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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung involvement was assessed in 30 consecutive patients with systemic lupus erythematosus (SLE), not selected by respiratory symptoms. Pulmonary function tests revealed a higher rate of abnormality than either clinical history or radiography. The single breath carbon monoxide diffusing capacity was below 80 per cent of the predicted value in 24 patients (80 per cent), and a reduced total lung capacity was present in 13 (43 per cent). There was a weak correlation between the severity of the functional defect and disease activity, assessed antinuclear factor and DNA binding. No correlation was found with serum complement of Clq precipitation. Since pulmonary fibrosis in SLE is uncommon it cannot account for the high frequency of abnormal findings, and the pathogenesis of the functional changes is probably multifactorial. In seven of the patients with the smallest lung volumes, measurements of static pressure volume curves and of maximum respiratory pressures indicated extrapulmonary volume restriction. In five of these patients, diaphragm function was specifically assessed and found to be grossly abnormal in four. The inability of the diaphragm to generate normal pressure may be due to either severe weakness or immobility following extensive pleural adhesions. The well recognized syndrome of "shrinking lungs" and high "sluggish" diaphragms with clear lung fields on radiography is probably due to dysfunction of the diaphragm rather than to primary intrapulmonary pathology.
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PMID:Diaphragm function and lung involvement in systemic lupus erythematosus. 60 14

Determinants of pulmonary fibrosis induced by inhaled mineral dusts include quantity retained, particle size, and surface area, together with their physical form and the reactive surface groups presented to alveolar cells. The outstanding problem is to ascertain how these factors exert their deleterious effects. Both compact and fibrous minerals inflict membrane damage, for which chemical mechanisms still leave uncertainty. A major weakness of cytotoxicity studies, even when lipid peroxidation and reactive oxygen species are considered, lies in tacitly assuming that membrane damage suffices to account for fibrogenesis, whereas the parallel occurrence of such manifestations does not necessarily imply causation. The two-phase procedure established that particles, both compact and fibrous, induce release of a macrophage factor that provokes fibroblasts into collagen synthesis. The amino acid composition of the macrophage fibrogenic factor was characterized and its intracellular action explained. Fibrous particles introduce complexities respecting type, durability, and dimensions. Asbestotic fibrosis is believed to depend on long fibers, but scrutiny of the evidence from experimental and human sources reveals that a role for short fibers needs to be entertained. Using the two-phase system, short fibers proved fibrogenic. Other mechanisms, agonistic and antagonistic, may participate. Growth factors may affect the fibroblast population and collagen production, with cytokines such as interleukin-1 and tumor necrosis factor exerting control. Immune involvement is best regarded as an epiphenomenon. Downregulation of fibrogenesis may follow collagenase release from macrophages and fibroblasts, while augmented type II cell secretion of lipid can interfere with the macrophage-particle reaction.
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PMID:Minerals, fibrosis, and the lung. 195 26

Clinical symptoms and signs and the frequency of abnormalities in the results of enzymatic, electromyographic, histological and serological tests were analysed in 50 patients, including 17 with polymyositis (PM) and 33 with dermatomyositis (DM), groups I and II according to Bohan's classification and followed-up for 25 years. Weakness of the proximal muscles of the extremities was present in both groups in all patients and in a high proportion of cases weakness involved also the distal muscles. Dysphagia was more frequent in DM patients (54.5%) than in PM (17.6%). In DM erythema and facial oedema as well as Gottron's sign were observed more frequently. In 11.8% of PM patients and 15.1% of DM patients deposition of calcium salts in subcutaneous tissue developed. Signs of vasculitis were found in 39.4% of DM cases and 17.6% of PM cases. In one-third of PM and in only 3 DM cases pitting oedema of the distal parts of the extremities was noted. Cardiovascular changes were disclosed in 82.3% of PM and 69.7% of DM patients. On the other hand, radiological signs of interstitial pulmonary fibrosis were noted more frequently in DM (36%) than in PM (23%). Increased serum activity of CPK, AspAT and ALAT was present with similar frequency in both groups from 71% to 81% of cases. EMG showed evidence of primary muscular changes in all PM patients and 69.6% of DM patients. Histological examination confirmed the diagnosis in the studied patients. Antinuclear antibodies were found relatively rarely, from 2% to 24% of PM/DM patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Polymyositis-dermatomyositis--a 25-year follow-up of 50 patients (analysis of clinical symptoms and signs and results of laboratory tests). 213 28

