scholarly journals The progress of traditional Chinese medicine in the treatment of aplastic anemia

2018 ◽  
Vol 6 (4) ◽  
pp. 159-164 ◽  
Author(s):  
Ningning Zhu ◽  
Dijiong Wu ◽  
Baodong Ye
Keyword(s):  
Bone Marrow ◽  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Aplastic Anemia ◽  
Peripheral Blood ◽  
Clinical Course ◽  
Hematologic Disease ◽  
Therapeutic Principle ◽  
The Past ◽  
Severity Of The Disease

Abstract Aplastic anemia (AA) is a common hematologic disease that is characterized by hematopoietic failure of the bone marrow and pancytopenia of the peripheral blood, which can be divided into severe and non-severe aplastic ane-mia, or acute and chronic aplastic anemia according to the severity of the disease and the progress of the clinical course. During the past years, the advantages of Traditional Chinese Medicine (TCM) on the treatment of AA have been well clarified and its theory system has been improved as well. This review is mainly on representing the pathogenesis, therapeutic principle and method, research progression, and advantages of TCM on AA.

scholarly journals Shen-Cao granules formulated based on traditional Chinese medicine alleviates bone marrow suppression caused by platinum-based anticancer reagents

Medicine ◽  
2017 ◽  
Vol 96 (19) ◽  
pp. e6818 ◽  
Author(s):  
Chunfeng Yu ◽  
Zhonghua Jiang ◽  
Aihua Hou ◽  
Yuejun Mu ◽  
Wei Liu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Bone Marrow Suppression

Aplastic Anemia: Pathogenesis and Treatment

Hematology ◽  
2007 ◽  
Vol 2007 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Andrea Bacigalupo
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Aplastic Anemia ◽  
Cell Biology ◽  
Short Interval ◽  
Treatment Strategies ◽  
Prognostic Indicators ◽  
Unrelated Donor ◽  
Allogeneic Bone ◽  
The Past

Abstract This review highlights some of the contributions that have appeared in the literature in the past decade on the pathogenesis and treatment of aplastic anemia (AA). This summary is brief because the field is vast, spaning from stem cell biology to stem cell disorders, from autoimmunity to transplantation, from graft-versus-host disease to late effects. The immune pathogenesis of AA is now based on several lines of evidence and will be discussed. Immunosuppressive therapy (IST) remains an important option for AA patients who are not candidates for transplantation. Favorable prognostic indicators for IST are young age and a short interval from diagnosis; the neutrophil count seems to have lost its predictive value with current antithymocyte globulin–cyclsoporin combination therapy. The outcome of allogeneic bone marrow transplantations has significantly improved in the past decade, particularly in the unrelated donor setting, to such an extent that treatment strategies may be affected. A short interval between diagnosis and treatment will also improve results for bone marrow transplantation; these rare patients should be referred to an experienced center immediately.

Parvovirus B19 and Aplastic Anemia: Case Control Study: Preliminary Report from the ITESM Hematology Study Group.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3765-3765
Author(s):  
Jose R. Borbolla Escoboza ◽  
Marcos E. Garza-Madrid ◽  
Luis Villela ◽  
Manuel A. Lopez-Hernandez ◽  
Jorge Vela-Ojeda
Keyword(s):  
Bone Marrow ◽  
Aplastic Anemia ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Parvovirus B19 ◽  
Bone Marrow Failure ◽  
Control Group ◽  
Number Of Patients ◽  
Two Samples ◽  
Sense Primer

