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  1. Article: Pharmacogenetics of asthma: where are we now?

    Larj, Michael J / Bleecker, Eugene R

    Clinics in chest medicine

    2006  Volume 27, Issue 1, Page(s) 109–17, vii

    Abstract: Pharmacogenetics adds value with improved clinical markers and increased ability to predict efficacy with greater clarity. This should lead to individualized and simplified dosing, improved efficacy with specific treatment, and enhanced safety. Improved ... ...

    Abstract Pharmacogenetics adds value with improved clinical markers and increased ability to predict efficacy with greater clarity. This should lead to individualized and simplified dosing, improved efficacy with specific treatment, and enhanced safety. Improved patient response should lead to enhanced patient compliance. Many challenges remain ahead including ethical issues related to patient confidentiality and banking of DNA. Regulatory issues and guidelines need to be discussed to establish reasonable boundaries. There is also a need for review of diagnosis and treatment combinations and Food and Drug Administration review of the process. Legal issues including patents and commercial issues concerning patient, physician, and managed care acceptance must be addressed.
    MeSH term(s) Arachidonate 5-Lipoxygenase/genetics ; Asthma/drug therapy ; Asthma/genetics ; Genotype ; Humans ; Polymorphism, Genetic ; Promoter Regions, Genetic/genetics ; Receptors, Adrenergic, beta-2/genetics ; Receptors, Corticotropin-Releasing Hormone/genetics ; Receptors, Glucocorticoid/genetics
    Chemical Substances CRF receptor type 1 ; Receptors, Adrenergic, beta-2 ; Receptors, Corticotropin-Releasing Hormone ; Receptors, Glucocorticoid ; Arachidonate 5-Lipoxygenase (EC 1.13.11.34)
    Language English
    Publishing date 2006-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 447455-7
    ISSN 1557-8216 ; 0272-5231
    ISSN (online) 1557-8216
    ISSN 0272-5231
    DOI 10.1016/j.ccm.2005.12.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Therapeutic responses in asthma and COPD. Corticosteroids.

    Larj, Michael J / Bleecker, Eugene R

    Chest

    2004  Volume 126, Issue 2 Suppl, Page(s) 138S–149S; discussion 159S–161S

    Abstract: The effects of inhaled corticosteroids (ICSs) in asthma include reduced severity of symptoms, improved pulmonary function, diminished bronchial hyperresponsiveness (BHR), prevention of exacerbations, and possible prevention of airway wall remodeling. ... ...

    Abstract The effects of inhaled corticosteroids (ICSs) in asthma include reduced severity of symptoms, improved pulmonary function, diminished bronchial hyperresponsiveness (BHR), prevention of exacerbations, and possible prevention of airway wall remodeling. Compared with an inhaled beta(2)-agonist, ICSs improve airway function and BHR, reduce bronchial-epithelium abnormalities, decrease bronchial inflammation, and reduce inflammatory-cell infiltration into the bronchial lamina propria; thus, they may prevent airway remodeling. In children, early use of ICSs may result in improved airway function over time. ICSs reduce use of prednisone, asthma medications, hospitalizations, and urgent-care visits. The primary side effects of ICSs in children are limited to transient reduction in growth. Compared with a leukotriene receptor antagonist (LTRA), ICSs produced a greater change from baseline in FEV(1) and greater reductions in symptoms. A long-acting beta(2)-agonist (LABA) combined with an ICS produced greater improvements than does therapy with ICSs even at higher doses. In COPD, the therapeutic value of ICSs is not as clear. While clinical trials in patients with mild COPD have not shown a reduction in decline in FEV(1) over time, other studies have shown that ICS therapy reduces exacerbations in patients with more severe COPD. Combination therapy with both ICS and LABA has recently been shown to be effective in COPD, where studies have documented additive improvement in FEV(1). Overall, the same therapeutic approaches show clinical effectiveness in both asthma and COPD. This supports the hypothesis that there are some similarities in these obstructive airway diseases. Future approaches should further define phenotypes, perhaps based in part on pharmacogenetic factors that will guide anti-inflammatory therapy in asthma and COPD.
    MeSH term(s) Adrenal Cortex Hormones/therapeutic use ; Anti-Inflammatory Agents/therapeutic use ; Asthma/drug therapy ; Asthma/physiopathology ; Drug Therapy, Combination ; Forced Expiratory Volume/drug effects ; Humans ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Receptors, Adrenergic, beta-2/therapeutic use ; Treatment Outcome
    Chemical Substances Adrenal Cortex Hormones ; Anti-Inflammatory Agents ; Receptors, Adrenergic, beta-2
    Language English
    Publishing date 2004-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.126.2_suppl_1.138S
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Effects of beta2-agonists on airway tone and bronchial responsiveness.

    Larj, Michael J / Bleecker, Eugene R

    The Journal of allergy and clinical immunology

    2002  Volume 110, Issue 6 Suppl, Page(s) S304–12

    Abstract: In evaluating the clinical consequences of beta(2)-agonist therapy, it is important to consider the possibility of reduced asthma control and increased bronchial responsiveness with regular or long-term use. Some studies have noted reductions in ... ...