A case of pneumonitis and pulmonary fibrosis occurring during long term treatment with amiodarone hydrochloride is described. The patient, a 68 year old woman, presented with severe dyspnoea and weakness 13 months after the institution of amiodarone therapy, 200 mg. bid 6 days/week. Chest x-ray showed patchy infiltrates involving the parahilar and medullary areas of both upper lobes. The clinical symptoms and the pulmonary signs improved only after amiodarone discontinuation and steroid treatment. Radiographic abnormalities gradually cleared over 45 days except for residual lines of fibrosis in the zones of previous alveolar consolidation still present 4 months later.
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PMID:Lung disease associated with amiodarone treatment. 405 92

A 64-year-old Black woman presented with high titer serum rheumatoid factor (RF), pelvic girdle weakness, sensory mononeuropathy, pulmonary fibrosis, and muscle histologic evidence of small artery necrotizing vasculitis. High dose corticosteroid therapy was followed by clinical improvement and reduction in serum RF titer. Four years later, and 9 months after discontinuance of corticosteroids, she developed an inflammatory polyarthritis, recurrent muscle weakness, and left foot drop, concomitantly with circulating immune complexes and extremely high titer serum RF. Necrotizing vasculitis is a distinctly rare presenting manifestation of rheumatoid disease.
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PMID:Necrotizing vasculitis as the initial manifestation of rheumatoid arthritis. 686 90

Twenty-four cases of polymyositis, 3 (12.5%) of them Dermatomyositis, have been treated and followed up for over 12 years. Majority (75%) were males. Inflammatory lesion was the cause in 18 (75%), collagen disease in 4 (16.7%) and malignancy in 2 (8.35%). Presenting features were fever (100%), proximal muscle weakness (95.8%) and tenderness (54.2%), facial and respiratory muscle weakness (4.2%). Raised CPK and transaminases, electromyogram abnormality and positive muscle biopsy were recorded in all. All were treated with steroids. Complication/associations noted were arthalgia (25%), dysphagia (20.6%), peripheral neuritis (8.35%), diabetes mellitus (4.2%), pulmonary fibrosis (4.2%) and malabsorption (4.2%). Fourteen cases (58%), all of inflammatory aetiology, recovered completely. Seven cases (29.2%) developed permanent atrophy of affected muscles. Cases with collagen disease and malignancy fared worse and deteriorated because of the primary disease.
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PMID:Polymyositis--a review and follow up study of 24 cases. 800 72

Over 100 cases of disorders closely resembling classic autoimmune diseases have been reported among patients who were injected or implanted with a diverse group of chemicals including paraffins, vegetable oils or silicone. Most cases have occurred in silicone breast implant recipients, especially those who received their prostheses 2-10 years prior to onset of symptoms. A high proportion of patients exhibit classic signs and symptoms of Sjogren's syndrome or scleroderma. Affected patients typically experience some combination of fatigue, myalgia, joint pain, sicca syndrome (dry eyes and mouth), synovitis, rash, alopecia, muscular weakness or lymphadenopathy, and autoantibody formation. Less commonly, patients may have the CREST syndrome (calcinosis, Raynaud's phenomena, esophageal hypomotility, sclerodactyly and telangiectasias), hypertension, pulmonary fibrosis, or central nervous system pathology.
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PMID:Silicone-reactive disorder: a new autoimmune disease caused by immunostimulation and superantigens. 828 1

