Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-dose methylprednisolone and antibiotics were used to treat 30 patients with aspiration pneumonia, in a prospective, randomized, double-blind trial with placebo control. All patients received clindamycin phosphate 1200 mg per day. In addition, 15 patients received methylprednisolone 20 mg per day for three days and the other 15 patients received placebo according to the same schedule. In the methyl prednisolone group, CRP had decreased (p < 0.05) from 12.7 +/- 9.8 to 6.4 +/- 5.4 mg/dl day 4, neutrophil elastase had decreased (p < 0.05) from 402 +/- 304 to 231 +/- 64 micrograms/dl by day 4 and to 184 +/- 59 micrograms/dl by day 7, maximum body temperature had decreased (p < 0.01) from 37.9 +/- 1.1 to 36.8 +/- 0.6 degrees C by day 7, and the pneumonia score had improved (p < 0.01) from 11.8 +/- 3.0 to 8.6 +/- 2.4 by day 4. In the placebo group, there were no significant improvements by those days. We conclude that low-dose methylprednisolone therapy with antibiotics is effective against aspiration pneumonia.
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PMID:[Treatment of aspiration pneumonia with low-dose methylprednisolone and antibiotics]. 769 68

Almost all respiratory diseases except benign lung tumors and lung dysplasia entail acute lung injury. The many clinical conditions associated with acute lung injury include aspiration pneumonia, bacterial pneumonia, and sepsis. The fundamental cause of acute lung injury is pulmonary vascular hyperpermeability. Pulmonary vascular hyperpermeability can be attenuated by nitric oxide and cyclic GMP, and potentiated by oxygen radicals and elastase released from neutrophils. Adhesion molecule inhibition could become an effective therapy against acute lung injury, because the adhesion molecules are very important in the pathogenesis of this condition. Adhesion molecules could also be useful markers of disease activity in various lung diseases. Neutrophil elastase inhibitors may become important as therapeutic agents against acute exacerbations of idiopathic interstitial pneumonia, because this pathological condition is a type of acute lung injury. Similarly, N-acetyl cysteine could also become a useful therapeutic agent against idiopathic interstitial pneumonia, because it is a precursor of glutathione, which is the major antioxidant in the fluid lining of the bronchial epithelium.
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PMID:[Pathophysiology of acute lung injury]. 921 75

Almost all of respiratory diseases except benign lung tumors and lung dysplasia entail acute lung injury (ALI). The many clinical conditions associated with acute lung injury include aspiration pneumonia, bacterial pneumonia and sepsis. Acute lung injury is the end results of common pathways initiated by a variety of local or systemic insults leading to diffuse damage to the pulmonary parenchyma. Despite the accumulation of abundant information regarding the physiological and cellular basis of lung injury and increasing sophisticated intensive care, an improvement in prognosis has lagged behind. It has become clear that there is not one mediator responsible for ALI, but rather a complex interplay exists between diverse proinflammatory (e.g., lipopolysaccharide, complement products, cytocains, chemocains, reactive oxygen species and arachidonic acid products) and anti-inflammatory (IL-10, IL-1-RA, PGI2) mediators. Early in the course of ALI, large numbers of neutrophils are sequestered in and emigrate from the pulmonary capillaries. The fundamental cause of ALI is pulmonary vascular hyperpermeability caused by the activated neutrophils which release oxygen radicals and proteases. In these processes several adhesion molecules play very important roles. Neutrophil elastase inhibitors become very useful therapeutic agents against acute exacerbation of idiopathic interstitial pneumonia (IIP), because this pathological conditions is a type of ALI. Similarly, N-acetyl cystein could also become a useful therapeutic agent against IIP, because it is a precursor of glutathione, which is the major antioxidant in the fluid lining of the bronchial epithelium.
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PMID:[The 74th Annual Meeting President Lecture. Pathogenesis and therapy of acute lung injury]. 1053 83