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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eosinophilia of synovial fluid is uncommon. Using the identification of Charcot-Leyden crystals to alert for the presence of eosinophils, we have increased by a factor of 5 the detection rate of synovial fluid eosinophilia. We describe here our clinical and laboratory findings in 7 patients with this feature. We believe they constitute a defined syndrome. Typically, the patients were young (ages 18-51) and had a personal and family history of allergy. They developed an acute, painless monarthritis after a minor trauma, and had no concurrent allergic symptoms. Each episode resolved in 1-2 weeks without therapy, and 3 patients had recurrences. All had pronounced dermatographism. The synovial fluid was mildly inflammatory: 10,850 +/- 3,665 white blood cells/mm3, with 41 +/- 5% eosinophils (mean +/- SEM). The cellularity and chemistry of the peripheral blood was unremarkable, except for a mild elevation of IgE levels (370 +/- 104 IU/ml). The exact pathophysiologic mechanism underlying this benign entity is not clear, but we suspect a nonimmunologic triggering event is operant, i.e., synovial trauma which mimics the cutaneous dermatographism.
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PMID:Eosinophilic synovitis: clinical observations on a newly recognized subset of patients with dermatographism. 375 40

Eosinophilia within the first 6 weeks of life was studied prospectively in 10 premature neonates. Mean birthweight was 1229 +/- 314 g, and mean gestational age 31.5 +/- 1.8 weeks. Simultaneous changes in eosinophil, neutrophil, total lymphocyte, suppressor and helper T-cell counts and IgE levels were monitored. Infants were designated as responders (eosinophils greater than 1000/microliter for greater than 5 days) and non-responders. In the 6 responders eosinophils increased from 353 +/- 76 (mean +/- SEM) at birth to a peak of 2783 +/- 430/microliter at 20-25 days. Responders had significantly lower neutrophil counts at birth (P less than 0.05), and in 5 of the 6 responders neutrophils increased by more than 100% within 10-15 days; this did not occur in any of the 4 non-responders (P less than 0.025). Lymphocytes and suppressor and helper T cells increased progressively in both groups over the period of study with no differences between responders and non-responders. Birthweight and gestational age were similar in both groups, and there were no apparent causes for the lower neutrophil counts in responders at birth. Eosinophilia was not related to an IgE response. The incidence of eosinophilia in this study is similar to that reported previously, and appears to be part of a biphasic granulopoietic response.
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PMID:Eosinophilia in premature neonates. Phase 2 of a biphasic granulopoietic response. 662 38

Eosinophilia has been reported during exacerbations of bronchitis, but the mechanisms of tissue recruitment of eosinophils are unclear. We quantified eosinophils and the concurrent expression of cytokines and chemokines probably responsible for the tissue eosinophilia in bronchial biopsies obtained from three groups of nonatopic subjects: (1) healthy nonsmokers (n = 7; FEV1 % predicted = 108 +/- 4 [mean +/- SEM]); (2) nonasthmatic smokers with chronic bronchitis (CB) in a stable phase of their disease (n = 11; FEV1 % predicted: 75 +/- 5); and (3) nonasthmatic subjects with CB who sought medical advice for an exacerbation of their condition (n = 9; FEV(1) % predicted: 61 +/- 8). We applied anti-EG2 antibody and immunostaining to detect and count eosinophils. We performed in situ hybridization to visualize and enumerate cells expressing the genes for interleukin (IL)-4 and IL-5 and the eosinophil chemokines eotaxin, monocyte chemoattractant protein (MCP)-4, or regulated on activation, normal T-cell expressed and secreted (RANTES). We confirmed an increase in EG2-positive eosinophils in patients with CB in exacerbation. We found messenger RNA (mRNA) positivity for IL-4 and IL-5 in CB, but the between-group differences were not statistically significant. However, the numbers of lymphomononuclear cells expressing eotaxin mRNA were significantly greater in the smokers with CB than in the healthy nonsmokers without CB (p < 0.01). Following an exacerbation, RANTES expression was upregulated and this chemokine was strongly expressed in both the surface epithelium and in subepithelial lymphomononuclear cells: only RANTES showed a significant positive correlation with the increasing number of EG2-positive cells (r = 0.51; p < 0.03). In conclusion, an allergic profile of inflammation can also occur in CB: the marked upregulation of RANTES in the epithelium and subepithelium most likely accounts for the increased eosinophilia associated with an exacerbation of bronchitis.
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PMID:Exacerbations of Bronchitis: bronchial eosinophilia and gene expression for interleukin-4, interleukin-5, and eosinophil chemoattractants. 1143 30