Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:031673 (collagen)
 124,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary disease has been associated with several chemotherapeutic agents but has not been reported in patients receiving the alkylating agent mitomycin (Mutamycin). We describe here the cases of three patients who developed interstitial pneumonia while receiving mitomycin therapy. Their clinical features including dyspnea, cough, and occasionally fever; reticular infiltrates were seen on chest roentgenogram. Histologically, diffuse alveolar septal edema, mononuclear-cell interstitial infiltrates, hypertrophy of alveolar lining cells, and alveolar septal collagen deposition were characteristic. Treatment with corticosteroids was associated with a rapid therapeutic response in all three patients.
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PMID:Interstitial pneumonia from mitomycin. 68 48

In a series of 2150 patients subjected to bronchoscopy 94 (4.5%) were found to have tracheobronchomalacia. Tracheomalacia alone was diagnosed in 21 patients (22%), tracheobronchomalacia in 59 (63%) and bronchomalacia alone in 14 (15%). Mild malacic changes were noted in 44 patients (47%), moderate in 38 (40.5%) and severe in 12 (12.5%). The main symptoms were dyspnoea (63%), chronic cough with expectoration (49%) and haemoptysis (33%), and the most frequent concurrent diseases chronic bronchitis (53%), bronchial cancer (27.5%) and pulmonary tuberculosis (19%). Bronchoscopy performed under local anaesthesia enabled the dynamics of the tracea and bronchi to be observed during spontaneous breathing and during coughing, and it is the best available diagnostic procedure. Histologically the number of longitudinal elastic fibres in the pars membranacea was clearly reduced throughout the whole tracheal area in one patient with tracheomalacia but no differences were found in the amount of collagen, mucopolysaccharides and elastin in the cartilages of trachea and bronchi. This disease seems to be associated with chronic obstructive pulmonary diseases such as chronic bronchitis, and it apparently shares the same aetiological factors.
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PMID:Acquired tracheobronchomalacia. 88 58

Interstitial lung disease (ILD) has been recognized as a manifestation of polymyositis or dermatomyositis (PM/DM). Patients with PM/DM with anti-Jo-1 antibody had a higher incidence of ILD. Thirty-five patients with PM/DM were studied the antibodies. Six (16.1%) were found to have them. ILD occurred in all 6 anti-Jo-1 positive patients, as opposed to 10 (34.5%) of 29 anti-Jo-1 negative patients. Only 2 cases of undifferentiated connective tissue disease among 1320 patients with various kinds of collagen vascular diseases other than PM/DM were positive for anti-Jo-1 antibody. These two patients also had lung involvement. Among six PM/DM patients with anti-Jo-1 antibody, dyspnea preceded proximal muscle weakness in three patients. In one case, the anti-Jo-1 antibody had been detected one month prior to the onset of myositis. Anti-Jo-1 antibody is a useful marker for PM/DM with ILD.
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PMID:Anti-Jo-1 antibody in patients with polymyositis/dermatomyositis. 130 48

Since July 1988, a total of 92 transbronchial biopsies (TBB) have been performed in 18 patients (aged 3-16 years). Twelve patients (67%) were heart-lung transplant (HLT) recipients undergoing surveillance for pulmonary graft rejection and infection. The remainder included immunocompromised patients at risk of opportunistic infections (n = 4), patients with fibrosing alveolitis (n = 1) and a collagen vascular disorder with suspected lung involvement (n = 1). TBB was performed through either a fiberoptic (n = 50) or a rigid (n = 41) bronchoscope, all under general anesthesia. On one occasion a cardiac bioptome was used through an endotracheal stent. The sensitivity of TBB for diagnosing acute and chronic rejection in HLT patients was 88% and 60%, respectively (specificity, 91% and 100%). Definitive diagnoses were made in 4 (67%) of the non-HLT group. Bronchoalveolar lavage (BAL) was performed during each procedure for microbiological and cytological examination. Thirty-four pathogenic organisms including Pseudomonas aeruginosa (16/34), Staphylococcus aureus (8/34), and Candida albicans (5/34) were isolated from BAL culture. Complications included pneumothorax (8%), transient pyrexia (7%), and dyspnea (2%).
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PMID:Technique and use of transbronchial biopsy in children and adolescents. 161 50

