Candida glabrata demonstrated increased fluconazole resistance (>256 μg/mL), with extensive cross-resistance to ketoconazole (0.38-3.0 μg), itraconazole (8 to >32 μg), and voriconazole (0.125-1.5 μg). Morphologically dissimilar colonies on RPMI/fluconazole agar demonstrated variable chromosomal profiles compared with the control isolate. Stable chromosomal changes were associated with a significantly higher (P<0.05) mRNA level of the hemolysin gene compared with the control. Phenotypic switching on CuSO4 agar was associated with variable metallothionein mRNA transcription levels. The proteome analysis of a fluconazole-resistant offshoot demonstrated a total of 98 protein spots, 25 showing a twofold upregulation.
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Experiments are described of the treatment of two patients with cryptococcal meningitis using antifungal drugs and amphotericin B. The first patient was a 56-year-old man with a slight azotaemia caused by hypertensive nephrosclerosis. Lumbar puncture revealed a positive India ink stain and a positive culture for Cryptococcus neoformans; serum titre for cryptococcal antigen was elevated. Amphotericin B was not administered because of the patient's slight azotaemia. After admission, the patient received oral and intravenous fluconazole (400 mg per day), for a total dose of 40 g of fluconazole over 103 days from October 1 while simultaneously receiving treatment with oral itraconazole (200 mg per day) from October 1 to December 5. In addition, he was given intravenous miconazole (600-1000 mg per day, total 74.4 g) and intrathecal miconazole (5-20 mg per day, total 375 mg) from December 1 to March 4 1990. Concomitantly, oral flucytosine (6 g per day) was given from December 5 to March 1 1990. Lumbar puncture performed at the completion of these treatments indicated the India ink stain still was positive and the serum titre for cryptococcal antigen high. Finally, amphotericin B alone was administered to the patient intravenously and intrathecally from March 4 to May 1, with an initial dose of 5 mg i.v. gradually increasing by 5 mg increments up to 50 mg per day. The patient's clinical symptoms immediately improved; the India ink stain became negative for the first time after admission and the serum titre for cryptococcal antigen also gradually decreased. On May 1, the patient was completely cured of cryptococcal meningitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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Many prospective randomized studies from our center have been reported between March 1976 and 2016, with more than 2700 renal transplant procedures conducted. The first study was a prospective randomized trial of azathioprine versus cyclosporine. The second study compared triple therapy (prednisolone + azathioprine + cyclosporine) versus conventional therapy (prednisolone + azathioprine). The third study was a cost-saving study, in which 100 patients received ketoconazole along with the triple regimen. Another trial demonstrated the advantages of a microemulsion form of cyclosporine. A subsequent trial compared calcineurin inhibitor minimization versus avoidance protocols. Rescue therapies were carried out to intensify immunosuppressive regimens after repeated rejection. In addition, steroid-free regimens were evaluated during both short- and long-term treatment. A recent trial reported a step-forward avoidance protocol with a calcineurin inhibitor and a steroid-free regimen, whereas another current study is the TRANSFORM one. The rationale behind antibody therapy was tho roughly evaluated among living-donor renal trans plant recipients with different agents, including basiliximab, daclizumab, antithymocyte globulin, and alemtuzumab.
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An open, comparative, randomized study was conducted using griseofulvin or itraconazole for the treatment of onychomycosis of the foot. Group I (45 patients) received itraconazole and Group II (45 patients) received griseofulvin. Each group was divided into three subgroups that received different topical treatment: antimycotic cream (isoconazole 1%), keratolytic cream (urea 40%), or placebo cream. The itraconazole group showed complete clearance in combination with isoconazole cream in 73.3% (11 of 15 patients), in combination with keratolytic cream in 78.5% (11 of 14 patients), and in combination with placebo cream in 91.6% (11 of 12 patients). The griseofulvin group showed complete clearance in combination with isoconazol cream in 46.1% (7 of 15 patients), in combination with keratolytic cream in 42.8% (6 of 15 patients), and in combination with placebo cream in 26.6% (4 of 15 patients). The itraconazole group showed better results compared with the griseofulvin group when the chi-square statistical method was used.
