Red cell distribution width is an inflammatory predictor marker of contrast induced nephropathy in patients undergoing percutaneous coronary intervention.

Red blood cell distribution width (RDW) is an inflammatory biomarker reported in complete blood cell (CBC) counts. High RDW defines a proinflammatory state. Contrast-induced nephropathy (CIN) is an important and common complication in percutaneous coronary intervention (PCI) treated patients. The current study was conducted to evaluate the role of RDW as a simple predictive inflammatory marker of CIN in PCI treated patients. The current prospective study enrolled 126 PCI treated patients. Laboratory investigations included CBC, liver function test, (HbA1C), lipid profile and serological tests. Serum urea and creatinine levels were obtained at baseline and 48 to 72 hours after PCI procedure, used to categorize for CIN. Diabetes mellitus, hypertension, and ischemic heart disease were present in 39 (31%), 44 (34.9%), and 23 (18.3%) patients, respectively. Of the studied patients, only 19 (15.1%) patients developed CIN. The hemoglobin level was significantly higher in the non-CIN group (13.49 ± 1.63 vs. CIN group 12.56 ± 1.62 mg/dl; p= 0.02). RDW was significantly higher among CIN group than non-CIN group (16.20 ± 2.60 vs. 13.83 ± 2.19 % (p < 0.001). Delta creatinine (% change in creatinine level after 48 hour) was significantly higher in patients with CIN (59.17 ± 28.89 vs. non-CIN 33.62 ± 9.76; p < 0.001). Predictors for CIN in patients who underwent PCI were old age high RDW high delta creatinine and amount of dye. At cut off > 14.5%, RDW had 79% sensitivity, 70% specificity and 71.3% overall accuracy at AUC of 0.76. In conclusion, RDW may be simple and immediately available inflammatory biomarker and predictor for development of CIN in patients undergoing PCI.

Kinetic of liver enzymes and serum electrolytes in HCV, HBV, and HIV negative chronic phase chronic myeloid leukemia patients treated with imatinib or nilotinib.

The outcome for chronic phase (CP) chronic myeloid leukemia (CML) patients was changed dramatically since the introduction of tyrosine kinase inhibitor (TKI) therapy. This study intended to evaluate side effects of TK Imatinib or Nilotinib on liver enzymes and serum electrolytes in relation to hematologic and molecular response in HCV-, HBV-, and HIV-, CP-CML patients. The study was a quasi-experimental pre-post single group design, included 38 HCV-, HBV-, and HIV-newly diagnosed Philadelphia positive CP-CML patients with normal hepatic and renal function. They were divided equally into two groups, 19 received Nilotinib, and 19 received Imatinib. Hematologic, BCR-ABL gene expression by RT-PCR, electrolytes and liver enzymes were measured at baseline and after 6 months of treatment. Patients age ranged between 20 and 62 years. Anemic manifestations represented the highest rate (n=23, 60.5%). The mean WBCs count was significantly reduced after treatment (p < 0.001). The WBCs count was significantly reduced in the Nilotinib group than the Imatinib group (97% and 94%, respectively, p=0.049). The mean hemoglobin level was significantly increased after treatment (p=0.010). The mean platelet level did not change over the treatment period. The mean AST, ALT, and ALP levels were significantly increased after treatment, (p=0.014, p=0.002, and p=0.047, respectively). The ALP level was significantly increased in both groups (p=0.001). The mean sodium potassium, phosphorous, and calcium level was not changed over the treatment period. The mean BCR-ABL gene expression was sharply decreased after treatment (p < 0.001). A higher reduction was observed in the Nilotinib group (99%) than the Imatinib group (91.5%) (p=0.025). Imatinib resulted in rise of AST and ALP levels than Nilotinib, while both had the same effect on the ALT level. Higher reduction in BCR-ABL gene expression was achieved by Nilotinib. Nilotinib and Imatinib did not affect serum levels of sodium, potassium, phosphorous, or calcium.

Can platelets indices and blood neutrophil to lymphocyte ratio be used as predictors for diagnosis of spontaneous bacterial peritonitis in decompensated post hepatitis liver cirrhosis?

