Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism causing finger clubbing in patients with lung cancer (LC) is still unclear. We compared age, cigarette consumption, data on blood gas analysis and pulmonary function tests among patients with LC with clubbing (n = 30) and without clubbing (n = 28) and among patients with pulmonary emphysema (PE) with (n = 11) and without clubbing (n = 17). We also examined serum concentrations of transforming growth factor beta 1 (TGF beta 1) and insulin-like growth factor-I (IGF-I) in the patients and healthy volunteers (n = 21). There were no differences in age or cigarette consumption. LC groups showed normal levels of Pao2 and Paco2, suggesting that neither hypoxaemia nor hypercapnia caused clubbing in these patients. The level of serum TGF beta 1 in patients with LC with clubbing was significantly higher than in other groups (P < 0.005), whereas levels of IGF-I did not differ among the groups. Our data suggest that TGF beta 1 may play a role in the mechanism of clubbing in patients with LC.
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PMID:Elevated serum transforming growth factor beta 1 level in primary lung cancer patients with finger clubbing. 888 46

There are several unsolved clinical findings in patients with idiopathic pulmonary fibrosis (IPF); (i) predominance of fibrosis in the lower lung fields, (ii) digital clubbing, and (iii) patchy distribution of pulmonary fibrosis. To explain these unsolved problems, we hypothesized that regenerated or premature bronchoepithelial cells may circulate in the blood in patients with IPF. To prove this, we performed the reverse transcriptase-polymerase chain reaction (RT-PCR) for cytokeratin 19 (CK19) and pulmonary surfactant protein A (SPA) in peripheral blood in patients with IPF and pulmonary fibrosis associated with collagen vascular disorders. In addition, 20 patients with chronic pulmonary emphysema as a disease control and 19 normal volunteers were also evaluated for the existence of circulating bronchoepithelial cells. RT-PCR analysis showed that CK19 was expressed in 12 of 38 blood samples (31.6%) of IPF and pulmonary fibrosis associated with collagen vascular disorders, seven of 20 (35.0%) blood samples of chronic pulmonary emphysema, and four of 19 (21.1%) blood samples of normal volunteers. mRNA for SPA was positive in eight of 38 (21.1%) blood samples of IPF. In contrast, SPA expressing cells were not detected in any blood samples obtained from patients with chronic pulmonary emphysema or normal volunteers. This evidence suggests that there were some circulating bronchoepithelial cells expressing mRNA for SPA in peripheral blood of patients with IPF and pulmonary fibrosis associated with collagen vascular disorders.
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PMID:Circulating bronchoepithelial cells expressing mRNA for surfactant protein A in patients with pulmonary fibrosis. 1086 11

Cystic fibrosis (CF) is an autosomal recessive disorder that is rarely found in Asians. Only four cases of CF from four different families have been reported in Taiwan. We report two cases of CF involving two teenage siblings. Both presented with repeated airway infections, poor weight gain, clubbing of the fingers, hypoxemia, and obstructive ventilatory impairment. Multiple focal bronchiectases and emphysema were demonstrated on high-resolution computed tomography. Sweat chloride concentrations, as measured using the modified sweat chloride test in a closed space with a heater, were 327 mmol/L and 276 mmol/L, respectively. To confirm the CF diagnosis, DNA mutation analysis was performed. All 27 exons of the CF transmembrane conductance regulator (TR) gene and their flanking intron sequences were screened for nucleotide sequence alterations, and the mutations were then identified by direct DNA sequence analysis. Both siblings carried 1898 + 5G-->T; a mutation previously identified in Taiwan. In addition, the mutation analysis identified a new single-base-insertion mutation in exon 13 on the second CFTR allele of these patients. This mutation, named 2215insG, is expected to cause a significant disruption of CFTR function. The 1898 + 5G-->T/2215insG genotype is thus consistent with the CF diagnosis. A new missense mutation, S895N, in exon 15 of the CFTR gene, which cosegregated with 2215insG, was also identified in both of these patients.
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PMID:Novel cystic fibrosis mutation (2215insG) in two adolescent Taiwanese siblings. 1092 68

