Validity of B-Type Natriuretic Peptide, Growth Differentiation Factor 15, and High-Sensitivity Troponin I Levels in Ischemic Heart Failure.

BACKGROUND: Heart failure (HF) is a major medical, and epidemiological problems with ischemic heart disease (IHD) is the most common cause of HF. We aimed to assess the plasma B-type natriuretic peptide (BNP) levels, serum growth differentiation factor 15 (GDF15), and high-sensitivity troponin I (hsTnI) in HF patients with and without IHD. METHODS: The study included 120 HF patients, categorized into 51 patients with IHD and 69 patients without apparent IHD. Clinical and echocardiographic assessments of the included patients were performed. ELISA assays of plasma BNP and serum GDF15 were done, while serum hsTnI was measured using chemiluminescent immunoassay. RESULTS: There were significantly higher median values of serum levels for GDF15 (pg/mL) and hsTnI (pg/mL) among IHD group (1,630.5 and 141.8, respectively) compared to non-IHD group (895 and 14.3, respectively, p ˂ 0.05 for both), with non-significant differences regarding to the BNP plasma levels (p ˃ 0.05). In the IHD group, significant positive correlations were observed between GDF15 with both BNP (r = 0.655, p = < 0.001) and hsTnI (r = 0.496, p = < 0.001). Serum GDF15 at a cutoff of ≤ 717 pg/mL has the highest specificity [85.51% vs. 50.72% for BNP (at cutoff > 264 pg/mL) and 59.42% for hsTnI]. Additionally, hsTnI at a cutoff of > 45.2 pg/mL has the highest sensitivity (70.59% vs. 68.63% for BNP and 33.33% for GDF15) in discriminating heart failure with IHD from heart failure without IHD. CONCLUSIONS: A multimarker approach, particularly GDF15 and hsTnI, is helpful in identifying HF patients with underlying IHD, thus enabling their proper management.

Expression analysis of two SLAM family receptors, SLAMF2 and SLAMF7, in patients with multiple myeloma.

Monoclonal antibodies against surface antigens on MM cells, such as anti-SLAMF7 and anti-CD38 antibodies, represent an attractive therapeutic modality for the eradication of multiple myeloma (MM) cells. However, further exploration of target molecules is urgently needed for the development of more effective therapies. In the present study, we studied the expression of CD48 in a total of 74 primary MM samples derived from patients to evaluate SLAMF2 (CD48) as a candidate in mAb therapy for MM. Of 74 samples, 39 were subjected to SLAMF7 analysis. Most of the MM cells, defined as CD38 and CD138 double-positive cells, showed strong expression of CD48 or SLAMF7 independent of disease stage or treatment history. In these 39 samples, most MM cells showed expression of both SLAMF7 and CD48; however, several samples showed expression of either only CD48 or only SLAMF7, including seven cases that were only highly positive for SLAMF7, and five that were only highly positive for CD48. Our study demonstrates that the immune receptor CD48 is overexpressed on MM cells together with SLAMF7, and that CD48 may be considered as an alternative target for treatment of MM in cases showing weak expression of SLAMF7.