Several substances with different inhibitory effects on adrenal steroid biosynthesis were investigated in patients with Cushing's syndrome. It has been shown that trilostane, a 3 beta-hydroxysteroid-dehydrogenase inhibitor, is not potent enough to block cortisol biosynthesis in patients with hypercortisolism. Aminoglutethimide inhibits side chain cleavage of cortisol synthesis, but it has been demonstrated that the blocking effect on cortisol secretion is not strong enough to normalize urinary cortisol excretion in patients with Cushing's disease. For metyrapone, an inhibitor of adrenal 11 beta-hydroxylase, promising results were reported for the treatment of Cushing's syndrome. However, the drug has several side effects and depending on the definition of the desired reduction of cortisol secretion a true remission was only found in a minority of patients. The antifungal drug ketoconazole in vitro predominantly blocks 17,20-desmolase (IC50 1 microM) and to a lesser extent 17 alpha-hydroxylase (IC50 10 microM) and 11 beta-hydroxylase (IC50 15-40 microM). Therefore, ketoconazole in vivo most potently suppresses androgen secretion and only to a lesser extent cortisol biosynthesis. Several therapeutic trials with ketoconazole treatment in patients with pituitary Cushing's disease showed various remission rates between 30 and 90%. In contrast, in almost all patients with benign, primary adrenal Cushing's syndrome cortisol levels were normalized. In patients with ectopic ACTH syndrome ketoconazole was effective in about 50% of all reported cases, while cortisol hypersecretion due to adrenocortical carcinoma was only rarely inhibited by ketoconazole. The main side effect of ketoconazole treatment was liver toxicity which occurred in 12% of all treated patients. In contrast to ketoconazole, the narcotic drug etomidate shows a strong inhibitory effect on 11 beta-hydroxylase (IC50 0.03-0.15 microM) but only a weak inhibition of 17,20 desmolase (IC50 380 microM). This correlates with in vivo studies where even low, non-hypnotic doses of etomidate induced a pronounced fall in serum cortisol levels in normals and in patients with Cushing's syndrome. However, its clinical use is limited by its mandatory intravenous application and its sedative effects. In conclusion, ketoconazole remains the only available steroid-inhibitory drug for a therapeutic trial in patients with Cushing's syndrome who cannot be treated definitively by surgery.
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This report is a description of two Ohio cases of acquired immunodeficiency syndrome (AIDS) and disseminated histoplasmosis, with discussion of diagnosis and treatment of this combination. The patient in case 1 developed disseminated histoplasmosis as the first significant symptomatic medical condition of his life. The patient in case 2 presented with severe pharyngitis, but without signs or symptoms specific to the lungs. Amphotericin B alone does not eradicate histoplasmosis in an AIDS patient. The best therapy at present is a full course of amphotericin B followed by a lifetime regimen of ketoconazole to prevent relapse. Family physicians in the District of Columbia, Texas, Maryland, Louisiana, Missouri, Illinois, Arizona, and Puerto Rico should be particularly vigilant in looking for the combination of these two diseases.
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Cilnidipine was rapidly metabolized to three metabolites. They are dehydrogenated metabolite of dihydropyridine ring of cilnidipine (M1), demethylation metabolite of lateral chain of dihydropyridine ring of cilnidipine (M2), and the dehydrogenation and demethylation metabolite of cilnidipine (M3). Ketoconazole (Ket) competitively inhibited the dehydrogenation of dihydropyridine ring of cilnidipine and lowered the metabolic rate of cilnidipine while alpha-naphthoflavone (alpha-Naph), sulfaphenazole (Sul), quinidine (Qui), diethyldithiocarbamate (DDC), and tranylcypromine (Tra) had a little or no inhibitory effects on the dehydrogenation of cilnidipine.
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Ketoconazole, an imidazole is a powerful antimycotic that has recently been used in the treatment of endocrinological and lipid metabolism disorders as well as in anti-cancer chemotherapy. When rat mammosomatotropic cells are treated for 30 hrs., this drug produces different effects depending on whether cells are normal or tumoral (GH3/B6). A dose of 10 microM had no effect in normal cells, however, in tumoral cells it had dramatic effects: (i) 50% of the cells are killed and those which survive no longer proliferate and they secrete GH but not PRL; (ii) they respond to GHRH in a dose-dependent manner, while normal cells do not under similar culture conditions; (iii) the lipid composition of the membrane is modified as indicated by the increase in arachidonic acid turn-over and the dramatic change in the distribution of its metabolites. For the moment we cannot explain these data.
