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BackgroundDepression in congestive heart failure (CHF) patients can increase morbidity and mortality. Given the ever-rising prevalence of CHF patients with depression, it is vital that we understand the predictors of depression in these patients to identify and better manage these patients. The main objective of this study was to evaluate the frequency and predictors of depression in CHF patients.MethodsA cross-sectional study was conducted in a tertiary care hospital. Patients with a diagnosis of CHF for more than 6 months based on signs and left ventricular ejection fraction <40% were included. Patients were interviewed with the Patient Health Questionnaire-9 (PHQ-9) consisting of nine items in line with the Diagnostic and Statistical Manual (DSM) - IV criteria to assess depression. Each item was scored from 0 to 3, and a PHQ-9 score of 10 or greater suggested clinical depression. Data were analyzed on SPSS, v22, and a p < 0.05 was considered significant.ResultsOf 170 participants, 102 (60%) had depression. Among these 102 patients, 42% (n = 43) had mild depression, and the rest (n = 59) had moderate-to-severe depression. Predictors of depression were New York Heart Association stage 3 or 4 (p = 0.001), previous myocardial infarction (p = 0.001), living without a partner (p = 0.001), lack of a joint family system (p = 0.001), sedentary lifestyle (p = 0.001), aged 70 years or more (p = 0.01), and having been admitted in a hospital at least once in the past two months (p = 0.002).ConclusionDepression is common among patients with CHF. It is associated with multiple factors and needs to be addressed and targeted urgently.

Chronic lymphocytic leukemia (CLL) has a highly variable clinical course. About 2-10% of CLL patients develop aggressive histological transformation, most commonly to diffuse large B cell lymphoma (DLBCL), historically called Richter transformation (RT). Clinical features suggestive of RT include elevated LDH and non-specific symptoms such as fever, weight loss, and lymphadenopathy. 18-fluorodeoxyglucose (18-FDG) uptake is increased on PET scan (standardized uptake value max most commonly ≥ 10). PET/CT study can identify optimal site for excisional biopsy, which is the gold standard for RT diagnosis, as well as aid in disease staging and prognostication. In addition to clinical prognostic features such lactate dehydrogenase level, platelet count, and performance status, important predictors of poor outcome in RT are TP53 disruption and clonal relationship of DLBCL to underlying CLL. Chemoimmunotherapy constitutes the standard treatment for RT, followed by stem cell transplant (SCT) in eligible patients. However, the majority of patients do not proceed to allogeneic SCT, either due to inadequate disease control with initial therapy, poor performance status, or lack of donor availability. Overall outcome is dismal. Some novel agents under investigation, particularly PD-1 inhibitors, are showing clinical activity in Phase I and II trials. An ongoing incidence of RT has been noted in studies of previously treated patients receiving targeted therapies such as ibrutinib and venetoclax; the frequency of RT in patients initially treated with novel agents rather than chemoimmunotherapy will be important to determine with longer follow-up. This review focuses on the development, clinicopathologic features, and treatment of RT in the context of novel therapies.

Mixed phenotype acute leukemia (MPAL) is an uncommon diagnosis, representing only about 2-5% of acute leukemia cases. The blast cells of MPAL express multilineage immunophenotypic markers and may have a shared B/T/myeloid phenotype. Due to historical ambiguity in the diagnosis of MPAL, the genetics and clinical features of this disease remain poorly characterized. Based on the 2008 and 2016 World Health Organization classifications, myeloid lineage is best determined by presence of myeloperoxidase, while B and T lymphoid lineages are demonstrated by CD19 and cytoplasmic CD3 expression. MPAL typically carries a worse prognosis than either acute myeloid leukemia (AML) or acute lymphoid leukemia (ALL). Given the rarity of MPAL, there is a lack of prospective trial data to guide therapy; treatment generally relies on ALL-like regimens followed by consolidation chemotherapy or hematopoietic stem cell transplant (HSCT). Here, we review the updated classification, biology, clinical features, and treatment approach to MPAL.