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The Hospital at Home (HaH) model has been positioned as an appropriate therapeutic strategy for selected patients undergoing an autologous hematopoietic stem cell transplantation (ASCT). This care model provides hospital equivalent care, both in quality and quantity, with medical and nursing staff that go to the patient's home. We describe our experience with a full at home model for patients undergoing ASCT during the phase of aplasia.Patients who met the eligibility criteria between January 1997 and December 2019, were discharged from the hospital and admitted into the HaH-ASCT program on the same day they in which hematopoietic stem cells were infused.84 patients were included. The median age was 54 [16-74]. The median duration of admission in the HaH program was 17 [3-86] days. Only 10 of these patients (12%) required hospital re-admission in the hematology department, 9 of them due to sepsis and one because of family care support claudication. 72 patients (86%) had a neutropenic fever episode during the HAH admission with a median duration of 2 [1-11] days. Empiric intravenous antimicrobial therapy was prescribed in all of them. Most patients (88%) presented with mucositis (44% grade 3-4). Parenteral nutrition was administered in 26% of patients for a median of 6 [1-12] days. 94% of patients required at least one blood product transfusion at home. There was no transplant related mortality during the HaH-ASCT program or in the patients readmitted.With a careful selection of patients and a comprehensive and well experienced multidisciplinary team (doctors, nurses, auxiliary nurses) in the HaH department and in close collaboration with the hematology department, allows a complete at home management of ASCT patients immediately after the HSC infusion. This allows patients undergoing an aggressive procedure such as ASCT to remain in their own familiar environment providing a better quality of life, with a program that has demonstrated to be effective and safe, with a low incidence of complications and with no associated mortality.

Background Patients undergoing hematopoietic stem cell transplantation (HSCT) are at high risk of multiple complications being graft versus host disease (GvHD) one of the most concerning. Addition of anti-T-lymphocyte globulin (ATG-Fresenius ®) reduces the incidence of acute and chronic GvHD however, optimal dose has not yet been established. Standard dose (60 mg/kg) has shown a significantly lower moderate-severe cGvHD yet its effect in Progression Free Survival (PFS) and Overall Survival (OS) is contradictory. Our primary objective was to analyze the efficacy of low ATG dose (21 mg/kg) in the prophylaxis of acute and chronic GvHD. As secondary objective we analyzed non-relapse mortality (NRM), infectious and non-infectious complications, GvHD and relapse free survival (GRFS), overall survival and progression free survival in high risk patients undergoing HSCT. Patients and methods We retrospectively analyzed 57 patients who underwent HSCT in our center from 2012 to 2017, receiving a total dose of 21 mg/kg (7 mg/kg on day -3, -2 and -1) of ATG as part of the GvHD prophylaxis, associated to cyclosporine/tacrolimus and MMF/short course-MTX. The conditioning regimen were myeloablative in 42 patients (73.7%). The donor was unrelated in 46 cases (80.7%). Seventeen (29.9%) had a mismatch (16 unrelated, 1 sibling). Stem cell source was peripheral blood in 51 patients (89.4%). Forty six (80.7%) patients were positive for CMV, from these 17 (36.9%) were paired with seronegative donors. The median age was 57 years old (18-70), 38(66.7%) were males. The most frequent diagnosis were Acute Myeloblastic Leukemia (40.4%), myelofibrosis (17.5%) and myelodisplastic syndrome (14%); 28 (49%) had a HCTI score ≥ 3 and 16 (29%) a high risk DRI score. Thirty patients (52.6%) were in complete remission at the moment of HSCT. (Table 1) Results Hematopoietic engraftment was observed in 54 patients (94.7%). The median neutrophil and platelet engraftment were 14 (10-34) and 15 (9-28) days, respectively. Primary graft failure occurred in 3 patients (2 myelofibrosis, 1 AML). Twenty (39.2%) out of 51 evaluable patients developed grade 2-4 acute GvHD. The cumulative incidence of grade 3-4 aGvHD was 8.8% (95% CI, 3.2-17.9%). Skin was the most affected organ (62%). We found a cumulative incidence of moderate to severe cGvHD of 35.2% (95% CI 22.7-47.9%), only 5 cases (10.6%) were severe, with a median onset at day 177 (57-893). The median duration of immunosuppresive systemic therapy was 488 days (207-2046) in the group of patients with moderate to severe cGvHD. Twelve patients died due to transplant related events, 7 were reported before day 100, all of infectious etiology. The NRM at two years was 21.9% (95% CI, 12-33.7%). Eleven patients (19.2%) had at least two episodes of CMV reactivation and one had cytomegalic gastrointestinal disease. One patient developed postransplantation lymphoproliferative disorder associated to Epstein Barr virus. Twenty patients (35%) developed noninfectious complications, being hemorrhagic diathesis, hepatotoxicity and severe mucositis the most frequents. With a median follow up of 28 months in alive patients (3-67), the GRFS at one year, OS and PFS at two years were 47.6% (95% CI, 42.8-52.2%), 59% (95% CI, 54.5-63.2%) and 52% (95% CI, 46.9-56.5%), respectively. The relapse incidence at two years was 26.3% (95% CI 14.7-39.4%). Conclusions In our center, the use of low ATG doses is protective against severe forms of acute GvHD, offering also a moderate protection against chronic GvHD in a cohort with high prevalence of mismatched unrelated donors, high median age and high risk DRI and HCTI. This approach doesn't seem to have a significant negative impact neither in GRFS, OS and PFS at two years. Disclosures No relevant conflicts of interest to declare.

Activation of pancreatic β-cell proliferation has been proposed as an approach to replace reduced functional β-cell mass in diabetes. Quiescent fibroblasts exit from G0 (quiescence) to G1 through pRb phosphorylation mediated by cyclin C/cdk3 complexes. Overexpression of cyclin D1, D2, D3, or cyclin E induces pancreatic β-cell proliferation. We hypothesized that cyclin C overexpression would induce β-cell proliferation through G0 exit, thus being a potential therapeutic target to recover functional β-cell mass. We used isolated rat and human islets transduced with adenovirus expressing cyclin C. We measured multiple markers of proliferation: [3H]thymidine incorporation, BrdU incorporation and staining, and Ki67 staining. Furthermore, we detected β-cell death by TUNEL, β-cell differentiation by RT-PCR, and β-cell function by glucose-stimulated insulin secretion. Interestingly, we have found that cyclin C increases rat and human β-cell proliferation. This augmented proliferation did not induce β-cell death, dedifferentiation, or dysfunction in rat or human islets. Our results indicate that cyclin C is a potential target for inducing β-cell regeneration., This work was supported by grants from ISCIII-Subdirección General de Evaluación y Fomento de la Investigación, Spain (PS09/00671); Programa Ramón y Cajal (RYC-2011-08101) Ministerio de Economía y Competitividad, Spain; and Europe-FP7 Marie Curie grant (IRG-247835) to I. Cózar-Castellano, by Europe-FP7 Marie Curie grant (IRG-256369) to G. Perdomo, by National Institute of Diabetes and Digestive and Kidney Diseases Grants (RO1-DK-073716;, DK-084236) and Juvenile Diabetes Research Foundation (17-2013-416) to E. Bernal-Mizrachi, and by a Minority Postdoctoral Fellowship from the American Diabetes Association to M. Jiménez-Palomares.