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

Irwin and co-workers have designed an anatomic approach to the diagnosis and treatment of cough. In their hands, diagnosis was consistently determined and treatment successful almost without exception, if sustained. We reviewed the results of a similar approach in 139 consecutive and unselected patients referred to pulmonary specialists in two community hospitals. Thirty-nine patients demonstrated hyperreactive airways (HA) by carbachol inhalation and/or eucapnic hyperventilation of cold air. Twenty-seven of 78 without HA had postnasal drip, and 13 of 78 had a persistent cough following acute upper airway inflammation. Other less common diagnoses included chronic bronchitis, gastro-esophageal reflux, occupational bronchitis, interstitial lung disease, and psychologic causes. We were able to find the cause of cough 88 percent of the time. Treatment adjusted for noncompliance was not always a success. While all patients with HA improved, 8 percent of patients without HA or specific diagnosis did not have an improvement in their cough upon retrospective inquiry. Based on this analysis, we find that the diagnosis and treatment of cough may not be as successful as originally reported using Irwin's approach.
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PMID:Chronic persistent cough. Experience in diagnosis and outcome using an anatomic diagnostic protocol. 292

Four cases of interstitial lung disease caused by chronic inhalation of paraffin oil are reported. The disease is facilitated by disorders of deglutition or gastro-oesophageal reflux. The diagnosis is confirmed by chromatography on a thin slice of silica gel of the lipid extract of broncho-alveolar lavage fluid.
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PMID:[Biochemical and cytological study of the alveolar lavage fluid in 4 cases of lipid pneumopathy]. 294 81

Systemic sclerosis (SSc) is a heterogenous disease with a morbidity and mortality that varies widely. Nonetheless, the future clinical course of an individual patient can be estimated based on the severity of skin and internal organ involvement within the first several years of the disease. Patients with limited cutaneous SSc (ISSc) have skin thickening below the elbows or knees and may have face and neck involvement. Patients with this subtype of SSc have Raynaud's phenomenon, digital ulcers, and esophageal dysfunction. Significant morbidity and mortality arises in those patients with ISSc who develop interstitial lung disease or pulmonary artery hypertension. Patients with diffuse cutaneous SSc (dSSc) have skin thickening above the elbows and knees or on the trunk. These patients have a more abrupt onset of disease, often with constitutional symptoms and arthalgias. Severe heart, lung, gut, and renal involvement, if it occurs, tends to develop within the first 5 years of disease, especially within the first several years. Patients with significant internal organ involvement have a poorer prognosis than patients who do not. The goals of the initial history and physical and laboratory examinations are to classify the type of scleroderma as ISSc or dSSc, to estimate disease duration, and to define the extent and severity of organ involvement. Treatment of SSc is organ based. Treatment may reduce morbidity associated with Raynaud's phenomenon, digital ulcers, esophageal dysmotility, esophageal reflux, gut dysmotility, arthralgias, myositis, and pulmonary artery hypertension. Therapy may stabilize lung function in patients with interstitial lung disease with alveolitis and stabilize renal function in patients with renal crisis. The overall prognosis for patients with SSc appears to be improving. Patients with early dSSc should be considered for enrollment onto protocol testing of potential disease-modifying therapies.
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PMID:Clinical approach to scleroderma. 975 79

Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal interstitial lung disease (ILD) of unknown etiology. Introduction of acid into the respiratory tree can produce pulmonary fibrosis. Gastroesophageal reflux (GER) has previously been associated with several other respiratory conditions, including pneumonia, bronchitis, and asthma. To investigate prospectively the possible association of GER and IPF, 17 consecutive patients with biopsy-proven IPF and eight control patients with ILD other than IPF underwent dual-channel, ambulatory esophageal pH monitoring. Sixteen of 17 patients with IPF had abnormal distal and/or proximal esophageal acid exposure compared with four of eight control patients (p = 0.02). In the patients with IPF, mean percent distal total (13.6 versus 3.34, p = 0.006), distal upright (12.4 versus 5.1, p = 0.04), distal supine (14.7 versus 0.88, p = 0.02), and proximal supine (7.48 versus 0.24, p = 0.04) esophageal acid exposure times were significantly greater than those in control patients. Only four patients with IPF (25%) with increased acid exposure had typical reflux symptoms such as heartburn or regurgitation. Patients with IPF have a high prevalence of increased esophageal acid exposure, usually without typical GER symptoms. GER in these patients tends to occur at night and extend into the proximal esophagus. Acid reflux may be a contributing factor in the pathogenesis of IPF.
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PMID:Increased prevalence of gastroesophageal reflux in patients with idiopathic pulmonary fibrosis. 984 71

Systemic sclerosis (SS) is characterized by sclerosis of the dermis and internal organs and by vascular abnormalities. Although the pathophysiology of the disease has been partly elucidated, the efficacy of long-term treatments remains limited, with no significant increase in survival in prospective studies. Conventional drug treatments are disappointing in clinical practice, and in a recent prospective randomized study standard-dose D-penicillamine was not more effective than mini-dose D-penicillamine. New long-term treatments are emerging for diffuse SS, including cyclophosphamide for patients with progressive interstitial lung disease or stem cell transplantation for those with early organ involvement. The most effective treatments remain symptomatic, such as angiotensin-converting enzyme inhibitors for acute renal crisis, calcium channel antagonists for Raynaud's phenomenon, and proton pump inhibitors for the complications of gastroesophageal reflux. This review article focuses on long-term treatments that are most likely to be effective and suggests symptomatic treatment strategies tailored to specific organ involvements.
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PMID:Treating systemic sclerosis in 2001. 1170 5

