Publications by authors named "Joe C Huang"

5 Publications

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Frailty in Chronic Obstructive Pulmonary Disease and Risk of Exacerbations and Hospitalizations.

Int J Chron Obstruct Pulmon Dis 2020 11;15:1967-1976. Epub 2020 Aug 11.

Department of Health Services Research and Development, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.

Background: Frailty is a complex clinical syndrome associated with vulnerability to adverse health outcomes. While frailty is thought to be common in chronic obstructive pulmonary disease (COPD), the relationship between frailty and COPD-related outcomes such as risk of acute exacerbations of COPD (AE-COPD) and hospitalizations is unclear.

Purpose: To examine the association between physical frailty and risk of acute exacerbations, hospitalizations, and mortality in patients with COPD.

Methods: A longitudinal analysis of data from a cohort of 280 participants was performed. Baseline frailty measures included exhaustion, weakness, low activity, slowness, and undernutrition. Outcome measures included AE-COPD, hospitalizations, and mortality over 2 years. Negative binomial regression and Cox proportional hazard modeling were used.

Results: Sixty-two percent of the study population met criteria for pre-frail and 23% were frail. In adjusted analyses, the frailty syndrome was not associated with COPD exacerbations. However, among the individual components of the frailty syndrome, weakness measured by handgrip strength was associated with increased risk of COPD exacerbations (IRR 1.46, 95% CI 1.09-1.97). The frailty phenotype was not associated with all-cause hospitalizations but was associated with increased risk of non-COPD-related hospitalizations.

Conclusion: This longitudinal cohort study shows that a high proportion of patients with COPD are pre-frail or frail. The frailty phenotype was associated with an increased risk of non-COPD hospitalizations but not with all-cause hospitalizations or COPD exacerbations. Among the individual frailty components, low handgrip strength was associated with increased risk of COPD exacerbations over a 2-year period. Measuring handgrip strength may identify COPD patients who could benefit from programs to reduce COPD exacerbations.
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http://dx.doi.org/10.2147/COPD.S245505DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7429100PMC
June 2021

Evaluation of Treatment Candidacy in Older Adults With Cancer.

Int J Radiat Oncol Biol Phys 2017 07;98(4):891-892

Department of Radiation Oncology, University of Washington School of Medicine, Seattle, Washington.

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http://dx.doi.org/10.1016/j.ijrobp.2016.11.024DOI Listing
July 2017

The clinical diagnosis of heparin-induced thrombocytopenia in patients receiving continuous renal replacement therapy.

J Thromb Thrombolysis 2009 May 17;27(4):406-12. Epub 2008 May 17.

Department of Medicine, Division of Hematology & Oncology, University of Vermont College of Medicine, Burlington, VT 05401, USA.

Background: Thrombocytopenia is common in critically ill patients who receive continuous renal replacement therapy. Often, these patients receive heparin therapy and the diagnosis of heparin induced thrombocytopenia (HIT) is considered as a potential etiology. No data regarding the clinical diagnosis of HIT is available for patients receiving continuous renal replacement therapy.

Patients And Methods: We performed a retrospective study of 29 consecutive patients who received CRRT in a medical-surgical intensive care unit (ICU) and determined trends in platelet counts following CRRT and the frequency of meeting platelet based clinical criteria for consideration of a HIT diagnosis.

Results: For patient exposures to CRRT concurrent with heparin, 54% met at least one clinical threshold for consideration of the diagnosis of HIT. In 31% of exposures, both a platelet count <100,000/mm3 and a >50% decrease from baseline were seen. In contrast, the majority (73-85%) of patients receiving CRRT had a low pre-test probability of HIT using the "4T's" scoring system. Mean platelet counts while on CRRT concurrent with heparin were significantly lower than when patients received heparin alone (P < 0.02).

