Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 68-year old man experienced a progressive proximal tetraparesis with anhidrosis and a single episode of horizontal diplopia before presenting exertional dyspnea; pulmonary investigations revealed a small cell carcinoma of the lung. Clinical and electrophysiological investigations with abnormal SFEMG, repetitive stimulations and autonomic assessment pointed to a pre-synaptic neuromuscular dysfunction compatible with a Lambert-Eaton syndrome. Antibodies to acetylcholine receptors and calcium channels were negative. Thoracic radiotherapy combined with chemotherapy produced marked improvement: repeated electrophysiological evaluations showed a strong correlation between median nerve CMAP amplitude and clinical course. This case prompted us to discuss current concepts of pre-synaptic dysfunction, and paraneoplastic syndrome, and to review therapeutic strategies, in the light of recent studies of Lambert-Eaton syndrome.
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PMID:[Lambert-Eaton myasthenic syndrome. Physiopathological aspects and therapeutic modalities]. 136 69

Of 60 cases with pericardial metastatic disease, 26 had significant effects on the cardiovascular system. Pericardial metastases were suspected in 18 of these cases before death. The most common features reported were dyspnea on exertion and pleural effusion. While these were nonspecific for circulatory disturbance, ECG features of ST-T changes and low voltage QRS complexes were helpful in suspecting pericardial metastases. Thoracic roentgenograms were not helpful unless there was a large pericardial effusion. Echocardiography reported in one case promises a higher incidence of suspicion in the future.
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PMID:Clinical and pathologic features of metastatic neoplasms of the pericardium. 705 81

Restrictive lung disease is often first detected when patients complain of dyspnea on exertion. Many forms of exercise testing are available, from simple hallway oximetry to the more formal and more complex cardiopulmonary exercise test. Although the use of exercise for diagnosis, treatment, and predicting outcomes is largely understudied in this population, it has recently been shown to be of value in some settings. Exercise testing may be a valuable diagnostic tool in determining the extent of lung disease in sarcoidosis. Medinger et al. reported that the symptom-limited exercise test detected pulmonary dysfunction earlier than history, physical examination, chest radiography, and spirometry alone. Furthermore, Delobbe et al. noted that in patients with biopsy-proved sarcoidosis, cardiopulmonary exercise testing was a more sensitive indicator of early lung disease than pulmonary function tests. The American College of Chest Physicians/American Thoracic Society have published an updated consensus statement for cardiopulmonary exercise testing. Christensen et al. reported that patients with restrictive lung disease may be at risk for hypoxemia with light exercise while on an airplane, and suggest that these patients be considered for in-flight oxygen therapy. Lastly, Herridge and the Canadian Critical Care Trial Group used the 6-minute walk test to prove that survivors of acute respiratory distress syndrome have significant functional limitation 1 year after discharge from the intensive care unit largely secondary to neuromuscular sequelae. Exercise testing appears to be a valuable tool in evaluating, treating, and predicting outcomes in patients with restrictive lung disease. Further study will help to support its use in other restrictive lung diseases.
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PMID:Role of exercise evaluation in restrictive lung disease: new insights between March 2001 and February 2003. 1290 12

We report a case of delayed bronchial stenosis after blunt chest trauma with right aortic arch. A 21-year-old male passenger was involved in a traffic accident. He was brought to an emergency hospital with severe chest pain and dyspnea, and diagnosed with multiple rib fractures, right hemopneumothorax and chylothorax. He was treated with chest tube drainage and the symptoms subsided. About 9 weeks later, he complained of exertional dyspnea and was referred to our hospital. Bronchoscopy demonstrated circumferential stenosis of the right main bronchus approximately 1 cm distal to the carina. Thoracic computed tomography and magnetic resonance imaging revealed the right aortic arch. Successful resection of the bronchial stenotic lesion was performed followed by end-to-end anastomosis through midsternotomy due to the associated right aortic arch. Postoperative bronchoscopy revealed that the site of the anastomosis was patent and his symptoms were relieved.
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PMID:Delayed bronchial stenosis after blunt chest trauma with right aortic arch. 1499 77

