G M Turino

St. John's University, New York City, New York, United States

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Publications (144)720.48 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Desmosine-CH2, an analog of the elastic tissue degradation biomarker desmosine, can be regarded as a potential internal standard for precise quantification of desmosines by LC-MS/MS. In this study, the chemical synthesis of desmosine-CH2 was completed in 22% overall yield in five steps. The LC-MS/MS analysis of desmosine-CH2 was also achieved.
    Organic & Biomolecular Chemistry 10/2014; · 3.49 Impact Factor
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    ABSTRACT: To the Editor:Most individuals carry two wild-type M alleles of the SERPINA1 gene which encodes α1-antitrypsin. 95% of severe deficiency of α1-antitrypsin is associated with the Z allele (Glu342Lys; denoted PiZZ in the homozygote), and with the retention and polymerisation of α1-antitrypsin within hepatocytes (1). These polymers are contained within periodic acid-Schiff-positive, diastase-resistant inclusions that are associated with neonatal hepatitis, cirrhosis and hepatocellular carcinoma. The concomitant lack of circulating α1-antitrypsin predisposes the Z α1-antitrypsin homozygote to early-onset emphysema. Polymers of α1-antitrypsin form within the lung as a result of local inflammation and exposure to cigarette smoke (2). They have also been identified in the skin of an individual with α1-antitrypsin deficiency and panniculitis (3) and in a renal biopsy from an individual with α1-antitrypsin deficiency and vasculitis (4). It is unknown whether these polymers form locally or are deposited in these tissues from a circulating source, and whether extrahepatic polymers are associated with any disease phenotypes. We have assessed whether polymers of α1-antitrypsin are present within serum, from where they originate, and whether they are associated with clinical features in individuals with PiZZ α1-antitrypsin deficiency. In this investigation we used ELISA with the anti-α1-antitrypsin polymer monoclonal antibody (2C1) (5) to assess.
    European Respiratory Journal 03/2014; · 7.13 Impact Factor
  • J O Cantor, S Ma, G M Turino
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    ABSTRACT: Damage to the lung elastic fiber network is largely responsible for the distention and rupture of alveolar walls in chronic obstructive pulmonary disease (COPD). It has therefore been suggested that blood or urine levels of the unique elastic fiber crosslinks, desmosine and isodesmosine (DID), may serve as a biomarker for the progression of the disease. The prognostic value of DID may be limited, however, by the large degree of variance associated with their measurement in patients with COPD. To overcome this problem, we propose that specific patterns of DID release from damaged elastic fibers, rather than their absolute quantity, may provide a better indication of morphological changes in the lungs of patients with COPD. Using percolation theory to model the elastic fiber network in the lung, it will be shown that the relative amounts of damaged and intact elastic fibers may be reflected at the molecular level by urinary levels of free and peptide-bound DID, respectively. The self-similar nature of percolation networks further suggests that detachment of crosslinks from elastic fibers may be analogous to the rupture of alveolar walls in COPD. Consequently, the ratio of free to bound DID may be a measure of emphysematous changes in this disease.
    Medical Hypotheses 06/2013; · 1.15 Impact Factor
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    ABSTRACT: Chemical synthesis of the deuterium isotope, desmosine-d4, has been achieved. This isotopic compound possesses all four deuterium atoms at the alkanyl carbons of the alkyl amino acid substitution in the desmosine molecule and is stable toward acid hydrolysis, this is required in the measurement of two crosslinking molecules, desmosine and isodesmosine, as biomarkers of elastic tissue degradation. The degradation of elastin occurs in several widely prevalent diseases. The synthesized desmosine-d4 is used as the internal standard to develop an accurate and sensitive isotope-dilution liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis which can serve as a generalized method for an accurate analysis of desmosine and isodesmosine as biomarkers in many types of biological tissues involving elastin degradation.
