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)

The eosinophilia-myalgia syndrome (EMS) is a unique entity associated with products that contain L-tryptophan (L-trp). Studies of the underlying etiopathogenic processes are underway. EMS is a distinct syndrome, but shares features with eosinophilic fasciitis and other variants of systemic sclerosis. A wide spectrum of clinical manifestations has been described, but there is no consensus regarding treatment. We report the clinical and laboratory features of 12 patients. All were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and analgesics with transient or minimal effect. Two received D-penicillamine (DP) and colchicine, with minimal improvement; one had no response to azathioprine (AZA). Eleven received corticosteroids and had improvement of general symptoms, arthralgias, arthritis, myalgias, skin changes, eosinophilia, and leukocytosis. Nevertheless, all but the latter two findings recurred when corticosteroids were tapered. Seven patients who were unresponsive to the former treatments received low-dose pulse oral methotrexate. Six exhibited continued improvement after a mean follow-up of 4.5 months, with good drug tolerance. Corticosteroids were tapered and, in some instances, discontinued without relapse or complications. One patient improved but later died of aspiration pneumonia. We conclude that methotrexate (MTX) is a therapeutic alternative for patients with severe or refractory EMS.
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PMID:Treatment of the eosinophilia-myalgia syndrome. 174 39

We studied all patients with community-acquired pneumonia who were admitted to our 800-bed adult acute care hospital from 1 November 1981 to 15 March 1987. The 719 patients had a mean age of 63.2 years; 18% were admitted from nursing homes, and 18% required ventilatory assistance as part of the therapy for pneumonia. Patients with nursing home-acquired pneumonia were significantly older; had a higher mortality (40% vs. 17%); were more likely to be admitted in January; were less likely to complain of cough, fever, anorexia, chills, headache, nausea, sore throat, myalgia, or arthralgia; and were more likely to be confused than those admitted from the community. Pneumonia of unknown etiology and aspiration pneumonia were more common and Mycoplasma pneumoniae infection less common among those with nursing home-acquired pneumonia. Streptococcus pneumoniae accounted for 58% of the 48 cases of bacteremia. None of the bacteremic patients received antibiotics before admission, compared with 34% of the nonbacteremic patients. Aerobic gram-negative rod bacteremia was not more frequent among nursing home patients than among those from the community. The overall mortality was 21% (8.5% for those less than 60 years of age and 28.6% for those greater than 60 years old). By multivariate analysis the following variables were significant predictors of mortality: number of lobes involved by the pneumonic process, number of antibiotics used to treat the pneumonia, age, admission from a nursing home, ventilatory support, and the number of complications that occurred while the patient was in the hospital.
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PMID:Community-acquired pneumonia requiring hospitalization: 5-year prospective study. 277 65

Three hundred seventeen patients with toxic oil syndrome caused by ingestion of denatured rapeseed oil were followed up after one year. Total mortality for the 317 patients was 4.4%. After 12 months, 3.2% of the surviving patients have a severe motor neuropathy, 52.9% are asymptomatic, and the remaining 39.4% have mild residual myalgia. The cause of death in seven patients during the acute phase of toxic oil syndrome was respiratory failure due to interstitial pneumonitis with cerebral edema. The death of five patients in the second phase was due to motor neuropathy that involved respiratory muscles and was complicated by aspiration pneumonia.
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PMID:Evolution of the alimentary toxic oil syndrome due to ingestion of denatured rapeseed oil. 669 59

Polymyositis was diagnosed in nine dogs. Factors utilized in making the diagnosis included (1) muscle pain or weakness, (2) high concentrations of serum muscle enzymes, (3) electromyographic abnormalities, and (4) histopathologic evidence of muscle necrosis and inflammation. Clinical signs included muscle pain, weakness, stilted gait, and pyrexia. Serum muscle enzyme concentrations were high in only three dogs. There was no apparent correlation between enzyme concentrations and severity of clinical involvement or degree of muscle necrosis on biopsy. Electromyographic changes included polyphasic motor unit potentials, fibrillation potentials, and positive waves. Variable degrees of muscle regeneration, degeneration, and inflammation were seen. Prednisone (2.2 mg/kg, OD, per os) was used effectively to treat four dogs. One dog improved initially but was euthanatized later when clinical signs became more pronounced. Three other dogs developed aspiration pneumonia secondary to megaesophagus and either died or were euthanatized.
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PMID:Polymyositis in dogs. 698 2

A four-month-old female Dobermann presented with myalgia, dysphagia, progressive weakness and loss of body condition. Diagnostic evaluation at nine months of age revealed markedly elevated serum creatine kinase activity, electromyographic abnormalities and histological evidence of chronic-active muscle necrosis. Imaging confirmed dysphagia and aspiration pneumonia. Muscular dystrophy was suspected and immunohistochemical staining of muscle cryosections demonstrated reduced sarcoglycans. Treatment consisted of gastrostomy, and over the next 5 months the dog gained weight, despite continued loss of muscle mass. The dog died at 14 months of age after developing clinical signs of aspiration pneumonia. To the authors' knowledge, this is the first report of muscular dystrophy in a Dobermann and only the second detailed report of a canine sarcoglycanopathy. Supportive care resulted in an acceptable quality of life for 10 months after clinical signs were first observed.
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PMID:Muscular dystrophy due to a sarcoglycan deficiency in a female Dobermann dog. 2548 56

Polymyositis is an idiopathic inflammatory myopathy of unknown aetiology that affect skeletal muscles causing symmetrical, proximal muscle weakness, and also other internal organs. The investigations reveal elevated skeletal muscle enzyme levels and characteristic electromyography (EMG) and muscle biopsy findings. Pulmonary involvement in polymyositis includes respiratory muscle weakness, aspiration pneumonia, interstitial lung disease, infection and drug-induced pneumonia. We expose the case of a young woman (47 years old) who presented to the Pulmonology Clinic with fever, cough, purulent sputum, discrete myalgia, being diagnosed at that moment with interstitial lung disease and treated with antibiotics, low dose of corticosteroids and symptomatic drugs. The evolution was slowly favorable for the respiratory impairment, but the patient developed exacerbated myalgia, muscle weakness, reaching even the impossibility of maintaining orthostatism, and also joint pain. Biological investigations revealed an important hepatocytolysis syndrome and also increased levels of muscle enzyme. The hypothetical diagnosis was polymyositis and to sustain this theory it was performed a muscle biopsy. The patient was transferred afterwards to the Rheumatology Clinic, in order to perform other specific investigations. In our clinic the patient maintained elevated levels of skeletal muscle enzymes and the muscle biopsy revealed polymyositis findings. Also immunological investigations objectified the presence of Jo1 antibodies. Therefore we pleaded for the diagnosis of idiopathic polymyositis, acute form. A multidisciplinary approach is needed in order to establish an accurate diagnosis and to institute a proper treatment.
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PMID:A CASE OF POLYMYOSITIS WITH INTERSTITIAL LUNG DISEASE ONSET. 2679 49