Abstract Aplastic anemia (AA) is a classic bone marrow failure syndrome simply defined as peripheral blood pancytopenia and a hypocelular bone marrow, yet the diagnosis must be made by excluding other causes of bone marrow failure. The incidence rate of AA reported by the International Aplastic Anemia and Agranulocytosis Study (IAAAS) in the 1980s was 2 cases per 1 million people. This disease is known to be caused by exposure to radiation, chemotherapy and some viral agents, yet most of the cases are idiopathic. Epstein Barr virus and non-A, non-B or non-C Hepatitis virus have classically been related to the development of some AA cases. Recently there have been some reports of AA following Parvovirus B19 (PvB19) infection. This virus, the only parvoviridae virus capable of infecting humans, attacks erythrocyte precursors attaching to the P antigen in their surface and requiring Beta1 integrin for viral entry. Although PvB19 seems to infect only erytroid precursors, it is widely recognized that the infection with this virus can cause not only anemia, but neutropenia and thrombocytopenia as well, producing aplastic crisis of varying intensity. A correlation has recently been found between PvB19 DNA in peripheral blood and AA in children. We pretend to corroborate this observation and include adult patients in order to improve our understanding of the relationship between PvB19 and AA. So far we have taken peripheral blood samples from 9 AA patients and 9 controls paired by age, sex and community; we plan to include 100 AA patients and their controls from several hospitals around Mexico. DNA was extracted using the PUREGENE DNA extraction kit (Gentra, Minneapolis MN). Nested PCR was performed using the sense primer (P1) 5-AATACACTGTGGTTTTATGGGCCG-3, antisense (P2) 5-CCATTGCTGGTTATAACCACAGGT-3 for the first round and the sense primer (P3) 5-AATGAAAACTTTCCATTTAATGATGTAG-3 and antisense primer (P4) 5-CTAAAATGGCTTTTGCAGCTTCTAC-3for the second round. A DNA sample from a patient with active infectious mononucleosis with positive IgG and IgM against PvB19 in serum was used as positive control. Two samples from the AA group (22%) and 1 from the control group (11%) have turned positive for PvB19 DNA. The reported incidence for the presence of this virusDNA in the peripheral blood of the population is 3%. We expect that, as the number of patients grows, the percentage of positive samples in the control group will decrease, while the percentage of positive samples in the AA group will rise or be sustained. Our partial results point towards a possible relationship between AA and the presence of PvB19 DNA in the peripheral blood cells. It is possible that this virus is one of many factors capable of precipitating the development of AA by limiting the bone marrows capacity to produce blood cells. We are in the process of gathering more samples to prove if a relationship really exists and, if so, future studies will likely shed light upon the mechanism by which PvB19 contributes to the development of AA and other marrow failure syndromes.

Thrombocytosis as a Presenting Feature in Myelodysplastic Syndromes (MDS) in Adults - 40 Year Experience from a Single Institution in the USA.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4831-4831
Author(s):  
Dhatri Kodali ◽  
Hector Mesa ◽  
Ajay Rawal ◽  
Pankaj Gupta
Keyword(s):  
Bone Marrow ◽  
Myelodysplastic Syndromes ◽  
Peripheral Blood ◽  
Myeloid Leukemia ◽  
Who Classification ◽  
Clinical Course ◽  
Refractory Anemia ◽  
Risk Category ◽  
Platelet Counts ◽  
Hydroxyurea Treatment

Abstract Thrombocytosis at presentation is uncommon in the myelodysplastic syndromes (MDS), and its influence on the clinical course of the disease and on prognosis is uncertain. To determine the clinical course and long-term outcomes of patients (pts) with thrombocytosis at initial diagnosis of MDS, we conducted a retrospective analysis of 503 pts diagnosed with MDS between Jan 1966 and July 2006 at the Minneapolis VA Medical Center. Original bone marrow and peripheral blood slides and reports were reviewed with a hematopathologist (H.M.) in all pts with high platelet counts (> 400 × 103/μL) and evidence of dysplasia. Clinico-pathological correlation was obtained by chart review. Patients with inadequate data, secondary causes of thrombocytosis, transient thrombocytosis, and those without evidence of dysplasia were excluded. Of 503 pts, 41 (8.2%) were found to have thrombocytosis at presentation. Their median age was 74 years. The spleen was enlarged (by imaging) in 6 pts. Peripheral blood counts (mean; range) at diagnosis were: hemoglobin (10.9 g/dL; 7.4 – 17.1), absolute neutrophils (7.9 × 103/μL; 0.8 – 30.7) and platelets (627 × 103/μL; 402 – 1231). The cases were re-classified according to the WHO classification of myeloid disorders as follows: chronic myelomonocytic leukemia-1 (CMML-1) = 17 (41%), refractory anemia with ringed sideroblasts and thrombocytosis (RARS-T) = 13 (32%) and others = 11 (27%; including 2 pts each with RA, MDS/myeloproliferative disorder-unclassified [MDS/MPD-U] and 5q- syndrome, and 1 pt each with RA with excess blasts [RAEB-1], therapy related MDS [tMDS], refractory cytopenia with multilineage dysplasia [RCMD], MDS-U and atypical chronic myeloid leukemia [Aty CML]). Bone marrow fibrosis was increased in 3 pts with CMML-1 and 1 with RARS-T, and was normal or only focally increased in all other pts. The IPSS risk category was Low in 15 pts, Int-1 in 3 pts and Int-2 in 2 pts. Cytogenetic data was not available in the other pts. Jak-2 mutation analysis was positive in 2 pts with RARS-T, negative in 1 pt each with RARS-T and MDS/MPD-U, and is pending in others. On follow-up, 2 pts with CMML-1 and 1 pt with Aty CML transformed to acute myeloid leukemia (AML) and both pts with 5q- syndrome transformed to CMML-2. Two pts with RARS-T progressed to RAEB-2 and 1 pt with CMML-1 progressed to CMML-2. One pt with CMML-1 developed marked myelofibrosis. Marked thrombocytosis required hydroxyurea treatment in 5 pts. One MDS-U pt received 5-azacytidine. Four of 41 (10%) pts experienced major bleeding events; 3 were receiving aspirin. Five pts required ongoing red cell transfusions. The median survival (MS) was 36 months in RARS-T, 60 months in CMML-1 and 27 months in others; the MS of all 41 pts was 48 months. Causes of death were AML in 3 pts, cytopenias due to MDS in 6 pts and unrelated/unknown in 21 pts. Eleven pts are currently alive. In conclusion, the majority of pts presenting with myelodysplasia and thrombocytosis fall in the MDS/MPD category of the new WHO classification (most commonly CMML or RARS-T), be older, and have low-risk features (IPSS Low or Int-1). The risks of spontaneous bleeding, transformation to AML, progression of disease or myelofibrosis are low, and the overall prognosis is relatively favorable. Platelet counts may reach levels requiring cytoreductive therapy. This study helps better understand the natural history and prognosis of this varied spectrum of MDS and overlap syndromes.

