Reduction in Unnecessary Red Blood Cell Folate Testing by Restricting Computerized Physician Order Entry in the Electronic Health Record.

PURPOSE: The red blood cell (RBC) folate test is a laboratory test with limited clinical utility. Previous attempts to reduce physician ordering of unnecessary laboratory tests, including folate levels, have resulted in only modest success. The objective of this study was to assess the effectiveness and impacts of restricting RBC folate ordering in the electronic health record (EHR). METHODS: This was a retrospective observational study that took place from January 2010 to December 2016 at a large academic healthcare network in Toronto, Canada. All inpatients and outpatients who underwent at least 1 RBC folate or vitamin B12 test during the study period were included. Ordering an RBC folate test was restricted to clinicians in gastroenterology and hematology. The option to order the test was removed from other physicians' computerized order entry screens in the EHR in June 2013. RESULTS: RBC folate testing decreased by 94.4% during the study, from a mean of 493.0 ± 48.0 tests per month prior to intervention to 27.6 ± 10.3 tests per month after intervention (P < .001). CONCLUSIONS: Restricting RBC folate ordering in the EHR resulted in a large and sustained reduction in RBC folate testing. Significant cost savings, estimated at more than a quarter of a million Canadian dollars over 3 years, were achieved. There was no significant clinical impact of the intervention on the diagnosis of folate deficiency.

Folate testing in hospital inpatients.

INTRODUCTION: Since Canada began fortifying grain products with folic acid in 1998, the rate of folate deficiency in outpatients has decreased substantially. Limited data exist on the prevalence of folate deficiency in Canadian hospital inpatients. METHODS: The electronic patient record at a large urban academic institution was reviewed for all red blood cell folate and vitamin B12 level tests performed on inpatients between January 1 and December 31, 2010. Chart reviews were performed on patients found to have folate deficiency to determine the indication for folate testing and the etiology of deficiency. RESULTS: There were 2563 red blood cell folate and 3154 vitamin B12 level tests performed in 2010. Of these, only 4 (0.16%) red blood cell folate levels were in the deficient range (<254 nmol/L), compared with 98 (3.1%) and 426 (13.5%) vitamin B12 levels that were in the deficient (<138 pmol/L) and intermediate (138-221 pmol/L) range, respectively. Of the 4 patients with folate deficiency, the etiology appeared to be alcohol abuse in one, a malabsorption syndrome in the second, decreased oral intake due to schizophrenia in the third, with the final low folate level appearing to be spurious. At a cost of $12.54 per test, $32,140 could be saved each year at this institution if red blood cell folate testing on inpatients was restricted. CONCLUSION: Folate deficiency in inpatients is nearly nonexistent, while an appreciable number of patients have low/intermediate vitamin B12 levels. Significant savings could be achieved by eliminating folate testing on inpatients.

An atypical cause of atypical chest pain.

The present report describes a case involving a 57-year-old HIV-positive man who presented with acute retrosternal chest pain accompanied by 24 h of fever. Septic arthritis of the manubriosternal joint was diagnosed based on magnetic resonance imaging findings in addition to Staphylococcus aureus bacteremia. To the authors' knowledge, the present case is only the 12th reported case of manubriosternal septic arthritis, and the first in an HIV-positive patient. Early diagnosis and treatment can circumvent the need for surgical intervention. Based on the present case report and review of the literature, the authors summarize the epidemiology, appropriate imaging and suggestions for antibiotic therapy for this rare presentation.

Le présent rapport décrit le cas d'un homme de 57 ans atteint du VIH qui a consulté en raison d'une douleur thoracique rétrosternale aiguë accompagnée de fièvre depuis 24 heures. Les résultats de l'imagerie par résonance magnétique ont permis de diagnostiquer une arthrite septique de l'articulation manubrio-sternale, ainsi qu'une bactériémie à Staphylococcus aureus. En autant que le sache les auteurs, il s'agit du 12e cas déclaré d'arthrite septique manubrio-sternale seulement, et le premier auprès d'un patient positif au VIH. Grâce à un diagnostic et un traitement rapides, on peut éviter l'intervention chirurgicale. Compte tenu du présent rapport de cas et de l'analyse bibliographique, les auteurs résument l'épidémiologie, l'imagerie pertinente et les suggestions d'antibiothérapie de cette présentation rare.

Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of Coxsackievirus B3-induced myocarditis and influences type I interferon production.

BACKGROUND: Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown. METHODS AND RESULTS: We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-type mice after exposure to Coxsackievirus B3 (CVB3). MyD88(-/-) mice showed a dramatic higher survival rate (86%) in contrast to the low survival (35%) in the MyD88(+/+) mice after CVB3 infection (P<0.0001). Pathological examination showed a significant decrease of cardiac and pancreatic inflammation in the MyD88(-/-) mice. Viral concentrations in the hearts were significantly decreased in the MyD88(-/-) mice. Cardiac mRNA levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and IL-18 were significantly decreased in the MyD88(-/-) mice. Similarly, serum levels of T-helper 1 cytokines were significantly decreased in the MyD88(-/-) mice. In contrast, cardiac protein levels of the activated interferon regulatory factor (IRF)-3 and IFN-beta were significantly increased in the MyD88(-/-) mice but not other usual upstream signals to IRF-3. The cardiac expression of coxsackie-adenoviral receptor and p56(lck) were also significantly decreased. CONCLUSIONS: MyD88 appears to be a key contributor to cardiac inflammation, mediating cytokine production and T-helper-1/2 cytokine balance, increasing coxsackie-adenoviral receptor and p56(lck) expression and viral titers after CVB3 exposure. Absence of MyD88 confers host protection possibly through novel direct activation of IRF-3 and IFN-beta.