Systemic Sclerosis is a multisystemic disease characterized by sclerosis of the skin and visceral organs, vasculopathy (Raynaud's phenomenon) and autoantibodies. The criteria for the classification of the disease requires either proximal scleroderma (major criteria) or the presence of 2 of the 3 minor features namely sclerodactyly, digital pitting scars and bibasilar pulmonary fibrosis. There are 3 subsets of this condition--diffuse variant, limited variant (CREST syndrome) and Overlap Syndrome (where patients have features of other rheumatic diseases). There are localized forms of scleroderma and pseudoscleroderma states. The presenting features of Systemic Sclerosis are usually Raynaud's, skin changes and arthralgia. Systemic complaints like breathlessness, dyspepsia, etc depending on the organ involved may be present. Management starts with patient education regarding the disease, skin care, exercises and regular medical check-up. There is no miracle cure but much can be done to improve the quality of life of the patient. Nifedepine and other drugs may improve Raynaud's phenomenon. Drugs can be used to treat other complications. Various medication have been tested as disease modifying drugs for scleroderma. These include drugs which inhibit collagen like D-penicillamine, colchicine, and immunosupressive drugs like cyclosporin. Ketotifen, a mast cell stabilizer has been reported to be effective in scleroderma. As it is a relatively safe drug, clinical trials are underway.
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PMID:Systemic sclerosis. 162 Nov 27

A previously healthy 16-year-old girl complaining of fever, hemosputum, chest pain and dyspnea was hospitalized. On admission, physical examination revealed mental confusion, holosystolic heart murmur, and swelling of the left foot. Laboratory investigations showed anemia, leukocytosis, thrombocytopenia, activation of inflammatory reactions, prolongation of PT and APTT, and hypoxia. Antinuclear antibody test was negative. There were no other findings suggestive of collagen diseases such as SLE. Chest X-ray showed consolidation in the left lower lung field and pleural effusion. Echocardiography disclosed a mass lesion in the left atrium in contact with the mitral valve, and mitral regurgitation. No findings indicative of an infectious etiology were present. The patient rapidly improved with high dose corticosteroid and anticoagulant therapy. A venogram of the lower extremity disclosed deep venous thrombosis. A lung ventilation-perfusion scan revealed multiple pulmonary thromboemboli. Elevation of anticardiolipin antibody was noted. Based on these findings, the diagnosis of primary antiphospholipid syndrome was made. Further administration of steroid and anticoagulant resulted in decrease of the titer of anticardiolipin antibody. This is the second report of primary antiphospholipid syndrome in Japan. The clinical significance of this disease is also discussed.
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PMID:[A case of primary antiphospholipid syndrome with fever, pulmonary thromboembolism and endocardial lesion]. 162 84

