Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An assessment of pulmonary mechanics revealed weakness of inspiratory and expiratory muscles as cause of the restrictive ventilatory defect (vital capacity: 47 +/- 10 percent predicted) in seven (ages 33 to 62 years) out of 26 consecutive patients with systemic lupus erythematosus (SLE). Maximal inspiratory transdiaphragmatic pressures were reduced mainly due to the markedly increased (more positive) esophageal pressures. During maximal expiratory efforts, esophageal and gastric pressures were grossly decreased. These abnormalities probably may be considered part of a more generalized, yet subclinical muscle disorder due to the SLE with, however, predominant involvement of the respiratory muscles. The abnormalities were not related to the use of corticosteroids or generalized inanition. The static expiratory lung compliance was reduced in all patients (55 +/- 18 percent predicted), but normalized immediately following passive inflation of the lungs to transpulmonary pressures of more than 30 cm H2O in two of the three subjects tested. The volume restriction was not progressive over a period of 38.5 patient-years.
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PMID:Respiratory muscle dysfunction in systemic lupus erythematosus. 687 96

To investigate further the modulation of autoimmune disease by nutritional means, the influence of zinc deprivation upon the development of the immunopathology of MRL/I mice was studied. Because some effects of zinc deficiency may be due to associated inanition and consequent caloric deprivation, mice with similarly restricted food intake but adequate zinc intake were also studied. Zinc restriction was introduced at either 4 or 10 wk of age and was continued throughout the study. When zinc deficiency was introduced at 4 wk of age, a significant delay in the appearance of the physical findings of MRL/I mice, including open sores, necrotic ears, arthritis, and end-stage cachexia, was noted. In addition, zinc deficiency introduced at this age resulted in a lower incidence and titer of antibodies to dsDNA and less severe glomerulonephritis than control mice. Furthermore, the immune response of zinc-deprived MRL/I mice was better preserved than control animals, and most importantly, survival was significantly prolonged. Pair-fed controls also showed delayed progression of their disease, but animals restricted isocalorically from 4 wk of age experienced a more rapid onset of the lupus-like syndrome than did their zinc-deprived counterparts. In contrast, when zinc deprivation was introduced at 10 wk of age, it had little beneficial effect upon disease progression. Indeed, caloric restriction introduced at this age had a greater impact than did zinc deficiency. Nonetheless, despite the variable influence of zinc deprivation and pair-feeding on autoimmune disease, zinc deprivation, whether introduced at 4 or 10 wk of age, resulted in a significantly greater reduction of lymphoproliferation. Successful modulation of disease activity by nutritional changes will depend on understanding the mechanisms of these differential pathologic processes.
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PMID:Nutritional factors and autoimmunity. III. Zinc deprivation versus restricted food intake in MRL/1 mice--the distinction between interacting dietary influences. 698 39