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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steroids are used in progressive lung sarcoid despite arguments that spontaneous remission occur and therapy may not alter outcome. We studied a unique group of 6 patients with dyspnea and advancing pulmonary sarcoid, who had documented untreated progressive disease for 6.8 +/- 2.4 years. Raised SACE, Ga 67 lung uptake, and lymphocyte counts in lung lavage fluid indicated continued active alveolitis. After 3-6 months on steroid, MRC dyspnea grade fell from 2.5 to 0.3 and FVC, FEV, and DLCO increased by 36%, 27% and 16% respectively. This was associated with a fall in small opacity profusion scores on x-ray lung uptake of Ga 67 and serum ACE. These improvements were sustained for the duration of follow up (mean 22 months). These data show that steroids can alter the natural history of progressive sarcoid and reversible alveolitis may coexist with established fibrosis.
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PMID:Evidence that steroids alter the natural history of previously untreated progressive pulmonary sarcoidosis. 357 16

Idiopathic pulmonary haemosiderosis (IPH) is a rare disease characterized by recurrent episodes of intrapulmonary bleeding, chronic iron deficiency anaemia and pulmonary fibrosis. IPH is a diagnosis made by exclusion of other causes. It occurs in both adults and children. Other conditions than IPH can cause pulmonary haemosiderosis. The etiology is unknown, but might be an immunological mechanism causing a defect in the basement membrane of the pulmonary capillary. IPH should be suspected in patients with recurrent episodes of coughing, haemoptysis, dyspnoea and anaemia. Chest X-ray shows pulmonary infiltrates during an acute attack. Examination of sputum or lung biopsy discloses large numbers of haemosiderin-laden pulmonary macrophages. The mortality-rate is high, but the prognosis is difficult to evaluate because many patients survive for a long time either with a course of recurrent attacks or with chronic symptoms, such as dyspnoea and persistent anaemia. Steroids may improve the condition of the patient during a bleeding episode.
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PMID:[Idiopathic pulmonary hemosiderosis]. 863 26

Adult respiratory distress syndrome (ARDS) is the pulmonary response to systemic inflammation precipitated by local or systemic tissue hypoxia, or ischaemia and reperfusion. ARDS is a dynamic, pathological process with a multifactorial etiology. The main clinical manifestations of ARDS are dyspnoea, non-cardiogenic pulmonary oedema, and hypoxia due to increased pulmonary capillary permeability, pulmonary vasoconstriction and diminished pulmonary vascular reactivity. Eventually this pulmonary pathology results in first, oedema, pulmonary hypertension, and increased ventilation-perfusion inequality and later, pulmonary remodelling and irreversible pulmonary hypertension. The inflammatory mechanisms involved in acute lung injury are complex and include activation of polymorphonuclear neutrophils, endothelial cells, and synthesis of free radicals, predominantly derived from oxygen. Cytokines synthesized by macrophages maintain and regulate the inflammatory host response. Immune-modulating therapy in ARDS is yet experimental. Accordingly, treatment in ARDS is supportive, directed towards pulmonary oedema, pulmonary hypertension and hypoxaemia. The use of low tidal volumes and low inspiratory pressures in mechanical ventilation is established therapy. The goal in haemodynamic monitoring by applying a Swan-Ganz catheter is to obtain a low pulmonary capillary wedge pressure (< 12-15 mmHg) without compromising adequate delivery of oxygen to vital organs. For treatment of pulmonary hypertension nitric oxide is useful. Change of position and inhalation with beta2-agonists are therapeutic possibilities. Steroids may be of benefit in the late proliferative phase of ARDS.
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PMID:[Acute respiratory distress syndrome. Pathogenesis and therapy of acute pulmonary failure]. 869 17

Chronic obstructive pulmonary disease (COPD) remains difficult to manage. Patients with COPD present with progressive dyspnea; difficulty in stopping smoking; recurrent exacerbations; and, ultimately, respiratory failure. Because of the lack of proven treatments for COPD and because inhaled corticosteroids can prevent airway inflammation and permanent lung damage in patients with asthma, it has become common practice to prescribe inhaled corticosteroids for patients with COPD despite a lack of data suggesting that these agents have any long-term benefit in these patients. In the past 12 months, three randomized, double-blind, placebo-controlled clinical trials (the European Respiratory Society Study on Chronic Obstructive Pulmonary Disease, the Copenhagen City Lung Study, and the Inhaled Steroids in Obstructive Lung Disease study) designed to assess the long-term effect of inhaled corticosteroids in patients with varying severity of airway obstruction have been presented. The results of these studies have been disappointing; they show little to suggest that any long-term benefit is gained from using inhaled corticosteroids in most patients with COPD, whether they continue to smoke or not.
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PMID:Inhaled steroid therapy in chronic obstructive pulmonary disease. 1074 68