To investigate the physiologic impairment and the role played by pulmonary function tests in interstitial lung disease (ILD), we performed spirometry tests and tested the single-breath carbon monoxide diffusing capacity of 27 patients with diffuse interstitial pulmonary fibrosis (DIPF) and 35 patients with collagen vascular disease (CVD). All of the patients showed irregular linear opacities on their chest X-ray films. Corresponding chest roentgenograms for each patient were evaluated according to the International Labour Organization (ILO) classification. A modified Baseline Dyspnea Index (BDI), which incorporate a patient's physical activity into the recording, was used to quantitate dyspnea. Patients with DIPF demonstrated a comparable reduction in both lung volumes and diffusing capacity. In contrast, patients with CVD had a greater reduction in diffusing capacity than in forced vital capacity (FVC) and total lung capacity (TLC). There were no significant correlations between the type of linear opacities and the severity of the pulmonary function abnormalities, or between the opacities and the dyspnea in either disease group. The profusion of pulmonary infiltrates also did not affect the lung function except for diffusing capacity in patients with DIPF. However, there was a significant loss of FVC, TLC, forced expiratory volume in one second (FEV1) and diffusing capacity with increasing levels of dyspnea. We conclude that pulmonary function parameters may not be equally affected in DIPF and CVD. Approaches using the ILO classification for analysis of chest roentgenograms provide limited information regarding the functional status of patients. Pulmonary functions are significantly related to the extent of a patient's physical activity, if the severity of dyspnea is evaluated carefully using a quantifiable system.
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PMID:Lung volume, diffusing capacity, chest roentgenogram and dyspnea index in interstitial lung disease. 167 99

A 19-year-old male was admitted to Teikyo University Hospital because of dyspnea. The chest film revealed pneumothorax of the right side. The patient was tall and thin, with long tapered extremities. The lens showed ectopia lentis. Echography of the heart showed dilatation of the aorta. A diagnosis of Marfan's syndrome was established on the basis of characteristic skeletal, ocular and cardiovascular findings. At thoracotomy, several bullae were removed by wedge resection. Collagen type distribution in the lung was investigated by an indirect immunohistochemical study using type-special antibody of type I collagen. There were no significant differences in collagen type I in the lung between Marfan's syndrome and control. This suggests that type I collagen in Marfan's syndrome cannot be distinguished from normal collagen I by indirect immunochemical study.
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PMID:[A case report of spontaneous pneumothorax in Marfan's syndrome and an immunohistochemical study of type I collagen in lung tissue]. 175 46

Sarcoidosis is a granulomatous multisystemic disorder, of unknown origin, that commonly affects young adults between 20-40 years of age. The disease usually manifests itself with changes in the chest which are radiologically visible in 90% of the patients in the form of bilateral hilar lymphadenopathy to interstitial infiltrates in the lungs and bronchi. Once the diagnosis of sarcoidosis has been established, the next step is to evaluate the activity and stadium of the disease. These activity markers include clinical, biochemical and immunological parameters. The clinical criteria include symptoms which indicate the clinical manifestation of sarcoidosis, as well as symptoms which are of prognostic importance for the further course of the disease: dry cough, dyspnea, erythema nodosum, posterior uveitis, polyarthralgia, myopathy, cardiac, renal or nervous system involvement, lymphadenopathy, skin lesions, splenomegaly, enlarged parotid and lacrimal glands, changes in chest x-ray and changes in pulmonary function tests. Biological criteria: biochemical markers in serum which are related to: macrophage and epithelioid cell activity, to lymphocyte activity, to granuloma activity and to collagen metabolism alterations; isotopic markers--67 gallium scan and cellular and soluble components in bronchoalveolar lavage fluid (BAL).
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PMID:[Sarcoidosis activity markers]. 180 91

Pulmonary lymphangioleiomyomatosis (p.l.) is a rare disease of unknown etiology, and restricted to fertile women. It is characterized by a nodular proliferation of smooth muscle cells in the peribronchial, perivascular and perilymphatic lung tissue, accompanied by cystic dilations of the alveoles, rupture of the alveolar wall, lymphangiectasis, and septal collagen fiber deposition. Radiological-alterations range from enhanced interstitial shadowing to honey comb lung. Common clinical symptoms are progressive dyspnea, pneumothorax, chylous pleural effusion and hemoptysis. Here we present the case of a 43 years old woman, undergoing nephrectomy because of hamartoma of the left kidney, with recurrent pneumothorax and progressive dyspnea, verifying the diagnosis of p.l. by open lung biopsy. Pathogenesis of the disease, differential diagnosis and possible therapeutic approaches are discussed.
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PMID:[A rare interstitial lung disease]. 194 56


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