Tiotropium bromide (Spiriva) is a long-acting anticholinergic bronchodilator that maintains bronchodilation for at least 24 hours, allowing once-daily administration. The active moiety is the tiotropium cation (tiotropium); tiotropium bromide 22.5 micrograms is equivalent to 18 micrograms of tiotropium cation. Greater improvements in lung function from baseline (primary endpoint mean trough FEV(1)) were observed with inhaled tiotropium 18 micrograms once daily than with placebo in 6-month and 1-year randomized, double-blind trials in patients with COPD. Tiotropium improved lung function (trough FEV(1) response) more effectively than ipratropium bromide (ipratropium) 40 micrograms four times daily in 1-year clinical trials, and was at least as effective as salmeterol 50 micrograms 12-hourly in 6-month trials. Preliminary data suggest that tiotropium alone or in combination with once-daily formoterol has a greater bronchodilator effect than twice-daily formoterol in patients with COPD. Improvements in patients' perception of health-related quality of life (HR-QOL) or dyspnea were greater with tiotropium than with placebo or ipratropium, and were similar to those with salmeterol. Reductions in the frequency and severity of acute exacerbations and in the use of rescue medication were also greater with tiotropium than with ipratropium or placebo. There was no evidence of tachyphylaxis with tiotropium during 1-year clinical trials. Inhaled tiotropium was generally well tolerated in clinical trials. Apart from dry mouth, the type and incidence of adverse events with tiotropium were similar to those with ipratropium, salmeterol or placebo in patients with COPD. In conclusion, inhaled tiotropium 18 micrograms once daily improved lung function, dyspnea, and HR-QOL, and decreased the incidence of acute COPD exacerbations and the use of rescue medication relative to placebo or ipratropium in clinical trials in patients with COPD. Tiotropium was at least as effective as salmeterol in terms of bronchodilator efficacy and improvements in dyspnea or HR-QOL. With the exception of dry mouth, the tolerability profile of tiotropium was similar to that with placebo, ipratropium, or salmeterol. Consequently, inhaled tiotropium is likely to be a valuable option for first-line, long-term maintenance therapy in the management of bronchoconstriction in patients with symptomatic COPD. Tiotropium bromide has a quaternary ammonium structure and acts as an anticholinergic bronchodilator; the active moiety is the tiotropium cation (tiotropium). A 22.5 micrograms dose of tiotropium bromide provides 18 micrograms of tiotropium. Orally inhaled tiotropium bromide antagonizes the muscarinic M(1), M(2), and M(3) receptors located in airway smooth muscle, reversing vagally mediated bronchoconstriction. Receptor binding assays and in vitro tests indicate that tiotropium bromide is kinetically selective for M(1) and M(3) receptors over the M(2) receptor, unlike ipratropium bromide, which is nonselective. Animal and in vitro studies showed that tiotropium bromide was more potent ( approximate, equals 20-fold) than ipratropium bromide in displacing [(3)H]N-methylscopolamine (NMS) from muscarinic receptors, and had a more sustained protective effect (>70% inhibition) against NMS binding. Tiotropium bromide was a more potent inhibitor of bronchial contraction than atropine ( approximate, equals 23-fold), and had a slower onset and markedly longer duration of action than atropine or an equipotent dose of ipratropium bromide. Aerosol particle penetration is improved with tiotropium, without delaying mucus clearance from the lungs. Tiotropium 4.5-36 micrograms once daily for 4 weeks increased mean trough and average FEV(1) and FVC and mean PEFR values from baseline compared with placebo, with no evidence of tachyphylaxis. Improvements in trough FEV(1) from baseline with tiotropium 4.5-36 micrograms were not dose dependent. Based on a lack of dose response, the optimal once-daily tiotropium dosage is 18 micrograms. Steady-state trough FEV(1) values are achieved within 48 hours of commencing tiotrochodilation (for >/=24 hours) and an attenuation of the nocturnal decline in FEV(1) that were unaffected by timing of the daily tiotropium dose were seen in randomized, double-blind, placebo-controlled studies in patients with stable COPD. The drug improved static and dynamic lung hyperinflation (evidenced by reduced trapped air volume and increased tidal volume and end-of-exercise inspiratory capacity), and improved exertional dyspnea (during activities of daily living and exertion) and exercise tolerance compared with placebo in randomized, double-blind studies. In patients with stable COPD, improved sleep-related oxygen desaturation that was unaffected by the timing of the daily dose was seen with tiotropium but not with placebo. Clinically significant treatment-related disorders of conduction or rhythm, or changes in heart rate were not observed with tiotropium in this patient group. Mean maximal plasma concentrations (C(max)) were observed within 5 minutes of inhalation of a single dose of tiotropium 18 micrograms in patients with COPD. Plasma drug levels declined to minimum concentrations (C(min)) within 1 hour of treatment in healthy volunteers. Mean steady-state C(max) concentrations (16 ng/L) were achieved after 2-3 weeks of once-daily inhaled tiotropium 18 micrograms in elderly patients with COPD; tiotropium does not appear to accumulate once steady-state has been achieved.The estimated absolute bioavailability of tiotropium at steady state in healthy volunteers was approximately 20-25%, and approximately 72% of the drug is bound to plasma proteins. Excretion of tiotropium is predominantly renal (through active secretion by the kidneys), although in vitro studies suggest that cytochrome P450 (CYP) oxidation (possibly involving CYP2D6 and CYP3A4 enzymes) may have a minor role. In patients with COPD, renal excretion of the unchanged drug at 24 hours (Ae(24)) was approximately 7%. The mean plasma elimination half-life after single or multiple doses in healthy volunteers and elderly patients with COPD was approximately 5-6 days. The renal clearance and urinary excretion of tiotropium decrease with increasing age; however, these changes are not considered to be clinically significant. Because of altered steady-state C(max), C(min), area under the concentration-time curve, and Ae(24) values, caution is required with tiotropium administration in patients with moderate-to-severe renal impairment. The pharmacokinetics of tiotropium in patients with severe renal or hepatic impairment have not been studied. Tiotropium does not interact with drugs such as cimetidine or ranitidine, which are also eliminated by active renal secretion. Orally inhaled tiotropium bromide has been evaluated as a bronchodilator for the management of patients with COPD in randomized, double-blind 6-month and 1-year trials, and in several shorter studies. In clinical trials, COPD was diagnosed according to the American Thoracic Society guidelines. The bronchodilator effect was expressed as the trough FEV(1) response (the mean change in FEV(1) from baseline measured 1 hour prior to and immediately before a scheduled dose), and was the primary endpoint in all but two clinical trials. The bronchodilator effect with tiotropium 18 micrograms once daily was superior to that with placebo in several well designed trials in patients with COPD. Moreover, greater improvements in mean peak and average FEV(1) responses occurred with tiotropium but not with placebo. Mean trough, peak, and average FVC responses, and weekly mean morning and evening PEFR values were also improved to a greater extent with tiotropium than with placebo. Tiotropium demonstrated a greater bronchodilator effect than ipratropium bromide (hereafter referred to as ipratropium when used at approved dosages) 40 micrograms four times daily in two 1-year trials in patients with COPD. Mean peak and average FEV(1), mean trough FVC responses, and weekly mean morning and evening PEFR values were also increased to a greater extent with tiotropium than with ipratropium. In one of the two 6-month trials that compared the efficacy of tiotropium with that of inhaled salmeterol 50 micrograms twice daily, greater improvements from baseline in mean trough, peak, and average FEV(1) and FVC responses were seen with tiotropium than with salmeterol. Increases in weekly mean evening, but not morning, PEFR values were generally greater with tiotropium than salmeterol. In the second trial, improvement in the primary endpoint (mean trough FEV(1) response from baseline) with tiotropium or salmeterol was similar, although peak and average responses were superior with tiotropium. Preliminary results from a 6-week crossover study in patients with COPD suggested that tiotropium alone or in combination with once-daily formoterol improved mean trough and average FEV(1) and trough FVC values from baseline to a greater extent than twice-daily formoterol. More patients achieved a clinically important improvement (increase of >/=1 unit) in the transitional dyspnea index focal score (a measure of dyspnea-related impairment) with tiotropium than with placebo in the 1-year trials. Tiotropium was superior to ipratropium in 1-year trials, and was at least as effective as salmeterol in 6-month trials, in achieving a clinically important improvement in focal scores. Tiotropium recipients experienced fewer COPD exacerbations than placebo or ipratropium recipients and had fewer and shorter COPD-related hospitalizations compared with placebo recipients. Unlike salmeterol, tiotropium lengthened the time to onset of the first exacerbation and decreased the number of exacerbations compared with placebo in two 6-month trials. Similar proportions of tiotropium, salmeterol, and placebo recipients required COPD-related hospitalizations. (ABSTRACT TRUNCATED)
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PMID:Tiotropium bromide. A review of its use as maintenance therapy in patients with COPD. 1535 Jan 63