    Analytical Biochemistry 05/2013; · 2.31 Impact Factor
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    ABSTRACT: Abstract Background: Intravenous alpha-1 antitrypsin protein (AAT) augmentation is a prescribed therapy for severe, genetically determined, alpha-1 antitrypsin deficiency (AATD), a genetic basis for pulmonary emphysema. AAT, a predominant systemic inhibitor of neutrophil elastase thus far has not been shown to decrease elastin degradation in a significant number of patients on this therapy. The objective of this study was to compare levels of biomarkers of elastin degradation in plasma, bronchoalveolar lavage (BALF) fluid and urine before and after beginning AAT augmentation therapy in patients with AATD. Methods: Desmosine and isodesmosine (DI), which occur only in elastin, are amino acid cross-links in mature elastin. Levels of DI in body fluids measure degradation of elastin and can be measured more specifically by mass spectrometry. This method was used to measure DI levels in plasma, bronchoalveolar lavage fluid and urine in cohorts of severe AATD patients on augmentation, not on augmentation and before and after the initiation of augmentation therapy. Results: Statistically significant reductions in plasma DI and in BALF DI were demonstrated in AATD patients receiving intravenous (IV) augmentation therapy as compared with those not receiving it. Administration by aerosol also produced statistically significant reductions in levels of DI in BALF. Conclusions: Results indicate that the currently prescribed doses of AAT augmentation inhibit neutrophil elastase adequately to reduce elastin degradation, both systemically and in the lung per se. The currently prescribed doses did not reduce elastin degradation to control levels, which may be possible with higher doses.
    COPD Journal of Chronic Obstructive Pulmonary Disease 04/2013; · 2.73 Impact Factor
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    Robert A. Sandhaus, Gerard Turino
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    ABSTRACT: Elastases of both the neutrophil and macrophage have been implicated in lung disease initiation and progression. Although it is unlikely that these proteases evolved for the purpose of injuring lung tissue, the elastin-rich connective tissue framework of the lungs appears to be particularly susceptible to the action of elastolytic proteases. Assuming that neutrophil elastase most likely plays a role in the migration of neutrophils toward a site of inflammation and degradation of proteins from invading organisms or other products of the inflammatory response, it is the role of inhibitors of this protease to protect normal tissues from its effects. In alpha-1 antitrypsin deficiency we find an experiment of nature that disrupts this protease-anti-protease balance, resulting in an increased risk of destructive lung disease.
    COPD Journal of Chronic Obstructive Pulmonary Disease 03/2013; 10(S1). · 2.62 Impact Factor
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    ABSTRACT: Alpha-1 antitrypsin (AAT) deficiency and tobacco smoking are confirmed risk factors for Chronic Obstructive Pulmonary Disease. We hypothesized that variable DNA methylation would be associated with smoking and inflammation, as reflected by the level of C-Reactive Protein (CRP) in AAT-deficient subjects. Methylation levels of 1,411 autosomal CpG sites from the Illumina GoldenGate Methylation Cancer Panel I were analyzed in 316 subjects. Associations of five smoking behaviors and CRP levels with individual CpG sites and average methylation levels were assessed using non-parametric testing, linear regression and linear mixed effect models, with and without adjustment for age and gender. Univariate linear regression analysis revealed that methylation levels of 16 CpG sites significantly associated with ever-smoking status. A CpG site in the TGFBI gene was the only site associated with ever-smoking after adjustment for age and gender. No highly significant associations existed between age at smoking initiation, pack-years smoked, duration of smoking, and time since quitting smoking as predictors of individual CpG site methylation levels. However, ever-smoking and younger age at smoking initiation associated with lower methylation level averaged across all sites. DNA methylation at CpG sites in the RUNX3, JAK3 and KRT1 genes associated with CRP levels. The most significantly associated CpG sites with gender and age mapped to the CASP6 and FZD9 genes, respectively. In summary, this study identified multiple potential candidate CpG sites associated with ever-smoking and CRP level in AAT-deficient subjects. Phenotypic variability in Mendelian diseases may be due to epigenetic factors.
    Epigenetics: official journal of the DNA Methylation Society 07/2012; 7(7):720-8. · 5.11 Impact Factor
  • COPD Journal of Chronic Obstructive Pulmonary Disease 06/2012; 9(4):435-8. · 2.73 Impact Factor
  • American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012
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    ABSTRACT: The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2).We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. FEV1 percent of predicted and FEV1/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator FEV1 percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator FEV1 percent of predicted and pre-bronchodilator FEV1/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact.
