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Posaconazole has become an important part of the antifungal armamentarium in the prophylaxis and salvage treatment of invasive fungal infections (IFIs). Structurally related to itraconazole, posaconazole displays low oral bioavailability due to poor solubility, with significant drug interactions and gastrointestinal disease also contributing to the generally low posaconazole plasma concentrations observed in patients. While therapeutic drug monitoring (TDM) of plasma concentrations is widely accepted for other triazole antifungal agents such as voriconazole, the utility of TDM for posaconazole is controversial due to debate over the relationship between posaconazole exposure in plasma and clinical response to therapy. This review examines the available evidence for a relationship between plasma concentration and clinical efficacy for posaconazole, as well as evaluating the utility of TDM and providing provisional target concentrations for posaconazole therapy. Increasing evidence supports an exposure-response relationship for plasma posaconazole concentrations for prophylaxis and treatment of IFIs; a clear relationship has not been identified between posaconazole concentration and toxicity. Intracellular and intrapulmonary concentrations have been studied for posaconazole but have not been correlated to clinical outcomes. In view of the high mortality and cost associated with the treatment of IFIs, increasing evidence of an exposure-response relationship for posaconazole efficacy in the prevention and treatment of IFIs, and the common finding of low posaconazole concentrations in patients, TDM for posaconazole is likely to be of significant clinical utility. In patients with subtherapeutic posaconazole concentrations, increased dose frequency, administration with high-fat meals, and withdrawal of interacting medications from therapy are useful strategies to improve systemic absorption.
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This study identified Cryptococcus neoformans varieties isolated from 35 patients at teaching hospital of the Federal University of the Triângulo Mineiro and evaluated the susceptibility to antifungal agents among these samples using the protocol M27-A2 from the National Committee for Clinical Laboratory Standards. The gattii variety was identified in 11.4% of the cases (n = 4). The minimum inhibitory concentration (mg/ml) of Cryptococcus neoformans neoformans isolates ranged from 0.062 to 2.000 (amphotericin B), 0.250 to 8.000 (fluconazole), 0.062 to 1.000 (itraconazole) and 0.125 to 1.000 (ketoconazole). The gattii variety presented a minimum inhibitory concentration range of 0.125 to 2.000 (amphotericin B), 0.250 to 16.00 (fluconazole), 0.062 to 1.000 (itraconazole) and 0.125 to 4.000 (ketoconazole). Two isolates resistant to itraconazole and two resistant to amphotericin B (one isolate of each variety per antifungal agent) were found. These data show the importance of determining the variety and minimum inhibitory concentration of Cryptococcus neoformans isolates, in order to monitor resistance development and enable better treatment for cryptococcosis.
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To describe the clinical presentation and outcomes of treatment with itraconazole in patients with sporotrichosis.
Eosinophilic pustular folliculitis (EPF), also known as Ofuji disease, is a disease that manifests with follicular papules or pustules. Its variants include a classic type that occurs most commonly in Japan, an HIV-associated type, an infantile type, a type that occurs on the palms and soles, a rare medication-associated variant, and a rare neoplasia-associated variant.A wide range of medications has been used to treat EPF. Topical corticosteroids are the first-line treatment option for EPF. Topical tacrolimus seems to be useful initial therapy as well. Oral indometacin (50-75 mg/day) is an effective treatment of classic EPF although it can induce peptic ulcers. For treatment of HIV-associated EPF when topical corticosteroids and indometacin do not work, various other treatments should be considered. These treatment options include cetirizine 20-40 mg/day, metronidazole 250 mg three times a day, itraconazole starting at a dosage of 200 mg/day and increasing to 300-400 mg/day, and topical permethrin. If these treatments do not work phototherapy with UVB is the 'gold standard' of treatment and is often curative. Treatments with less certain risk-benefit ratios but with some efficacy include PUVA (psoralen + UVA) photochemotherapy, oral corticosteroids, synthetic retinoids (i.e. isotretinoin 1 mg/kg/day), and acitretin (0.5 mg/kg/day), oral cyclosporine (ciclosporine) 5 mg/kg/day, interferon (IFN)-alpha-2b, and IFNgamma. Minocycline 100mg twice daily and dapsone 50-100mg twice daily have been used with some effect. The use of highly active antiretroviral therapy for HIV has resulted in the amelioration of EPF as CD4 cell counts rise above 250/mm(3). The diversity of clinical presentations and affected populations make it seem that EPF is a reaction pattern as much as a disease and that therapy should be tailored to the variant of EPF and the underlying etiology.
