Dialysis access as a source of infective endocarditis in dialysis patients.

The incidence of Infective Endocarditis (IE) is higher in dialysis patients compared to the general population. A major risk factor for IE in this group stems from bacterial invasion during repeated vascular access. Previous studies have shown increased risk of bacteremia in patients with indwelling dialysis catheters compared to permanent vascular access. However, association between the development of IE and the type of dialysis access is unclear. We aimed to examine the associated types of intravascular access and route of infection in dialysis patients who were admitted with infective endocarditis at our center. All patients admitted to Albert Einstein Medical Center in Philadelphia with a diagnosis of infective endocarditis who were on chronic hemodialysis were identified from the hospital database for the period of 1/1/07 to 12/31/18. Modified Duke criteria was used to confirm the diagnosis of infective endocarditis. A total of 96 cases were identified. Of those, 57 patients had an indwelling dialysis catheter while the other 39 had permanent dialysis access. In 82% of patients with dialysis catheters, their dialysis access site was identified as the primary source of infection compared to 30% in those with permanent dialysis access (p<0.001). The number of dialysis catheters placed in the preceding 6 months was strongly associated with endocarditis resulting from the dialysis access site (OR = 3.202, p=0.025). Dialysis catheters are more likely to serve as the source of infection in dialysis patients developing IE compared to permanent dialysis access. Increased awareness of risk of IE associated with dialysis catheters is warranted.

Transthyretin Cardiac Amyloidosis and Aortic Stenosis: Connection and Therapeutic Implications.

BACKGROUND: There is a growing interest in the observed significant incidence of transthyretin cardiac amyloidosis in elderly patients with aortic stenosis. Approximately, 16% of patients with severe aortic stenosis undergoing aortic valve replacement have transthyretin cardiac amyloidosis. Outcomes after aortic valve replacement appear to be worst in patients with concomitant transthyretin cardiac amyloidosis. METHODS: Publications in PubMed, Cochrane Library, and Embase databases were systematically searched from January 2012 to September 2018 using the keywords transthyretin, amyloidosis, and aortic stenosis. All studies published in English that reported the prevalence, association and outcomes of transthyretin cardiac amyloidosis in patients with aortic stenosis undergoing were included. RESULTS/CONCLUSION: The relationship between aortic stenosis and transthyretin cardiac amyloidosis is not well understood. A few studies have proven successful surgical management when both conditions coexist. This systematic review suggests that transthyretin cardiac amyloidosis is common in elderly patients with aortic stenosis and tend to have high mortality rates after AVR. The significant incidence of the two diseases occurring simultaneously warrants further investigation to improve management strategies in the future.

Gomisin A Suppresses Colorectal Lung Metastasis by Inducing AMPK/p38-Mediated Apoptosis and Decreasing Metastatic Abilities of Colorectal Cancer Cells.

Gomisin A (G.A) is a dietary lignan compound from Schisandra chinensis. In this study, the effect of G.A on the proliferation and metastasis of colorectal cancer (CRC) cells was investigated using several CRC cell lines and a lung metastasis mouse model. Both oral and intraperitoneal administration of G.A (50 mg/kg) inhibited lung metastasis of CT26 cells. Various concentrations of G.A were incubated with CRC cell lines and their viability was determined using a cell counting kit-8 assay. G.A significantly decreased the viability of various CRC cell lines, whereas it did not change the proliferation of normal colon cells. G.A induced G0/G1 phase arrest and apoptosis of CT26 and HT29 cells by regulating cyclin D1/cyclin-dependent kinase 4 (CDK4) expression and apoptotic proteins such as caspases and B-cell lymphoma-2 (Bcl-2) family proteins, respectively. G.A-induced apoptosis was mediated by AMPK/p38 activation in CRC cells. A non-cytotoxic concentration of G.A inhibited epithelial-mesenchymal transition of CRC cells by modulating E-cadherin and N-cadherin expression levels. Moreover, the migration and invasion of CRC cells were reduced by G.A treatment. Especially, G.A decreased matrix metalloproteinase (MMP)-2 and MMP-9 expressions and activities. G.A ameliorated lung metastasis of CRC cells by decreasing cell survival and metastatic abilities of CRC cells. Thus, G.A might be a potential novel therapeutic agent for metastatic CRC.