Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pertussis, or "whooping cough," is a highly communicable disease caused by the coccobacillus Bordetella pertussis. Pertussis remains one of the most common causes of death from infectious diseases worldwide. We describe a 5-week-old infant girl who presented with severe pertussis infection associated with extreme leukocytosis and required prolonged extracorporeal membrane oxygenation (ECMO). Nitric oxide therapy resolved the pulmonary hypertension, and she was successfully weaned from ECMO and discharged home after 3 months. We report successful application of ECMO for severe pertussis-induced respiratory failure despite multiple grave prognostic indicators (<1 year age, leukocytosis, pulmonary hypertension) and discuss the role of extracorporeal life support in treating pertussis.
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PMID:Pertussis with severe pulmonary hypertension and leukocytosis treated with extracorporeal membrane oxygenation. 1593 56

Diffuse pulmonary hemorrhage leading to death is a syndrome which may develop in leptospirosis, but its pathophysiology is not well documented. We report an autopsy case of leptospirosis. A healthy 41-year-old man presented with low back myalgia, dry cough and fever for 4 days and a normal chest X-ray on admission. Acute respiratory failure developed hours later. Profuse bloody fluid appeared in the endotracheal tube immediately after intubation. Chest X-ray showed whiteness across all lung fields. He died of persistent shock 16 h after the onset of acute respiratory failure. Autopsy revealed diffuse pulmonary hemorrhage with hyaline-membrane formation, myocarditis, interstitial nephritis and hepatitis. Silver stain of lung and kidney tissue demonstrated leptospires. Immunohistochemical staining showed inducible nitric oxide synthase in alveolar macrophages. Immunofluorescein staining showed immunoglobulin in alveolar septum and alveolar space. This case suggests that hemorrhagic diffuse alveolar damage with persistent shock is related to over-production of nitric oxide and immunoglobulin deposition in fatal leptospirosis.
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PMID:Nitric oxide production and immunoglobulin deposition in leptospiral hemorrhagic respiratory failure. 1638 81

Angiotensin-converting enzyme (ACE) inhibitors may induce cough and rhinopharyngeal inflammation. Obstructive sleep apnea (OSA) is characterized by upper airway inflammation. We describe a patient who, during enalapril treatment, developed cough, upper airway symptoms, and diurnal sleepiness, with an increased number of obstructive apnea-hypopnea episodes (apnea-hypopnea index [AHI], 25) during sleep. Her symptoms and AHI improved 1 month after enalapril was discontinued and diuretic therapy (hydrochlorothiazide-spironolactone) was initiated. Similar findings were observed in 4 other patients with OSA who had ACE inhibitor-induced cough. The mean +/- SD AHI was 33.8+/-21.0 during enalapril treatment and 20.0+/-17.0 after withdrawal of this drug (P = .04). Exhaled nitric oxide, a marker of airway inflammation, was increased during enalapril treatment (15.0 +/- 4.3 parts per billion) and decreased after discontinuation of this drug (9.0 +/- 2.6; P = .03). No significant difference in the AHI and exhaled nitric oxide was observed in 4 patients with OSA who did not experience cough, before or after withdrawal of ACE inhibitor treatment. These findings suggest that ACE inhibitor treatment may contribute to OSA by inducing upper airway inflammation.
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PMID:Angiotensin-converting enzyme inhibitors and obstructive sleep apnea. 1643 79

Suppurative cough can be defined as a cough where purulent sputum is produced. Chronic suppurative cough may be associated with the destruction of the bronchial wall (bronchiectasis). As mild forms of the disease are not associated with respiratory limitation or failure to thrive, such children may not present for investigation and therefore the true incidence of suppurative cough is difficult to gauge. Chronic suppurative cough remains an important health problem in developing countries and some indigenous populations of developed countries. The purpose of this review is to present the appropriate investigations and evaluate the evidence for current management strategies in children with suppurative cough. To accomplish this, a brief discussion on the aetiology of suppurative cough in childhood is presented. The most commonly identifiable cause of suppurative cough is cystic fibrosis. A detailed discussion on cystic fibrosis is beyond the scope of this review. Other causes of chronic suppurative cough in pre-school children may be classified according to congenital malformations of the airway, immunodeficiency, ciliary dysfunction and, unusually, acquired causes. Microbiology of sputum culture or bronchoalveolar lavage, assessment of immune function, the role of exhaled nitric oxide and ciliary studies, and medical imaging are discussed in detail. One can conclude that the evidence for management strategies for children with suppurative cough is, at best, level 3 evidence, i.e. non-randomised, controlled or cohort studies.
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PMID:Investigation and management of suppurative cough in pre-school children. 1647 11