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Seventy-one allograft recipients receiving voriconazole, in whom complete clinical, microbiologic and pharmacokinetic data were available, were studied to determine the efficacy of voriconazole in preventing fungal infections. The length of voriconazole therapy was 6-956 days (median 133). The total number of patient-days on voriconazole was 13 805 ( approximately 38 years). A total of 10 fungal infections were seen in patients on voriconazole (18% actuarial probability at 1 year): Candida glabrata (n=5), Candida krusei (n=1), Cunninghamella (n=1), Rhizopus (n=2) and Mucor (n=1). Two of the four zygomycosis cases were preceded by short durations of voriconazole therapy, but prolonged itraconazole prophylaxis. The plasma steady-state trough voriconazole levels around the time the infection occurred were <0.2, <0.2, 0.33, 0.55, 0.63 and 1.78 microg/ml in the six candidiasis cases. Excluding the four zygomycosis cases, all the six candidiasis cases were seen among the 43 patients with voriconazole levels of < or =2 microg/ml and none among the 24 with levels of >2 microg/ml (P=0.061). We conclude that voriconazole is effective at preventing aspergillosis. However, breakthrough zygomycosis is seen in a small proportion of patients. The role of therapeutic voriconazole monitoring with dose adjustment to avoid breakthrough infections with fungi that are otherwise susceptible to the drug needs to be explored prospectively.
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We performed a systematic review and meta-analysis of randomized controlled trials that compared different antifungal agents for the treatment of candidemia and other forms of invasive candidiasis. Two reviewers independently appraised the quality of trials and extracted data. The primary outcome was all-cause mortality, and secondary outcomes were microbiological failure, treatment failure, and adverse events. Relative risks (RRs) with 95% confidence intervals (CIs) were pooled.
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Cerebral endothelial cells in the rat, pig, and, most recently, human have been shown to express several types of receptors specific for glutamate. High levels of glutamate disrupt the cerebral endothelial barrier via activation of N-methyl-d-aspartate (NMDA) receptors. We have previously suggested that this glutamate-induced barrier dysfunction was oxidant dependent. Here, we provide evidence that human cerebral endothelial cells respond to glutamate by generating an intracellular oxidant stress via NMDA receptor activation. Cerebral endothelial cells loaded with the oxidant-sensitive probe dihydrorhodamine were used to measure intracellular reactive oxygen species (ROS) formation in response to glutamate receptor agonists, antagonists, and second message blockers. Glutamate (1 mM) significantly increased ROS formation compared with sham controls (30 min). This ROS response was significantly reduced by 1) MK-801, a noncompetitive NMDA receptor antagonist; 2) 8-(N,N-diethylamino)-n-octyl-3,4,5-trimethoxybenzoate, an intracellular Ca(2+) antagonist; 3) LaCl(3), an extracellular Ca(2+) channel blocker; 4) diphenyleiodonium, a heme-ferryl-containing protein inhibitor; 5) itraconazole, a cytochrome P-450 3A4 inhibitor; and 6) cyclosporine A, which prevents mitochondrial membrane pore transition required for mitochondrial-dependent ROS generation. Our results suggest that the cerebral endothelial barrier dysfunction seen in response to glutamate is Ca(2+) dependent and may require several intracellular signaling events mediated by oxidants derived from reduced nicotinamide adenine dinucleotide oxidase, cytochrome P-450, and the mitochondria.
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Sporotrichosis occurs after fungal implantation of Sporothrix spp. in the skin, and is the main subcutaneous mycosis in Latin America. Here we describe three atypical cases of the disease. The first case report an extra-cutaneous occurrence of the disease with joint infection; the second one describes a patient with bilateral lymphocutaneous form of sporotrichosis; and the third shows a zoonotic cutaneous case with the development of an erythema nodosum as a hypersensitivity reaction. These cases show the disease importance on the region and the necessity of fungal culture to the diagnosis confirmation.
The objectives of this retrospective study were to examine the relationship between the bioavailability of itraconazole and the type of food consumed and to determine the effects of food consumption on the pharmacokinetic parameters following a single oral dose of itraconazole in healthy volunteers.
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A transversal survey on the habits was conducted from March to May 2001, using a questionnaire mailed to 200 intensive care units.
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Disseminated histoplasmosis can have a varied presentation when it affects the skin. Presentation mimicking a cutaneous neoplasm is an uncommon manifestation. We present the case of an 86-year-old man presenting with a cutaneous lesion clinically suspicious for malignancy that was ultimately determined to be his first clinical manifestation of disseminated histoplasmosis after biopsy for histopathologic analysis. Microscopically, the lesion was a nodule with an eroded epidermis overlying a dense dermal inflammatory process. The infiltrate was characterized by numerous epithelioid histiocytes admixed with acute and chronic inflammation. On closer inspection, numerous 2-4 mum intracellular spores surrounded by a clear halo were identified. The organisms were highlighted with periodic acid schiff (PAS) stain. We present this case to highlight a unique presentation of disseminated histoplasmosis. Although this presentation is uncommon, it serves as a reminder that histopathologic confirmation of clinical diagnoses is important before undertaking more invasive procedures such as excision.