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Clinical samples were collected from 50 clinically suspected cases of systemic mycosis and subjected to smear, culture, antifungal sensitivity and PCR (based on 18S rRNA gene).
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A pooled analysis of 2 trials comparing mycological cure rates from continuous treatment with terbinafine (250 mg/d for 12 weeks) and continuous treatment with itraconazole (200 mg/d for 12 weeks) found a statistically significant difference in 11- and 12-month outcomes in favor of terbinafine (risk difference, -0.23 [95% confidence interval, -0.32 to -0.15]; number needed to treat, 5 [95% confidence interval, 4 to 8]). An analysis of clinical cure rates was not possible because of the diversity of definitions used in researching the effectiveness of oral antifungal drugs for onychomycosis. Only 3 trials gave a clear definition of clinical cure and presented data for these outcomes.
A total of 20 new phenylenedithiourea derivatives was synthesized by reaction of phenylenediisothiocyanates with aromatic amines as aminobenzoic, aminosalicylic acid and their derivatives. Their chemical structures were confirmed by elemental analysis, IR spectrometry and 1H NMR. The compounds were screened for in vitro antifungal, antibacterial activities and some of them have strong antifungal activities comparable to the activity observed for ketoconazole.
Fungal infections have dramatically increased in recent years, along with the increase of drug-resistant isolates in immunocompromised patients. Ninety eight Candida species obtained from blood cultures at the Tri-Service General Hospital, Taiwan, from 1998 to 2000 were studied. These included 50 Candida albicans, 13 Candida glabrata, 24 Candida tropicalis and 11 Candida parapsilosis isolates. To investigate their susceptibility to commonly used antifungal drugs, minimum inhibitory concentrations (MIC) of amphotericin B, fluconazole, flucytosine, and ketoconazole were determined. Both the National Committee for Clinical Laboratory Standards reference broth macrodilution method and E-test were used in parallel. Ninety five isolates (95/98, 96.94%) were susceptible to amphotericin B at a concentration < or = 1 microg/mL. All isolates (100%, 98/98) were susceptible to flucytosine. Approximately 30% of these Candida isolates were resistant to fluconazole. The MIC for 90% of isolates (MIC90) values for both methods for these isolates were 0.5 microg/mL for amphotericin B, 32 microg/mL for fluconazole, 0.25 microg/mL for flucytosine (0.125 microg/mL by E-test method), and 4 microg/mL for ketoconazole. MIC for 50% of isolates (MIC50) values for these agents were 0.25, 2, 0.06, and 0.06 microg/mL, respectively. The essential agreement of MIC values within 2 dilutions for the 2 methods was 99.0% for amphotericin B, 90.8% for ketoconazole, 92.9% for fluconazole, and 91.8% for flucytosine. This study showed that E-test has equivalent performance to the broth macrodilution method and can be used as an alternative MIC technique for antifungal susceptibility testing.
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Forty sequential isolates of Trichophyton rubrum were obtained from patients suffering from onychomycosis at two time points, before and after antifungal oral therapy. Strain differentiation by specific amplification of the two tandemly repeated elements (TRS-1 and TRS-2) of the ribosomal DNA of T. rubrum was performed. In addition, susceptibility tests were executed by the microdilution method with nine antifungal drugs: ketoconazole, itraconazole, fluconazole, miconazole, clotrimazole, isoconazole, griseofulvin, cyclopiroxolamine and terbinafine. The combination of TRS-1 with TRS-2 PCR amplification patterns configured 11 T. rubrum genotypes and the three most prevalent (genotypes 1-I, 5-I and 2-I) accounted for 67.5% of the isolates. Seven isolates (35%) obtained before antifungal oral therapy exhibited genotype 1-I compared to the 11 (55%) obtained after the treatment. Twelve patients exhibited different strains before and after the antifungal therapy. With respect to in vitro susceptibility testing, terbinafine was the most potent agent, followed by itraconazole, clotrimazole, isoconazole, miconazole, cyclopiroxolamine, ketoconazole, griseofulvin and fluconazole. Furthermore, an increase in the minimum inhibitory concentrations (MIC) were observed for most of the azole agents when testing isolates obtained post-treatment from four patients. This increase in MIC occurred concomitantly with the major occurrence of genotype 1-I for isolates obtained after oral therapy. These data attempt to consider the relevance of in vivo drug resistance for onychomycosis caused by T. rubrum.
