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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tracheobronchial aspiration of gastric secretions has been suggested in published reports as a possible cause for idiopathic pulmonary fibrosis. Forty-eight of 131 patients with roentgenographic evidence of pulmonary fibrosis had no established etiologic diagnosis after individualized evaluations. They were prospectively studied by upper gastrointestinal series to determine the incidence of gastroesophageal reflux. The incidence of both hiatal hernia and reflux were statistically higher in the study group than in a group of 270 age-matched controls who had upper gastrointestinal series for the usual indications; (2) a subgroup of 15 patients who had pulmonary fibrosis and serologic evidence which suggested immune-mediated diseases; and (3) a subgroup of 23 patients with pulmonary fibrosis of established etiology. The patients in the study group could be further characterized by clinical and roentgenographic presentations, low maximum-mid-expiratory flow rates, and lung biopsies compatible with interstitial fibrosis. These observations and other cited evidence are supportive of the concept that repeated, small tracheobronchial aspirations of gastric acid secretions over a long period of time may cause interstitial pulmonary fibrosis.
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PMID:Pulmonary fibrosis associated with tracheobronchial aspiration. A study of the frequency of hiatal hernia and gastroesophageal reflux in interstitial pulmonary fibrosis of obscure etiology. 126 17

Gastroesophageal diseases with reflux can cause numerous pulmonary complications (bronchospasm crisis, bronchitis, pneumonias, lung abscesses). These manifestations are very frequent in the hiatal hernias and in some series have reached up to 46 percent of the cases studied. Recently it has been suggested that microaspirations, repeated over a long period of time, may cause an alteration of the pulmonary interstitium and the consecutive development of a clinical and roentgenologic picture similar to pulmonary fibrosis. The aspirations are produced more frequently at night, favoured by the lying down position and because of it the patients present attacks of nocturnal cough. In this paper, two patients who presented the association of pulmonary fibrosis and hiatal hernia with esophageal relux are described. The first case was diagnosed early; he had minimal radiographic anomalies and the disappearance of the respiratory symptomatology was achieved by means of the medical treatment of the esophageal reflux. The second case was in a very advanced stage with severe respiratory insufficiency and gastrointestinal manifestations of many years' evolution. Both patients had been diagnosed as having idiopathic pulmonary fibrosis. Although there is no experimental proof of the "reflux-fibrosis" theory, we think that this possibility should be kept in mind before diagnosing the interstitial pulmonary pattern as idiopathic, especially in the cases of only slight radiographic and functional involvement susceptible to improvement with correction of the esophageal reflux.
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PMID:[The association of diffuse pulmonary fibrosis and hiatal hernia: a simple coincidence? (author's transl)]. 736 85

Interstitial lung diseases (ILD) are disorders of the lower respiratory tract, characterized by chronic inflammation of the lung parenchyma, varying degree of fibrosis, derangement of the alveolar walls and loss of the functional alveolar capillary units. ILD are relatively uncommon in children. Most of the interstitial lung diseases have no known etiology. In children, common diseases associated with ILD include viral respiratory tract infections (RSV, parainfluenza, etc.), gastroesophageal reflux, idiopathic pulmonary fibrosis, pulmonary hemosiderosis, eosinophilic pneumonia, pneumonitis associated with AIDS, etc. Chronic inflammation of the alveoli (alveolitis), the initial injury in ILD, and several mediators released from inflammatory cells (eosinophils, neutrophils and macrophages) can cause fibrosis and derangement of alveolar walls. Dyspnea and a non-productive cough are the cardinal symptoms of ILD. Other findings include chest pain, hemoptysis and weight loss. Clubbing of fingers occur in approximately 50 per cent of cases. Diagnosis is based on a combination of history, clinical findings, radiographic findings, pulmonary function tests and histologic findings. Open lung biopsy has been very helpful in providing information regarding the extent and nature of the damage, prognosis and response to therapy. There are 3 main aspects in the treatment of ILD. The most important step is to identify and eliminate the cause. The second is suppression of the inflammation. The third is supportive and symptomatic treatment. Corticosteroids are the drugs commonly used for suppression of inflammation. Immunosuppressive drugs (azathioprine, cyclophosphamide) have also been tried. Lung transplantation and heart transplantation have been successfully achieved in selected patients. The results of therapy should be regularly monitored by clinical symptoms, chest radiographs and serial pulmonary function studies.
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PMID:Interstitial lung diseases in children: a review. 764 31