Conclusions: The clinical diagnosis of HIT in ICU patients initiating CRRT is challenging given the decrease in platelet counts seen following CRRT initiation in the majority of patients. A prospective study in this population is needed to optimize patient outcomes.
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http://dx.doi.org/10.1007/s11239-008-0228-8DOI Listing
May 2009

Tamoxifen and aromatase inhibitors differentially affect vascular endothelial growth factor and endostatin levels in women with breast cancer.

Clin Cancer Res 2008 May;14(10):3070-6

Department of Medicine, University of Vermont, Burlington, Vermont, USA.

Purpose: Circulating and cellular proangiogenic and antiangiogenic proteins such as vascular endothelial growth factor (VEGF) and endostatin contribute to the local angiogenic balance. We explored the effects of tamoxifen and aromatase inhibitors on concentrations of VEGF and endostatin in plasma, serum, and platelet releasate (induced by platelet activation).

Experimental Design: VEGF and endostatin concentrations were measured with a quantitative immunoassay before and after 1 to 5 weeks of treatment in 30 women with breast cancer treated with either tamoxifen (n = 14) or aromatase inhibitors (n = 16). Platelet activation was induced by a thrombin receptor agonist.

Results: Tamoxifen therapy resulted in an increase in platelet releasate concentrations of VEGF (P = 0.01) but no change in plasma VEGF. In contrast, aromatase inhibitor therapy did not affect serum, plasma, or platelet releasate VEGF. In univariate analysis, aspirin use attenuated the tamoxifen-associated increase in VEGF in the platelet releasate and decreased serum levels of VEGF (P = 0.03). Aromatase inhibitor therapy resulted in a decrease in serum endostatin concentrations (P = 0.04), whereas plasma concentrations of endostatin tended to be higher during treatment with aromatase inhibitors (P = 0.06). Tamoxifen therapy resulted in no change in serum or plasma endostatin concentrations. Platelet releasate concentrations of endostatin did not change with either treatment. Interindividual variability was noted among both aromatase inhibitor--and tamoxifen-treated patients.

Conclusions: Tamoxifen and aromatase inhibitor therapy affect VEGF and endostatin levels and likely contribute to the angiogenic balance in breast cancer patients. Aspirin decreased the proangiogenic effects of tamoxifen, suggesting that antiplatelet and/or antiangiogenic therapy might improve the effectiveness of tamoxifen in women with breast cancer.
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http://dx.doi.org/10.1158/1078-0432.CCR-07-4640DOI Listing
May 2008

Differences between smokers and nonsmokers in regional gray matter volumes and densities.

Biol Psychiatry 2004 Jan;55(1):77-84

Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, California 90095, USA.

Background: Magnetic resonance imaging (MRI) studies have demonstrated large-scale brain abnormalities in cigarette smokers, such as ventricular enlargement and atrophy. Converging lines of evidence point to functional differences between smokers and nonsmokers in specific brain regions, namely the lateral prefrontal cortex (PFC), anterior cingulate cortex (ACC), ventral striatum, and thalamus. Using MRI, we examined these regions for differences in gray matter between smokers and nonsmokers.

Methods: Thirty-six otherwise healthy adults (19 smokers and 17 nonsmoking control subjects) underwent three-dimensional Fourier-transform spoiled-gradient-recalled acquisition MRI of the brain. Both hand-drawn regions of interest and the computer program voxel-based morphometry were used to assess group differences in regional gray matter volumes and densities, respectively.

Results: Smokers had smaller gray matter volumes and lower gray matter densities than nonsmokers in the PFC bilaterally, along with smaller volumes in the left dorsal ACC and lower gray matter densities in the right cerebellum. Smokers also had negative associations between pack-year smoking history and PFC gray matter densities.

Conclusions: Smokers and nonsmokers differed in regional gray matter in brain areas previously linked with nicotine dependence. These findings might reflect effects of chronic smoking, predisposing traits that lead to smoking, or some combination of these factors.
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http://dx.doi.org/10.1016/s0006-3223(03)00610-3DOI Listing
January 2004