Disease relevance of Paracoccidioidomycosis

• Itraconazole is also effective in lymphocutaneous and visceral sporotrichosis, in paracoccidioidomycosis, for Penicillum marneffei infection, and is an alternative to amphotericin B for Histoplasma duboisii infection [1].
• Sera from 46 patients with paracoccidioidomycosis or other mycoses and sera from healthy individuals were evaluated by the inh-ELISA; overall sensitivity was 80.4% (37 of 46 paracoccidioidomycosis patients tested positive), and specificity compared with that of normal controls from areas of endemicity was 81.4% [2].
• OBJECTIVE: Paracoccidioidomycosis is an important cause of Addison's disease in South America. We have carried out an extensive and prospective study on paracoccidioidomycosis comparing glucocorticoid, mineralocorticoid and androgen function with adrenal regulators, ACTH/beta-LPH and plasma renin activity (PRA) [3].
• Comparison of the mean results of routine pulmonary function studies of 17 patients with diffuse pulmonary paracoccidioidomycosis (PM) and manifestations of chronic obstructive pulmonary disease (COPD) to those of 17 matched patients with pure COPD showed no significant differences [4].
• In systemic infections, clinical trials have led to recommendations that itraconazole is the current drug of choice for blastomycosis, histoplasmosis, paracoccidioidomycosis, lymphocutaneous sporotrichosis, chronic disseminated aspergillosis and many cases of phaeohyphomycosis [5].

High impact information on Paracoccidioidomycosis

• Miconazole in paracoccidioidomycosis [6].
• The 43,000-Da glycoprotein (gp43) of Paracoccidioides brasiliensis is an immunodominant antigen for antibody-dependent and immune cellular responses in patients with paracoccidioidomycosis [7].
• Treatment of paracoccidioidomycosis with ketoconazole: a three-year experience [8].
• Absence of interleukin-4 determines less severe pulmonary paracoccidioidomycosis associated with impaired Th2 response [9].
• Tumor necrosis factor in paracoccidioidomycosis patients [10].

Chemical compound and disease context of Paracoccidioidomycosis

• The role of C5 in experimental murine paracoccidioidomycosis [11].
• The usual therapy for paracoccidioidomycosis is sulfonamides, amphotericin B, and azole derivatives (ketoconazole, itraconazole, and fluconazole) [12].
• Following definitive diagnosis of paracoccidioidomycosis, he was treated initially with trimethoprim/sulphamethoxazole, but there was no clinical improvement [13].
• The findings in a patient with paracoccidiodomycosis (South American blastomycosis) diagnosed by open-lung biopsy and treated successfully with a combination of trimethoprim and sulfamethoxazole are reported, and the clinical spectrum of the disease is reviewed [14].
• Effect of anti-IL-4, interferon-gamma and an antifungal triazole (SCH 42427) in paracoccidioidomycosis: correlation of IgE levels with outcome [15].

Biological context of Paracoccidioidomycosis

• Six patients with multisystem paracoccidioidomycosis proven by serology and culture or smear were treated with relatively brief courses of intravenous miconazole [16].
• Isoniazid acetylating phenotype in patients with paracoccidioidomycosis and its relationship with serum sulfadoxin levels, glucose-6-phosphate dehydrogenase and glutathione reductase activities [17].
• Normal human sera, in contrast to paracoccidioidomycosis sera, were unreactive with gp43 but recognized epitopes of FNPA susceptible to alkaline hydrolysis and pronase treatment [18].

Anatomical context of Paracoccidioidomycosis

• The results indicate that progression of chronic disseminated paracoccidioidomycosis was associated with the development of T-cell suppressor activity for Con A responses of PBL, and that DTH responses to antigen were depressed by the administration of serum with specific high titer antibodies [19].
• Programmed cell death in thymus during experimental paracoccidioidomycosis [20].
• An inhibition assay was performed and it was verified that anti-gp43 serum and a pool of sera from individuals with paracoccidioidomycosis were able to inhibit the adhesion of P. brasiliensis to the Vero cells [21].
• Immunocytochemical localization of cytokines and inducible nitric oxide synthase (iNOS) in oral mucosa and lymph nodes of patients with paracoccidioidomycosis [22].
• The erythro-immunoassay, a new serological procedure in which a hybrid antibody conjugate is able to bind erythrocytes, was used for the titration of antibodies against P. brasiliensis in sera from patients with paracoccidioidomycosis [23].

Gene context of Paracoccidioidomycosis

• Modulation of CD28 and CD86 expression in patients with paracoccidioidomycosis in different periods of treatment [24].
• In an attempt to understand better the immunoregulatory disorders in paracoccidioidomycosis (PCM), the possible correlation between interleukin pattern, lymphoproliferation, C-reactive protein (CRP) and specific antibody levels was investigated in the polarized clinical forms of this disease [25].
• The presence of 9 HLA-A and 14 HLA-B specificities was determined in 83 patients with paracoccidioidomycosis [26].
• High serum interleukin-10 and tumor necrosis factor alpha levels in chronic paracoccidioidomycosis [27].
• Production of IFN-gamma is impaired in patients with paracoccidioidomycosis during active disease and is restored after clinical remission [28].

Analytical, diagnostic and therapeutic context of Paracoccidioidomycosis

• In the immunodiffusion test, the rapidly produced antigen demonstrated a sensitivity of 90% by detecting antibody in sera from 103 of 114 proven cases of paracoccidioidomycosis [29].
• In conclusion, we have shown that paracoccidioidomycosis-related Th1 immunosuppression is associated with down-modulation of the IL-12 pathway, that IL-10 may participate in this process, and that patients cured from paracoccidioidomycosis may not fully recover their immune responsiveness [30].
• An acidic glycolipid (Band 1), purified from P. brasiliensis by a combination of ion exchange chromatography, HPLC, and HPTLC, was found to be reactive with sera of all patients with paracoccidioidomycosis (PCM) [31].
• Western immunoblot experiments demonstrated that the recombinant protein and the native HSP60 were recognized by sera from humans with paracoccidioidomycosis (PCM) [32].
• 1. Indirect immunofluorescence was used to compare reticulin antibodies, endocardium-vessel-interstitium (EVI) antibodies and heterophilic antibodies in serum samples from patients with degenerative and inflammatory diseases, Chagas' disease, or paracoccidioidomycosis and from healthy blood donors [33].

References