scholarly journals Unusual Case of Hepatic Sinusoidal Obstruction Syndrome Induced By Low Dose Oral Cyclophosphamide

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 37-37
Author(s):  
Pramod Gaudel ◽  
Jordan Snyder ◽  
Abdulraheem Yacoub
Keyword(s):  
Bone Marrow ◽  
Low Dose ◽  
Left Ventricular ◽  
High Dose ◽  
Sinusoidal Obstruction Syndrome ◽  
Oral Cyclophosphamide ◽  
Publicly Traded ◽  
Hematopoietic Stem ◽  
Hepatic Sinusoidal Obstruction Syndrome ◽  
Dose Oral

Hepatic sinusoidal obstruction syndrome (SOS) has been reported in patients receiving high dose intravenous (IV) cyclophosphamide especially as a part of preparative regimen for hematopoietic stem cell transplantation. Hepatic SOS from low dose oral cyclophosphamide has not been reported. Here we present a rare case of hepatic SOS induced by low dose oral cyclophosphamide. A 78-year-old male with history of coronary artery disease status post coronary artery bypass graft (CABG) was initially seen in hematology clinic for evaluation of normocytic anemia. During workup, bone marrow biopsy revealed NK cell large granular lymphocytic leukemia (LGL). He was then started on low dose oral cyclophosphamide 50 mg daily. After 2 months, his dose was reduced to 25 mg daily due to severe neutropenia. He then tolerated cyclophosphamide well and his hemoglobin (Hb) improved from his baseline 8 gm/dl to 12 gm/dl in 4 months. After 6 months of treatment, he was admitted to the hospital for abdominal distension, ascites and 15 pounds weight gain over 3 weeks. Labs most prominent on admission were Hb of 12.5 gm/dL , WBC 5.3 x 103/µL, Platelets 197 x 103/µL, total bilirubin 1.6 mg/dL, aspartate aminotransferase (AST) 89 U/L , alanine aminotransferase (ALT) 35 U/L and alkaline phosphatase (ALP) 283 U/L. Workup of ascites included abdominal paracentesis which revealed serum ascites albumin gradient(SAAG) <1.1 and fluid cytology was negative for carcinoma. Ultrasound of abdomen showed diffuse parenchymal heterogeneity and increased echogenicity of liver with patent hepatic vessels with normal direction of blood flow. Echocardiogram revealed preserved left ventricular systolic function with estimated left ventricular ejection fraction of 60%. He then underwent transjugular liver biopsy which revealed chronic lymphoproliferative disorder of NK cells, prominent centrilobular sinusoidal dilatation and congestion, lobular disarray, cholestasis and sinusoidal fibrosis suggestive of veno-occlusive disease secondary to drug/toxin induced liver injury. The Naranjo adverse drug reaction probability scale indicated a probable relationship between hepatic SOS and cyclophosphamide. Cyclophosphamide was held. Bone marrow biopsy showed the patient was in remission. His liver enzymes are improving and hematologic counts continue to be stable while on observation. High dose of IV cyclophosphamide given as myeloablative therapy in combination of total body irradiation or busulfan (or other agents) in preparation for hematopoietic stem cell transplantation can induce hepatic SOS, which can be severe leading to acute liver failure and death. The diagnosis is usually based on clinical features of tender hepatomegaly, weight gain, ascites and jaundice. Liver biopsy is usually diagnostic. Mechanism of injury is related to direct toxic effects of cyclophosphamide on sinusoidal cells in the liver, causing their necrosis and release into the sinusoids, obstruction and obliteration of hepatic veins. This case demonstrates that hepatic SOS can also be caused by low dose oral cyclophosphamide. Given this rare occurrence, it is prudent for the clinicians to keep an open mind and consider hepatic SOS as a potential side effect even with oral cyclophosphamide. Disclosures Yacoub: Novartis: Speakers Bureau; Agios: Honoraria, Speakers Bureau; Incyte: Speakers Bureau; Hylapharm: Current equity holder in private company; Cara Therapeutics: Current equity holder in publicly-traded company; Ardelyx: Current equity holder in publicly-traded company; Dynavax: Current equity holder in publicly-traded company; Roche: Other: Support of parent study and funding of editorial support.

