Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Control of breathing, bronchomotor tone and lung function are inferior to circadian rhythms, which can already be demonstrated at healthy subjects. They get relevant especially at patients with obstructive airway disease and sleep disturbances. Particularly in the early morning hours flow resistance in the airways and in the nose rises. Several different mechanisms are suspected to be responsible: Allergen exposure in bed, supine position, interruption of the bronchodilator therapy, gastro-oesophageal reflux, tenseness of the airways and secretory accumulation. Connected to nocturnal asthma might also be an increased airway responsiveness. Several factors contribute to nocturnal asthma, but they don't constitute a general concept for the explanation of nightly exacerbations. Many hormonal neural cellular and humoral factors show diurnal fluctuations which favour a constrictive bronchial response in the night. Diurnal or ultradian changes in O2 and CO2 sensitivity only play a minor role. However, we have to realise alterations in the responses of the central neuronal control mechanisms of breathing within the respiratory cycle. Oscillations of arterial CO2 partial pressure or pH-values influence tidal volume and ventilation directly. Circadian changes of different vital functions cause minor alterations in airway responsiveness and airway resistance in normal subjects, however in patients with asthma they are enlarged in amplitude and become relevant especially in the night and early morning hours.
 ...
PMID:[Chronobiology of the bronchial system]. 924 91

Eosinophil infiltration into the esophagus is observed in diverse diseases including gastroesophageal reflux and allergic gastroenteritis, but the processes involved are largely unknown. We now report an original model of experimental esophagitis induced by exposure of mice to respiratory allergen. Allergen-challenged mice develop marked levels of esophageal eosinophils, free eosinophil granules, and epithelial cell hyperplasia, features that mimic the human disorders. Interestingly, exposure of mice to oral or intragastric allergen does not promote eosinophilic esophagitis, indicating that hypersensitivity in the esophagus occurs with simultaneous development of pulmonary inflammation. Furthermore, in the absence of eotaxin, eosinophil recruitment is attenuated, whereas in the absence of IL-5, eosinophil accumulation and epithelial hyperplasia are ablated. These results establish a pathophysiological connection between allergic hypersensitivity responses in the lung and esophagus and demonstrate an etiologic role for inhaled allergens and eosinophils in gastrointestinal inflammation.
 ...
PMID:An etiological role for aeroallergens and eosinophils in experimental esophagitis. 1113 83

Eosinophilic esophagitis (EE) is increasingly recognized in adults. It is an inflammatory disease of the esophageal mucosa, with variable presentation, unresponsive to acid suppression therapy. The diagnosis requires histological confirmation of intense eosinophilic infiltration on esophageal biopsy specimen, however exact criteria required to make a diagnosis of EE is still being debated and a clear differentiation from gastroesophageal reflux disease (GERD) is important. Allergen elimination or anti-inflammatory therapy may be effective in such patients. The imperfect diagnostic criteria for EE mandate an understanding of the immunology and the pathophysiology of the disease. It may facilitate the introduction of novel treatment modalities in an individual unresponsive to acid suppression therapy. This paper describes basic elements of the immune-mediated injury to the esophageal mucosa and management aspects to provide a better understanding of the condition.
 ...
PMID:Role of mucosal inflammation in eosinophilic esophagitis: review of the literature. 2199 11

The goals of treatment are prevention of fatalities, hospitalizations, and emergency department visits, along with achieving good long-term control of asthma, with reduction of symptoms, maintenance of normal activity level, prevention of exacerbations, and accelerated loss of pulmonary function (forced expiratory volume in 1 second [FEV(1)]) as well as avoiding harm from therapies. Treatment often is initiated based on severity of symptoms, physical examination findings, and, for some patients, the FEV(1) or peak expiratory flow rates. Comorbidities such as gastroesophageal reflux disease and laryngopharyngeal reflux, rhinitis or rhinosinusitis, sleep apnea, recurrent infections, smoking, and substance abuse should be addressed. Two treatment modalities are indicated only for individuals with allergic asthma: allergen-specific immunotherapy, commonly known as allergy shots, and omalizumab. Allergen immunotherapy is effective in decreasing symptoms and medication use in selected patients with mild-to-moderate allergic asthma. In addition, patients receiving allergen immunotherapy for allergic rhinitis may have a decreased risk of developing asthma. Omalizumab, a recombinant humanized monoclonal anti-IgE antibody indicated for persistent moderate-to-severe allergic asthma, has been shown to improve asthma-related quality of life, decrease clinically significant exacerbation rates, number of courses of oral corticosteroids, and reduce the severity of exacerbations. It is administered every 2-4 weeks subcutaneously, and improvement should be ascertained after 4-6 months.
 ...
PMID:Chapter 12: Asthma: principles of treatment. 2279 85

Triggers and precipitating factors as well as comorbid conditions are associated with asthma and severe asthma. They interfere with the potential to control the disease and represent an additional burden for the patients. Allergen exposure is well known to induce loss of control and exacerbations. Comorbid conditions belong to various fields of medicines including cardiovascular diseases, osteoporosis, obesity and sleep apneas and GERD. They should be diagnosed and treated for themselves according to the best state of the art. Their precise role et their contribution to severe asthma pathophysiology is largely unknown and longitudinal cohort studies are needed to better understand and treat the patients with severe asthma.
 ...
PMID:[How to consider triggers and comorbid conditions in severe asthma in adults]. 2754 6

The goals of treatment are prevention of fatalities, hospitalizations, and emergency department visits, along with achieving good long-term control of asthma, with reduction of symptoms, maintenance of normal activity level, prevention of exacerbations and accelerated loss of pulmonary function (forced expiratory volume in the first second of expiration [FEV1]), and avoidance of harm from therapies. Treatment is often initiated based on the severity of symptoms, physical examination findings, and, for some patients, the FEV1 or peak expiratory flow rates. Comorbidities such as gastroesophageal reflux disease and laryngopharyngeal reflux, rhinitis or rhinosinusitis, sleep apnea, recurrent infections, smoking, and substance abuse should be addressed. Two treatment modalities are indicated only for individuals with allergic asthma: allergen-specific immunotherapy (commonly known as allergy shots), and biologic therapies that target type-2 (T2) inflammation. Allergen immunotherapy is effective in decreasing symptoms and medication use in select patients with mild-to-moderate allergic asthma. In addition, patients who receive allergen immunotherapy for allergic rhinitis may have a decreased risk of developing asthma. Omalizumab, mepolizumab, reslizumab, benralizumab, and dupilumab are monoclonal antibodies that target T2 inflammation and are indicated for either moderate-to-severe or severe asthma. These have been well studied to improve asthma symptoms and have specific characteristics unique to each individual medication. A focus on adherence can be considered in choosing therapy because it is not clear which biologic to choose in T2 high asthma at this time.
 ...
PMID:Asthma in adults: Principles of treatment. 3169 Mar 79