Spontaneous bacterial peritonitis (SBP) is most common infection in patients with liver cirrhosis with ascites. SBP is diagnosed by the presence of ≥250 polymorphonuclear leukocyte (PMNL)/mm3 in the ascetic fluid with absence of surgical and treatable causes of intra-abdominal infection. This study intended to evaluate platelet indices and neutrophil to lymphocyte ratio (NLR) as predictors marker of SBP. This study included 106 patients: 53 cirrhotic with SBP, 53 cirrhotic without SBP and 53 sex and age matched normal non cirrhotic controls. The mean platelet volume (MPV), platelet distribution width (PDW), platelet crit (PCT), NLR and C reactive protein (CRP) were compared between study groups. Patients with SBP had significantly higher MPV, PDW, PCT NLR and platelet-lymphocyte ratio (PLR) than patients without SBP (P< 0.001 for all). Patients with SBP had significantly higher MPV, PDW, PCT NLR and PLR than the control group (P< 0.001). MPV, PDW, PCT, PLR, and NLR had positive significant correlations with CRP and ascetic fluid PMNL (P< 0.001). In conclusion, our study findings indicated that platelet indices in cirrhotic patients may be novel, simple, low-cost, non-invasive, and valuable diagnostic marker for diagnosis of SBP. They could be considered reliable and surrogate marker for PMNL.

sVCAM-1, and TGFß1 in chronic phase, chronic myeloid leukemia patients treated with tyrosine kinase inhibitors.

The outcome for chronic phase (CP) chronic myelogenous leukemia (CML) patients has changed dramatically since the introduction of tyrosine kinase inhibitor (TKI) therapy. We examined the characteristics of CML patients during TKI therapy by determining the plasma concentrations of soluble vascular cell adhesion molecule 1 (sVCAM-1), and transforming growth factor (TGFß1) biomarkers. The plasma levels of sVCAM-1 and TGFß1 were measured by ELISA at baseline and after 3 months of TKI treatment. The levels of sVCAM-1, and TGFß1 were significantly elevated in patients with CML (P< 0.01). Dasatinib treatment was associated with a significant reduction in the levels of these biomarkers (P< 0.01). In conclusion, plasma levels of sVCAM-1 and TGFß1 could have a role in the pathogenesis of CML and may be used as predictors of hematological and molecular responses to TKIs. A favorable outcome for Dasatinib therapy was observed.

T-lymphocytes Expression of Toll-like Receptors 2 and 4 in Acute Myeloid Leukemia Patients with Invasive Fungal Infections.

Background: Invasive fungal infections (IFIs) are important cause of mortality in acute myeloid leukemia (AML) patients on treatment with intensive induction chemotherapy. Toll-like receptors, mainly Toll-like receptors 2 and 4 (TLR2 and TLR4), play a considerable role in the host defense against microorganisms. The involvement of TLR signaling in modulation of innate immune response is extensively discussed, but the TLR expressions profiling on adaptive immune cells are not specified. Also, the expressions of TLRs and their association with the occurrence of IFIs in patients with AML are not studied. So, the novel aim of this study was to investigate the associations between the T-lymphocyte expression of TLR2 and TLR4 and the occurrence of IFIs in AML patients treated with intensive induction chemotherapy. Materials and Methods: One hundred twenty two newly diagnosed AML patients were evaluated. The laboratory diagnostic techniques for IFIs include culture, microscopic examination, histopathology, galactomannan assay and PCR. The expressions of TLR2 and TLR4 were analyzed by flow cytometry. The Control group included 20 age and sex-matched individuals. Results: There was a significant increase in the expression of TLR4 in AML patients with IFI compared to healthy controls (p = 0.001). TLR2 and TLR4 expressions increased significantly in AML patients with mixed fungal and bacterial infection compared to healthy controls (p= 0.002 and p=0.001, respectively). Conclusion: TLRs expressions could be important biological markers for the occurrence of IFI in non-M3 AML patients after intensive induction chemotherapy.