Publications

High resolution CT (HRCT) scanning has contributed significantly to the evaluation of patients with interstitial lung disease and is particularly useful in the diagnosis of idiopathic pulmonary fibrosis (IPF). The characteristic radiographic features of the idiopathic interstitial pneumonias on HRCT scans have been increasingly analysed and are now fairly well described. Based on current data, HRCT scanning can provide a confident, highly specific diagnosis of IPF in many patients with diffuse lung disease. This article reviews an organised approach to HRCT scanning and identifies the features that allow an accurate diagnosis of the idiopathic interstitial pneumonias to be made. The role of surgical lung biopsy is discussed in the diagnosis of cases when a definite HRCT diagnosis cannot be made.

BACKGROUND

Certain hospitals play a central role in ensuring Medicaid-insured patients' access to care. Their quality of care is critical to evaluate.

OBJECTIVE

To determine whether hospitals for which Medicaid patients represent a high percentage of total discharges provide a different quality of care than other hospitals.

RESEARCH DESIGN

Cross-sectional analysis.

SUBJECTS

Acute care hospitals participating in the first Hospital Compare public report (released November 2004) and the 2004 American Hospital Association hospital survey.

MEASURES

Hospitals serving 1 standard deviation above the national mean percentage of Medicaid patients were designated high Medicaid hospitals. Performance was assessed using percent compliance with 10 processes of care for 3 conditions: myocardial infarction, congestive heart failure, and community-acquired pneumonia.

RESULTS

Among the 2874 nonteaching hospitals, high Medicaid hospitals had lower adherence (P < 0.01) than other nonteaching hospitals on all 10 indicators. Of particular clinical importance, high Medicaid nonteaching hospitals less frequently prescribed beta-blockers (83% vs. 90%%, P < 0.0001) and aspirin at discharge in myocardial infarction (85% vs. 91%%, P < 0.0001), and administered antibiotics on time in CAP (68% vs. 75%, P < 0.0001). Among teaching institutions, there were few differences between high Medicaid and other hospitals.

CONCLUSIONS

Among hospitals publicly reporting on the Hospital Compare Web site, nonteaching hospitals treating a high percentage of Medicaid patients had lower adherence to quality indicators than other nonteaching hospitals on 10 indicators. Further research is needed to determine what factors contribute to differences in reported quality.

BACKGROUND

Idiopathic pulmonary fibrosis (IPF) is characterized by the insidious onset of dyspnea or cough. However, a subset of patients has a short duration of symptoms with rapid progression to end-stage disease. In this study, we evaluated clinical and molecular features of "rapid" and "slow" progressors with IPF.

METHODS AND FINDINGS

26 patients with <6 months of symptoms before first presentation [rapid progressors] and 88 patients with >24 months of symptoms [slow progressors] were studied. Survival was analyzed by the Kaplan-Meyer method and proportional hazard's model. Lung microarrays and tissue proteins were measured in a subset of patients. No differences were found in age, physiologic impairment and bronchoalveolar lavage (BAL) cellular profile. There were more males (OR = 6.5; CI:1.4-29.5; p = 0.006) and smokers (OR = 3.04; CI:1.1-8.3; p = 0.04) in the rapid progressors group. Survival from the beginning of symptoms was significantly reduced in rapid progressors (HR = 9.0; CI:4.48-18.3; p<0.0001) and there was a tendency for decreased survival from the time of diagnosis (HR = 1.5; CI:0.81-2.87; p = 0.18). We identified 437 differentially expressed genes. Lungs of rapid progressors overexpressed genes involved in morphogenesis, oxidative stress, migration/proliferation, and genes from fibroblasts/smooth muscle cells. Upregulation of two of these genes, adenosine-2B receptor and prominin-1/CD133, was validated by immunohistochemistry and were expressed by alveolar epithelial cells. BAL from rapid progressors showed a >2-fold increase of active matrix metalloproteinase-9, and induced a higher fibroblast migration compared with slow progressors and controls [238+/-98% versus 123+/-29% (p<0.05) and 30+/-17% (p<0.01)].

CONCLUSIONS/SIGNIFICANCE

A subgroup of IPF patients, predominantly smoking males, display an accelerated clinical course and have a gene expression pattern that is different from those with slower progression and longer survival. These findings highlight the variability in the progression of IPF, and may explain, in part, the difficulty in obtaining significant and reproducible results in studies of therapeutic interventions in patients with IPF.

We analyzed the clinical factors associated with late cytomegalovirus (CMV) reactivation in a group of 269 consecutive recipients of allogeneic stem cell transplant (SCT) for hematological malignancies. Eighty-four subjects (31%) experienced late CMV reactivation, including 64 with prior early reactivation and 20 with isolated late reactivation. Multivariate analyses were conducted in patients with early CMV reactivation to identify factors associated with late recurrence. Important risk factors included lymphoid diagnosis, occurrence of graft-versus-host disease (GVHD), greater number of episodes of early reactivation, persistent day 100 lymphopenia and the use of a CMV-seronegative donor graft. We combined these risk factors in a predictive model to identify those at relatively low, intermediate and high risk. The low-risk group (15% cumulative incidence, CI) encompassed patients without early CMV reactivation, and subjects transplanted for a myeloid malignancy from a matched-related (MR) donor without subsequent acute GVHD. The high-risk patients (73% CI) met all of the following criteria: (1) received an MR graft but developed GVHD, or received a non-MR graft irrespective of GVHD; (2) had more than two episodes of early reactivation; and (3) received a CMV-seronegative graft and/or remained persistently lymphopenic at day 100 after SCT. The remaining patients had an intermediate incidence of 32%.

After inoculation of Leishmania major, a rapid production of IL-4 by LACK-specific CD4+ T cells has been shown to drive Th2 cell development in susceptible mice i.e. BALB/c and C57BL/6 mice rendered susceptible by neutralization of IFN-gamma at the onset of infection. Here, we showed that peptide AA 156-173 induced an early IL-4 mRNA expression not only in BALB/c mice but also in resistant B10.D2 mice when IFN-gamma is neutralized. Epitope mapping of LACK protein demonstrated that peptide containing AA 293-305 induced early IL-4 mRNA transcripts in susceptible H-2b mice i.e. BALB/b and resistant C57BL/6 mice when IFN-gamma is neutralized. Stringently, the early IL-4 response to the H-2d (AA 156-173) or the H-2b (AA 293-305) epitopes occurred in V beta 4 V alpha 8 CD4+ T cells from either H-2d or H-2b susceptible mice, respectively.