Vitamin D level and risk of community-acquired pneumonia and sepsis.

Previous research has reported reduced serum 25-hydroxyvitamin D (25(OH)D) levels is associated with acute infectious illness. The relationship between vitamin D status, measured prior to acute infectious illness, with risk of community-acquired pneumonia (CAP) and sepsis has not been examined. Community-living individuals hospitalized with CAP or sepsis were age-, sex-, race-, and season-matched with controls. ICD-9 codes identified CAP and sepsis; chest radiograph confirmed CAP. Serum 25(OH)D levels were measured up to 15 months prior to hospitalization. Regression models adjusted for diabetes, renal disease, and peripheral vascular disease evaluated the association of 25(OH)D levels with CAP or sepsis risk. A total of 132 CAP patients and controls were 60 ± 17 years, 71% female, and 86% Caucasian. The 25(OH)D levels <37 nmol/L (adjusted odds ratio (OR) 2.57, 95% CI 1.08-6.08) were strongly associated with increased odds of CAP hospitalization. A total of 422 sepsis patients and controls were 65 ± 14 years, 59% female, and 91% Caucasian. The 25(OH)D levels <37 nmol/L (adjusted OR 1.75, 95% CI 1.11-2.77) were associated with increased odds of sepsis hospitalization. Vitamin D status was inversely associated with risk of CAP and sepsis hospitalization in a community-living adult population. Further clinical trials are needed to evaluate whether vitamin D supplementation can reduce risk of infections, including CAP and sepsis.

Prospective comparison of curbside versus formal consultations.

BACKGROUND: Curbside consultations are commonly requested during the care of hospitalized patients, but physicians perceive that the recommendations provided may be based on inaccurate or incomplete information. OBJECTIVE: To compare the accuracy and completeness of the information received from providers requesting a curbside consultation of hospitalists with that obtained in a formal consultation on the same patients, and to examine whether the recommendations offered in the 2 consultations differed. DESIGN: Prospective cohort. SETTING: University-affiliated, urban safety net hospital. MAIN OUTCOME MEASURES: Proportion of curbside consultations with inaccurate or incomplete information; frequency with which recommendations in the formal consultation differed from those in the curbside consultation. RESULTS: Curbside consultations were requested for 50 patients, 47 of which were also evaluated in a formal consultation performed on the same day by a hospitalist other than the one performing the curbside consultation. Based on information collected in the formal consultation, information was either inaccurate or incomplete in 24/47 (51%) of the curbside consultations. Management advice after formal consultation differed from that given in the curbside consultation for 28/47 patients (60%). When inaccurate or incomplete information was received, the advice provided in the formal versus the curbside consultation differed in 22/24 patients (92%, P < 0.0001). CONCLUSIONS: Information presented during inpatient curbside consultations of hospitalists is often inaccurate or incomplete, and this often results in inaccurate management advice.

Transfer of the cholera toxin A1 polypeptide from the endoplasmic reticulum to the cytosol is a rapid process facilitated by the endoplasmic reticulum-associated degradation pathway.

The active pool of internalized cholera toxin (CT) moves from the endosomes to the Golgi apparatus en route to the endoplasmic reticulum (ER). The catalytic CTA1 polypeptide is then translocated from the ER to the cytosol, possibly through the action of the ER-associated degradation (ERAD) pathway. Translocation was previously measured indirectly through the downstream effects of CT action. We have developed a direct biochemical assay for CTA1 translocation that is independent of toxin activity. Our assay is based upon the farnesylation of a CVIM motif-tagged CTA1 polypeptide (CTA1-CVIM) after it enters the cytosol. When expressed from a eukaryotic vector in transfected CHO cells, CTA1-CVIM was targeted to the ER, but was not secreted. Instead, it was translocated into the cytosol and degraded in a proteosome-dependent manner. Translocation occurred rapidly and was monitored by the appearance of farnesylated CTA1-CVIM in the detergent phase of cell extracts generated with Triton X-114. Detergent-phase partitioning of CTA1-CVIM resulted from the cytoplasmic addition of a 15-carbon fatty acid farnesyl moiety to the cysteine residue of the CVIM motif. Our use of the CTA1-CVIM translocation assay provided supporting evidence for the ERAD model of toxin translocation and generated new information on the timing of CTA1 translocation.