A Novel Ex Vivo Immunotherapy for Some Hematopoietic and Blood Deficient Disorders.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4218-4218
Author(s):  
Jiayu Chen ◽  
Weiwei Liu ◽  
Lingzhen Chen ◽  
Xiaohuai Wang ◽  
Weimin Zhang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Aplastic Anemia ◽  
Immune Cells ◽  
Clinical Studies ◽  
Partial Remission ◽  
Bone Marrow Failure ◽  
Idiopathic Thrombocytopenia ◽  
Severity Of The Disease ◽  
Idiopathic Thrombocytopenia Purpura

Abstract We have developed a novel cell-based immunotherapy for treatment of some hematopoietic and blood deficient diseases such as aplastic anemia, chemotherapy-induced severe myelosuppression, idiopathic thrombocytopenia purpura and autoimmunity-induced cytopenia. Autologous and/or allogeneic peripheral blood mononuclear cells were cultured in vitro with a combination of cytokines and a calcium mobilizing agent for 2 days before given to patients via intravenous infusion. The immunotherapy has been shown to have potent activities in stimulating multi-lineage hematopoiesis and blood production including platelet production, which remains a major clinical problem to be solved. The immunotherapy is more effective for treatment of chronic and severe bone marrow failure and inefficient blood production than currently available growth factors of G-CSF, GM-CSF, Erythropoietin and IL-11. The mechanism of the immunotherapy is yet completely clear to us, however, some evidence suggests that in vitro activated immune cells produce and secrete multiple cytokines, working in concert, these cytokines released by the infused cells in organs important for hematopoiesis and blood production such as bone marrow, liver and spleen have remarkable effects on target cells, resulting in improved hematopoiesis, blood cell differentiation and maturation. In the preliminary clinical studies, more than 100 patients with aplastic anemia, severe chemotherapy-induced myelosuppression, systemic lupus erythematosus-associated cytopenia and idiopathic thrombocytopenia refractory to conventional therapies have been treated with the immunotherapy and the results have been encouraging. In severe idiopathic and benzene-induced aplastic anemia, 90% patients have complete or partial remission after the immunotherapy and one and half year survival is 90%. We have used 2–5x108in vitro activated allogeneic immune cells per infusion per day for 5 consecutive days, followed by small numbers of autologous infusions (1 to 10 million from approximately 50 ml of peripheral blood, depending on the severity of the disease, once a week for 4 weeks). This cycle of therapy is repeated till patient’s absolute neutrophil count is more than 0.5x109/L. The duration of the immunotherapy required for patients with AA to significantly improve ranges from two months to two years depending on the severity of the disease. Idiopathic thrombocytopenia is as difficult as aplastic anemia to treat for the immunotherapy and also requires relatively long time (several months to a year) for patients to respond to the therapy. Approximately 50% adult patients treated with the immunotherapy have complete or partial remission. In severe myelosuppression induced by chemotherapy in leukemia patients, the immunotherapy is highly effective and capable of reducing infection, bleeding and blood transfusion. The recovery of severe myelosuppression (from a few days to a month depending on the severity) after the immunotherapy is much quicker than that of aplastic anemia and idiopathic thrombocytopenia purpura. In conclusion, animal and preliminary human clinical studies suggest that the immunotherapy is highly effective for some bone marrow failure and blood deficient disorders, which are usually difficult to treat with the conventional therapies. The immunotherapy described here merits further investigation.