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States, and it accounts for approximately 500,000 hospitalizations for exacerbations each year. New definitions of acute COPD exacerbation have been suggested, but the one used by Anthonisen et al. is still widely accepted. It requires the presence of one or more of the following findings: increase in sputum purulence, increase in sputum volume, and worsening of dyspnea. Patients with COPD typically present with acute decompensation of their disease one to three times a year, and 3% to 16% of these will require hospital admission. Hospital mortality of these admissions ranges from 3% to 10% in severe COPD patients, and it is much higher for patients requiring ICU admission. The etiology of the exacerbations is mainly infectious (up to 80%). Other conditions such as heart failure, pulmonary embolism, nonpulmonary infections, and pneumothorax can mimic an acute exacerbation or possibly act as "triggers." Baseline chest radiography and arterial blood gas analysis during an exacerbation are recommended. Oxygen administration through a venturi mask seems to be appropriate and safe, and the oxygen saturation should be kept just above 90%. Either a short acting beta 2-agonist or an anticholinergic is the preferred bronchodilator agent. The choice between the two depends largely on potential undesirable side effects and the patient's coexistent conditions. Adding a second bronchodilator to the first one does not seem to offer much benefit. The evidence suggests similar benefit of MDIs when compared with nebulized treatment for bronchodilator delivery. If MDIs are to be used, spacer devices are recommended. Steroids do improve several outcomes during an acute COPD exacerbation, and a 10- to 14-day course seems appropriate. Antibiotic use has been shown to be beneficial, especially for patients with severe exacerbation. Changes in bacteria strains have been documented during exacerbations, and newer generations of antibiotics might offer a better response rate. There is no role for mucolytic agents or chest physiotherapy in the acute exacerbation setting. Noninvasive positive pressure ventilation might benefit a group of patients with rapid decline in respiratory function and gas exchange. It has the potential to decrease the need for intubation and invasive mechanical ventilation and possibly decrease in-hospital mortality.
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PMID:Evidence-based approach to acute exacerbations of COPD. 1257 91

Organising pneumonia (OP) is a rare syndrome that has been associated with a variety of underlying disorders, including infections, collagen vascular diseases, toxic fumes, cancer, drugs and radiotherapy. Cryptogenic form is also observed. Steroids are usually effective in the treatment of OP, but other treatment regimens have been used as well. We present 5 women with OP, age ranged 57-76 years (mean - 67 years). Two of them were smokers and three were non-smokers. One patient was treated because of hyperthyreosis, one of COPD, and four had a hypertension. Four of them were diagnosed by the open lung biopsy and one by transbronchial lung biopsy. Dyspnoea (100%), cough (100%), fever (80%), weight loss (40%), chest pain (20%), were the most frequently noticed symptoms. All patients had bilateral consolidations with areas of ground glass attenuations at chest x-ray and HRCT. Migratory pattern of them was observed in four patients. Significant elevation of antibodies titers against Chlamydia pneumoniae was revealed in two patients. In all patients clarithromycin in a dose 0.5 g b.d. was administrated. Complete clinical and radiological remission was obtained after 3 months of clarithromycin therapy in 3 patients (one had Chlamydia antibodies). Two patients had not obtained significant improvement during the first two weeks of therapy so prednisolone in a dose 0.5 mg/kg/d was introduced. Also complete remission was noticed in these patients. The observation period ranged from 8 months to 4 years (mean - 34 months). Our study confirms that OP can be treated by the use of clarithromycin. It may be the alternative treatment, particularly for patients in whom probability of adverse reactions in the course of steroid treatment is high.
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PMID:[Organizing pneumonia--own experiences with clarithromycin treatment]. 1632 49