One hundred and twenty two patients who were presenting with chronic persistent cough for more than 3-4 weeks were studied. Using anatomical and stepwise approach, we could identify the cause of chronic cough in 96% of the patients. The most common causes were due to postnasal drip syndrome (PND) (45%) and bronchial asthma (26%). We also demonstrated the important role of methacholine inhalation challenge in the diagnostic work up. The procedure could identify the patients who had bronchial hyperresponsiveness (BHR) in 52% of the cases. The severity degree of the BHR was classified into three levels. Mild or nonspecific BHR was defined as PC20 16-25 mg/ml. This could be found in many diseases such as PND and bronchiectasis. Moderate degree of BHR (PC20 8-16 mg/ml) was found in patients with PND and asthma. PC20 of less than 8 mg/ml was considered to be the most severe degree and it seemed to be specific for the diagnosis of asthma (positive predictive value 100%). Other condition that caused chronic cough were drug-induced, especially angiotensin-converting enzyme inhibitors, gastroesophageal reflux disease (GERD), idiopathic pulmonary fibrosis, subgottic cancer and idiopathic cough. These conditions may require invasive diagnostic work up, such as fiberoptic bronchoscopy and tissue biopsy. The treatment of chronic cough was according to the etiology. Thus, the patients presenting with chronic cough should be investigated to identify the cause, and it was not just only the administration of cough suppressant drugs in these patients.
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PMID:The role of the methacholine inhalation challenge in adult patients presenting with chronic cough. 925 42

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

Gastroesophageal reflux disease (GERD) can present with both typical symptoms such as heartburn and regurgitation as well as atypical symptoms. These symptoms may include chest pain, asthma, chronic cough, hoarseness, otitis media, atypical loss of dental enamel, idiopathic pulmonary fibrosis, recurrent pneumonia, chronic bronchitis and even sudden infant death. The diagnosis of GERD in these patients can often present a challenge and usually requires a combination of selected testing and therapeutic trials. Acid suppression by using proton pump inhibitors remains the treatment of choice in GERD, but some patients will also respond well to antireflux surgery. This article addresses the presentations, diagnostic challenges, and therapeutic opportunities in GERD patients with atypical presentations.
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PMID:Gastroesophageal reflux disease: extraesophageal manifestations and therapy. 1121 55

Gastroesophageal reflux (GER) has been associated with a number of interstitial lung diseases, including systemic sclerosis and idiopathic pulmonary fibrosis. Systemic sclerosis results in both pulmonary and esophageal manifestations, and studies have shown a correlation, but no causal relation, between GER and pulmonary fibrosis in this condition. The role of GER in idiopathic pulmonary fibrosis has recently been studied using esophageal pH monitoring, and the results show high prevalence of GER compared with normal individuals and patients with other interstitial lung diseases of known cause. Aggressive, long-term therapy of GER and evaluation of its effect on pulmonary disease will allow determination of the real influence of GER on idiopathic pulmonary fibrosis. Additional outcomes-based studies and therapeutic trials are needed to clarify the association between GER and interstitial lung diseases.
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PMID:Interstitial lung disease and gastroesophageal reflux. 1174 23