A 65-year-old female had been diagnosed with right lung cancer by her family physician, and she was introduced to our Department of Thoracic Surgery at Matsuyama Red Cross Hospital in May 2004. She underwent a right upper lobectomy and wedge resection of S6 with the systematic dissection of her mediastinal lymph nodes. The patient made an uneventful recovery and was discharged on postoperative day 19. However, chylothorax was detected on a chest roentgenogram when she consulted our outpatient clinic again for dyspnea on exertion and chest pain. Chylothorax occurred in postoperative day 34. The patient initially received conservative therapy, but subsequently underwent surgical treatment and fibrin glue intubation when conservative therapy proved to be unsuccessful.
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PMID:Late-period-onset chylothorax after a pulmonary resection for lung cancer: a case report. 1795 94

Unilateral diaphragm paralysis (UDP) is an important and often unrecognized cause of dyspnea. We report a 72-year-old man in whom UDP was incidentally detected by transthoracic echocardiography. He was asymptomatic at rest, but experienced dyspnea on exertion. Chest radiography was not pathognomonic in this case because the heart silhouette obscured the left diaphragmatic contour. Transthoracic echocardiography showed an extrinsic compression to the right atrium. Right atrial collapse was obvious during heart movements with variation upon respiratory movements. There was no pericardial effusion nor any solid mass lesion. Fluoroscopic sniff test demonstrated a significant paradoxical elevation of the paralyzed right diaphragm in inspiration. Thoracic and abdominal computed tomography scans did not show any other pathology. The diagnosis was made as idiopathic UDP.
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PMID:Right atrial compression due to idiopathic right diaphragm paralysis detected incidentally by transthoracic echocardiography. 1915 48

A 44-year-old woman was admitted to our hospital because of a 15-month history of exertional dyspnea, nonproductive cough and fever. Thoracic high-resolution computed tomography (HRCT) showed centrilobular ground-glass opacities distributed in bilateral lung fields. She had worked at a down quilt factory and had been exposed to a large amount of feathers for 5 years. A peripheral lymphocyte proliferation test by positive was positive for pigeon serum. We diagnosed bird-related hypersensitivity pneumonia. After quitting her job, improvement of her clinical symptoms and chest imaging findings were observed and she has been free of relapse.
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PMID:[A case of acute hypersensitivity pneumonia in a worker at a feather duvet factory]. 2140 Sep 4

We report a case showing delayed hemothorax superimposed on extrapleural hematoma after blunt chest injury. The patient was a 56-year-old man with a medical history of alcoholic hepatopathy who presented with a chief complaint of dyspnea on exertion. One month prior to presentation, he had sustained a fall that had resulted in left simple rib fracture. A chest radiograph taken at the time of injury showed notable reduction in the permeability of the left lung field along with high pulmonary collapse as well as rightward deviation of the shadow of the inferior mediastinum. Chest CT images showed a region of low absorption in the thoracic cavity with septi. Thoracic drainage was performed (1,300 mL total) and hemothorax was diagnosed. Thoracoscopic examination was then performed. When the inside of the thorax was observed, what had been presumed to be the septi of a multilocular fluid collection was found to be actually the parietal pleura, and a hematoma was confirmed inside the extrapleural cavity. The hematoma inside the extrapleural cavity was managed with lavage and drainage, and drainage tubes were placed inside both the thoracic cavity and extrapleural cavity at the end of the procedure. The patient's postoperative course was uneventful, and he was discharged on postoperative day 4.
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PMID:Delayed hemothorax superimposed on extrapleural hematoma after blunt chest injury: a case report. 2403 Apr 85