Congenital left atrial appendage ostial stenosis in an extremely premature infant diagnosed by transthoracic echocardiography

Congenital left atrial appendage ostial stenosis is a very rare congenital cardiac condition. We present the case of an extremely premature infant with congenital left atrial appendage ostial stenosis diagnosed by transthoracic echocardiographic imaging.     

Role of S100A8 and S100A9 in neutrophil recruitment in response to monosodium urate monohydrate crystals in the air‐pouch model of acute gouty arthritis

Objective

To examine the role of chemokines, S100A8, and S100A9 in neutrophil accumulation induced by the causative agent of gout, monosodium urate monohydrate (MSU) crystals.

Methods

MSU crystal–induced neutrophil migration was studied in the murine air‐pouch model. Release of chemokines, S100A8, S100A9, and S100A8/A9 in response to MSU crystals was quantified by enzyme‐linked immunosorbent assays. Recruited cells were counted following acetic blue staining, and the subpopulations were characterized by Wright‐Giemsa staining of cytospins.

Results

MSU crystals induced the accumulation of neutrophils following injection in the air pouch, which correlated with the release of the chemokines CXCL1, CXCL2, CCL2, and CCL3. However, none of these was found to play an important role in neutrophil migration induced by MSU crystals by passive immunization with antibodies directed against each chemokine. S100A8, S100A9, and S100A8/A9 were also found at high levels in the pouch exudates following injection of MSU crystals. In addition, injection of S100A8, S100A9, or S100A8/A9 led to the accumulation of neutrophils in the murine air pouch, demonstrating their proinflammatory activities in vivo. Passive immunization with anti‐S100A8 and anti‐S100A9 led to a total inhibition of the accumulation of neutrophils. Finally, S100A8/A9 was found at high concentrations in the synovial fluid of patients with gout.

Conclusion

S100A8 and S100A8/A9 are essential to neutrophil migration induced by MSU crystals. These results suggest that they might be involved in the pathogenesis of gout.

     

Changes in bone mineral density following discontinuation or continuation of alendronate therapy in glucocorticoid‐treated patients: A retrospective,observational study

Objective

To evaluate the effects of discontinuing or continuing alendronate (ALN) therapy on bone mineral density (BMD) after patients on a long‐term regimen of glucocorticoids (GCs) completed a 1‐year treatment period with ALN.

Methods

Eligible patients were individuals with GC‐induced osteoporosis who had received ALN (5 or 10 mg) for 1 year in a prior clinical trial and, at the end of the year, were still taking GCs at an average daily dose of ≥7.5 mg of prednisone or equivalent. Patients were contacted 3–5 years after completion of the prior ALN trial for followup measurements of the lumbar spine BMD and hip BMD, and retrospective information was collected about serious or drug‐related adverse experiences and concomitant medication use. Some patients remained on GCs, and some remained on ALN, either alone or in combination with other drugs. The primary response parameter was the percentage change in lumbar spine BMD from the end of year 1 to the followup visit. Change in BMD at the hip was a secondary response parameter.

Results

Ninety (49.2%) of the eligible 183 patients participated in the retrospective study. The followup period, which began at the end of year 1 of the original clinical trial, ranged from 3.3 years to 4.6 years. The mean number of days of treatment with ALN was 507. Fifty patients were included in the analysis because they had received supraphysiologic doses of GCs (doses above the lowest tertile of GC use for the study population; that is, higher than ∼6 mg/day), and they had not taken (defined as <6 months of use) other bone‐affecting agents except ALN. Eleven of the 50 patients discontinued taking ALN (duration of use <90 days), 8 took ALN between 90 days and 300 days, and 31 continued to take ALN for >300 days after year 1 of the clinical trial. GC users who discontinued treatment with ALN (<90 days of therapy) had numerically greater decreases in BMD at the lumbar spine, femoral neck, and total hip from the end of year 1 (mean change −5.1%, −9.2%, and −6.6%, respectively), compared with patients who continued to take ALN for >300 days (mean change 0.1%, −0.9%, and 1.8%, respectively).

Conclusion

Substantial loss of BMD in the lumbar spine and hip was seen in patients who discontinued treatment with ALN but who continued to take >6 mg/day of GCs. However, patients receiving GCs who remained on the ALN regimen appeared to benefit from continued ALN treatment, since BMD was maintained in this latter group.

     

A failure in the medication delivery system—how disclosure and systems investigation improve patient safety

A recent medication error at Vanderbilt University Medical Center contributed to the death of a patient. The ensuing criminal indictment of the administering nurse has shaken the medical community. This has led to clinical staff questioning whether they can disclose patient safety incidents without fear of criminal prosecution. However, because of the publicity of this case, hospitals can benefit from the lessons learned and mitigate the risk of this and similar events at their facilities. To uncover the most impactful and relevant safety recommendations, the Vanderbilt case is examined from a systems investigation perspective using the available public information gathered from media reports, the Tennessee Bureau of Investigation report, and Vanderbilt's corrective action plan submitted to CMS. We present an example of how hospitals can benefit from disclosure: Henry Ford Health used the Vanderbilt case study as part of its medication safety continuous improvement initiatives, which are underpinned by available medication safety recommendations from the Institute for Safe Medication Practices. Using this experience and the lessons learned from the Vanderbilt case, a proactive action plan is presented for hospitals nationwide to prevent the recurrence of this medication error. Without disclosure, these analyses and safety recommendations would not have been possible.