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Target Concepts:
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Query: UMLS:C0024312 (
lymphopenia
)
4,859
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Strenuous exercise is followed by
lymphopenia
, neutrophilia, impaired natural immunity, decreased lymphocyte proliferative responses to mitogens, a low level of secretory immunoglobulin A in saliva, but high circulating levels of pro- and anti-inflammatory cytokines. These exercise-induced immune changes may provide the physiological basis of altered resistance to infections. The mechanisms underlying exercise-induced immune changes are multifactorial and include neuroendocrinological and metabolic mechanisms. Nutritional supplementation with glutamine abolishes the exercise-induced decline in plasma glutamine, but does not influence post-exercise immune impairment. However, carbohydrate loading diminishes most exercise effects of cytokines, lymphocyte and neutrophils. The diminished neutrophilia and elastase (
EC 3.4.21.37
) responses to eccentric exercise in elderly subjects were enhanced to levels comparable with those of young subjects by fish oil or vitamin E supplements. However, although vitamin C supplementation may diminish the risk of contracting an infection after strenuous exercise, it is not obvious that this effect is linked to an effect of vitamin C on exercise-induced immune changes. In conclusion, it is premature to make recommendations regarding nutritional supplementation to avoid post-exercise impairment of the immune system.
...
PMID:Exercise and immune function: effect of ageing and nutrition. 1060 10
In an effort to further elucidate the complex changes in the complement-leukocyte system during cardiopulmonary bypass (CPB), plasma levels of C3d, C5a, and
granulocyte elastase
bound to alpha1-proteinase inhibitor (E-alpha1 PI) were followed prior to, during, and after CPB. Leukocyte and differential cell counts and granulocyte migration were also determined. Complement activation was documented during CPB by an increase in plasma C3d corrected for hemodilution. Significant amounts of C5a were not revealed. Cell counts decreased during CPB but, if corrected for hemodilution, remained unchanged apart from a slight decrease in lymphocyte count after 60 minutes. Eighteen hours after CPB, neutrocytosis and
lymphopenia
occurred. Plasma E-alpha1 PI increased during CPB, reflecting release of granulocyte lysosomal enzymes. Granulocyte migration was transitorily depressed during CPB, and it was shown that this was due to the appearance of an intrinsic cellular defect. CPB is associated with acute changes in cells and plasma, resembling an acute whole-body inflammatory response, with transitory impairment of granulocyte migration. The clinical significance of these observations remains to be determined.
...
PMID:Complement and leukocytes during cardiopulmonary bypass: effects on plasma C3d and C5a, leukocyte count, release of granulocyte elastase and granulocyte chemotaxis. 1717 7
A 22-year-old man was admitted to our hospital with fever, cough and dyspnea. His chest radiograph showed diffuse ground-glass attenuation in both lung fields. Arterial blood gas analysis showed hypoxemia (PaO2 28.7 Torr breathing room air) and he required mechanical ventilation within 6 hours after admission. Gomori methenamine silver (GMS) stain of the bronchoalveolar lavage (BAL) fluid smear showed round and indented organisms, and polymerase chain reaction revealed pneumocystis jirovecii in the BAL fluid. The HIV antibody was positive and peripheral blood CD4-positive
lymphocytes decreased
to 4.0%. Pneumocystis pneumonia complicated with acquired immunodeficiency syndrome (AIDS) was diagnosed. There was no four-fold rise in screen viral titers. We treated him with antibiotics, trimethoprim-sulfamethoxazole, ganciclovir, fos-fluconazole, steroid pulse therapy and sivelestat sodium hydrate. Respiratory failure was relieved within 5 days following treatment. The percentage of neutrophils in the BAL fluid was elevated (44.6%). Neutrophil elastase on admission was increased and improved to the normal range after treatment. Sivelestat sodium hydrate is an anti-
neutrophil elastase
inhibitor and may be one of the treatment options for acute respiratory failure due to pneumocystis pneumonia in AIDS patients.
...
PMID:[Acute respiratory failure due to pneumocystis pneumonia successfully treated with combined use of sivelestat sodium hydrate]. 1859 91