This investigation examined a possible correlation between lipopolysaccharide (LPS)-induced pulmonary neutrophilia and cough. Conscious male guinea pigs were acutely exposed to aerosolized LPS and thereafter at various times challenged with citric acid aerosol (CA; 250mM) to induce cough followed by bronchoalveolar lavage (BAL) to quantitate inflammatory cell accumulation. LPS caused a hyporesponsive cough at 24h post-LPS with neutrophilia apparent from 2h post-LPS. By 96h post-LPS both cough and neutrophilia had returned towards normal. Dexamethasone (DEX, 2mgkg(-1)/day for 3 days prior) did not affect the cough hyporesponsiveness at 24h; however it attenuated LPS-induced BAL fluid neutrophilia. Since LPS can stimulate inducible nitric oxide synthase (iNOS) we hypothesized that the cough hyporesponsiveness may involve nitric oxide. To investigate this we treated animals with an aerosolized iNOS inhibitor 1400W (1mM) immediately prior to LPS. 1400W had no significant effect on either cough hyporesponsiveness or BAL fluid neutrophilia at 24h post-LPS. Despite differing effects on neutrophilia, these findings clearly indicate that neither DEX nor iNOS inhibition had any direct effect on LPS-induced cough hyporesponsiveness. The mechanism underlying the LPS-induced cough hyporesponsiveness does not appear to be directly linked to LPS-induced neutrophilic inflammation.
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PMID:Modulation of citric acid-induced cough following lipopolysaccharide-mediated neutrophilia in the guinea pig. 1648 Dec 6

Licorice, the roots of Glycyrrhiza inflata, is used by practitioners of alternative medicine to treat individuals with gastric or duodenal ulcers, bronchitis, cough, arthritis, adrenal insufficiency, and allergies. We investigated the anti-inflammatory properties of 4 licorice extracts: extracts of roasted licorice obtained by ethanol (rLE) or water extraction (rLW) and extracts of raw licorice obtained by ethanol (LE) or water extraction (LW). rLE demonstrated strong anti-inflammatory activity through its ability to reduce nitric oxide and prostaglandin E(2) production in the LPS-stimulated mouse macrophage cell, RAW264.7. It also inhibited the production of pro-inflammatory cytokines and CD14 expression on the LPS-stimulated RAW264.7 cells. Further study indicated that LPS-induced degradation and phosphorylation of Ikappa-Balpha, along with DNA-binding of NF-kappaB, was significantly inhibited by rLE exposure in RAW264.7 cells. In the murine model, we found that in vivo exposure to rLE-induced an increase in the survival rate, reduced plasma levels of TNF-alpha and IL-6, and increased IL-10 production in LPS-treated mice. Collectively, these data suggest that the use of rLE may be a useful therapeutic approach to various inflammatory diseases.
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PMID:Anti-inflammatory effect of roasted licorice extracts on lipopolysaccharide-induced inflammatory responses in murine macrophages. 1671 55

The prevalence of gastroesophageal reflux disease (GERD) is increasing. GERD is a chronic disease and its treatment is problematic. It may present with various symptoms including heartburn, regurgitation, dysphagia, coughing, hoarseness or chest pain. The aim of this study was to investigate if a dietary supplementation containing: melatonin, l-tryptophan, vitamin B6, folic acid, vitamin B12, methionine and betaine would help patients with GERD, and to compare the preparation with 20 mg omeprazole. Melatonin has known inhibitory activities on gastric acid secretion and nitric oxide biosynthesis. Nitric oxide has an important role in the transient lower esophageal sphincter relaxation (TLESR), which is a major mechanism of reflux in patients with GERD. Others biocompounds of the formula display anti-inflammatory and analgesic effects. A single blind randomized study was performed in which 176 patients underwent treatment using the supplement cited above (group A) and 175 received treatment of 20 mg omeprazole (group B). Symptoms were recorded in a diary and changes in severity of symptoms noted. All patients of the group A (100%) reported a complete regression of symptoms after 40 days of treatment. On the other hand, 115 subjects (65.7%) of the omeprazole reported regression of symptoms in the same period. There was statiscally significant difference between the groups (P < 0.05). This formulation promotes regression of GERD symptoms with no significant side effects.
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PMID:Regression of gastroesophageal reflux disease symptoms using dietary supplementation with melatonin, vitamins and aminoacids: comparison with omeprazole. 1694 79

