Patient populations, including those with hematological malignancies, have different responses to COVID-19 vaccines. This study aimed to quantitatively analyze the efficacy and safety of COVID-19 mRNA vaccines in patients with hematological malignancies. Studies reporting on the efficacy and safety of COVID-19 mRNA vaccines in cohorts with hematological malignancies compared to healthy controls were systematically searched in four databases. Meta-analysis and subgroup analyses were performed to generate quantitative synthesis. Fifteen studies with 2,055 cohorts with hematological malignancies and 1,105 healthy subjects as control were included. After two doses of COVID-19 vaccination, only 60% of cohorts with hematological malignancies were seroconverted compared to healthy controls (RR 0.60; 95%CI 0.50–0.71). A single dose of the vaccine resulted in a significantly lower seroconversion rate (RR 0.30; 95%CI 0.16–0.54). Non-Hodgkin lymphoma cohorts had the lowest rate of seroconversion (RR 0.5; 95%CI 0.35–0.71) and those who received active treatments had lower immunological responses (RR 0.59; 95%CI 0.46–0.75). Antibody titers were lower in cohorts with hematological malignancies without any differences in adverse effects in both groups. In conclusion, cohorts with hematological malignancies showed a lower seroconversion rate and antibody titers after receiving COVID-19 mRNA vaccines. The type of malignancy and the status of treatment had a significant impact on the response to vaccination. The vaccines were shown to be safe for both patients with hematological malignancies and healthy controls. Booster doses and stricter health protocols might be beneficial for patient populations.

Introduction: Patients with deep vein thrombosis (DVT) pose high morbidity and mortality risk thus needing fast and accurate diagnosis. Wells clinical prediction scores with D-dimer testing are traditionally used to rule out patients with low probability of DVT. However, D-dimer testing has a few limitations regarding its relatively low specificity. Neutrophillymphocyte ratio (NLR), a marker of inflammation, was found to increase in DVT. Hence, we aimed to evaluate the role of NLR for DVT diagnosis. Methods: Data were collected from medical records of patients with suspected DVT at Cipto Mangunkusumo National General Hospital during January-December 2014. Diagnosis of DVT was conducted using lower limb ultrasonography. Diagnostic values for NLR, D-dimer, and NLR + D-dimer were determined by receiver operating characteristic (ROC) analysis to obtain area under the curve (AUC), sensitivity, specificity, negative predictive value, and positive predictive values. Sensitivity and specificity analyses of NLR and D-dimer were also conducted based on Wells score and divided into groups of low and high probability of DVT. Results:The AUC values for NLR, D-dimer, and NLR + D-dimer were 72.6%, 70.4%, and 76.1%, respectively. The optimal cut-off value determined for NLR was 5.12 with sensitivity of 67.7%, specificity of 67.9%, PPV of 68.85%, and NPV of 64.91% in differentiating subjects with and without DVT. This study also found that D-dimer had sensitivity of 69.4%, specificity of 71.4%, PPV of 72.88%, and NPV of 67.8%. Meanwhile, the NLR + D-dimer combination had sensitivity of 66.1% and specificity of 72.6%. Multivariate analysis showed that NLR (OR: 2.636; 95% CI: 1.144-6.076; p: 0.023) and D-dimer (OR: 4.175; 95% CI: 1.810-9.633; p: 0.001) were associated with DVT. Conclusion: NLR value has wider AUC than D-Dimer and is relatively easier to obtain and does not require specific assay, thus enabling rapid evaluation of symptomatic patients suspected of having DVT. Adding NLR to D-dimer increased AUC to detect DVT. Therefore, NLR could serve as a complementary diagnostic tool for D-dimer to exclude DVT, especially in low clinical probability patients.

