Search PubMed⌕ Search

PubMed · 385382

[Fungal maxillary sinusitis].

Abstract

Since 1969, 600 patients suffering from maxillary sinusitis have been systematically controlled clinically as well as mycologically. We discovered 81 cases of maxillary sinusitis (13,4%). Aspergillus fumigatus and Candida albicans were the most frequently isolated fungi. Three clinical forms could be distinguished: (1) a muco-purulent form (35 cases); (2) a budding and/or caseous form (22 cases), and (3) a pseudotumoral form (24 cases). 42 patients treated with a 1% econazol (base) solution were healed.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D Grigoriu, J Bambule, J Delacrétaz, M Savary. 1979. [Fungal maxillary sinusitis].. https://pubmed.ncbi.nlm.nih.gov/385382/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Variable number of tandem repeats of TNF receptor type 2 promoter as genetic biomarker of susceptibility to develop invasive pulmonary aspergillosis.

Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin alpha (LT-alpha) are pivotal mediators of inflammatory responses in fungal infection diseases. We hypothesized that polymorphisms in genes of these cytokines or their receptors might increase the susceptibility of hematologic patients to develop invasive pulmonary aspergillosis (IPA). One hundred two hematologic patients and 124 age-matched controls were enrolled in the study, and the following standard single nucleotide polymorphisms were investigated: TNF-alpha -308 and +489, LT-alpha +252 and Tumor Necrosis Factor Receptor 2 (TNFR2) +676. Variable number of tandem repeats (VNTRs) at position -322 of the TNFR2 gene were also studied. Genotypic and allelic frequencies were similar between patients and controls. IPA was diagnosed in 54 of the 102 patients according to consensus criteria published by the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group. TNF-alpha and LT-alpha polymorphisms were not associated with presence of IPA. Susceptibility to IPA was strongly associated with VNTR at position -322 in the promoter region of the TNR2 gene (p = 0.029) but was not associated with the presence of TNFR2 +676 polymorphism. A genetic difference in TNFR2 promoter VNTR may play a major role in susceptibility to IPA infection.

Aspergillosis↗