Invasive splenic mucormycosis due to Rhizopus microsporus during chemotherapy for acute monocytic leukemia: a case report and literature review.

Mucormycosis is a rare opportunistic fungal infection associated with high mortality that typically occurs in immunocompromised patients. It is difficult to diagnose owing to non-specific clinical manifestations, the serologic index, imaging features, and the limitations of diagnostic methods. The incidence of invasive splenic mucormycosis is extremely rare, with only a few cases documented in the literature. We report a survival case of invasive splenic mucormycosis involving the liver caused by Rhizopus microsporus in a patient during consolidation therapy for acute monocytic leukemia (AML-M5). The patient initially presented with recurrent fever and splenomegaly accompanied by multiple focal hypodensities unresponsive to empiric anti-infective treatment. Splenic mucormycosis was diagnosed by Contrast-Enhanced Ultrasonography (CEUS) and metagenomic next-generation sequencing (mNGS). However, surgical intervention carries a high risk due to the progressive involvement of the liver in invasive splenic mucormycosis. Fortunately, monotherapy with amphotericin B was effective, and the patient underwent allo-HSCT. This case aims to emphasize the importance of utilizing mNGS and CEUS for the timely diagnosis of mucormycosis to help clinicians identify splenic mucormycosis and initiate appropriate therapy as soon as possible to improve therapeutic efficacy and prognosis.

Differential Expression of TXNIP Isoforms in the Peripheral Leukocytes of Patients with Acute Myocardial Infarction.

BACKGROUND: Acute myocardial infarction (AMI) is the most serious type of coronary atherosclerotic heart disease (CAD). The pathological changes are characterized by atherosclerosis. Oxidative stress plays an important role in atherosclerosis. Thioredoxin-interacting protein (TXNIP), an endogenous inhibitor and regulator of thioredoxin, could bind thioredoxin to regulate its expression and antioxidant activity negatively. The NCBI data show that there are two isoforms in TXNIP gene, namely, TXNIP1 and TXNIP2. Our previous studies have shown that TXNIP expression levels in patients with unstable angina pectoris (UAP) were increased compared with controls (CTR). However, no upregulation of TXNIP was detected in AMI patients. METHODS: The leucocytes were isolated from peripheral venous blood, and total RNA of the leucocytes was extracted. Then, real-time quantitative PCR was performed. RESULTS: mRNA levels of TXNIP2 in AMI were significantly increased compared with CTR (P < 0.05). However, the expression of TXNIP1 was downregulated in AMI, but the difference was not statistically significant (P > 0.05). Logistic regression analysis showed that TXNIP2 mRNA levels were significantly associated with AMI (OR = 2.207, P < 0.05). CONCLUSIONS: The expression of TXNIP2, not TXNIP1, is upregulated in leukocytes of AMI patients, indicating that only TXNIP2 in circulating leucocytes may be involved in the pathogenesis of AMI.

Altered Expression of TXNIP in the peripheral leukocytes of patients with coronary atherosclerotic heart disease.

BACKGROUND: Coronary atherosclerotic heart disease (CAD) is mainly caused by atherosclerosis, an inflammatory disease characterized by plaque formation in arteries. Reactive oxygen species caused structural damage and dysfunction of arterial endothelial cells. Thioredoxin-interacting protein (TXNIP) is the endogenous inhibitor and regulator of thioredoxin, a major cellular antioxidant and antiapoptotic system. In order to explore the role of TXNIP in the occurrence and development of CAD, we detected the TXNIP expression and discussed its molecular mechanisms in CAD. METHODS: The mRNA levels of TXNIP gene in peripheral leucocytes were detected in CAD and healthy controls (CTR) by quantitative real-time polymerase chain reaction. And TXNIP proteins were detected by western blotting. RESULTS: TXNIP gene expression levels in patients with unstable angina pectoris (UAP, n = 96) were significantly increased compared with those of CTR (n = 192, P < .05). However, the situation is different in acute myocardial infarction (n = 96, P > .05). Logistic regression analysis showed that TXNIP levels were significantly positive correlated with UAP (OR = 1.728, P < .05). CONCLUSIONS: TXNIP gene expression in the peripheral leucocytes was increased in patients with UAP, indicating that TXNIP in circulating leucocytes may be involved in the pathogenesis of UAP.

Effect of Angiotensin-Converting Enzyme Inhibitors in Contrast-Induced Nephropathy: A Meta-Analysis.

AIMS: The purpose of this study was to evaluate the effect of angiotensin-converting enzyme inhibitors (ACEIs) on contrast-induced nephropathy (CIN) in patients undergoing coronary angiography or percutaneous coronary intervention (PCI). METHODS: We searched the Medline, Embase, Cochrane Library, China National Knowledge Infrastructure, Chongqing VIP database and Wanfang database up to December 2014. Pooled risk ratios (RRs) or weighted mean difference (WMD) with their 95% CIs for the CIN incidence, serum creatinine (SCr), estimated glomerular filtration rate (eGFR) and blood urea nitrogen (BUN) of the patients were collected and calculated using the software Review Manager 5.2. RESULTS: A total of 12 separate studies including 1,868 patients (1,011 ACEI cases and 857 controls) were considered in the meta-analysis. The overall RR of the incident CIN in the ACEI group vs. the control group was 0.95 (95% CI 0.57-1.58), and the total WMDs of the x0394;SCr, x0394;eGFR and x0394;BUN were -0.01 (95% CI -0.04 to 0.02), 5.71 (95% CI -0.66 to 12.09) and 0.78 (95% CI -0.16 to 1.73), respectively. Besides, the RR of CIN incidence in the captopril group vs. the control group was 0.72 (95% CI 0.25-2.05, p = 0.54), and the pooled WMD of the x0394;SCr was -0.13 (95% CI -0.21 to -0.06, p < 0.01). CONCLUSION: This meta-analysis suggests that ACEIs administration has no significant influence in the CIN of patients undergoing coronary angiography or PCI; however, captopril might have the potential to prevent CIN.

TAK-242 suppresses lipopolysaccharide-induced inflammation in human coronary artery endothelial cells.

TAK-242 (resatorvid), a novel small-molecule cyclohexene derivative, inhibits TLR4 signaling selectively. TAK-242 blocked the Toll-like receptor (TLR) 4-triggered inflammatory signaling by binding directly to a specific amino acid Cys747 in the intracellular domain of TLR4. The present study was designed to examine the effects of TAK-242 on vascular inflammatory responses in human coronary artery endothelial cells (HCAECs) challenged by lipopolysaccharide (LPS, a TLR4 ligand). The results show that TAK-242 attenuated the LPS-induced expression of interleukin (IL)-6, IL-8 and monocyte chemoattractant protein 1 both at the transcription and translation levels in HCAECs. LPS-induced endothelial cell adhesion molecules, intercellular adhesion molecular-1 and vascular cell adhesion molecule-1 expressions were also reduced by treatment with TAK-242. In addition, coincubation with TAK-242 did not effect the expression of TLR4 in LPS-activated HCAECs. Furthermore, TAK-242 efficiently suppressed LPS-induced phosphorylation of nuclear factor κB (NF-κB) and IL-1 associated kinase-1 (IRAK-1) in HCAECs. These findings show that TAK-242 can suppress endothelial cell inflammation, suggesting that TAK-242 might be suitable for development as a therapeutic agent for inflammatory cardiovascular disease.