The Experts below are selected from a list of 10086 Experts worldwide ranked by ideXlab platform

Joseph R. Pisegna - One of the best experts on this subject based on the ideXlab platform.

David C Metz - One of the best experts on this subject based on the ideXlab platform.

Duncan F Rogers - One of the best experts on this subject based on the ideXlab platform.

  • treatment of airway mucus Hypersecretion
    Annals of Medicine, 2006
    Co-Authors: Duncan F Rogers, Peter J Barnes
    Abstract:

    Airway mucus Hypersecretion is now recognized as a key pathophysiological feature in many patients with asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis. Consequently, it is important to develop drugs that inhibit mucus Hypersecretion in these susceptible patients. Conventional therapies, including anticholinergics, ss2-adrenoceptor agonists, corticosteroids, mucolytics and macrolide antibiotics, have variable efficacy in inhibiting airway mucus Hypersecretion, and are less effective in COPD than in asthma. Novel pharmacotherapeutic targets are being investigated, including inhibitors of nerve activity (e.g. large conductance calcium-activated potassium, BKCa, channel activators), tachykinin receptor antagonists, epoxygenase inducers (e.g. benzafibrate), inhibitors of mucin exocytosis (e.g. anti-myristoylated alanine-rich C kinase substrate (MARCKS), peptide and Munc-18B blockers), inhibitors of mucin synthesis and goblet cell hyperplasia (e.g. epidermal growth factor (EGF), receptor tyrosine kinase inhibitors, p38 mitogen-activated protein (MAP), kinase inhibitors, MAP kinase kinase/extracellular signal-regulated kinase (MEK/ERK), inhibitors, human calcium-activated chloride (hCACL2), channel blockers and retinoic acid receptor-a antagonists), inducers of goblet cell apoptosis (e.g. Bax inducers or Bcl-2 inhibitors), and purinoceptor P(2Y2) antagonists to inhibit mucin secretion or P(2Y2) agonists to hydrate secretions. However, real and theoretical differences delineate the mucus hypersecretory phenotype in asthma from that in COPD. More information is required on these differences to identify specific therapeutic targets which, in turn, should lead to rational design of anti-hypersecretory drugs for treatment of airway mucus Hypersecretion in asthma and COPD.

  • airway mucus Hypersecretion in asthma an undervalued pathology
    Current Opinion in Pharmacology, 2004
    Co-Authors: Duncan F Rogers
    Abstract:

    Airway mucus Hypersecretion is a feature of many patients with asthma. It is indicative of poor asthma control and contributes to morbidity and mortality. Excess mucus not only obstructs airways but also contributes to airway hyperresponsiveness. Furthermore, asthma might have a specific mucus hypersecretory phenotype. Goblet cell hyperplasia and submucosal gland hypertrophy are shared with other hypersecretory diseases, such as chronic obstructive pulmonary disease; however, some features are different, including mucus plugging, mucus "tethering" to goblet cells, plasma exudation, and increased amounts of a low charge glycoform of mucin (MUC)5B and the presence of MUC2 in secretions. Experimentally, most of the inflammatory mediators and neural mechanisms implicated in the pathophysiology of asthma impact upon the mucus hypersecretory phenotype. There is currently huge research interest in identifying targets involved in inducing mucus abnormalities, which should lead to the rational design of anti-hypersecretory drugs for treatment of airway mucus Hypersecretion in asthma.

  • mucus pathophysiology in copd differences to asthma and pharmacotherapy
    Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace Fondazione clinica del lavoro IRCCS [and] Istituto di clinica tisiolo, 2000
    Co-Authors: Duncan F Rogers
    Abstract:

    Patients with chronic obstructive pulmonary disease (COPD) exhibit characteristics of airway mucus Hypersecretion, including sputum production, increased luminal mucus, goblet cell hyperplasia and submucosal gland hypertrophy. These features are not common to all patients and the impact of Hypersecretion on morbidity and mortality is a matter for debate. However, current evidence indicates that airway Hypersecretion has pathophysiological and clinical significance in COPD, particularly as patients age or are prone to respiratory tract infection. This suggests that it is important to develop drugs that inhibit mucus Hypersecretion in these patients. A number of drugs are currently available that may be of therapeutic benefit in hypersecretory disorders of the airways, e.g. glucocorticosteroids and anticholinergics. Novel compounds are undergoing preclinical research, e.g. inhibitors of epidermal growth factor receptor tyrosine kinase and antisense oligomers. However, preliminary data indicate that the mucus in COPD differs to that in asthma in that: 1) it is less viscous and without marked plasma exudation, 2) the ratio of mucin (MUC) 5AC:MUC5B may be reduced, and 3) there is full release of mucin into the airway lumen rather than "tethering" of mucus as in asthma. Consequently, future research should determine whether there really is an intrinsic abnormality specific to mucus in chronic obstructive pulmonary disease. Based upon this information, appropriate suppressers of mucus Hypersecretion in chronic obstructive pulmonary disease can be developed.