scholarly journals Sinusoidal Obstruction Syndrome Following Myeloablative Therapy and Tranexamic Acid Treatment for Hemorrhage in Two Patients with Neuroblastoma

Children ◽  
2020 ◽  
Vol 7 (11) ◽  
pp. 198
Author(s):  
Felix Zirngibl ◽  
Carina Flemmig ◽  
Peter Lang ◽  
Annette Künkele ◽  
Angelika Eggert ◽  
...  
Keyword(s):  
Tranexamic Acid ◽  
Clinical Course ◽  
Young Patients ◽  
High Dose Chemotherapy ◽  
High Dose ◽  
Sinusoidal Obstruction Syndrome ◽  
Causal Association ◽  
Hematopoietic Stem ◽  
Hepatic Sinusoidal Obstruction Syndrome ◽  
Short Time

Adverse thromboembolic events following administration of the anti-fibrinolytic agent tranexamic acid (TA), used to prevent/treat excessive blood loss, are rare. We present the clinical course of two young patients (22 and 56 months) receiving busulfan/melphalan (Bu/Mel) high-dose chemotherapy with autologous hematopoietic stem cell transplantation (HSCT) to treat high-risk neuroblastoma, who developed hepatic sinusoidal obstruction syndrome (SOS) within 48 h after systemic TA treatment for a hemodynamically relevant hemorrhage. Defibrotide treatment resolved hepatic SOS, but the short time between TA administration and SOS onset suggests a causal association.

Bortezomib in Combination with High-Dose Dexamethasone and Continuous Low-Dose Oral Cyclophosphamide for Relapsed Multiple Myeloma.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2549-2549 ◽  
Author(s):  
Martin Kropff ◽  
Guido Bisping ◽  
Peter Liebisch ◽  
Orhan Sezer ◽  
Hermann Einsele ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Low Dose ◽  
Response Rate ◽  
Single Agent ◽  
Median Number ◽  
High Dose ◽  
Oral Cyclophosphamide ◽  
Minor Response ◽  
Chromosome 13 ◽  
Dose Oral

Abstract Single agent bortezomib treatment yields ≥ partial responses (PR) in 24% of patients with relapsed, refractory multiple myeloma (MM) and 38% of patients who had received 1 – 3 previous therapies. Dexamethasone (DEX) adds to anti-myeloma activity of bortezomib. The present phase II trial was intitiated to study bortezomib combined with DEX and continuous low-dose oral cyclophosphamide (CY). 50 patients with advanced MM were scheduled to receive bortezomib 1.3 mg/m2 IV days 1, 4, 8, and 11 q 3 weeks for 8 cycles in combination with DEX 20 mg PO on the day of bortezomib injection and the day thereafter, and CY 50 mg PO daily; followed by 3 cycles bortezomib 1.3 mg/m2 IV days 1, 8, 15, and 22 q 5 weeks in combination with corresponding DEX and CY schedules. Patient characteristics included median age 63 years; B2M > 3,0 mg/L, 64%; CRP > 3,0 mg/L, 25%; deletion of chromosome 13, 46%; median number of prior regimens, 2 (range 1 – 9), and prior standard therapy > 12 mo, 94 %. 78% of patients had relapsed after high-dose melphalan. The EBMT criteria were used for definition of response. Five patients (10%) achieved a complete response, 33 (66%) a PR, and 6 (12%) a minor response (MR) resulting in an overall response rate (≥MR) of 88%. On an intention-to-treat basis, median event-free survival (EFS) with this combination was 10 months. After a median follow-up of 10 months, median overall survival has not been reached. Notably, chromosome 13 deletion was predictive of a favorable outcome (higher response rate, longer EFS) in this setting. The median number or treatment cycles given was 6. 56% of the patients terminated study treatment prematurely, mainly for disease progression (10%) or adverse events (34%). Grade 4 neutropenia during at least one treatment cycle occurred in one patient (2%), grade 4 thrombocytopenia in 17%; one thrombocytopenic bleeding. Grade 3/4 non-hematologic toxicities requiring dose or schedule modifications included infections (26%), peripheral neuropathy (25%), fatigue (15%), herpes zoster (13%), and cardiovascular events (11%). One patient succumbed to infection without predisposing neutropenia. Bortezomib in combination with DEX and CY appears to be a highly active regimen without increased toxicity compared to a single agent treatment with bortezomib. Maintenance treatment might be required for prolonged EFS.

