheral blood ALC was recorded before and after ATG treatment on days 1, 3, 5, 7, and 14, and at months 1, 2, 3, and 12. Statistical analysis was carried out using SPSS version 17.0 statistical software. (SPSS Inc., Chicago, IL). To compare the differences between the ATG-F and R-ATG groups, Nonparametric Wilcoxon's rank sum test, χ2, or Fisher's exact test were used for categorical variables. Student's t test was used to compare the changes of lymphocyte counts after ATG therapy. All p values represented were two-sided, with p < 0.05 indicating statistical significance. As shown in Table 3, all 53 patients received IST, and the response rates up to the endpoint of follow-up were as follows: 16 (30.19%) patients achieved complete remission (CR), 21 (39.62%) patients partial remission (PR), the remaining 16 (30.19%) no response (NR). The overall response rate was 69.81% (n = 37). The comparison of response rates among groups is shown in Table 4. Of 53 patients, 42 patients were diagnosed with SAA and VSAA. The overall response rate of SAA and VSAA patients was 71.43% (n = 30), with 14 (33.33%) patients achieving CR, 16 (38.09%) PR, and the remaining 12 (28.57%) NR. The survival rate was 80.95% (n = 34). Among the 11 patients diagnosed with NSAA, the overall response rate was 81.82% (9/11). There was no statistically significant difference in the overall response rates between the SAA/VSAA and NSAA groups (x2 = 0.049, p > 0.05). As shown in Table 3, time to the first response of IST treatment was 3 months. The response rates at 3, 6, and 12 months after treatment were 37.74% (n = 20), 54.72% (n = 29), and 73.84% (n = 39), respectively. Relapse occurred in two patients in the second year after IST treatment; therefore, the overall response rate was 69.81% (n = 37). Of all 16 nonresponders and relapsed patients (30.19%), two cases received matched unrelated donor (MUD) transplantation and achieved hematopoietic reconstitution with normal peripheral hemogram; 8 nonresponders died of infection and bleeding (mortality = 15.09%); the other six patients are alive and dependent on component blood transfusion and supportive care. One SAA patient achieved complete remission, but died of aneurysm rupture. Therefore, the overall survival rate was 83.02% (n = 44).Table 3Responses of patients with childhood AA to ATG-F and R-ATG therapyTotal (n = 53)ATG-F (n = 24)R-ATG (n = 29)p valueOverall response rate (%)37 (69.81)17 (70.83)20 (68.97)0.883 CR (%)16 (30.19)7 (29.17)9 (31.03)0.883 PR (%)21 (39.62)10 (41.67)11 (37.93)0.782 NR (%)16 (30.19)7 (29.17)9 (31.03)0.883Survival rate (%)44 (83.02)20 (83.33)24 (82.76)1.000Response rate after treatment Three months (%)20 (37.74)9 (37.50)11 (37.93)0.974 Six months (%)29 (54.72)13 (54.17)16 (55.17)0.942 Twelve months (%)aAt twelve months after ATG treatment, 39 cases were responsive and relapse occurred in 2 cases.39 (73.84)19 (79.17)20 (68.97)0.402ATG-induced adverse reactions Anaphylactoid reactions (%)20 (37.74)9 (37.50)11 (37.93)0.974 Platelet transfusion (%)13 (24.53)6 (25.00)7 (29.17)0.942 Serum sickness (%)21 (39.63)9 (37.50)12 (50.00)0.774 Infection within one month (%)10 (18.68)4 (16.67)6 (20.69)0.984AA = aplastic anemia; ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; CR = complete remission; NR = no response; PR = partial remission; R-ATG = rabbit antithymocyte globulin.a At twelve months after ATG treatment, 39 cases were responsive and relapse occurred in 2 cases. Open table in a new tab Table 4Efficacy of ATG-F and R-ATG for the treatment of childhood SAA/VSAATotal (n = 42)ATG-F (n = 17)R-ATG (n = 25)p valueOverall response rate (%)30 (71.43)12 (70.59)18 (72.00)1.000 CR (%)14 (33.33)5 (29.41)9 (36.00)0.657 PR (%)16 (38.09)7 (58.33)9 (36.00)0.735 NR (%)12 (28.57)5 (29.41)7 (28.00)1.000Survival rate (%)34 (80.95)14 (82.35)20 (80.00)1.000ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; CR = complete remission; NR = no response; PR = partial remission; R-ATG = rabbit antithymocyte globulin; VSAA = very severe aplastic anemia. Open table in a new tab AA = aplastic anemia; ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; CR = complete remission; NR = no response; PR = partial remission; R-ATG = rabbit antithymocyte globulin. ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; CR = complete remission; NR = no response; PR = partial remission; R-ATG = rabbit antithymocyte globulin; VSAA = very severe aplastic anemia. As outlined in Table 3, 24 patients were included in the ATG-F group, with seven (29.17%) patients achieving CR, 10 (41.67%) patients PR, and the remaining seven (29.17%) patients NR. The overall response rate in the ATG-F group was 70.83% (n = 17). In addition, there were 29 patients in the R-ATG group, consisting of nine (31.03%) patients achieving complete remission, 11 (37.93%) patients partial remission, and nine (31.03%) patients no response. The overall response rate in the R-ATG group was 68.97% (n = 20). No significant differences were observed in the response rate, number of responders, and the survival rate between these two groups. Similarly, the two groups showed no significant differences in the response rate or the survival rate at 3, 6, and 12 months after ATG therapy. Further, there was no difference in the recovery of HB, ANC, ARC, and platelet (Plt) between Rabbit Anti-Human T-lymphocyte Immunoglobulin-Fresenius (F-ATG) and Rabbit Anti-human Thymocyte Immunoglobulin-Genzyme (G-ATG) groups at 12 months after ATG therapy (Table 5).Table 5Recovery of blood counts in childhood AA treated with R-ATG and ATG-FDataF-ATG (x ± s)G-ATG (x ± s)tp valueHB (g/L)95.4583 ± 5.7319396.9655 ± 6.05730−0.1780.859ANC (× 109/L)1.6750 ± 0.245191.8931 ± 1.49450−0.5770.567ARC (× 109/L)35.2500 ± 3.9751342.5517 ± 8.22207−0.7490.457Plt (× 109/L)73.0833 ± 12.6977073.5517 ± 13.04951−0.0250.980AA = aplastic anemia; ANC = absolute neutrophil count; ARC = absolute reticulocyte count; ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; HB = hemoglobin; Plt = platelet; R-ATG = rabbit antithymocyte globulin. Open table in a new tab AA = aplastic anemia; ANC = absolute neutrophil count; ARC = absolute reticulocyte count; ATG-F = Jurkat cell-reactive anti-t lymphocyte globulin; HB = hemoglobin; Plt = platelet; R-ATG = rabbit antithymocyte globulin. As shown in Table 4, 17 patients were included in the ATG-F group, with five (29.41%) patients achieving complete remission, seven (58.33%) patients partial remission, and the remaining five (29.41%) patients no response. The overall response rate in the ATG-F group was 70.95% (n = 12). Additionally, there were 25 patients in the R-ATG group, consisting of nine (36.00%) patients achieving CR, nine (" @default.
• W2080965265 created "2016-06-24" @default.
• W2080965265 creator A5020600851 @default.
• W2080965265 creator A5026192010 @default.
• W2080965265 creator A5066866428 @default.
• W2080965265 creator A5069931477 @default.
• W2080965265 creator A5075218317 @default.
• W2080965265 date "2014-06-01" @default.
• W2080965265 modified "2023-09-27" @default.
• W2080965265 title "Comparison of rabbit antithymocyte globulin and Jurkat cell-reactive anti-t lymphocyte globulin as a first-line treatment for children with aplastic anemia" @default.
• W2080965265 cites W101289525 @default.
• W2080965265 cites W1964220731 @default.
• W2080965265 cites W1999427257 @default.
• W2080965265 cites W2005518037 @default.
• W2080965265 cites W2011605963 @default.
• W2080965265 cites W2016231795 @default.
• W2080965265 cites W2016759622 @default.
• W2080965265 cites W2018493712 @default.
• W2080965265 cites W2023640756 @default.
• W2080965265 cites W2024481101 @default.
• W2080965265 cites W2029335286 @default.
• W2080965265 cites W2035442779 @default.
• W2080965265 cites W2036245297 @default.