Robert T Jensen - One of the best experts on this subject based on the ideXlab platform.

  • pharmacotherapy of zollinger ellison syndrome
    Expert Opinion on Pharmacotherapy, 2013
    Co-Authors: Tetsuhide Ito, Hisato Igarashi, Hirotsugu Uehara, Robert T Jensen
    Abstract:

    Introduction: The role of pharmacotherapy in the management of patients with Zollinger–Ellison syndrome (ZES) is often equated with the medical management of acid Hypersecretion. However, pharmacotherapy is also increasingly involved in the other management areas of these patients. Areas covered: This paper reviews the role of pharmacotherapy in all aspects of the management of patients with ZES. Newer aspects are emphasized. This includes the difficulty of diagnosing ZES in patients taking proton pump inhibitors. Also covered is the role of pharmacotherapy in controlling acid Hypersecretion and other hormonal hypersecretory states these patients may develop, including hyperparathyroidism in patients with multiple endocrine neoplasia type 1 and ZES; tumor localization; and the treatment of advanced metastatic disease. The last includes chemotherapy, liver-directed therapies, biotherapy (somatostatin/interferon), peptide radio-receptor therapy and molecular-targeted therapies including the use of mTor inhi...

  • mechanism of acid Hypersecretion post curative gastrinoma resection
    Digestive Diseases and Sciences, 2011
    Co-Authors: Jeremiah V Ojeaburu, Tetsuhide Ito, Pellegrino Crafa, Cesare Bordi, Robert T Jensen
    Abstract:

    Some patients with Zollinger-Ellison syndrome post curative gastrinoma resection continue to show gastric acid Hypersecretion; however, the mechanism is unknown. The aim of this study was to prospectively study acid secretion following curative gastrinoma resection and analyze factors contributing in patients with Zollinger-Ellison syndrome. Fifty patients cured post gastrinoma resection were studied with serial assessments of acid secretory status, cure status and ECL-cell status/activity (with serial biopsies, CgA, urinary N-MIAA). Correlative analysis was performed to determine predictive factors. Hypersecretion occurred in 31 patients (62%) and 14 had extreme-Hypersecretion. There was an initial decline (3–6 months) in BAO/MAO, which then remained stable for eight years. Preoperative BAO correlated with the postoperative secretion, but not other clinical, tumoral, laboratory variables, the degree of postoperative acid suppression or type of antisecretory drug needed. Hypersecretors had greater postoperative ECL changes (P = 0.005), serum CGA (P = 0.009) and 24-h urinary N-MIAA (P = 0.0038). Post curative resection, gastric Hypersecretion persists long term (mean 8 years) in 62% of patients and in 28% it is extreme, despite normogastrinemia. No preoperative variable except BAO correlates with postresection Hypersecretion. The persistent increased ECL-cell extent post curative resection suggests prolonged hypergastrinemia can lead to changes in ECL-cells that are either irreversible in humans or sustained by unknown mechanisms not involving fasting hypergastrinemia and which can result in Hypersecretion, in a proportion of which it can be extreme. Whether similar findings may occur in patients with idiopathic GERD treated for prolonged periods (>10 years) with PPIs, at present, is unknown.

  • helicobacter pylori infection a reversible cause of hypergastrinemia and hyperchlorhydria which may mimic zollinger ellison syndrome
    Digestive Diseases and Sciences, 1995
    Co-Authors: Christian H Weber, Irina A Lubensky, Murray Orbuch, Doris B Strader, Robert T Jensen
    Abstract:

    The present report describes two patients with fasting hypergastrinemia, gastric acid Hypersecretion, andHelicobacter pylori gastritis. Provocative testing for Zollinger-Ellison syndrome was negative and imaging studies did not demonstrate an intra-abdominal mass. Following eradication of theHelicobacter pylori infection, the fasting hypergastrinemia resolved in both patients and in one patient the gastric acid Hypersecretion also resolved. The implications of this case on the differential diagnosis of Zollinger-Ellison syndrome are discussed.

Chris E Forsmark - One of the best experts on this subject based on the ideXlab platform.