    Respiratory research 02/2012; 13:16. · 3.38 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a major health problem worldwide and is now the third leading cause of death in the United States. There is a lack of therapies that can stop progression of the disease and improve survival. New drug discovery can be aided by the development of biomarkers, which can act as indicators of severity in the course of the disease and responses to therapy. This perspective brings together the laboratory and clinical evidence, which suggest that elastin degradation products can fulfill the need for such a biomarker. Elastin is a recognized target for injury in COPD. The amino acids desmosine and isodesmosine exist only in matrix elastin; can be measured specifically and sensitively in plasma, urine, and sputum; and indicate changes in the systemic balance between elastase activity and elastase inhibition brought on by the systemic inflammatory state. The biomarker levels in sputum reflect the state of elastin degradation in the lung specifically. Clinical data accumulated over several decades indicate correlations of desmosine and isodesmosine levels with COPD of varying severity and responses to therapy.
    American Journal of Respiratory and Critical Care Medicine 07/2011; 184(6):637-41. · 11.04 Impact Factor
  • Shuren Ma, Gerard M Turino, Yong Y Lin
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    ABSTRACT: The aim of this study is to develop a standardized LC-MS/MS method for accurate measurement of desmosine (DES) and isodesmosine (IDS) in all body fluids as biomarkers for in vivo degradation of matrix tissue elastin in man and animals. A reproducible three-step analytical procedure: (1) sample hydrolysis in 6N HCl, (2) SPE by a CF1 cartridge with addition of acetylated pyridinoline as internal standard (IS), and (3) LC/MSMS analysis by SRM monitoring of transition ions; DES or IDS (m/z 526-481+397) and IS (m/z 471-128) was developed. The method achieves accurate measurements of DES/IDS in accessible body fluids (i.e. urine, plasma, and sputum). LOQ of DES/IDS in body fluids is 0.1 ng/ml. The % recoveries and reproducibility from urine, plasma, and sputum samples are above 99 ± 8% (n = 3), 94 ± 9% (n = 3) and 87 ± 11% (n = 3), with imprecision 8%, 9% and 10%, respectively. The proposed method was applied to measure DES/IDS in body fluids of patients with chronic obstructive pulmonary disease (COPD) and healthy controls. Total DES/IDS in sputum and plasma is increased over normal controls along with the free DES/IDS in urine in patients. DES/IDS can be used to study the course of COPD and the response to therapy. This practical and reliable LC-MS/MS method is proposed as a standardized method to measure DES and IDS in body fluids. This method can have wide application for investigating diseases which involve elastic tissue degradation.
    Journal of chromatography. B, Analytical technologies in the biomedical and life sciences 07/2011; 879(21):1893-8. · 2.78 Impact Factor
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    ABSTRACT: Tobacco smoke is a major risk factor in the development of COPD. Secondhand smoke (SHS) exposure is a known risk factor in asthma, bronchitis, and coronary artery disease. Elastin is a recognized target for injury in COPD, and the amino acids desmosine and isodesmosine (D/I), which are specific for elastin degradation, are elevated in COPD. This study determined whether exposure to SHS affects elastin degradation in asymptomatic individuals. Two cohorts of asymptomatic individuals without evidence of respiratory or circulatory disease, exposed to SHS, were studied. Both cohorts comprised normal nonsmokers, active smokers, and those exposed to SHS. D/I were measured in plasma and quantified by high-performance liquid chromatography and tandem mass spectrometry by published methods. Plasma cotinine, a metabolite of nicotine, was also measured. In each cohort, the levels of D/I in plasma were statistically significantly higher in secondhand-smoke-exposed subjects than in the normal nonexposed subjects. Smokers had the highest levels of D/I but their levels were not statistically significantly higher than those of the secondhand-smoke-exposed. Cotinine levels were elevated in secondhand-smoke-exposed subjects and active smokers but not in most nonsmoking control subjects. Results indicate a tissue matrix effect of degradation of body elastin from SHS exposure and possible lung structure injury, which may result in COPD. Long-term studies of individuals exposed to SHS for the development of COPD are warranted.
