Hyperfibrinolysis secondary to acquired factor XIII deficiency A case report.

INTRODUCTION: Hyperfibrinolysis induced by factor XIII deficiency (FXIIID) is extremely rare, and patients with no manifestations of active bleeding can easily and frequently be neglected in clinical practice, leading to a missed diagnosis. Herein, we report a rare case of idiopathic FXIIID with secondary hyperfibrinolysis. PATIENT CONCERNS: A 69-year-old man presented with ecchymosis of the right arm and chest wall. DIAGNOSIS: Considering the clinical picture, coagulation function test results, and FXIII activity, the patient was finally diagnosed with hyperfibrinolysis secondary to acquired factor XIII deficiency. INTERVENTIONS: The patient was treated with fresh frozen plasma, aminomethylbenzoic acid, a prothrombin complex, etamsylate, dexamethasone, and cryoprecipitate. OUTCOMES: The patient improved and was discharged after factor replacement therapy, and no further bleeding was reported 1 month after discharge. CONCLUSION: This case report illustrates that the complications of Factor XIII deficiency may include hyperfibrinolysis. Since timely diagnosis of FXIIID is challenging, detailed coagulation factor examinations are needed for definitive diagnosis. It has been suggested that gene testing and antibody testing can help in diagnosis. If ideal treatment is not available, alternative treatment should be provided to reduce bleeding.

Intermediate dose cytarabine improves survival and relapse-free rate compared with standard-dose cytarabine as post-remission treatment for acute myeloid leukemia: A retrospection study.

ABSTRACT: The exact dose of cytarabine still remain controversial for the management of patients with acute myeloid leukemia (AML) after complete remission (CR), but recent studies favor lower doses. This study aimed to investigate the toxic effects of single-intermediate dose (ID) cytarabine in patients with AML after achieving CR, compared with standard-dose cytarabine.In this retrospective study, AML patients who achieved CR after consolidation therapy before enrollment between 07/2008 and 05/2019 were included. All patients were divided into single-ID cytarabine and standard-dose cytarabine. The Kaplan-Meier method was used to compare overall survival (OS) and relapse-free time (RFS). Cox regression models were used to assess factors independently associated with OS and RFS. The toxic side effects of hematology and non-hematology were observed.52 patients were enrolled. There were 33 in ID group, 19 in Standard dose group. The 3-year RFS rate (40.4% vs 22.2%, P = .031) was better in the ID group than in the standard-dose group, while the 3-year OS rate was not different between the 2 groups (50.2% vs 27.8%, P = .074). Treatment stratage of ID cytarabine chemotherapy significantly improve the prognosis of AML regardless of patient age, risk grade, WBC count. There were no significant differences between the 2 groups in grade 3 to 4 bone marrow suppression, gastrointestinal symptoms, blood transfusion, infections.Patients with AML receiving ID cytarabine showed better survival and similar toxicity profiles compared with patients who received standard-dose cytarabine.

[The influence of induced autophagy in vitro on proliferation of multiple myeloma cells].

OBJECTIVE: To investigate the influence of autophagy on the survival and proliferation of multiple myeloma (MM) cells. METHODS: Multiple myeloma (MM) cell line U266 cell autophagy was induced by serum-free culture condition, and adding rapamycin or 3-MA respectively. The cells proliferation was observed. U266 cells, lymphoma cell Jurket under normal culture condition, and serum-free cultured Jurket cell were used as control group. The proliferation and apoptosis of cells were determined by CCK8 and flow cytometry, respectively. MDC staining were employed to detect the autophagy. The mRNA expression of Mtor and Beclin1 gene of U266 cells were assayed by RT-PCR. Protein LC3I/LCII and LAMP1 was analyzed by western blot. RESULTS: There was low level of autophagy in U266 cells, sera starvation increased the level of autophagy. Rapamycin upregulated autophagy of the U266 cells and stimulated their proliferation. But the autophagy level of sera starvation and rapamycin group declined when culture for 96h.3-MA had the same effects on U266 cells, although it was on 24 h. But rapamycin and 3-MA could inhibit cell proliferation under normal culture condition. Compared with normal culture condition, apoptosis of U266 cells increased significantly after 24h incubation in medium without sera \[(1.33 ± 0.09)% and (17.90 ± 1.46)%, respectively\] (P < 0.01). Rapamycin and 3-MA could inhibit the serum-free induced apoptosis \[(6.23 ± 0.12)% and (6.97 ± 0.03)%, respectively\](P < 0.01), but cell apoptosis was at the same level after 72 hour incubation \[(30.37 ± 0.27)%, (30.13 ± 1.93)% and (28.57 ± 2.83)%, respectively\] (P > 0.05). However, apoptosis of U266 cells decreased to 18.7% and 12.6% after removal of rapamycin and 3-MA. CONCLUSION: There is basically level of autophagy in MM cells which is higher than those in the Jurkat cells. Both Rapamycin and 3-MA can inhibit the cells proliferation under normal culture condition. Up-regulated autophagy promotes survival and proliferation of MM cells under sera deletion. Rapamycin strengthens this effect with limited duration. 3-MA has dual effects on cell autophagy.