Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Older patients may be excluded from intensive care units because of the perception that they will benefit less than younger patients. To determine if advanced age is associated with increased mortality independent of severity of illness, we compared older and middle-aged patients admitted to a medical intensive care unit. We reviewed the charts of 130 patients age 75 years or older and 135 patients age 55 to 65 admitted over a 30-month period. We controlled for severity of illness using the Acute Physiology Assessment and Chronic Health Evaluation (APACHE II) system without including points for age (APACHE IIM). The groups were similar with regard to gender, whether or not they had a private attending physician, mean APACHE IIM score, and diagnoses, except that older patients had more chronic obstructive pulmonary disease. Hospital stay was slightly longer in the older group (37 vs. 39 days, rank sum, P less than .02). Hospital mortality was significantly greater in the older group (39% vs. 51%, Chi-square P less than .05) with a crude relative risk of 1.32 (95% confidence interval [CI]: 1.01, 1.73). However, the relation of age group to mortality differed for patients with different diagnoses. When we used logistic regression to adjust for APACHE IIM, whether the patient had a private attending physician, primary admitting diagnosis, or presence of cancer, older patients did not have a significantly greater risk of dying (adjusted relative risk, 1.05; 95% CI: 0.97, 1.12). When pulmonary artery catheterization was added to the model, it independently predicted mortality adjusted relative risk, 1.47; 95% CI: 1.05, 2.06.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Are elderly people less responsive to intensive care? 235 23

Oxidative stress may differentially regulate protein loss within peripheral muscles of severe chronic obstructive pulmonary disease (COPD) patients exhibiting different body composition. Oxidation levels of proteins, myosin heavy chain (MyHC) and myonuclei, superoxide anion, antioxidants, actin, creatine kinase, carbonic anhydrase-3, ubiquitin-proteasome system, redox-signalling pathways, inflammation and muscle structure, and damage were quantified in limb muscles of severe COPD patients with and without muscle wasting, and in sedentary controls. Compared with controls, in the quadriceps of muscle-wasted COPD patients, levels of protein carbonylation, oxidation of MyHC and myonuclei, superoxide anion production, superoxide dismutase, total protein ubiquinitation, E2(14k), atrogin-1, FoxO1 and p65 were higher, while content of MyHC, creatine kinase, carbonic anhydrase-3, myogenin, and fast-twitch fibre size were decreased. Importantly, in nonwasted COPD patients, where MyHC was more oxidised than in controls, its content was preserved. Muscle inflammation and glutathione levels did not differ between patients and controls. In all patients, muscle structure abnormalities were increased, while muscle force and exercise capacity were reduced. In severe COPD, while muscle oxidative stress increases regardless of their body composition, protein ubiquitination and loss of MyHC were enhanced only in patients exhibiting muscle atrophy. Oxidative stress does not seem to directly modulate muscle protein loss in these patients.
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PMID:Does oxidative stress modulate limb muscle atrophy in severe COPD patients? 2240 99

This review presents an analysis of the literature on the topic of respiratory muscle (RM) dysfunction in various forms of respiratory pathology: chronic obstructive pulmonary disease (COPD), asthma, community-acquired pneumonia, idiopathic pulmonary fibrosis (IPF), sarcoidosis and interstitial lung diseases (ILD), associated with systemic connective tissue diseases (polymyositis, dermatomyositis and systemic lupus erythematosus - SLE). Various clinical and pathophysiological aspects of RM dysfunction and general patterns of its pathogenesis were examined. It was proved that the role of RM in the development of respiratory failure depends on the form and stage of the pulmonary pathology and the severity of systemic manifestations of these diseases: excessive proteolysis, oxidative stress, hypoxia, chronic systemic inflammation. These factors modify the morphofunctional status of RM, worsens their contractile function, which is contributed to the development of respiratory failure. In some cases, the primary weakness of RM precedes the clinical manifestation of pulmonary pathology, which is distinctive for some variants of myositis-associated ILD and SLE. Endogenous intoxication syndrome plays a significant role in the development of RM dysfunction during community-acquired pneumonia. It is noted that sarcoid pulmonary ventilation disorders associate with the RM weakness, but not with the degree of lung damage. In most cases, secondary RM dysfunction predominates that contributes to respiratory failure progression, which is especially noticeable in case of COPD, asthma and IPF.
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PMID:Respiratory muscles dysfunction and respiratory diseases. 3109 66