Much of the clinical data evaluating the efficacy and safety of antifungal prophylaxis has been generated in cancer patients. The choice of antifungal agent for prophylaxis in this population remains controversial. However, azole compounds such as clotrimazole, ketoconazole and fluconazole appear to be more effective and better tolerated than nystatin suspension. Although ketoconazole has been shown to reduce fungal colonization in surgical patients, current data do not support the routine use of antifungal prophylaxis in this population. In renal transplant recipients, clotrimazole troches have been shown to be more effective than placebo or nystatin suspension. Selective bowel decontamination with nonabsorbable antibiotics and nystatin may be useful in reducing Candida colonization in liver transplant patients but no definitive recommendations may be made at this time regarding optimal antifungal prophylaxis in these patients. In patients with advanced HIV disease or history of prior fungal disease prophylaxis for oropharyngeal candidiasis is indicated, although the agent of choice remains controversial. Fluconazole is the drug of choice for prevention of relapse of cryptococcal meningitis in patients with AIDS. Finally, only limited data exist assessing the relationship between local colonization and systemic fungal infection. Adverse effects associated with antifungal prophylaxis, generally limited to nausea and vomiting and transient elevations in hepatic transaminases, occur with similar frequency among available oral or topical agents. However, the incidence of nausea and vomiting with resultant poor patient tolerance and compliance is usually higher with nystatin.
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Maduromycosis is a chronic granulomatous condition caused by fungal infection and is rarely encountered in Europe. To our knowledge, this is the first report of a case of maduromycosis affecting the chest wall in the United Kingdom. Conservative excision and drainage of the lesion combined with ketoconazole treatment in a dose 400 mg daily for several months failed to cure the condition. However, radical excision of the lesion combined with myoplastic repair of the defect in the chest wall eradicated the disease. Maduromycosis can occur in the chest wall and should be suspected in the immigrant population from tropical and subtropical areas. We recommend radical resection of similar lesions, combined with prolonged treatment with an antifungal agent e.g. ketoconazole when the causative organism is madurella mycetomis.
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A series of 2-(2,4-difluorophenyl)-2-hydroxy-3-(1H-1,2,4-triazol-1-yl)propyl dithiocarbamates as new analogs of fluconazole were synthesized and their antifungal activities were evaluated. Among these compounds, 2a-f and 3a-q exhibited higher activities than fluconazole against nearly all fungi tested except Aspergillus fumigatus. Noticeably, the in vitro biological activities of 2b, 3a, 3c, 3h-k, and 3o-q against Candida species were much better than those of fluconazole and ketoconazole. Also, 2a-d, 3a-d, 3e-f, 3h-k, 3p and 3q showed higher activities against A. fumi than fluconazole. Computational docking experiments indicated that the inhibition of CYP51 involved a coordination bond with iron of the heme group, the hydrophilic H-bonding region, the hydrophobic region, and the narrow hydrophobic cleft.
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We report a case of refractory Fusarium paronychia in a 42-year-old man with Behçet's disease receiving oral cyclosporin and corticosteroid. Symptoms resembling candidal paronychia of his little finger could not be cured by topical ketoconazole and oral terbinafine. The pathogen was identified as Fusarium solani species complex by gene analysis, and was multiple drug resistant. The case eventually resolved by occlusive dressing therapy with 0.5% amorolfine cream for 3 months.
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Fusarium proliferatum caused endophthalmitis after cataract surgery. Diagnosis was established by classical microbiology and molecular biology methods (PCR and DNA typing). The treatment with local amphotericin B, oral ketoconazole, and topical natamycin was successful.