BackgroundRace and ethnicity, typically defined as how individuals self-identify, are complex social constructs. Self-identified racial/ethnic minorities are less likely to receive preventive care and more likely to report healthcare discrimination than self-identified non-Hispanic whites. However, beyond self-identification, these outcomes may vary depending on whether racial/ethnic minorities are perceived by others as being minority or white; this perception is referred to as socially-assigned race.PurposeTo examine the associations between socially-assigned race and healthcare discrimination and receipt of selected preventive services.MethodsCross-sectional analysis of the 2004 Behavioral Risk Factor Surveillance System “Reactions to Race” module. Respondents from seven states and the District of Columbia were categorized into 3 groups, defined by a composite of self-identified race/socially-assigned race: Minority/Minority (M/M, n = 6,837), Minority/White (M/W, n = 929), and White/White (W/W, n = 25,913). Respondents were 18 years or older, with 61.7% under age 60; 51.8% of respondents were female. Measures included reported healthcare discrimination and receipt of vaccinations and cancer screenings.ResultsRacial/ethnic minorities who reported being socially-assigned as minority (M/M) were more likely to report healthcare discrimination compared with those who reported being socially-assigned as white (M/W) (8.9% vs. 5.0%, p = 0.002). Those reporting being socially-assigned as white (M/W and W/W) had similar rates for past-year influenza (73.1% vs. 74.3%) and pneumococcal (69.3% vs. 58.6%) vaccinations; however, rates were significantly lower among M/M respondents (56.2% and 47.6%, respectively, p-values<0.05). There were no significant differences between the M/M and M/W groups in the receipt of cancer screenings.ConclusionsRacial/ethnic minorities who reported being socially-assigned as white are more likely to receive preventive vaccinations and less likely to report healthcare discrimination compared with those who are socially-assigned as minority. Socially-assigned race/ethnicity is emerging as an important area for further research in understanding how race/ethnicity influences health outcomes.

Late human gestation is associated with an increase in the concentration of cortisol (F) in the fetal circulation and amniotic fluid. It had been assumed that most of the F measured in the amniotic fluid came from the fetal adrenal gland. However, local production of F can also occur in human intrauterine tissues from inactive cortisone under the influence of the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1. Recent studies have shown that 11beta-HSD 1 activity is up-regulated by prostaglandins (PG) E2 and F2alpha, hormones that are produced in the fetal membranes (FM) at term. In the present study, we hypothesized that 11beta-HSD 1 expression would increase in FM during pregnancy and at labor, creating the potential for local increase in F production at term. We examined 11beta-HSD 1 expression in placenta and FM obtained during normal pregnancy from nonlaboring women [26-28 wk (n = 3); 29-30 wk (n = 3); 32-33 wk (n = 3); 35-36 wk (n = 3)] and from uncomplicated term pregnancies after elective cesarean section (n = 6). 11beta-HSD 1 expression was also examined in amnion and chorionic tissues in relation to term labor (n = 12). Immunohistochemistry and Western blot analysis were used to examine 11beta-HSD 1 localization and expression. 11beta-HSD 1 activity was also measured in microsomal fractions prepared from whole fetal membranes. At term, immunoreactive 11beta-HSD 1 expression was localized predominantly to the chorion trophoblast cells, attached decidua, and amnion epithelial cells. 11beta-HSD 1 expression in FM increased with gestational age and reflected increased enzyme reductase activity. No change in 11beta-HSD 1 expression was found in placental tissue from the same patients. There was a significant increase in 11beta-HSD 1 expression in amnion but not in chorion with the onset of labor. We suggest that increases in 11beta-HSD 1 expression/activity by intrauterine membranes during late gestation may result in increased potential for a local increase in F production and that FM should be considered as an extraadrenal source of F during late gestation. This local F production may be involved in different pathways contributing to the regulation of parturition.

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Spontaneous bacterial peritonitis (SBP) has a high mortality rate; early antimicrobial therapy is essential for improving patient outcomes. Given that cirrhotic patients are often coagulopathic, the perceived risk of bleeding may prevent providers from performing a paracentesis and ruling out this potentially deadly disease.We examine the pathophysiology and risk factors for SBP, and current guidelines for its diagnosis and treatment. We then review the time-sensitive nature of performing a paracentesis, and the current controversies and contraindications for performing this procedure in patients at risk for SBP.Cirrhotic patients with ascites and clinical suspicion for SBP—abdominal pain or tenderness, fever or altered mental status—should have a diagnostic paracentesis. Although most patients with cirrhosis and liver dysfunction will have prolonged prothrombin time, paracentesis is not contraindicated. Limited data support platelet administration prior to paracentesis if <40,000-50,000/μL. Timely antimicrobial therapy includes a third-generation cephalosporin for community-acquired infection; nosocomial infections should be treated empirically with a carbapenem or with piperacillin-tazobactam, or based on local susceptibility testing. Patients with gastrointestinal (GI) hemorrhage should receive ceftriaxone prophylactically for GI hemorrhage.SBP has a high mortality rate. Early diagnosis and antimicrobial therapy are essential for improving patient outcomes. Cirrhotic patients with ascites with clinical suspicion for SBP, abdominal pain or tenderness, altered mental status or fever should have a diagnostic paracentesis performed prior to admission unless platelets <40,000-50,000/μL.