scholarly journals Low Dose Umbilical Cord Blood Transplant Results in Skewed Immune Cell Composition Which May Impact Immune Reconstitution after Allogeneic Hematopoietic Stem Cell Transplantation

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5672-5672
Author(s):  
Chi Hua Sarah Lin ◽  
Beth Shaz ◽  
Rona Singer Weinberg
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
T Cell ◽  
Cell Population ◽  
Peripheral Blood ◽  
Low Dose ◽  
High Dose ◽  
Hematopoietic Stem ◽  
Nsg Mice ◽  
Cd34 Cells

Abstract Introduction Reconstitution of donor-derived immune system after allogeneic hematopoietic stem cell transplantation (HSCT) is essential for recovery and long-term survival. Despite routine use of human umbilical cord blood (hUCB) as a stem cell source for allogeneic HSCT, much remains unknown regarding the kinetics of immune recovery and correlation with different transplant cell dosages. To study the hUCB repopulating potential, different hUCB CD34+ cell dosages were transplanted into immune deficient NSG mice; hematopoietic cells were then collected and engraftment was analyzed. Methods NOD/SCID/IL-2Rγnull recipient (NSG) mice (Jackson Laboratories, Bar Harbor, ME) were kept in pathogen-free facilities. CD34+ cells were isolated from a pool of six hUCB donors using a CD34+ microbead kit (Miltenyi Biotec). Each sublethal irradiated (220 or 300 cGy) 8 week old female NSG mice received either low dose (15x103, N=15) or high dose (75x103, N=15) CD34+ cells transplanted intravenously via retro-orbital route. Animal experiments were performed in accordance with Institutional Animal Care and Use Committee guidelines. Statistical analysis was performed with Prism software (GraphPad Software, Inc) and Excel. Data are presented as mean ± standard error of the mean (SEM). Results To determine the effects of hUCB CD34+ cell dosages on the rate of engraftment, NSG mice were transplanted with low doseor high dose CD34+ cells. The transplanted CD34+ cell dosages were comparable to clinical dosages based on body weight (Mavroudis et al. 1996). The engrafted cells were analyzed for expression of surface markers that define human hematopoietic cells. During the follow up period of up to 18 weeks, the high dose infused group had increased hUCB engraftment compared with the low dose infused group in peripheral blood (Fig 1A), bone marrow (Fig 1B & 1C) and spleen (Fig 1D), which is consistent with reported clinical observations that infused cell dosage is inversely correlated with time to engraftment (Migliaccio et al. 2000 Blood). Interestingly, we observed different lymphoid subset frequencies between low and high dose infused groups at the post-engraftment stage (18 weeks post transplantation) (data not shown). To investigate different lymphoid subset engraftment frequencies in low and high dose hUCB transplanted recipient mice at early engraftment stage, peripheral blood and hematopoietic organs were collected and analyzed up to 10 weeks post transplantation. The low dose infused group had significantly lower CD3+ (T cells) and CD56+ (NK cells) frequency in peripheral blood at 4 and 8 weeks (Fig 2A & 3A). More importantly, CD3+ (T cells) frequency was close to non-detectable in the bone marrow and spleen in the low dose infused group (Fig 2B & 2C), and CD56 (NK cells) frequency was decreased in the low dose infused group compared with the high dose infused group (Fig 3B & 3C). The absolute CD3+ and CD56+ number, displayed as fold difference, were even more dramatically decreased in the femur (Fig 2D & 3D) and the spleen (Fig 2E & 3E) of low dose infused group. Because of the substantial difference in T cell subset frequencies between the two dosage groups in bone marrow and spleen, thymuses were collected and analyzed to study T cell development and maturation. Engraftment of hCD45+ cells in the thymuses were observed in 10 out of 15 animals (66.7%) in the low dose infused group and 12 out of 14 animals (85.7%) in the high dose infused group. Interestingly, in animals with high hCD45+ frequency, the total thymocyte CD3+ frequency was lower in the low dose infused group (Fig 4A). Additionally, the low dose infused group had lower CD3+CD4+ T cell frequency (Fig 4B) and higher CD3+CD4+CD8+ T cell frequency (Fig 4C), suggesting low dose infused group had a decreased mature T cell population and increased immature T cell population in the thymus. In contrast, the low dose hUCB CD34+ cells infused group had increased hCD19 (B cells) frequency in the peripheral blood, bone marrow and spleen (Fig 5A-5C), while the absolute hCD19 (B cells), displayed as fold difference, did not show a statistically significant difference between the two groups (Fig 5D & 5E). Conclusions In summary, our findings suggest that (1) transplanted hUCB cell dosage is inversely correlated with time to engraftment (2) low transplanted hUCB cell dosage resulted in skewed immune cell population which may contribute to delayed immune recovery after allogeneic HSCT. Disclosures No relevant conflicts of interest to declare.

