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PubMed2000

[Pleurisy: diagnostic and therapeutic management].

Diagnosis of pleural effusion is difficult in children. The etiologies are numerous; however, infectious agents are more frequent. Thoracocentesis proves to be the first-line diagnostic tool. Light's criteria are the best for distinguishing whether the effusion is a transudate or an exudate. If the patient has an exudative pleural effusion, other tests are indicated to determine the etiology and in some cases the treatment: macroscopic appearance, cytology and differential white cell count (level of glucose, lactate dehydrogenase, adenosine deaminase, pH, bacterial cultures). Others investigations--biopsy of pleura by thoracoscopy or video-assisted thoracoscopy, bronchofibroscopy, CT scan--are sometimes useful. Intrapleural instillation of urokinase appears to be useful and safe. Evaluation is necessary for video-assisted thoracoscopy used early.

Age Factors↗
PubMed1986

Calculus revisited. A review.

Although there is no doubt that gingivitis can develop in the absence of supragingival calculus, it is not clear to what extent the presence of mineralized deposit enhances gingival inflammation. Partial inhibition of plaque mineralization can be accomplished by chemical agents, but there has been no demonstration in humans of a reduction in gingivitis. It remains to be established what level of inhibition (if any) is required to have more than a cosmetic effect. Since the accepted scenario is that apical growth of supragingival plaque precedes the formation of subgingival calculus, there is no longer an issue of whether subgingival calculus is the cause or the result of periodontal disease. Subgingival mineralization results from the interaction of subgingival plaque with the influx of mineral salts that is part of the serum transudate and inflammatory exudate. This chronology, however, should not be the basis for relegating calculus to the ash heap. Morphologic and analytical studies point to the porosity of calculus and retention of bacterial antigens and the presence of readily available toxic stimulators of bone resorption. When coupled with the increased build up of plaque on the surface of the calculus, the combination has the potential for extending (beyond that of plaque alone) the radius of destruction and the rate of displacement of the adjacent junctional epithelium. The centrality of thorough scaling and root planing in the successful maintenance of periodontal health supports the view that subgingival calculus contributes significantly to the chronicity and progression of the disease, even if it can no longer be considered as responsible for initiation.

Bacteria↗
PubMed1965

EXUDATIVE LESIONS IN DIABETES MELLITUS.

Exudative lesions and capsular drops have been examined in a renal biopsy series of 25 diabetics and a post-mortem series of 100 consecutive diabetics. Electron microscopy of a capsular drop and an exudative lesion is described. Exudative lesions were found in 48% of the biopsies and 47% of the necropsy material. Capsular drops were found in 60% of the biopsies and 29% of the necropsy material. No correlation with age, proteinuria, hypertension, or uraemia was noted. The incidence of both types of lesion increased with the known duration of the diabetes.

Adolescent↗
PubMed1992

Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema.

Interleukin-8 (IL-8), a potent neutrophil chemotactic peptide, has been found in association with human disease, but its contribution to chemotactic activity in humans is not yet known. We asked whether IL-8 is present in inflammatory human pleural effusions, and to what extent it contributes to pleural liquid neutrophil chemotactic activity. Because tumor necrosis factor alpha (TNF-alpha) is a strong inducer of IL-8, we also asked whether TNF-alpha was present. For this prospective study, we collected pleural liquid from 51 patients (empyema, 14; parapneumonic, four; tuberculous, eight; malignant, nine; miscellaneous exudative, seven; and transudative, nine), counted pleural neutrophils, and measured IL-8 and TNF-alpha concentrations in the supernatant. To determine the contribution of IL-8 to chemotactic activity in empyema, we measured the neutrophil migration induced by empyemic liquids before and after addition of anti-IL-8 F(ab')2 antibody fragments or control anti-IL-6 F(ab')2. We found that IL-8 concentrations were higher in empyema (61.3 +/- 21.0 ng/ml [SEM]) than in all other effusions (1.1 +/- 0.5 ng/ml) (p = 0.0001). All empyema liquids had IL-8 concentrations above 2.5 ng/ml, which was true for only three of the other 37 effusions (two parapneumonic, one tuberculous). IL-8 levels correlated with the pleural neutrophil count (r = 0.46; p = 0.007) and the neutrophil chemotactic activity of pleural liquid (r = 0.43; p = 0.008). Anti-IL-8 antibodies decreased chemotactic activity in empyema liquids by 65 +/- 5%, whereas the control antibody had no effect (0 +/- 5% decrease) (p = 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

Chemotaxis, Leukocyte↗
PubMed2000

Eotaxin levels in pleural effusions: comparison with monocyte chemoattractant protein-1 and IL-8.

OBJECTIVE: In order to investigate the role of eotaxin in pleural diseases, we measured eotaxin in pleural effusions and studied the relationship between eotaxin levels and recruitment of inflammatory cells, particularly eosinophils. Interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) levels were also measured for comparison. METHODS: We evaluated 47 pleural effusion samples, 7 transudates and 40 exudates. The exudates consisted of 19 malignant, 11 tuberculous, and 5 parapneumonic effusions, and 5 effusions of other etiologies. Chemokine levels were measured by specific sandwich enzyme-linked immunosorbent assays. RESULTS: Eotaxin was detected in all samples examined, but the levels did not differ significantly among the exudates. There was no significant correlation between the levels of eotaxin and MCP-1 or IL-8. The level of eotaxin but not the others was significantly higher in eosinophilic effusions (>10% eosinophils among white blood cells in the fluid) than in non-eosinophilic fluids. The number of eosinophils in pleural effusions was significantly correlated with the eotaxin levels, but not with the levels of other chemokines. The number of neutrophils was significantly correlated with IL-8 but not with the others. CONCLUSIONS: Results suggest that eotaxin contributes to the migration of eosinophils in pleural inflammation. Taken together with the correlation between IL-8 and neutrophils, it appears that the predominant type of pleural inflammatory infiltrate is controlled, at least in part, by the subgroup of chemokines expressed in the pleural space.

Chemokine CCL11↗