• W2080965265 cites W2036902889 @default.
• W2080965265 cites W2039007181 @default.
• W2080965265 cites W2050945312 @default.
• W2080965265 cites W2052285621 @default.
• W2080965265 cites W2055482423 @default.
• W2080965265 cites W2066484486 @default.
• W2080965265 cites W2067596358 @default.
• W2080965265 cites W2068866006 @default.
• W2080965265 cites W2076630716 @default.
• W2080965265 cites W2095276384 @default.
• W2080965265 cites W2114652933 @default.
• W2080965265 cites W2118999711 @default.
• W2080965265 cites W2131799119 @default.
• W2080965265 cites W2133676382 @default.
• W2080965265 cites W2136923772 @default.
• W2080965265 cites W2150570014 @default.
• W2080965265 cites W2334999848 @default.
• W2080965265 cites W4230817393 @default.
• W2080965265 cites W4255204353 @default.
• W2080965265 doi "https://doi.org/10.1016/j.exphem.2014.02.003" @default.
• W2080965265 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24582815" @default.
• W2080965265 hasPublicationYear "2014" @default.
• W2080965265 type Work @default.
• W2080965265 sameAs 2080965265 @default.
• W2080965265 citedByCount "6" @default.
• W2080965265 countsByYear W20809652652015 @default.
• W2080965265 countsByYear W20809652652017 @default.
• W2080965265 countsByYear W20809652652019 @default.
• W2080965265 countsByYear W20809652652020 @default.
• W2080965265 crossrefType "journal-article" @default.
• W2080965265 hasAuthorship W2080965265A5020600851 @default.
• W2080965265 hasAuthorship W2080965265A5026192010 @default.
• W2080965265 hasAuthorship W2080965265A5066866428 @default.
• W2080965265 hasAuthorship W2080965265A5069931477 @default.
• W2080965265 hasAuthorship W2080965265A5075218317 @default.
• W2080965265 hasBestOaLocation W20809652651 @default.
• W2080965265 hasConcept C179464577 @default.
• W2080965265 hasConcept C203014093 @default.
• W2080965265 hasConcept C2776090121 @default.
• W2080965265 hasConcept C2777761686 @default.
• W2080965265 hasConcept C2780007613 @default.
• W2080965265 hasConcept C2781440808 @default.
• W2080965265 hasConcept C71924100 @default.
• W2080965265 hasConcept C81358767 @default.
• W2080965265 hasConcept C8891405 @default.
• W2080965265 hasConceptScore W2080965265C179464577 @default.
• W2080965265 hasConceptScore W2080965265C203014093 @default.
• W2080965265 hasConceptScore W2080965265C2776090121 @default.
• W2080965265 hasConceptScore W2080965265C2777761686 @default.
• W2080965265 hasConceptScore W2080965265C2780007613 @default.
• W2080965265 hasConceptScore W2080965265C2781440808 @default.
• W2080965265 hasConceptScore W2080965265C71924100 @default.
• W2080965265 hasConceptScore W2080965265C81358767 @default.
• W2080965265 hasConceptScore W2080965265C8891405 @default.
• W2080965265 hasIssue "6" @default.
• W2080965265 hasLocation W20809652651 @default.
• W2080965265 hasLocation W20809652652 @default.
• W2080965265 hasOpenAccess W2080965265 @default.
• W2080965265 hasPrimaryLocation W20809652651 @default.
• W2080965265 hasRelatedWork W1990620909 @default.
• W2080965265 hasRelatedWork W2055118537 @default.
• W2080965265 hasRelatedWork W2080965265 @default.
• W2080965265 hasRelatedWork W2362205565 @default.
• W2080965265 hasRelatedWork W2391321166 @default.
• W2080965265 hasRelatedWork W2462714844 @default.
• W2080965265 hasRelatedWork W2548436607 @default.
• W2080965265 hasRelatedWork W3198685530 @default.
• W2080965265 hasRelatedWork W4235609713 @default.
• W2080965265 hasRelatedWork W607736087 @default.
• W2080965265 hasVolume "42" @default.
• W2080965265 isParatext "false" @default.
• W2080965265 isRetracted "false" @default.
• W2080965265 magId "2080965265" @default.
• W2080965265 workType "article" @default.