Pulmonary involvement in Sweet's syndrome (SS) is rare. We report a case of SS with severe respiratory involvement responding to corticosteroid therapy. A 82-year-old man presented fever of 39 degrees C associated with cough and dyspnea, and crackles in the left lung. The infection work-up was negative. Chest X-ray showed cardiomegaly and left lower lobe pulmonary infiltrates. Pulmonary signs did not improve on treatment with antibiotics, and after 1 week maculopapular lesions appeared, localized on the knees, the periombilical area and the back. The antibiotics were changed without improvement. A skin biopsy revealed infiltration by neutrophilic granulocytes and marked edema in the dermis, consistent with SS. The patient's condition progressively worsened, requiring high oxygenotherapy, and he was transferred to an intensive care unit. Chest X-ray revealed an important alveolar and interstitial syndrome. Bronchoalveolar lavage found 170 leukocytes with 30% neutrophils (N < 5%), 7% lymphocytes and 63% macrophages. A search for bacteria, viruses or parasites in bronchoalveolar lavage was negative. The patient was treated with antibiotics, a high dose of furosemide and steroids for 4 days. Because the patient improved dramatically within 5 days, with a negative infection work-up and a dramatic decrease of C-reactive protein, the antibiotics were stopped. Steroids were secondarily tapered very slowly. A chest computed tomography (CT) scan showed a substantial improvement of pulmonary lesions. We also review the 22 cases of pulmonary involvement of SS reported in the literature.
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PMID:Pulmonary involvement in Sweet's syndrome: a case report and review of the literature. 1679 26

A 78-year-old man with diabetes mellitus, hyperthyroidism and congestive heart failure was admitted to our hospital because of dyspnea on effort. He had been taking 200 mg/day amiodarone for 2 years, in order to treat a intermitted ventricular tachycardia. His chest X rays showed the appearance of diffuse consolidation in the right lung field. At first severe pulmonary infection was suspected, and he was treated with antibiotics. In spite of the treatment, the chest X-ray findings did not improved. We thought of the possibility of interstitial lung disease, and performed bronchoalveolar lavage (BAL) and transbronchial lung biopsy (TBLB) from the right middle lobe. TBLB revealed the organizing pneumonia (OP). At the same time we observed that he had temporary sinus arrest and entered a stated of shock requiring intubation, temporary pacing and intra-aortic balloon pumping (IABP) . The coronary angiography (CAG) revealed no abnormalities and cardiac function was normal. Within two days his sinus rhythm recovered spontaneously. After cessation of amiodarone and administering steroid therapy, pulmonary shadows resolved quickly. Since there were no laboratory signs of connective tissue or infectious disease such as a normal autoimmune serology, antibody titers against Mycoplasma pneumoniae, Clamydia species, and BAL, TBLB cultures, etc, we considered that unilateral organizing pneumonia and temporary sinus arrest could be induced by amiodarone. The amiodarone pulmonary toxicity (APT) commonly courses pleural effusion and while it may be strictly unilateral, there are often diminutive contralateral foci visible on HR-CT. Steroids should be given for months and tapered prudently, otherwise APT may recur owing to the persistence of amiodarone in lung.
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PMID:[Case of unilateral organizing pneumonia induced by amiodarone pulmonary toxicity]. 1951 1

An 84-year-old woman was referred to our hospital with fever and dyspnea. Her arterial oxygen partial pressure was 48.3 Torr. Chest computed tomography (CT) showed a foreign body incarcerated in the right truncus intermedius. Bronchoscopy revealed the incarceration of a dark red foreign body with an elliptical shape in the right truncus intermedius, and bronchoscopic removal was performed. The foreign body was an iron pill. Steroids were administered to prevent local inflammation and granulation of the bronchial mucosa. She recovered and was discharged on day 15. A patient with severe bronchial mucosal injury caused by iron pill aspiration was successfully treated by bronchoscopic removal.
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PMID:[A case of severe bronchial mucosal injury caused by iron pill aspiration]. 2018 43

Primary tracheal non-Hodgkin's lymphoma (NHL) is rare, with fewer than 30 cases reported to date. We review the clinical presentation, evaluation, and treatment of 2 cases of tracheal NHL mimicking granulation tissue. The first patient was a 67-year-old man with myelodysplastic syndrome and Crohn's disease who had a recurring lesion of the proximal trachea causing significant airway obstruction. The second patient was a 47-year-old man with a history of multiple intubations who presented with dyspnea and stridor due to circumferential tracheal stenosis. In both cases, bronchoscopy revealed abundant granulation tissue, and the initial biopsy results indicated benign disease. However, after requests from the diagnostic team to rule out lymphoma, additional immunohistochemical stains and polymerase chain reaction testing confirmed NHL. Radiotherapy was initiated. The first patient responded well and remains disease-free after 4 years. The second patient died of airway obstruction due to severe distal tracheal stenosis. Recurrent granulation tissue should raise the suspicion of malignancy and prompt further tissue evaluation for evidence of lymphoma. Steroids for airway compromise may cause progression to mature stenosis as prednisone is used in the treatment of lymphoma. Localized disease involving the central airways may be treated successfully with limited chemotherapy and radiotherapy.
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PMID:Tracheal non-Hodgkin's lymphoma masquerading as benign granulation tissue: a report of two cases. 2073 62


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