Following the experience of asthma, characterised by the presence of bronchial hyper-responsiveness, the notion has been accepted that the chronic cough of disease occurs as a result of altered sensitivity of the afferent limb of the cough reflex. Methods for testing for the 'threshold' for eliciting the cough reflex have also been borrowed from asthma care. In the main aerosols are inhaled that contain the relevant stimulus.A number of factors influence the cough response to inhaled aerosols. The distribution of the inhaled aerosol is important as certain chemically sensitive receptors are distributed in different regions of the lungs. The larynx and central airways are important but so too are the peripheral airways. The degree of bronchodilatation is also important as airway narrowing can, itself, induce coughing in man.Asthma, oesophageal reflux and rhinitis patients experience increased coughing, that is associated with increased sensitivity to inhaled capsaicin. In syndromes of chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) increased sensitivity to coughing with capsaicin is common. This appears a specific effect of the pathogenic process of the disease. Modification of the disease process can lessen coughing and the sensitivity to capsaicin.
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PMID:Chronic cough and the cough reflex in common lung diseases. 1209 71

The oxidation of proteins may play an important role in the pathogenesis of chronic inflammatory lung diseases, and may contribute to lung damage. However, the extent of oxidation and the distribution among proteins are not known for most pediatric lung diseases. In this work, protein oxidation was assessed as protein carbonyls. Bronchoalveolar lavages (BAL) from children with chronic lung diseases were investigated by dot-blot assay for content and for pattern of distribution of oxidized proteins by two-dimensional (2D) electrophoresis and Western blotting. Significantly higher levels of protein oxidation than in healthy controls were determined in groups of patients with interstitial lung disease, gastro-esophageal reflux disease, and pulmonary alveolar proteinosis. The proteins most sensitive to oxidation were serum albumin, surfactant protein A, and alpha1-antitrypsin. Our data show increased oxidative stress in lungs of children with chronic pulmonary diseases, with significant interindividual variations. The extent of protein oxidation was proportional to the count of neutrophilic granulocytes in BAL fluid. These findings strongly support the concept that an abundance of reactive oxygen species produced during neutrophilic inflammation may be a deleterious factor, leading to pulmonary damage in these patients.
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PMID:Protein oxidation by chronic pulmonary diseases in children. 1627 Mar 27

A causal link between chronic inflammation and carcinogenesis is explored by reviewing illustrative examples of specific cancers and causal agents and mechanisms. The causal agents or pathologic conditions include microbial agents, gastroesophageal reflux, chronic cholecystitis and cholelithiasis, inflammatory bowel disease, and specific agents that cause chronic obstructive or diffuse interstitial lung disease. The proportion of total cancer deaths attributable to infectious agents is estimated to be about 20% to 25% in developing countries and 7% to 10% in more industrialized countries. Recurrent or persistent inflammation may induce, promote, or influence susceptibility to carcinogenesis by causing DNA damage, inciting tissue reparative proliferation, and/or creating a stromal "soil" that is enriched with cytokines and growth factors. Future research on the complex cascade of cellular and humoral factors participating in the chronic inflammatory process will further understanding of the pathogenesis of various cancers and potentially provide a rationale for targeted chemopreventive interventions.
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PMID:Chronic inflammation: a common and important factor in the pathogenesis of neoplasia. 1651 35

Gastroesophageal reflux is a potential cause of allograft dysfunction after lung transplantation due to microaspiration, lung inflammation, and development of bronchitis obliterans. A 16-year-old Japanese boy who had been suffering from interstitial lung disease received bilateral lung transplant from a braindead donor in the United States. Three months after lung transplantation, his lung function has not increased as expected. Spirometory revealed forced vital capacity (FVC) of 1.11 l (33% of predicted) and forced expiratory volume in one second (FEV1.0) of 0.81 l (28% of predicted). All possible etiologies, including infection, acute and chronic rejection, and other abnormalities were investigated. The only positive finding was the presence of gastroesophageal reflux. He first underwent pyroloplasty which did not improve lung function. Twenty-four-hour pH monitor performed after surgery revealed frequent gastroesophageal reflux. He eventually underwent laparoscopic fundoplication 9 months after initial lung transplantation. His lung function gradually improving after fundoplication, an FVC was 1.56 l (44% of predicted) and FEV1 was 1.25 l (33% of predicted).
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PMID:[Gastroesophageal reflux as a cause of pulmonary dysfunction after lung transplantation]. 1792 4

Lansoprazole is an acid proton-pump inhibiting drug that is used for the treatment of duodenal or gastric ulcers, H. pylori infection, gastroesophageal reflux disease or Zollinger-Ellison syndrome. Although lansoprazole is well known for its gastrointestinal and dermatologic adverse effects, mild pulmonary symptoms are also known to develop from taking this drug. There have been no reports about lansoprazole-induced interstitial lung disease. We report here a case of lansoprazole-induced interstitial lung disease that developed in a 66-year-old man.
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PMID:Reversible lansoprazole-induced interstitial lung disease showing improvement after drug cessation. 1838 65


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