Hematologic Toxicity of High-Dose Iodine-131–Metaiodobenzylguanidine Therapy for Advanced Neuroblastoma

2004 ◽  
Vol 22 (12) ◽  
pp. 2452-2460 ◽  
Author(s):  
Steven G. DuBois ◽  
Julia Messina ◽  
John M. Maris ◽  
John Huberty ◽  
David V. Glidden ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Radiation Dose ◽  
Red Cells ◽  
Whole Body ◽  
High Dose ◽  
Hematologic Toxicity ◽  
Severe Thrombocytopenia ◽  
Hematopoietic Stem ◽  
Iodine 131 ◽  
Mibg Therapy

Purpose Iodine-131–metaiodobenzylguanidine (131I-MIBG) has been shown to be active against refractory neuroblastoma. The primary toxicity of 131I-MIBG is myelosuppression, which might necessitate autologous hematopoietic stem-cell transplantation (AHSCT). The goal of this study was to determine risk factors for myelosuppression and the need for AHSCT after 131I-MIBG treatment. Patients and Methods Fifty-three patients with refractory or relapsed neuroblastoma were treated with 18 mCi/kg 131I-MIBG on a phase I/II protocol. The median whole-body radiation dose was 2.92 Gy. Results Almost all patients required at least one platelet (96%) or red cell (91%) transfusion and most patients (79%) developed neutropenia (< 0.5 × 103/μL). Patients reached platelet nadir earlier than neutrophil nadir (P < .0001). Earlier platelet nadir correlated with bone marrow tumor, more extensive bone involvement, higher whole-body radiation dose, and longer time from diagnosis to 131I-MIBG therapy (P ≤ .04). In patients who did not require AHSCT, bone marrow disease predicted longer periods of neutropenia and platelet transfusion dependence (P ≤ .03). Nineteen patients (36%) received AHSCT for prolonged myelosuppression. Of patients who received AHSCT, 100% recovered neutrophils, 73% recovered red cells, and 60% recovered platelets. Failure to recover red cells or platelets correlated with higher whole-body radiation dose (P ≤ .04). Conclusion These results demonstrate the substantial hematotoxicity associated with high-dose 131I-MIBG therapy, with severe thrombocytopenia an early and nearly universal finding. Bone marrow tumor at time of treatment was the most useful predictor of hematotoxicity, whereas whole-body radiation dose was the most useful predictor of failure to recover platelets after AHSCT.

166Ho-DOTMP plus melphalan followed by peripheral blood stem cell transplantation in patients with multiple myeloma: results of two phase 1/2 trials

Blood ◽  
2003 ◽  
Vol 102 (7) ◽  
pp. 2684-2691 ◽  
Author(s):  
Sergio Giralt ◽  
William Bensinger ◽  
Mark Goodman ◽  
Donald Podoloff ◽  
Janet Eary ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Stem Cell ◽  
Hematopoietic Stem Cell Transplantation ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Phase 1 ◽  
High Dose ◽  
Two Phase ◽  
Hematopoietic Stem