We report a 79-year-old man who developed progressive gait disturbance and sensory loss. He had been doing well except for hepatitis B virus hepatitis until 72 years of age when he developed angina pectoris for which aorto-coronary bypass operation was performed when he was 73-year-old (1986). In 1990, he developed pulmonary fibrosis for which prednisolone was prescribed. His liver function deteriorated, and the liver function tests suggested liver cirrhosis. He noted an onset of gait disturbance in the middle of June in 1992 when he was 79-year-old. His gait disturbance deteriorated progressively, and he developed edema and loss of sensation in his both legs. He became unable to walk unassisted in the beginning of July. He fractured his right external malleolus after falling down from a chair. He became unable to stand by himself, and he was admitted to the cardiology service of our hospital on July 18, 1992, and the neurology service was asked to see the patient on July 30 of the same month. The patient was well developed and well nourished man in no acute distress. General physical examination revealed slight jaundice, left carotid bruit, and slight pitting pretibial edema. His temperature was 37.3 degrees C. On neurologic examination, he was alert and mentally sound without dementia. He showed a slight weakness in the facial muscles bilaterally and mild dysarthria and dysphagia, however, the other cranial nerves appeared intact. He was unable to stand unassisted. The muscle tone was hypotonic, however, no focal muscle atrophy was noted, nor was observed fasciculatory twitches.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 79-year-old man with rapidly progressive tetraparesis]. 829 70

To assess the feasibility of treatments for patients with small cell lung cancer (SCLC) showing a poor performance status (PS, Eastern Cooperative Oncology Group; ECOG 3 or 4), we retrospectively reviewed the outcome for 13 SCLC patients showing poor PS treated at the National Cancer Center Hospital between January 1984 and May 1994. The main factors which contributed to poor prognosis were superior vena cava (SVC) syndrome, massive pleural effusion, tracheal stenosis due to lymph node swelling, pericardial effusion and pulmonary fibrosis (causing dyspnea in combination), brain metastasis resulting in neurological disturbance, cachexia, Eaton-Lambert syndrome causing muscle weakness, retroperitoneal lymph node metastasis causing abdominal pain, peritoneal effusion due to abdominal lymph node swelling, vertebral metastasis causing paraplegia, and dermatomyositis/polymyositis (DM/PM) causing muscle weakness. All of the patients received chemotherapy with or without radiotherapy. The PS of 8 patients improved with treatment, but no improvement was seen in 5. We analyzed these 13 patients and considered the treatments for those with poor PS. Chemo-radiotherapy was tolerable in SCLC patients showing PS 3, and improved their PS if severe conditions or combined disease did not arise concurrently. It was further suggested that PS 4 patients with severe conditions or combined disease should not be given the treatments.
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PMID:Retrospective analysis of the treatment of patients with small cell lung cancer showing poor performance status. 865 51

A 56-year-old man experienced dyspnea since August 1995 and the chest X-ray film showed abnormal shadow. The diagnosis of bronchiolitis obliterans organizing pneumonia (BOOP) was established based on the histological findings of transbronchial lung biopsy. The patient was treated with prednisolone and symptoms improved. Myalgia and muscle weakness developed associated with relapse of BOOP after withdrawal of prednisolone. Patient was admitted to our department on December 1995 for further examination. An increased level of serum CPK, histological findings of muscle biopsy consistent with myositis, and positive anti-Jo-1 antibody were identified. Those findings supported a diagnosis of polymyositis (PM), and BOOP was considered as a pulmonary complication of PM. Myositis and pulmonary lesion improved after second course of steroid therapy and patient was discharged on May 1996. Both chronic pulmonary fibrosis and acute progressive interstital pneumonia are well known as pulmonary lesion associated with PM. The former is frequently recognized in cases of PM with anti-Jo-1 antibody and the latter is often observed in cases without autoantibodies. The association of PM and BOOP, however, has rarely been reported. The findings that BOOP frequently preceded PM and anti-Jo-1 antibody was positive in half of the cases were observed in the literature.
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PMID:[A case of polymyositis with anti-Jo-1 antibody preceded by BOOP]. 966 82


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