Introduction:Leukostasis is a medical emergency with high mortality which often occurs in acute myeloid leukemia patients with hyperleukocytosis. One of the therapies that can be used for leukostasis in acute myeloid leukemia is leukapheresis. However, whether leukapheresis can provide better survival benefit when compared with patients not receiving leukapheresis is still unclear. Hence, we aimed to evaluate the effect of chemotherapy plus leukapheresis combination versus chemotherapy only on 28-day survival of acute myeloid leukemia patients with leukostasis. Methods: This study was a dual-center retrospective cohort using secondary data from medical records collected from November 2018 to March 2019. Inclusion criteria were adult patients aged 18 years old or above, diagnosed with acute leukemia with hyperleukocytosis status defined by WBC count greater than 100,000/uL, and with symptoms of leukostasis. One-month survival analysis was conducted using Kaplan-Meier curve method. Univariate and multivariate analyses were then conducted using Cox proportional hazards model to obtain value of hazard ratio (HR) with a 95% confidence interval (CI). Results: A total of 38 patients were obtained for analysis. The median overall survival was 25 days (95% CI: 17.001-32.999 days) in the chemotherapy only group and 20 days (95% CI: 1.497-38.503) in the chemotherapy with leukapheresis group. The use of leukapheresis did not affect 28-day survival (HR: 1.140; 95% CI: 0.396-3.283; p value: 0.809) and 7-day survival (HR: 1.073; 95% CI: 0.277-4.152; p value: 0.919). In the multivariate analysis, age ≥60 years, blast percentage ≥90%, creatinine ≥1.4 mg/dL, and presence of disseminated intravascular coagulation were associated with worse 28-day survival. Conclusion: AML patients with leukostasis who received both chemotherapy and leukapheresis did not have better 28-day survival and 7-day survival when compared with patients receiving chemotherapy only. Old age, high blast percentage, high creatinine, and presence of disseminated intravascular coagulation were prognostic factors for worse 28-day survival.

Background. Acquired hemophilia A (AHA) is a potentially life-threatening autoimmune hemostatic disorder where autoantibodies that disrupt the functions of factor VIII (FVIII) are present in the circulation. The early diagnosis of AHA is difficult since the symptoms of AHA differ from those of congenital hemophilia A. Furthermore, the management of AHA is also more complex due to the presence of autoantibodies against FVIII (FVIII inhibitors). Here, we present three case reports and conduct a literature review of AHA with the aim to increase awareness and knowledge regarding the diagnosis and treatment of AHA. Case Presentations. We present three patients diagnosed with AHA in these case reports. The first patient was a young female, while the second and third patients were middle-aged and elderly males, respectively. All patients presented with a chief complaint of bruises without hemarthrosis and a history of bleeding. Laboratory examinations of the patients revealed isolated prolonged aPTT, normal PT, and the presence of autoantibodies against factor VIII, which are characteristics of AHA. Patients were then treated with corticosteroids to reduce the titer level of autoantibodies and received factor VIII transfusion to stop bleeding. Conclusion. AHA can be suspected in patients presenting with symptoms of bruises without hemarthrosis and without the history of bleeding. Isolated aPTT elevation with normal PT should raise high suspicion of AHA. The presence of FVIII inhibitors can help to confirm the diagnosis of AHA. Treatment consists of factor VIII transfusion and corticosteroid therapy. Bypassing agents are recommended as an alternative to FVIII transfusion.

Chronic myeloid leukemia (CML) is one of the most common leukemias occurring in the adult population. The course of CML is divided into three phases: the chronic phase, the acceleration phase, and the blast phase. Pathophysiology of CML revolves around Philadelphia chromosome that constitutively activate tyrosine kinase through BCR-ABL1 oncoprotein. In the era of tyrosine kinase inhibitors (TKIs), CML patients now have a similar life expectancy to people without CML, and it is now very rare for CML patients to progress to the blast phase. Only a small proportion of CML patients have resistance to TKI, caused by BCR-ABL1 point mutations. CML patients with TKI resistance should be treated with second or third generation TKI, depending on the BCR-ABL1 mutation. Recently, many studies have shown that it is possible for CML patients who achieve a long-term deep molecular response to stop TKIs treatment and maintain remission. This review aimed to provide an overview of CML, including its pathophysiology, clinical manifestations, the role of stem cells, CML treatments, and treatment-free remission.