Abstract Holmium-166 1, 4, 7, 10-tetraazcyclododecane-1, 4, 7, 10-tetramethylenephosphonate (166Ho-DOTMP) is a radiotherapeutic that localizes specifically to the skeleton and can deliver high-dose radiation to the bone and bone marrow. In patients with multiple myeloma undergoing autologous hematopoietic stem cell transplantation two phase 1/2 dose-escalation studies of high-dose 166Ho-DOTMP plus melphalan were conducted. Patients received a 30 mCi (1.110 Gbq) tracer dose of 166Ho-DOTMP to assess skeletal uptake and to calculate a patient-specific therapeutic dose to deliver a nominal radiation dose of 20, 30, or 40 Gy to the bone marrow. A total of 83 patients received a therapeutic dose of 166Ho-DOTMP followed by autologous hematopoietic stem cell transplantation 6 to 10 days later. Of the patients, 81 had rapid and sustained hematologic recovery, and 2 died from infection before day 60. No grades 3 to 4 nonhematologic toxicities were reported within the first 60 days. There were 27 patients who experienced grades 2 to 3 hemorrhagic cystitis, only 1 of whom had received continuous bladder irrigation. There were 7 patients who experienced complications considered to be caused by severe thrombotic microangiopathy (TMA). No cases of severe TMA were reported in patients receiving in 166Ho-DOMTP doses lower than 30 Gy. Approximately 30% of patients experienced grades 2 to 4 renal toxicity, usually at doses targeting more than 40 Gy to the bone marrow. Complete remission was achieved in 29 (35%) of evaluable patients. With a minimum follow-up of 23 months, the median survival had not been reached and the median event-free survival was 22 months. 166Ho-DOTMP is a promising therapy for patients with multiple myeloma and merits further evaluation. (Blood. 2003;102:2684-2691)

scholarly journals Ripk3 Signaling Regulates Hematopoietic Stem Cell Number and Function during Stress

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 3714-3714
Author(s):  
Lei Zhang ◽  
Huacheng Luo ◽  
Jing Li ◽  
Hong-Min Ni ◽  
Mark Sellin ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Low Dose ◽  
Conflicts Of Interest ◽  
Lymphoblastic Leukemia ◽  
High Dose ◽  
Low Doses ◽  
Hematopoietic Stem ◽  
Increased Risk ◽  
Leukemia Development ◽  
Serial Transplantation

Background: Among all tissues, bone marrow (BM) is the most sensitive tissue to ionizing radiation (IR)-induced acute tissue damage (ATD) and chronic long-term residual damage (LT-RD). BM failure and a significant reduction in blood cells (pancytopenia) often occurs within days after exposure to IR due to the massive death of proliferative hematopoietic progenitor cells (HPCs). However, due to their quiescent cell cycle status and reduced fidelity of DNA repair feature, many hematopoietic stem cells (HSCs) cannot fully eliminate such damage and enter senescence; this results in LT-RD. Abnormal dysplastic hematopoiesis is the most common LT-RD in most victims of IR, followed by an increased risk of leukemia/lymphoma development. Thus IR exposure is an established cause of BM failure and leukemia. A significant increase in the production of inflammatory cytokines is induced by IR which contributes to the pathogenesis of both ATD and LT-RD. Such inflammatory cytokines induce the activation of Ripk3-Mlkl-mediated necroptotic signaling in HSCs. However, the role of Ripk3-Mlkl signaling in IR-induced damage has not studied. Experimental procedures: The self-renewal capacity of HSCs among Ripk3-/-, Mlkl-/- and WT mice were examined and compared by serial transplantation assay. The phenotypes of ATD and LT-RD induced by different dosages of IR were compared among Ripk3-/-, Mlkl-/- and WT mice. The mechanism by which Ripk3 signaling prevents IR-induced leukemia development was studied. Results: Ripk3-Mlkl signaling is not required for hematopoiesis during homeostatic condition. However, during serial transplantation, inactivation of such signaling prevents stress-induced loss of HSCs. Interestingly, Ripk3 signaling also induces an Mlkl-independent ROS-p38-p16-mediated senescence in HSCs. Thus Ripk3-/- HSCs showed better competitive hematopoietic ability compared to Mlkl-/- and WT HSCs during serial transplantation. A sub-lethal dosage of IR (6Gy) induces Ripk3-dependent NF-κB activation and pro-survival gene expression in HSCs, which is necessary for the survival of damaged HSCs. After 6Gy IR, although DNA damage is repaired in most HSCs within 2 days, a proportion of HSCs in WT and Mlkl-/- mice fail to fully repair the damage and undergo p53-p21-dependent senescence. However such cells in Ripk3-/- mice die from apoptosis. Thus the remaining HSCs in Ripk3-/- mice should be functionally normal, while a proportion of the remaining HSCs in Mlkl-/- and WT mice remain damaged but senescent, all as demonstrated by competitive hematopoietic reconstitution assay. Multiple low-doses of IR (1.75Gy once week × 4) induce HSC exhaustion in WT mice but not in Ripk3-/- and Mlkl-/- mice. Interestingly, almost all Ripk3-/- mice develop acute lymphoblastic leukemia within 200 days after such low dose IR, while 45% of WT and 60% of Mlkl-/- mice develop thymomas within 360 days (see Figure). Mechanistically, such low-dose IR stimulates chronic inflammatory cytokine production. Such cytokines induce Ripk3-Mlkl-mediated necroptosis in response to HSC exhaustion observed in WT mice. These cytokines also induce Ripk3-ROS-p38-p16-mediated senescence in response to impaired HSC functioning observed in both WT and Mlkl-/- mice. In Ripk3-/- mice, due to the lack of both necroptotic and senescent signaling, mutant HSCs accumulate and leukemia development is accelerated. Conclusion: Ripk3 signaling plays distinct roles in HSCs in response to different doses of IR. High-dose IR induces Ripk3-dependent NF-κB/survival signaling, which is required for the survival of HSCs which fail to repair the damage. Thus temporal inhibition of Ripk3-NF-κB signaling might help to remove the damaged HSCs thus preventing the occurrence of LT-RD. However multiple low-doses of IR induces Ripk3 activation in HSCs which represses leukemia development by inducing both ROS-p38-p16-mediated senescence and Ripk3-Mlkl-mediated necroptosis. Induced activation of Mlkl-necroptosis might help to repress leukemia development by removing damaged HSCs. Disclosures No relevant conflicts of interest to declare.

