epiglucan has been researched along with Mycetoma* in 4 studies
4 other study(ies) available for epiglucan and Mycetoma
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Wako β-D-glucan assay can be used to measure serum β-D-glucan in Sudanese patients to aid with diagnosis of eumycetoma caused by Madurella mycetomatis.
Eumycetoma is a neglected tropical infection of the subcutaneous tissue commonly caused by the fungus Madurella mycetomatis. Previously, we demonstrated that β-D-glucan was present in the serum of eumycetoma patients.. To compare the performance of the recently approved easy-to-use Wako β-D-glucan assay to that of the Fungitell assay in eumycetoma patients.. Using sera obtained from 41 eumycetoma, 12 actinomycetoma and 29 healthy endemic controls, we measured the β-glucan serum concentrations using the Wako assay and compared the performance to that of the Fungitell assay.. With the Fungitell assay, median β-glucan serum concentrations of 208, 70 and 27 pg/ml were obtained for the 41 eumycetoma patients, the 12 actinomycetoma patients and the 29 healthy endemic controls, respectively. With the Wako assay these concentrations were 14.45, 11.57 and 2.5 pg/ml, respectively. We demonstrated that when using the optimized cut-off value (5.5 pg/ml) for the Wako assay, the Wako and Fungitell assays had comparable performance in terms of sensitivity and specificity.. The Wako assay is comparable to the Fungitell assay for measurement of serum β-glucan in mycetoma patients and hence can be used in combination with current diagnostic tools. However, this test should be used in combination with other tests to differentiate actinomycetoma from eumycetoma. Topics: beta-Glucans; Glucans; Humans; Madurella; Mycetoma; Sensitivity and Specificity | 2023 |
Detection of (1→3)-β-d-Glucan in Eumycetoma Patients.
Mycetoma can be caused by bacteria (actinomycetoma) or fungi (eumycetoma). Here, we demonstrated in 45 eumycetoma patients, 30 actinomycetoma patients, and 30 healthy controls that (1→3)-β-d-glucan detection in serum cannot reliably be used to discriminate between the two types of mycetoma. Topics: Adolescent; Adult; Aged; beta-Glucans; Child; Female; Healthy Volunteers; Humans; Male; Middle Aged; Mycetoma; Proteoglycans; Young Adult | 2016 |
Last generation triazoles for imported eumycetoma in eleven consecutive adults.
Optimal management of eumycetoma, a severely debilitating chronic progressive fungal infection of skin, disseminating to bone and viscera, remains challenging. Especially, optimal antifungal treatment and duration are ill defined.. We conducted a monocentric retrospective study of 11 imported cases of eumycetoma treated by voriconazole or posaconazole for at least 6 months. Response to treatment was assessed through evolution of clinical and magnetic resonance imaging (MRI). (1→3) ß-D-glucan (BG) and positron emission tomography using [18F] fluorodeoxyglucose (PET/CT) results were also assessed. Identified species were Fusarium solani complex (n = 3); Madurella mycetomatis, (n = 3), and Exophiala jeanselmei, (n = 1). Moreover, two coelomycetes and one phaeohyphomycetes strains without species identification were retrieved. Serum BG and PET/CT were abnormal in 7/8 and 6/6 patients tested, respectively. Patients received last generation azoles for a mean duration of 25.9±18 months. Complete response (major clinical and MRI improvement) was observed in 5/11 patients, partial response (minor MRI improvement or stable MRI findings) in 5 and failure (MRI evidence of disease progression) in one, with a 73±39 [6-132] months mean follow-up. Relapse occurred in 2 patients after treatment discontinuation. Optimal outcome was associated with fungal species, initiation of last generation triazole therapy (<65 months since first symptoms), negative serum BG and PET/CT normalization.. MRI, PET/CT and serum BG appear as promising tools to assess optimal time of antifungal treatment for eumycetoma. Topics: Adolescent; Adult; Antifungal Agents; beta-Glucans; Child; Exophiala; Fluorodeoxyglucose F18; Fusarium; Humans; Madurella; Magnetic Resonance Imaging; Male; Mycetoma; Positron-Emission Tomography; Proteoglycans; Retrospective Studies; Skin; Treatment Outcome; Triazoles; Voriconazole; Young Adult | 2014 |
Caspofungin-mediated beta-glucan unmasking and enhancement of human polymorphonuclear neutrophil activity against Aspergillus and non-Aspergillus hyphae.
We investigated whether caspofungin and other echinocandins have immune-enhancing properties that influence human polymorphonuclear neutrophil (PMN)-mediated mold hyphal damage.. Using aniline blue staining, we compared patterns of beta-glucan exposure in Aspergillus fumigatus, Aspergillus terreus, Rhizopus oryzae, Fusarium solani, Fusarium oxysporum, Scedosporium prolificans, and Scedosporium apiospermum hyphae after caspofungin exposure. We also determined PMN-mediated hyphal damage occurring with or without preexposure to caspofungin or with preexposure to the combination of caspofungin and anti-beta-glucan monoclonal antibody, using 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-sH-tetrazolium hydroxide (XTT) assay.. Preincubation with caspofungin (32 microg/mL for R. oryzae; 0.0625 microg/mL for other isolates) increased exposure to beta-glucan. PMN-induced damage increased after caspofungin exposure and was further augmented by the addition of anti-beta-glucan antibody. Preincubation with micafungin or anidulafungin had similar effects on PMN-induced damage of A. fumigatus hyphae. Finally, preexposure of A. fumigatus, but not S. prolificans, to caspofungin induced expression of Dectin-1 by PMN.. The results of the present study suggest inducement of beta-glucan unmasking by echinocandins and enhancement of PMN activity against mold hyphae, thereby supporting the immunopharmacologic mode of action of echinocandins. Topics: Aspergillus; Aspergillus fumigatus; beta-Glucans; Caspofungin; Cell Wall; Echinocandins; Fusarium; Humans; Hyphae; Lectins, C-Type; Lipopeptides; Membrane Proteins; Mycetoma; Nerve Tissue Proteins; Neutrophils; Reverse Transcriptase Polymerase Chain Reaction; Rhizopus; Scedosporium; Toll-Like Receptor 2; Toll-Like Receptor 4 | 2008 |