    Chest 03/2011; 140(4):946-53. · 7.13 Impact Factor
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    ABSTRACT: Aerosolized hyaluronan (HA) has been previously shown to prevent cigarette smoke-induced airspace enlargement and elastic fiber injury in mice when given concurrently with smoke. In the present study, a more stringent test of the therapeutic potential of HA was performed by delaying treatment with this agent for 1 month. After treatment with cigarette smoke for 3 h per day for 5 days per week for 1 month, mice (DBA/2J) began receiving aerosolized HA (0.1%) for 1 h prior to smoke exposure (controls were given aerosolized water). The results indicate that much of the damage to the lung elastic fibers occurred within the first several months of smoke exposure, as measured by levels of desmosine and isodesmosine (DID) in bronchoalveolar lavage fluid (BALF). In contrast to previously published studies, where concurrent administration of aerosolized HA significantly reduced BALF DID levels within 3 months of smoke exposure, the same effect was not seen until 6 months when HA treatment was delayed. However, despite the prolonged breakdown of elastic fibers in the current study, a significant reduction in airspace enlargement was observed after only 2 months of HA treatment. These findings provide further support for testing this agent in patients with pre-existing chronic obstructive pulmonary disease.
    Beiträge zur Klinik der Tuberkulose 02/2011; 189(1):51-6. · 2.17 Impact Factor
  • Jiangtao He, Gerard M Turino, Yong Y Lin
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    ABSTRACT: This study presents a method for detecting and characterizing peptides of elastin that result from lung matrix injury in chronic obstructive pulmonary disease (COPD). Lung elastin degradation was studied by two representative in vivo elastases, human neutrophil elastase (HNE) and macrophage metalloproteinase (MMP12). The resulting peptide mixtures were analyzed by high-performance liquid chromatography/electrospray tandem mass spectrometry (LC/MSMS) to characterize 40 elastin-derived peptides (EDPs), 24 from HNE and 16 from MMP12 digestions. The peptides constitute major EDPs that are solubilized by the enzymatic digestion. Using the selected reaction monitoring (SRM) from LC/MSMS analysis, the transition ions of the peptides were used to investigate the presence of the peptides in selected body fluids of chronic obstructive pulmonary disease (COPD) patients. Four peptides, GYPI, APGVGV, GLGAFPA, and VGVLPGVPT, were detected in plasma or sputum of some COPD patients but not in normal controls. A hexapeptide VGVAPG, which had been widely studied for its chemotactic activity for a possible pathogenic role in COPD, was not detected in lung EDPs by HNE or MMP12 digestion, but only by porcine pancreatic elastase (PPE) digestion. This study demonstrates a practical methodology to study peptides from matrix degradations in pulmonary disease and a means of investigating their pathogenesis.