The syndrome resulting from combined pulmonary fibrosis and emphysema has not been comprehensively described. The current authors conducted a retrospective study of 61 patients with both emphysema of the upper zones and diffuse parenchymal lung disease with fibrosis of the lower zones of the lungs on chest computed tomography. Patients (all smokers) included 60 males and one female, with a mean age of 65 yrs. Dyspnoea on exertion was present in all patients. Basal crackles were found in 87% and finger clubbing in 43%. Pulmonary function tests were as follows (mean+/-sd): total lung capacity 88%+/-17, forced vital capacity (FVC) 88%+/-18, forced expiratory volume in one second (FEV1) 80%+/-21 (% predicted), FEV1/FVC 69%+/-13, carbon monoxide diffusion capacity of the lung 37%+/-16 (% predicted), carbon monoxide transfer coefficient 46%+/-19. Pulmonary hypertension was present in 47% of patients at diagnosis, and 55% during follow-up. Patients were followed for a mean of 2.1+/-2.8 yrs from diagnosis. Survival was 87.5% at 2 yrs and 54.6% at 5 yrs, with a median of 6.1 yrs. The presence of pulmonary hypertension at diagnosis was a critical determinant of prognosis. The authors hereby individualise the computer tomography-defined syndrome of combined pulmonary fibrosis and emphysema characterised by subnormal spirometry, severe impairment of gas exchange, high prevalence of pulmonary hypertension, and poor survival.
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PMID:Combined pulmonary fibrosis and emphysema: a distinct underrecognised entity. 1645 4

Hypertrophic pulmonary osteoarthropathy (HPOA), also known as secondary hypertrophic osteoarthropathy, is a clinical syndrome characterized by proliferative periostitis of the long bones especially in the distal and periarticular aspects, proliferation of the synovial membranes, causing painful and swollen joints, and often with finger clubbing. It is associated with various underlying causes, including pulmonary, pleural, cardiac, abdominal and miscellaneous conditions. Its pulmonary causes include bronchogenic carcinoma, tuberculosis, pulmonary abscess, bronchiectasis, emphysema, etc. Its radiographic presentation involves periostitis in the lower extremities. We report one case that had an incidental finding of HPOA with initial complaint about an incidental solitary knee mass with painful swelling of right knee, leading to early diagnosis of occult bronchogenic carcinoma. The radiographs and magnetic resonance imaging (MRI) revealed periosteal reactions without definite intraosseous lesion. Chest radiography and CT scan disclosed an infiltrating right upper lobe lesion suspicious malignancy. Patient received right S2 segmentectomy of lung with pathological confirmation of adenocarcinoma of lung cancer. It is important for the clinician to be aware of the radiographic findings of periostitis of HPOA, which may be the clues leading to early detection of lung cancer without significant pulmonary symptoms and to avoid possible tumor progression and distant metastases.
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PMID:Incidental solitary knee mass as the first manifestation of hidden lung cancer. 1901 72

Combined pulmonary fibrosis and emphysema (CPFE) syndrome is an uncommon entity characterised by emphysema of the upper lobes and diffuse fibrosis of the lower lobes and carries a bad prognosis with the onset of pulmonary hypertension. Lung involvement due to exposures suffered by welders is generally considered benign though, rarely, a diffuse interstitial fibrotic disease has been reported. CPFE syndrome has however never been reported in welders. A 65-year-old man, welder by occupation and an ex-smoker, presented with progressive exertional dyspnoea associated with dry cough noticed for the last four months. On examination, there was mild tachypnea, clubbing and bilateral basal velcro crepitations on chest auscultation. Lung function test revealed mild mixed ventilatory impairment with severe diffusion defect. HRCT chest showed bilateral upper lobe emphysema and diffuse interstitial fibrosis in the lower lobes. Transbronchial lung biopsy revealed interstitial fibrosis, chronic inflammation and iron deposits. A diagnosis of combined pulmonary fibrosis with emphysema (CPFE) with interstitial pulmonary siderofibrosis (IPS) was established. A review of literature did not show any other report of a similar nature.
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PMID:Combined pulmonary fibrosis and emphysema in a welder. 2266 43