Pulmonary arterial hypertension (PH) is a pathologic condition in dogs characterized by abnormally high pressures in the pulmonary circulation and has been associated with a poor outcome. Sildenafil is a type V phosphodiesterase inhibitor that produces nitric oxide mediated vasodilatation. Sildenafil treatment decreases pulmonary arterial pressure and pulmonary vascular resistance in people with PH. The purpose of this study was to describe the clinical characteristics and outcome of dogs with PH treated with sildenafil. The cardiology database was searched for dogs with PH treated with sildenafil. PH was defined as systolic pulmonary arterial pressure (PAPs) > or = 25 mmHg at rest. Medical records were reviewed for the following information: signalment, duration and type of clinical signs before treatment, underlying disease, estimated or measured PAPs, dosage and dosing interval of sildenafil, and the effect of treatment on clinical signs and pulmonary arterial pressure and survival time. Thirteen affected dogs were identified. Clinical signs included collapse, syncope, respiratory distress, and cough. Duration of clinical signs before presentation ranged from 3 days to 5 months. An underlying cause was identified in 8 dogs. The median sildenafil dosage was 1.9 mg/kg. Ten dogs received concurrent medications. Median PAPs was 90 mmHg; 8 dogs were reevaluated after therapy, and the median decrease in PAPs was 16.5 mmHg. The median survival time of all dogs was 91 days. Sildenafil appeared to be well tolerated in dogs with PH and was associated with decreased PAPs and amelioration of clinical signs in most. Sildenafil represents a reasonable treatment option for dogs with pulmonary hypertension.
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PMID:Retrospective evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs. 1819 19

Data on the efficacy of corticosteroids on respiratory picornavirus-induced wheezing are limited. To determine whether prednisolone is effective in rhinovirus- or enterovirus-induced recurrent wheezing, we conducted a controlled trial comparing oral prednisolone (2 mg/kg/day in three divided doses for 3 days) with placebo in hospitalized wheezing children and studied post hoc virus-specific efficacy in early wheezing (<3 episodes, reported elsewhere) and in recurrent wheezing (>or=3 episodes). Virus-negative children where excluded. Our primary endpoint was the time until children were ready for discharge. Secondary endpoints included oxygen saturation and exhaled nitric oxide during hospitalization, duration of symptoms, blood eosinophil count, and impulse oscillometry 2 wk after discharge, and occurrence of relapses during the following 2 months. Virus-specific effects were analyzed with interaction analysis in a multivariate regression model. During the study period, 661 patients were hospitalized, 293 randomized, and 59 were accepted in this analysis (mean age 2.6 yr, s.d. 1.3). Prednisolone did not significantly decrease the time until ready for discharge in all patients (prednisolone vs. placebo, medians, 18 vs. 24 h, p = 0.11). However, prednisolone decreased the time until ready for discharge in children with picornavirus infection (respectively, 12 vs. 24 h, p = 0.0022) and more specifically, in children with enterovirus infection (6 vs. 35 h, p = 0.0007). In the secondary endpoints, prednisolone decreased the duration of cough and dyspnea in rhinovirus-affected children (p = 0.033 for both). Prospectively designed clinical trial is needed to test the hypothesis that prednisolone reduces symptoms in picornavirus-affected wheezing children.
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PMID:Efficacy of prednisolone in children hospitalized for recurrent wheezing. 1758 12

Asthma is one of the most common aetiologies of chronic cough. In a subgroup of asthmatics, cough may be the predominant or sole symptom. This condition is referred to as cough variant asthma (CVA). The diagnosis of CVA often presents a challenge since physical examination and spirometric tests may be normal. Up to 50% of patients with CVA have associated eosinophilic bronchitis, with the degree of eosinophilia being similar to that of other asthmatics. Demonstration of bronchial hyperresponsiveness by methacholine inhalation challenge, elevated level of exhaled nitric oxide and sputum eosinophilia support the presence of CVA, but the diagnosis is confirmed only upon resolution of the cough with specific antiinflammatory treatment.
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PMID:[Syndrom Corrao--cough variant asthma]. 1764 48


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