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BackgroundThe purpose of this study was to identify the clinical characteristics and outcomes of peripheral vascular catheter-related bloodstream infections (PVC-BSIs) and determine the risk of severe complications or death.MethodsWe performed a retrospective observational study from June 2010 to April 2015 at two regional university-affiliated hospitals in Tokyo. We studied the clinical manifestations, underlying diseases, laboratory results, treatment methods, recurrence rates, and complications in 62 hospitalized patients diagnosed with PVC-BSIs by positive blood cultures.ResultsThe median time from admission to bacteremia was 17 days (range, 3–142 days) and that from catheter insertion to bacteremia diagnosis was 6 days (range, 2–15 days). Catheter insertion sites were in the arm in 48 (77.4%) patients, in the foot in 3 (4.8%) patients, and in an unrecorded location in 11 (17.7%) patients. Additionally, the causative pathogens were Gram-positive microorganisms in 58.0% of cases, Gram-negative microorganisms in 35.8% of cases, Candida spp. in 6.2% of cases, and polymicrobials in 25.8% of cases. Eight (12.9%) patients died within 30 days of their blood culture becoming positive. Patients who died of PVC-BSIs had a higher proportion of Staphylococcus aureus infection than patients who survived (odds ratio, 8.33; p = 0.004).ConclusionsPVC-BSIs are a significant cause of health care-associated infection. We observed cases of severe PVC-BSI requiring intensive and long-term care along with lengthy durations of antibiotic treatment due to hematogenous complications, and some patients died. For patients with PVC-BSIs, S. aureus bacteremia remains a major problem that may influence the prognosis.

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Background and purpose:Various complications consequent on disordered calcium and phosphate homeostasis occur frequently in chronic kidney disease (CKD) patients. Particularly, vascular calcification has high morbidity and mortality rates. There is a clear need for a better CKD model to examine various aspects of this disordered homeostasis. Experimental approach: Oral dosing with adenine induced CKD in rats in only 10 days. Serum calcium, phosphate and parathyroid hormone were measured and calcification in aorta was assessed histologically. The effects of varying phosphorus content of diet or treatment with phosphate binders or active vitamin D3 on these parameters were examined. Key results: After adenine dosing, significant hyperphosphatemia, hypocalcemia and secondary hyperparathyroidism (2HPT) were observed during the experimental period of 15 weeks. Aortic calcification was detected in only some of the animals even at 15 weeks (~40%). Treatment with vitamin D3 for 18 days, even at a low dose (100 ng·kg -1 , 3-4 times week -1 , p.o), caused aortic calcification in all animals and increases in serum calcium levels up to the normal range. The vitamin D3-induced calcification was significantly inhibited by phosphate binders which lowered serum phosphate levels and the calcium ¥ phosphate product, although serum calcium levels were elevated. Conclusions: These data suggest that rats dosed orally with adenine provide a more useful model for analysing calcium/ phosphate homeostasis in severe CKD. Controlling serum calcium/phosphate levels with phosphate binders may be better than vitamin D3 treatment in hyperphosphatemia and 2HPT, to avoid vascular calcification.

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Interleukin-11 (IL-11) is a pleiotropic cytokine that supports various types of hematopoietic cell growth and is involved in bone resorption. We report here the involvement of recombinant human IL-11 (rHuIL-11) in osteoblast differentiation in mouse mesenchymal progenitor cells, C3H10T1/2. rHuIL-11 alone increased alkaline phosphatase (ALP) activity and upregulated expression levels of osteocalcin (OC), bone sialo protein (BSP), and parathyroid hormone receptor (PTHR) mRNA. rHuIL-11 had no effect on expression of type II collagen, peroxisome proliferator-activated receptor-gamma2 (PPAR-gamma2), adipocyte fatty acid-binding protein P2 (aP2), and myogenic MyoD protein (MyoD). Recombinant human bone morphogenetic protein (rHuBMP)-2 increased ALP activity and mRNA expression of these genes except for MyoD. The expression patterns of ALP activity and osteoblast-specific or chondrocyte-specific genes suggest that rHuIL-11 may be involved in early differentiation of osteoblasts at a step earlier than that which is affected by rHuBMP-2. In support of this hypothesis, combined treatment with rHuIL-11 and rHuBMP-2 synergistically increased ALP activity and mRNA expression of OC and type II collagen, rHuIL-11 also abrogated the increased levels of PPAR-gamma2, aP2 mRNA caused by rHuBMP-2. Our results suggest that rHuIL-11 alone and in combination with rHuBMP-2 can induce osteoblastic differentiation of progenitor cells and plays an important role in osteogenesis.

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