Evaluation of a calcium, magnesium and phosphate clinical ordering tool in the emergency department.

OBJECTIVE: We developed a clinical tool comprising patient risk factors for having an abnormal calcium (Ca), magnesium (Mg) or phosphate (PO4) level. We hypothesized that patients without a risk factor do not require testing. This study examined the tool's potential utility for rationalizing Ca, Mg and PO4 ordering in the emergency department (ED). METHODS: We undertook a retrospective observational study in a single metropolitan ED. Patients aged 18 years or more who presented between July and December 2019 were included if they had a Ca, Mg or PO4 test during their ED stay. Demographic and clinical data, including the presence of risk factors, were extracted from the medical record. The primary outcome was a clinically significant abnormal Ca, Mg or PO4 level (>0.2 mmol/l above or below the laboratory reference range). RESULTS: Calcium, Mg and PO4 levels were measured on 1426, 1296 and 1099 patients, respectively. The positive and negative predictive values and likelihood ratios of the tool identifying a patient with a Ca level > 0.2 mmol/l outside the range were 0.05, 0.99, 1.59 and 0.41, respectively. The values for Mg were 0.02, 1.00, 1.44 and 0.35 and those for PO4 were 0.15, 0.93, 1.38 and 0.57, respectively. The majority of patients not identified as having an abnormal level did not receive electrolyte correction treatment. Application of the tool would have resulted in a 35.8% cost reduction. CONCLUSION: The tool failed to predict a very small proportion of patients (approximately 1%) with an abnormal Ca or Mg level and for whom it would have been desirable to have these levels measured. It may help rationalize Ca and Mg ordering and reduce laboratory costs.

Author and journal self-citation in Emergency Medicine original research articles.

OBJECTIVE: To determine author and journal self-citation rates in a sample of original emergency medicine (EM) research articles. METHODS: We undertook a retrospective observational study of original research articles published in 2019 in the top six English language general EM journals. Data comprised the total numbers of articles, citations, authors and self-citations for each author (author self-citations) as well as the number of articles in the reference list that had been previously published in the same journal (journal self-citations). RESULTS: 3213 individual authors and 581 articles were examined. Most authors did not self-cite at all although 62 self-cited five or more times in a single article. The mean (SD) and median (IQR) numbers of individual author self-citations/article/year were 0.6 (1.3) and 0 (0-1), respectively. Overall, author self-citations accounted for 2.4% of all cited articles. There was a weak positive but significant correlation between the number of individual author self-citations/article/year and the number of articles published by the author (r = 0.38, p < 0.001). There was no correlation between the journal impact factor (IF) and the author self-citation rate (r = 0.14, p = 0.79). The journals differed significantly in their author self-citation rates (p < 0.001). Annals of Emergency Medicine had the highest journal self-citation rate at 8.1% (95%CI 7.0%-9.2%) self-citations/100 citations/year, almost twice that of some other journals. There was a large but non-significant positive correlation between the journal IF and journal self-citation rates (r = 0.78, p = 0.07). CONCLUSION: Both author and journal self-citation rates in the articles examined are relatively low compared to other medical and scientific disciplines.

Two pathways for cyclooxygenase-2 protein degradation in vivo.

COX-2, formally known as prostaglandin endoperoxide H synthase-2 (PGHS-2), catalyzes the committed step in prostaglandin biosynthesis. COX-2 is induced during inflammation and is overexpressed in colon cancer. In vitro, an 18-amino acid segment, residues 595-612, immediately upstream of the C-terminal endoplasmic reticulum targeting sequence is required for N-glycosylation of Asn(594), which permits COX-2 protein to enter the endoplasmic reticulum-associated protein degradation system. To determine the importance of this COX-2 degradation pathway in vivo, we engineered a del595-612 PGHS-2 (Delta 18 COX-2) knock-in mouse lacking this 18-amino acid segment. Delta 18 COX-2 knock-in mice do not exhibit the renal or reproductive abnormalities of COX-2 null mice. Delta 18 COX-2 mice do have elevated urinary prostaglandin E(2) metabolite levels and display a more pronounced and prolonged bacterial endotoxin-induced febrile response than wild type (WT) mice. Normal brain tissue, cultured resident peritoneal macrophages, and cultured skin fibroblasts from Delta 18 COX-2 mice overexpress Delta 18 COX-2 relative to WT COX-2 expression in control mice. These results indicate that COX-2 can be degraded via the endoplasmic reticulum-associated protein degradation pathway in vivo. Treatment of cultured cells from WT or Delta 18 COX-2 mice with flurbiprofen, which blocks substrate-dependent degradation, attenuates COX-2 degradation, and treatment of normal mice with ibuprofen increases the levels of COX-2 in brain tissue. Thus, substrate turnover-dependent COX-2 degradation appears to contribute to COX-2 degradation in vivo. Curiously, WT and Delta 18 COX-2 protein levels are similar in kidneys and spleens from WT and Delta 18 COX-2 mice. There must be compensatory mechanisms to maintain constant COX-2 levels in these tissues.