Perfect Engraftment after Fludarabine, Cyclophosphamide Plus Thymoglobulin Conditioning Regimen for Unrelated Transplantation in Severe Aplastic Anemia: Phase II Prospective Multi-Center Study in Korea

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3003-3003
Author(s):  
Hyoung Jin Kang ◽  
Hee Young Shin ◽  
Jun Eun Park ◽  
Young Tak Lim ◽  
Nak Gyun Chung ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Aplastic Anemia ◽  
Phase Ii ◽  
Peripheral Blood ◽  
Promising Result ◽  
Conditioning Regimen ◽  
Severe Aplastic Anemia ◽  
Once Daily ◽  
Donor Type ◽  
Mobilized Peripheral Blood

Abstract Anti-thymocyte globulin (ATG) has been used in severe aplastic anemia (SAA) as a part of the conditioning regimen. Among the many kinds of ATG preparations, thymoglobulin had been found to be more effective in preventing graft-versus-host disease (GVHD) and rejection of organ transplants. After the promising result of the pilot study (Bone Marrow Transplant. 2004. 34; 939), phase II prospective multi-center clinical trial was performed with fludarabine, cyclophosphamide plus thymoglobulin conditioning regimen to allow good engraftment in unrelated transplantation for SAA. Twenty-eight patients underwent bone marrow (N=15) or mobilized peripheral blood (N=13) transplantation with cyclophosphamide (50 mg/kg once daily i.v. on days −9, −8, −7 & −6), fludarabine (30 mg/m^2 once daily i.v. on days −5, −4, −3 & −2) and thymoglobulin (2.5 mg/kg once daily i.v. on days −3, −2 & −1) from HLA matched unrelated donors. GVHD prophylaxis regimen was composed of cyclosporine (or tacrolimus), methotrexate, with or without low dose thymoglobulin (1.25 mg/kg once daily i.v. on days 7, 9 and 11). The median infused cell dose of nucleated cells and CD34 positive cells were 6.8×10^8/kg (1.3– 39.9×10^8/kg) and 5.2×10^6/kg (1.2–27.0×10^6/kg), respectively. The median number of days required for ANC of more than 0.5×10^9/l and 1.0×10^9/l were 14 days (10–35 days) and 15 days (11–40 days), respectively. The spontaneous platelet recovery to more than 20×10^9/l required a median of 22 days (22–182 days). Donor type hematologic recovery (donor type chimerism more than 90%) was achieved in all patients. Fourteen patient developed grade II–IV acute GVHD. The event free survival (EFS) was 73% and all events were transplantation related mortality (TRM) which included coagulopathy (N=3), PTLD (N=2), pneumonia (N=1), and myocardiac infarction (N=1). The EFS of patients who received bone marrow (65%) was not different from that of patients who received mobilized peripheral blood (82%) (P=0.37), but the EFS of patients who received immunosuppressive therapy (IST) previously (55%) was lower than that of patients who didn’t receive IST (92%), significantly (P=0.04). Fludarabine, cyclophosphamide plus thymoglobulin conditioning allows for the promising result of very good engraftment, although serious events occurred in some patients. We are now planning to start new multicenter study to decrease TRM by reducing the dose of cyclophosphamide.

scholarly journals Aplastic anemia in China

2018 ◽  
Vol 6 (3) ◽  
pp. 134-137 ◽  
Author(s):  
Chunyan Liu ◽  
Zonghong Shao
Keyword(s):  
Bone Marrow ◽  
Autoimmune Disease ◽  
T Lymphocytes ◽  
Aplastic Anemia ◽  
Therapeutic Effect ◽  
Severe Aplastic Anemia ◽  
Hematologic Disease ◽  
Great Progress ◽  
Better Than

Abstract Aplastic anemia (AA) is a hematologic disease characterized by pancytopenia. Up to now, severe aplastic anemia (SAA) has been recognized by international and domestic scholars as an autoimmune disease with bone marrow (BM) failure mediated by the hyperfunctional T lymphocytes. The incidence of AA is more in China compared with other countries. In the recent years, both the pathogenesis and treatment of AA have made a great progress in our country. Thus, the therapeutic effect of AA was much better than before. Here, we conclude the researches of AA in China.

Sign in / Sign up

Export Citation Format

Share Document