    Experimental Lung Research 11/2010; 36(9):548-57. · 1.75 Impact Factor
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    ABSTRACT: Alpha1-antitrypsin (AAT) deficiency is characterized by low blood levels of alpha1-proteinase inhibitor (alpha₁-PI) and may lead to emphysema. Alpha₁-PI protects pulmonary tissue from damage caused by the action of proteolytic enzymes. Augmentation therapy with Prolastin® (Alpha₁-Proteinase Inhibitor [Human]) to increase the levels of alpha₁-PI has been used to treat individuals with AAT deficiency for over 20 years. Modifications to the Prolastin manufacturing process, incorporating additional purification and pathogen-reduction steps, have led to the development of an alpha₁-PI product, designated Prolastin®-C (Alpha₁-Proteinase inhibitor [Human]). The pharmacokinetic comparability of Prolastin-C to Prolastin was assessed in subjects with AAT deficiency. In total, 24 subjects were randomized to receive 60 mg/kg of functionally active Prolastin-C or Prolastin by weekly intravenous infusion for 8 weeks before crossover to the alternate treatment for another 8 weeks. Pharmacokinetic plasma samples were drawn over 7 days following last dose in the first treatment period and over 10 days following the last dose in the second period. The primary end point for pharmacokinetic comparability was area under the plasma concentration versus time curve over 7 days post dose (AUC₀₋₇ (days)) of alpha₁-PI determined by potency (functional activity) assay. The crossover phase was followed by an 8-week open-label treatment phase with Prolastin-C only. Mean AUC₀₋₇ (days) was 155.9 versus 152.4 mg*h/mL for Prolastin-C and Prolastin, respectively. The geometric least squares mean ratio of AUC₀₋₇ (days) for Prolastin-C versus Prolastin had a point estimate of 1.03 and a 90% confidence interval of 0.97-1.09, demonstrating pharmacokinetic equivalence between the 2 products. Adverse events were similar for both treatments and occurred at a rate of 0.117 and 0.078 per infusion for Prolastin-C (double-blind treatment phase only) and Prolastin, respectively (p = 0.744). There were no treatment-emergent viral infections in any subject for human immunodeficiency virus, hepatitis B or C, or parvovirus B19 during the course of the study. Prolastin-C demonstrated pharmacokinetic equivalence and a comparable safety profile to Prolastin. ClinicalTrials.gov Identifier: NCT00295061.
    BMC Clinical Pharmacology 09/2010; 10:13. · 1.36 Impact Factor
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    ABSTRACT: Abstract Background Alpha1-antitrypsin (AAT) deficiency is characterized by low blood levels of alpha1-proteinase inhibitor (alpha1-PI) and may lead to emphysema. Alpha1-PI protects pulmonary tissue from damage caused by the action of proteolytic enzymes. Augmentation therapy with Prolastin® (Alpha1-Proteinase Inhibitor [Human]) to increase the levels of alpha1-PI has been used to treat individuals with AAT deficiency for over 20 years. Modifications to the Prolastin manufacturing process, incorporating additional purification and pathogen-reduction steps, have led to the development of an alpha1-PI product, designated Prolastin®-C (Alpha1-Proteinase inhibitor [Human]). The pharmacokinetic comparability of Prolastin-C to Prolastin was assessed in subjects with AAT deficiency. Methods In total, 24 subjects were randomized to receive 60 mg/kg of functionally active Prolastin-C or Prolastin by weekly intravenous infusion for 8 weeks before crossover to the alternate treatment for another 8 weeks. Pharmacokinetic plasma samples were drawn over 7 days following last dose in the first treatment period and over 10 days following the last dose in the second period. The primary end point for pharmacokinetic comparability was area under the plasma concentration versus time curve over 7 days post dose (AUC0-7 days) of alpha1-PI determined by potency (functional activity) assay. The crossover phase was followed by an 8-week open-label treatment phase with Prolastin-C only. Results Mean AUC0-7 days was 155.9 versus 152.4 mg*h/mL for Prolastin-C and Prolastin, respectively. The geometric least squares mean ratio of AUC0-7 days for Prolastin-C versus Prolastin had a point estimate of 1.03 and a 90% confidence interval of 0.97-1.09, demonstrating pharmacokinetic equivalence between the 2 products. Adverse events were similar for both treatments and occurred at a rate of 0.117 and 0.078 per infusion for Prolastin-C (double-blind treatment phase only) and Prolastin, respectively (p = 0.744). There were no treatment-emergent viral infections in any subject for human immunodeficiency virus, hepatitis B or C, or parvovirus B19 during the course of the study. Conclusion Prolastin-C demonstrated pharmacokinetic equivalence and a comparable safety profile to Prolastin. Trial Registration ClinicalTrials.gov Identifier: NCT00295061
    BMC Clinical Pharmacology. 01/2010;
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    ABSTRACT: Alpha-1-antitrypsin deficiency is a genetic condition associated with severe, early-onset chronic obstructive pulmonary disease (COPD). However, there is significant variability in lung function impairment among persons with the protease inhibitor ZZ genotype. Early identification of persons at highest risk of developing lung disease could be beneficial in guiding monitoring and treatment decisions. Using a multicenter, family-based study sample (2002-2005) of 372 persons with the protease inhibitor ZZ genotype, the authors developed prediction models for forced expiratory volume in 1 second (FEV(1)) and the presence of severe COPD using demographic, clinical, and genetic variables. Half of the data sample was used for model development, and the other half was used for model validation. In the training sample, variables found to be predictive of both FEV(1) and severe COPD were age, sex, pack-years of smoking, bronchodilator responsiveness, chronic bronchitis symptoms, and index case status. In the validation sample, the predictive model for FEV(1) explained 50% of the variance in FEV(1), and the model for severe COPD exhibited excellent discrimination (c statistic = 0.88).