Fibroblast foci are indicative of idiopathic pulmonary fibrosis and appear to be a cellular attempt to repair the damaged alveolus. Although this progressive, often fatal, clinical syndrome is thought to be dependent on alveolar injury of unknown origin, significant clinical and preclinical evidence points to gastric acid as a causative harmful agent. Graded instillation of various forms of acid in several animal models resulted in aspiration-induced lung injury, including pulmonary fibrosis in pigs. Moreover, compelling clinical data suggest that a high percentage of patients with idiopathic pulmonary fibrosis also experience abnormal esophageal acid exposure, without necessarily experiencing the typical symptoms of gastroesophageal reflux disease (GERD). Aggressive, long-term therapeutic trials of patients with GERD and evaluation of the therapeutic effects on pulmonary disease will allow determination of the real influences of abnormal esophageal acid exposure in the development of idiopathic pulmonary fibrosis.
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PMID:The role of gastroesophageal reflux in idiopathic pulmonary fibrosis. 1292 77

Gastro-oesophageal reflux disease (GERD) has been associated with a variety of supra-oesophageal symptoms, including asthma, laryngitis, hoarseness, chronic cough, frequent throat clearing and globus pharyngeus. GERD may be overlooked as the underlying mechanism for these symptoms because typical GERD symptoms may be absent, despite abnormal oesophageal acid exposure. Two basic mechanisms linking GERD with laryngeal symptoms have been proposed: direct contact of gastric acid with the upper airway, in some cases due to micro-aspiration, and a vagovagal reflex triggered by acidification of the distal portion of the oesophagus. Gastro-oesophageal reflux (GER) during sleep is believed to be an important mechanism for the development of supra-oesophageal complications of GERD, such as asthma and idiopathic pulmonary fibrosis (IPF). Several physiological changes during sleep, including prolonged oesophageal acid contact time, decreased upper oesophageal sphincter pressure, increased gastric acid secretion, decreased salivation, decreased swallowing and a decrease in conscious perception of acid, render an individual more susceptible to reflux-induced injury. Supra-oesophageal symptoms often improve in response to aggressive acid-suppressive therapy. However, many unanswered questions remain regarding the appropriate approach to diagnosis and treatment of patients with GERD-related supra-oesophageal symptoms. In this article we review the relationship between supra-oesophageal symptoms and GERD and, where possible, highlight the evidence supporting the role of night-time reflux as a contributing factor to these symptoms.
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PMID:Review article: supra-oesophageal manifestations of gastro-oesophageal reflux disease and the role of night-time gastro-oesophageal reflux. 1552 62

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease limited to the lungs and associated with the histologic appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy. The estimated prevalence in the United States is between 35,000 and 55,000 cases,and evidence suggests that the prevalence is increasing for IPF. Risk factors associated with pulmonary fibrosis include smoking, environmental exposures, gastroesophageal reflux dis-ease, commonly prescribed drugs, diabetes mellitus, infectious agents, and genetic factors. The diagnosis requires a careful history and physical examination, characteristic physiological and radiological studies, and, in some cases, a surgical lung biopsy. The natural history of IPF is not known, but evidence supports the concept of a continuum of idiopathic interstitial pneumonias that may overlap in time. Most patients with IPF succumb to respiratory failure, cardiovascular disease, lung cancer, pulmonary embolism, infection, and other health problems. The median survival time for patients with IPF is less than 3 yr. Factors that predict poor outcome include older age, male gender, severe dyspnea, history of cigarette smoking, severe loss of lung function, appearance and severity of fibrosis on radiological studies, lack of response to therapy,and prominent fibroblastic foci on histopathologic evaluation. Conventional therapy (corticosteroids, azathioprine, cyclophosphamide) provides only marginal benefit. Lung transplantation should be considered for patients with IPF refractory to medical therapy. In light of the poor prognosis and lack of response to available anti-inflammatory therapy, alternative approaches to therapy are being pursued. Emerging strategies to treat patients with IPF include agents that inhibit epithelial injury or enhance repair, anti-cytokine approaches, agents that inhibit fibroblast proliferation or induce fibroblast apoptosis, and other novel approaches.
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PMID:Pulmonary fibrosis. 1613 Feb 30


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