scholarly journals Phase I Trial of Intra-arterial Administration of Autologous Bone Marrow-Derived Mesenchymal Stem Cells in Patients with Multiple System Atrophy

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Seok Jong Chung ◽  
Tae Yong Lee ◽  
Yang Hyun Lee ◽  
KyoungWon Baik ◽  
Jin Ho Jung ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Multiple System Atrophy ◽  
Phase I ◽  
Dose Group ◽  
Low Dose ◽  
Autologous Bone Marrow ◽  
High Dose ◽  
Autologous Bone

Background. This study is aimed at investigating the safety and tolerability of the intra-arterial administration of autologous bone marrow-derived mesenchymal stem cells (BM-MSCs) in patients with multiple system atrophy- (MSA-) cerebellar type (MSA-C). Methods. This was a single-center, open-label phase I clinical trial in patients with MSA-C. A three-stage dose escalation scheme (low-dose, 3.0 × 10 5 cells/kg; medium-dose, 6.0 × 10 5 cells/kg; high-dose, 9.0 × 10 5 cells/kg) was applied to determine the maximum tolerated dose of intra-arterial administration of BM-MSCs based on the no-observed-adverse-effect level derived from the toxicity study. The occurrence of adverse events was evaluated 1 day before and 1, 14, and 28 days after BM-MSC therapy. Additionally, we assessed changes in the Unified MSA Rating Scale (UMSARS) score 3 months after BM-MSC treatment. Results. One serious adverse drug reaction (ADR) of leptomeningeal enhancement following the intra-arterial BM-MSC administration occurred in one patient in the low-dose group. The safety review of the Internal Monitoring Committee interpreted this as radiological evidence of the blood-brain barrier permeability for MSCs. No other ADRs were observed in the medium- or high-dose groups. In particular, no ischemic lesions on diffusion-weighted images were observed in any of the study participants. Additionally, the medium- and high-dose groups tended to show a slower increase in UMSARS scores than the low-dose group during the 3-month follow-up. Conclusion. The present study confirmed that a single intra-arterial administration of autologous BM-MSCs is a safe and promising neuroprotective strategy in patients with MSA-C.

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