Chronic dyspnea is shortness of breath that lasts more than one month. The perception of dyspnea varies based on behavioral and physiologic responses. Dyspnea that is greater than expected with the degree of exertion is a symptom of disease. Most cases of dyspnea result from asthma, heart failure and myocardial ischemia, chronic obstructive pulmonary disease, interstitial lung disease, pneumonia, or psychogenic disorders. The etiology of dyspnea is multifactorial in about one-third of patients. The clinical presentation alone is adequate to make a diagnosis in 66 percent of patients with dyspnea. Patients' descriptions of the sensation of dyspnea may be helpful, but associated symptoms and risk factors, such as smoking, chemical exposures, and medication use, should also be considered. Examination findings (e.g., jugular venous distention, decreased breath sounds or wheezing, pleural rub, clubbing) may be helpful in making the diagnosis. Initial testing in patients with chronic dyspnea includes chest radiography, electrocardiography, spirometry, complete blood count, and basic metabolic panel. Measurement of brain natriuretic peptide levels may help exclude heart failure, and D-dimer testing may help rule out pulmonary emboli. Pulmonary function studies can be used to identify emphysema and interstitial lung diseases. Computed tomography of the chest is the most appropriate imaging study for diagnosing suspected pulmonary causes of chronic dyspnea. To diagnose pulmonary arterial hypertension or certain interstitial lung diseases, right heart catheterization or bronchoscopy may be needed.
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PMID:Causes and evaluation of chronic dyspnea. 2296 29

A syndrome associating an upper-lobe emphysema and pulmonary fibrosis of the lower lung was recently characterized. Few cases were identified in the literature. We report a case of a 68 year- old smoker man presented for exacerbation of a severe dyspnea. Physical examination revealed basal crackles and finger clubbing. Blood gas analysis showed hypoxemia. Chest radiography showed features compatible with emphysema of the upper lobes and fibrosis of the basis. Chest computed tomography confirmed chest radiography's findings and revealed fibrosis. The diagnosis of idiopathic pulmonary fibrosis was made. Pulmonary function tests showed obstructive pattern. Systolic pulmonary arterial pressure was elevated up to 87 mm Hg on heart ultrasonography. The authors emphasize the importance of the diagnosis of this entity made through chest computed tomography and the fact that it is characterized by severe impairment of gas exchange, the high prevalence of pulmonary hypertension and poor survival.
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PMID:The syndrome of combined pulmonary fibrosis and emphysema. 2519 78

A 50-year-old male, a tobacco smoker, who was known to have ulcerative colitis presented with dry cough, chest pain, dysponea and frequent passage of blood and mucous mixed stools. Physical examination revealed clubbing, subcutaneous emphysema of upper chest and auscultatory findings of crunching sound over pre-cordial area and basal crepitations. Spirometry was suggestive of restrictive pattern. High resolution computed tomography (HRCT) of thorax revealed pneumomediastinum, subcutaneous emphysema, bilateral diffuse centrilobular nodules and ground-glass haziness with mosaic pattern along with posterior basal fibrotic changes. The present case documents the uncommon pulmonary involvement of spontaneous pneumomediastinum and subcutaneous emphysema diffuse parenchymal lung disease, in a patient with ulcerative colitis.
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PMID:A rare case of ulcerative colitis with diffuse parenchymal lung disease, spontaneous pneumomediastinum and subcutaneous emphysema. 2523 May 52

PATIENT PRESENTATION AND DIAGNOSTIC WORK-UP: The patient is a 72-year-old man presenting with dyspnoea on exertion. He is a former heavy smoker (40 pack-years) and his father, now deceased, had rheumatoid arthritis (RA). On physical examination he had mild bi-basilar crackles but no finger clubbing. Autoimmune serology was positive for rheumatoid factor (RF: 25 IU/ml). Lung function tests showed normal FVC, a FEV1/FVC ratio of 72% and a TLCO of 49% predicted. Lung CT showed centrilobular and paraseptal emphysema, subpleural fine reticulation and traction bronchiolectasis, with no clear basal predominance (Figure 1). BAL cytology showed 83% alveolar macrophages, 12% lymphocytes, 3% neutrophils, and 2% eosinophils.
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PMID:Challenges in the classification of fibrotic ILD: Patient case 2. 2623 38


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