Publications

BACKGROUND

Although hypothesized to be a hazard of hospitalization, it is unclear whether hospital-acquired anemia (HAA) is associated with increased adverse outcomes following discharge.

OBJECTIVE

To examine the incidence, predictors, and postdischarge outcomes associated with HAA.

DESIGN

Observational cohort study using electronic health record data.

SUBJECTS

Consecutive medicine discharges between November 1, 2009 and October 30, 2010 from 6 Texas hospitals, including safety-net, teaching, and nonteaching sites. Patients with anemia on admission or missing hematocrit values at admission or discharge were excluded.

MEASURES

HAA was defined using the last hematocrit value prior to discharge and categorized by severity. The primary outcome was a composite of 30-day mortality and nonelective readmission.

RESULTS

Among 11,309 patients, one-third developed HAA (21.6% with mild HAA; 10.1% with moderate HAA; and 1.4% with severe HAA). The 2 strongest potentially modifiable predictors of developing moderate or severe HAA were length of stay (adjusted odds ratio [OR], 1.26 per day; 95% confidence interval [CI], 1.23-1.29) and receipt of a major procedure (adjusted OR, 5.09; 95% CI, 3.79-6.82). Patients without HAA had a 9.7% incidence for the composite outcome versus 16.4% for those with severe HAA. Severe HAA was independently associated with a 39% increase in the odds for 30-day readmission or death (95% CI, 1.09-1.78). Most patients with severe HAA (85%) underwent a major procedure, had a discharge diagnosis of hemorrhage, and/or a discharge diagnosis of hemorrhagic disorder.

CONCLUSIONS

Severe HAA is associated with increased odds for 30-day mortality and readmission after discharge; however, it is uncertain whether severe HAA is preventable. Journal of Hospital Medicine 2017;12:317-322.

PURPOSE

The aim of this study was to determine whether gadoxetate-enhanced magnetic resonance imaging (MRI) improves lesion characterization in patients at risk for hepatocellular carcinoma compared with computed tomography (CT).

MATERIALS AND METHODS

Forty-nine patients with indeterminate lesions found at contrast-enhanced CT were prospectively enrolled and imaged using gadoxetate-enhanced hepatobiliary phase (HBP) MRI within 30 days of their initial CT. Three readers graded each lesion at CT and MRI using the Liver Imaging Reporting and Data System (LI-RADS) v2014 major criteria and HBP characterization as an ancillary feature. Patients were followed for an average of 1.8 years to document growth or stability of each lesion.

RESULTS

The Liver Imaging Reporting and Data System categorization changed for 71% (52/73) of lesions based on HBP MRI compared with CT, with 30% (22/73) of lesions upgraded and 41% (30/73) of lesions downgraded. There was almost perfect agreement between readers for arterial phase hyperintensity and HBP hypointensity, with lower interreader agreement for washout and capsule appearance. On the basis of composite clinical follow-up, lesions that were subsequently classified as hepatocellular carcinoma were assigned a higher LI-RADS category on HBP MRI when compared with CT.

CONCLUSIONS

For patients with indeterminate lesions seen on contrast-enhanced CT, HBP MRI using gadoxetate improves lesion characterization when using LI-RADS v2014 criteria.

Context

Most cases of autosomal recessive hypoparathyroidism (HYPO) are caused by loss-of-function mutations in GCM2 or PTH.

Objective

The objective of this study was to identify the underlying genetic basis for isolated HYPO in a kindred in which 3 of 10 siblings were affected.

Subjects

We studied the parents and the three adult affected subjects, each of whom was diagnosed with HYPO in the first decade of life.

Methods

We collected clinical and biochemical data and performed whole exome sequencing analysis on DNA from the three affected subjects after negative genetic testing for known causes of HYPO.

Results

Whole exome sequencing followed by Sanger sequencing revealed that all three affected subjects were compound heterozygous for two previously reported mutations, c.967_979delCTGTCCCCTCCGC:p.(L323SfsX51) and c.995+(3_5)delGAGinsTAT, in AIRE, which encodes the autoimmune regulator protein that is defective in autoimmune polyglandular syndrome type 1 (APS-1). Each parent carries one mutation, and all of the children of the patients are either heterozygous for one mutation or wild type. The affected sister developed premature ovarian failure, but the two affected brothers have no other features of APS-1 despite elevated serum levels of anti-interferon-α antibodies.

Conclusions

Our findings indicate that biallelic mutations in AIRE can cause isolated HYPO as well as syndromic APS-1. The presence of antibodies to interferon-α provides a highly sensitive indicator for loss of AIRE function and represents a useful marker for isolated HYPO due to AIRE mutations.