Rationale: Some acute myeloid leukemia (AML) patients are unresponsive to treatment or have remission followed by worsening of disease (known as relapsed/refractory AML [R/RAML]) after standardized treatment. The CAG/HAG regimen is not often used clinically because heterogenous patient responses, resistance, and hematopoietic bone marrow dysfunction have been reported with its use. We present 2 cases of R/RAML treated with a new combined therapy (venetoclax+ hypomethylating agents [HMAs]) in which the HAG dose was adjusted and effective in the first course of treatment. Patient characteristics: Case 1 involved a 23-year-old man who had suffered from AML for >4 years, and his FLT3 mutation status was positive at the initial diagnosis. After the first course of treatment with the standard-dose “Da” plan, the patient experienced complete remission. During the subsequent courses of treatment, the patient experienced 6 recurrences and was treated with the “ID Ara-C + MIT + sidaaniline” and “CAG + sidaaniline” regimens. However, the disease did not respond. Case 2 involved a 26-year-old man who received chemotherapy with the “Da,” “ID Ara-C,” “decitabine + half-dose CAG,” and “HAE” regimens. In this patients, remission could not be achieved. Reintroduction of the “ia” scheme also failed after treatment in our hospital. Diagnosis: Two patients were diagnosed with R/RAML. Interventions: The patient in case 2 received chemotherapy interventions, whereas the patient in case 1 refused to receive medical services at our hospital. Outcomes: The patient in case 1 was discharged after complete response treatment due to economic reasons and relapsed 2 months later. The patient ultimately died of infection and heart failure. The patient in case 2 is receiving a second cycle of chemotherapy. Lessons: We recommend the “venetoclax + HMAs combined with dose-adjusted CAH/HAG” regimen as an effective treatment for adult R/RAML.
Objective. To explore the clinical value of specific miRNA in patients with acute promyelocytic leukemia. Methods. 129 patients with acute promyelocytic leukemia diagnosed in our hospital from January 2015 to January 2020 were selected as the observation group. At the same time, 74 patients with nonacute promyelocytic leukemia who underwent bone marrow aspiration were included as the control group. The expression levels of miR-126-5p and miR-13, different characteristic parameters, and prognosis were compared between the two groups, and the clinical significance of miR-126-5p and miR-13 in acute promyelocytic leukemia was analyzed. Results. The expression of miR-126-5p ( 12.31 ± 2.25 versus 17.30 ± 3.28 ) and miR-13 ( 16.05 ± 3.47 versus 21.66 ± 2.18) in the observation group was significantly lower than that in the control group ( P < 0.05 ). The expression level of miR-126-5p was significantly correlated with lactate dehydrogenase level, HGB level, NPM1 mutant type, and complete remission ( P < 0.05 ). The expression level of miR-13 was significantly correlated with HGB level, NPM1 mutant type, and complete remission ( P < 0.05 ). Both expression levels of miR-126-5p and miR-13 were not correlated with sex, age, WBC, PLT, proportion of bone marrow primordial cells, hepatomegaly, splenomegaly, lymph node enlargement, and FLT3-ITD ( P > 0.05 ). Cox multivariate regression analysis showed that peripheral blood WBC, bone marrow blast cell count, and miR-126-5p and miR-13 were prognostic factors in patients with acute promyelocytic leukemia ( P < 0.05 ). The sensitivity, specificity, accuracy, and AUC of serum miR-126-5p prediction were 75.83%, 84.56%, 82.17%, and 0.729, respectively. The sensitivity, specificity, accuracy, and AUC of serum miR-13 prediction were 78.64%, 88.49%, 86.20% and 0.882, respectively. Conclusion. Serum miR-126-5p and miR-13 are closely related to the prognosis of patients with acute promyelocytic leukemia. Serum miR-126-5p and miR-13 can be used as reliable indexes to predict the prognosis of patients.
3001 Poster Board II-978 Lipopolysaccsharide (LPS) is a principal outer membrane component of gram-negative bacteria. It initiates an inflammatory response to infection by activating Toll-like receptor-4 (TLR4) on various tissues or cells in host. Platelet contributes to the inflammation process through respond to invading pathogens, membrane adhesion molecule (CD62P, P-selectin) and CD40L on platelet are the indexes to determine platelet activation. The present experiment was designed to investigate the expression of Toll-like receptor 4 (TLR4) on platelet and to determine whether platelet TLR4 involves in platelet activation induced by Lipopolysaccsharide (LPS). Human platelet-rich plasma (PRP) and platelet suspension obtained from 15 healthy people were pretreated with a concentration of 0.2μg/ml of LPS in the presence or absence of thrombin (1 U/ml) for 1 hour. The expressions of TLR4,CD62P and CD40L on platelets were detected through flow cytometry, and platelet TLR4 was further determined by performing western blot analysis. The results show that the percentage of TLR4-positive platelet induced by thrombin was increased by 32.34% compared with the resting platelets (25.44%, P<0.01). TLR4 expression on platelets treated with LPS was remarkedly elevated in the presence or absent of thrombin. However, the expression level was much higher in presence of both than thrombin alone( 39.16%,P<0.01). Moreover, the similar results were found in Western blot analysis. Synchronously, the expressions of CD62P and CD40L on resting platelets were 6.39% and 2.45%, they were also markedly increased when treated with thrombin(42.68% and 14.80%) and LPS respectively, and the increase of CD62P was more significant when stimulated with both of LPS and thrombin(63.03%). Although anti-TLR4 antibody inhibited significantly the increases of TLR4, CD62P and CD40L on platelets induced by LPS, it didn't effect their increases induced by thrombin. The experiment results support the evidence that functional TLR4 can be expressed on human platelet. It may involve in platelet activation as an important mediator of LPS- induced CD62P and CD40L expressions on platelets. Disclosures: No relevant conflicts of interest to declare.
Lipopolysaccsharide (LPS) is a principal outer membrane component of gram-negative bacteria. It initiates an inflammatory response to infection by activating Toll-like receptor-4 (TLR4) in host. Infection increases risk for hemostasis, thrombosis, DIC, and tissue repair. Platelet contributes to the inflammation process through respond to invading pathogens, membrane adhesion molecule (P-selectin) is one of the indexes to determine platelet activation. Experiment was designed to study whether TLR4 is expressed on human platelet, and what is the function of TLR4 in platelet activation induced with LPS. Platelet suspensions from 10 heath people were treated with LPS of different concentrations for 1 hour, which were 0mg/L(control),0.1mg/L,0.5mg/L,1mg/L and 5mg/L, respectively. The expressions of TLR4, P-select on platelets and PAI-1 in platelets were detected through flow cytometry (FCM) and western blot(WB) methods. ADP-induced platelet aggregation was measured by LG-PABER aggregometer. Compared with control, the expressions of TLR4,P-selectin on platelets and PAI-1 in platelets after treated with LPS of 0.5mg/L,1mg/L and 5mg/L were increased (P<0.05). positive correlation was observed between TLR4 and P-selectin on platelets, but between TLR4 and PAI-1 in platelets. LPS of all concentrations did not affected ADP-induced platelet aggregation. Therefore, it is evident that functional TLR4 is expressed on human platelet. TLR4 on platelet might be one of the important intermedia between platelet activation and LPS or bacteria, and contribute to the inflammatory process in host. It is also worthy to study whether LPS affect platelet aggregation induced by other inductors.
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