    American journal of epidemiology 10/2009; 170(8):1005-13. · 4.98 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States but is often undertreated. COPD often overlaps with other conditions such as hypertension and osteoporosis, which are less morbid but may be treated more aggressively. We evaluated the prevalence of these comorbid conditions and compared testing, patient knowledge, and management in a national sample of patients with COPD. A survey was administered by telephone in 2006 to 1003 patients with COPD to evaluate the prevalence of comorbid conditions, diagnostic testing, knowledge, and management using standardized instruments. The completion rate was 87%. Among 1003 patients with COPD, 61% reported moderate or severe dyspnea and 41% reported a prior hospitalization for COPD. The most prevalent comorbid diagnoses were hypertension (55%), hypercholesterolemia (52%), depression (37%), cataracts (31%), and osteoporosis (28%). Only 10% of respondents knew their forced expiratory volume in 1 second (95% confidence interval [CI], 8-12) compared with 79% who knew their blood pressure (95% CI, 76-83). Seventy-two percent (95% CI, 69-75) reported taking any medication for COPD, usually a short-acting bronchodilator, whereas 87% (95% CI, 84-90) of patients with COPD and hypertension were taking an antihypertensive medication and 72% (95% CI, 68-75) of patients with COPD and hypercholesterolemia were taking a statin. Although most patients with COPD in this national sample were symptomatic and many had been hospitalized for COPD, COPD self-knowledge was low and COPD was undertreated compared with generally asymptomatic, less morbid conditions such as hypertension.
    The American journal of medicine 05/2009; 122(4):348-55. · 5.30 Impact Factor
  • Edward Eden, Gerard M Turino
    Chest 04/2009; 135(3):591-2. · 7.13 Impact Factor

Publication Stats

2k Citations
720.48 Total Impact Points

Institutions

  • 2004–2013
    • St. John's University
      New York City, New York, United States
  • 1997–2013
    • Aurora St. Luke's Medical Center
      Milwaukee, Wisconsin, United States
  • 1991–2012
    • Saint Luke's Hospital (NY, USA)
      New York City, New York, United States
  • 2006–2011
    • St. Luke School of Medicine
      New York City, New York, United States
    • Medical University of South Carolina
      • Department of Medicine
      Charleston, SC, United States
  • 2010
    • University of Texas Health Science Center at Tyler
      Tyler, Texas, United States
  • 1962–2009
    • Columbia University
      • • Department of Medicine
      • • College of Physicians and Surgeons
      New York City, NY, United States
  • 2008
    • Policlinico San Matteo Pavia Fondazione IRCCS
      Ticinum, Lombardy, Italy
  • 1991–2007
    • St. Luke's Hospital
      Cedar Rapids, Iowa, United States
  • 2000
    • Maimonides Medical Center
      Brooklyn, New York, United States
  • 1998
    • The Brooklyn Hospital Center
      New York City, New York, United States
  • 1977–1997
    • CUNY Graduate Center
      New York City, New York, United States
  • 1994
    • New York Medical College
      • Department of Medicine
      New York City, NY, United States
  • 1980
    • Royal College of Physicians and Surgeons of Glasgow
      Glasgow, Scotland, United Kingdom
  • 1974–1980
    • Devry College of New York, USA
      New York City, New York, United States
  • 1959–1970
    • New York Presbyterian Hospital
      • Department of Pain Medicine
      New York City, New York, United States