    Abstract In evaluating the clinical consequences of beta(2)-agonist therapy, it is important to consider the possibility of reduced asthma control and increased bronchial responsiveness with regular or long-term use. Some studies have noted reductions in protective effects but not complete loss of protection with short-acting beta(2)-agonist therapy. These reductions vary, depending on the use of nonspecific, indirect, or immunologic challenges, but it appears there is a greater loss of protective effect against indirect stimuli. Tachyphylaxis to the bronchodilatatory effects of long-acting beta(2)-agonists appears to be minimal. Individuals homozygous for arginine at locus 16 of the beta(2)-adrenergic receptor gene have a decline in pulmonary function during beta(2)-agonist use, and they are at greater risk of asthma exacerbations during beta(2)-agonist therapy than patients with other genotypes. Important questions for further research are whether small differences in tachyphylaxis and bronchoprotection have relevant clinical effects and to what extent tachyphylaxis and tolerance to bronchoprotection are caused by pharmacogenetic interactions.
    MeSH term(s) Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists/therapeutic use ; Asthma/drug therapy ; Bronchial Hyperreactivity/drug therapy ; Bronchoconstriction/drug effects ; Bronchodilator Agents/therapeutic use ; Humans ; Muscle, Smooth/drug effects
    Chemical Substances Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists ; Bronchodilator Agents
    Language English
    Publishing date 2002-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 121011-7
    ISSN 1085-8725 ; 1097-6825 ; 0091-6749
    ISSN (online) 1085-8725 ; 1097-6825
    ISSN 0091-6749
    DOI 10.1067/mai.2002.130045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Genetics of asthma and COPD. Similar results for different phenotypes.

    Meyers, Deborah A / Larj, Michael J / Lange, Leslie

    Chest

    2004  Volume 126, Issue 2 Suppl, Page(s) 105S–110S; discussion 159S–161S

    Abstract: Asthma and COPD are common respiratory diseases that are caused by the interaction of genetic susceptibility with environmental factors. Environmental influences are important in both diseases, and although there are differences in genetic ... ...

    Abstract Asthma and COPD are common respiratory diseases that are caused by the interaction of genetic susceptibility with environmental factors. Environmental influences are important in both diseases, and although there are differences in genetic susceptibilities, there are also similarities. Three examples of interest for both asthma and COPD patients are discussed. The first is the results of family studies, which have shown evidence for susceptibility loci for both asthma-related and COPD-related phenotypes in the same chromosomal region. Second, evidence for a gene-environment interaction with passive smoking for asthma patients compared with individual smoking for COPD patients will be covered. The third is an example of one candidate gene (interleukin-13), in which similar results have been observed for both asthma and COPD.
    MeSH term(s) Asthma/diagnosis ; Asthma/genetics ; Chromosomes, Human, Pair 2/genetics ; Clinical Trials as Topic ; Environmental Exposure/adverse effects ; Genetic Linkage/genetics ; Genetic Predisposition to Disease/epidemiology ; Genetic Predisposition to Disease/etiology ; Genetic Predisposition to Disease/genetics ; Genetic Testing ; Humans ; Interleukin-13/genetics ; Phenotype ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/genetics ; Smoking/adverse effects ; Smoking/genetics
    Chemical Substances Interleukin-13
    Language English
    Publishing date 2004-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.126.2_suppl_1.105S
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Long-acting beta agonists in asthma therapy.

    Rissmiller, Richard W / Larj, Michael J / Peters, Stephen P

    Current allergy and asthma reports

    2003  Volume 4, Issue 2, Page(s) 91–92

    MeSH term(s) Adrenal Cortex Hormones/therapeutic use ; Adrenergic beta-Agonists/therapeutic use ; Albuterol/analogs & derivatives ; Albuterol/therapeutic use ; Asthma/drug therapy ; Bronchodilator Agents/therapeutic use ; Ethanolamines/therapeutic use ; Formoterol Fumarate ; Humans ; Salmeterol Xinafoate ; Time Factors
    Chemical Substances Adrenal Cortex Hormones ; Adrenergic beta-Agonists ; Bronchodilator Agents ; Ethanolamines ; Salmeterol Xinafoate (6EW8Q962A5) ; Albuterol (QF8SVZ843E) ; Formoterol Fumarate (W34SHF8J2K)
    Language English
    Publishing date 2003-12-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2057370-4
    ISSN 1529-7322
    ISSN 1529-7322
    DOI 10.1007/s11882-004-0049-6
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  6. Article: Asthma exacerbations and formoterol.

    Rissmiller, Richard W / Larj, Michael J / Peters, Stephen P / Bleecker, Eugene R

    Chest

    2004  Volume 125, Issue 4, Page(s) 1590–1591

    MeSH term(s) Administration, Inhalation ; Adrenal Cortex Hormones/administration & dosage ; Adrenergic beta-Agonists/administration & dosage ; Adrenergic beta-Agonists/adverse effects ; Albuterol/administration & dosage ; Albuterol/analogs & derivatives ; Asthma/physiopathology ; Bronchodilator Agents/administration & dosage ; Bronchodilator Agents/adverse effects ; Drug Therapy, Combination ; Ethanolamines/administration & dosage ; Ethanolamines/adverse effects ; Formoterol Fumarate ; Humans ; Research Design ; Salmeterol Xinafoate
    Chemical Substances Adrenal Cortex Hormones ; Adrenergic beta-Agonists ; Bronchodilator Agents ; Ethanolamines ; Salmeterol Xinafoate (6EW8Q962A5) ; Albuterol (QF8SVZ843E) ; Formoterol Fumarate (W34SHF8J2K)
    Language English
    Publishing date 2004-04
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.125.4.1590
    Database MEDical Literature Analysis and Retrieval System OnLINE

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