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Nizoral (Ketoconazole)
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Nizoral

Nizoral is an extra-class medicine which is taken in treatment of infections such as throat yeast infections, vaginal yeast infections, fungal infections, esophagus. Nizoral is a helpful for patients with Cushing's syndrome, hair growth, prostate cancer, eumycetoma, tinea versicolor, leishmaniasis, high blood levels of calcium. Nizoral acts as an anti-fungal drug.

Other names for this medication:

Similar Products:
Grifulvin, Lamisil, Sporanox, Grifulvin V, Diflucan, Fluconazole, Sporanox PulsePak, Onmel, Amphocin, Voriconazole, Abelcet, Fungizone, Vfend, Onmel, Abelcet

 

Also known as:  Ketoconazole.

Description

Nizoral is developed with a help of medical professionals to fight with infections (throat yeast infections, vaginal yeast infections, fungal infections, esophagus), Cushing's syndrome, women hair growth, prostate cancer, eumycetoma, tinea versicolor, leishmaniasis, high blood levels of calcium. Target of Nizoral is to control, ward off, reduce and terminate fungi growth.

Nizoral acts as an anti-fungal drug. Nizoral operates by reducing fungi growth spreads by infection.

Nizoral is also known as Ketoconazole, Fung.

Nizoral is imidazole.

Dosage

You should take it by mouth with full glass of water.

Take Nizoral once a day at the same time.

If you want to achieve most effective results do not stop taking Nizoral suddenly.

Overdose

If you overdose Nizoral and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Nizoral overdosage: feeling lightheaded, diarrhea, migraine, abnormal pain, ears ringing, nausea, rething.

Storage

Store at room temperature between 15 and 25 degrees C (59 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Nizoral are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Nizoral if you are allergic to Nizoral components.

Do not take Nizoral if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not use Nizoral if you take astemizole (Hismanal), cisapride (Propulsid), midazolam (Versed), triazolam (Halcion).

Be careful if you are taking oral diabetes medicine as glipizide (Glucotrol), chlorpropamide (Diabinese), glyburide (Glynase, Diabeta, Micronase), tolazamide (Tolinase), tolbutamide (Orinase); tacrolimus (Prograf); rifampin (Rimactane, Rifadin); warfarin (Coumadin); cyclosporine (Neoral, Sandimmune); antacids; famotidine (Pepcid, AC Pepcid), cimetidine (Tagamet HB, Tagamet), ranitidine (Zantac 75, Zantac), nizatidine (Axid AR, Axid); digoxin (Lanoxicaps, Lanoxin); methylprednisolone (Medrol); phenytoin (Dilantin); rabeprazole (Aciphex), omeprazole (Prilosec), lansoprazole (Prevacid).

Be careful if you have liver disease, achlorhydria.

Avoid consuming alcohol.

Try to avoid machine driving.

It can be dangerous to stop Nizoral taking suddenly.

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Neoscytalidium dimidiatum is an opportunistic fungus causing cutaneous infections mostly, which are difficult to treat due to antifungal resistance. In Malaysia, N. dimidiatum is associated with skin and nail infections, especially in the elderly. These infections may be mistaken for dermatophyte infections due to similar clinical appearance. In this study, Neoscytalidium isolates from cutaneous specimens, identified using morphological and molecular methods (28 Neoscytalidium dimidiatum and 1 Neoscytalidium sp.), were evaluated for susceptibility towards antifungal agents using the CLSI broth microdilution (M38-A2) and Etest methods. Amphotericin B, voriconazole, miconazole and clotrimazole showed high in vitro activity against all isolates with MIC ranging from 0.0313 to 1 µg/mL. Susceptibility towards fluconazole and itraconazole was noted in up to 10% of isolates, while ketoconazole was inactive against all isolates. Clinical breakpoints for antifungal drugs are not yet available for most filamentous fungi, including Neoscytalidium species. However, the results indicate that clinical isolates of N. dimidiatum in Malaysia were sensitive towards miconazole, clotrimazole, voriconazole and amphotericin B, in vitro.

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Fluconazole and itraconazole are two investigational triazole antifungal agents that are currently undergoing clinical trials in the United States. Both are active orally, have favorable pharmacokinetics (i.e., good bioavailability, long half-life, low plasma protein binding), and possess activity against several systemic fungal pathogens. In addition, preliminary information suggests that these agents are substantially less toxic than currently available azole compounds. Fluconazole and, to a lesser degree, itraconazole have been shown to be highly effective for the treatment of cryptococcal meningitis. The potential for drug interactions is much lower with these agents compared to drugs such as ketoconazole.

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Five patients with African histoplasmosis were treated with ketoconazole. Three of these were children with disseminated disease and 2 were adults with localized cutaneous disease. Both patients with cutaneous disease responded to treatment, although one was lost to follow-up. Of the 3 children with disseminated disease, one was apparently cured, one responded well but subsequently relapsed, and one failed to respond in spite of having blood levels of ketoconazole within the therapeutic range. Further studies are needed to determine the optimum dosage and duration of treatment with ketoconazole for this condition.

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Metabolism of a new antitumor agent, CAI (NSC 609974), was investigated in human liver tissue in vitro and in plasma and urine of patients receiving CAI. Metabolites identified by HPLC following C-labeled CAI incubation with human liver microsomes and reported as percentage of total metabolites formed were M1 (0-3.4%), M2 (4. 5-33%), M3 (60-79%), and M4 (7.2-19%). Ketoconazole, an inhibitor of cytochrome P450 3A4, prevented formation of M1, M3, and M4 (concentration of drug that inhibited metabolite formation by 50% when compared to maximum uninhibited activity, 3.0 &mgr;M), but only weakly inhibited formation of M2 (concentration of drug that inhibited metabolite formation by 50% when compared to maximum uninhibited activity, >50&mgr;M). CAI incubated with recombinant human P450 3A4 microsomes produced metabolites M3 and M4. Conjugation of M3, most likely a glucuronide, was observed after incubation of C-labeled CAI and UDP-glucuronic acid with human liver 13,000 x g supernatant. Plasma samples from patients receiving CAI contained CAI (3.1-5.0 &mgr;g/ml), M1 (0.9-2.6 &mgr;g/ml), and M2 (1. 0-2.2 &mgr;g/ml). CAI and M3 but not M4 were observed in the urine samples. After incubation of the urine samples withbeta-glucuronidase, CAI concentrations increased 67%, M3 increased up to 9-fold, and M4 was detected. CAI is metabolized in vitro and in vivo by both Phase I and Phase II enzymes and is metabolized to M3 and M4 by P450 3A4. These studies suggest that elevated levels of CAI may result from P450 3A4 inhibition by ketoconazole if these two drugs are coadministered. Correlation between CAI metabolism in vitro and results obtained in patients demonstrates the usefulness of liver metabolism studies in vitro in the early stages of drug development.

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Aminobenzolamide (5-sulfanilylamido-1,3,4-thiadiazole-2-sulfonamide) is a potent inhibitor of the zinc enzyme carbonic anhydrase (CA, EC 4.2.1.1), being at the same time structurally similar to the antimicrobial sulfonamides. Here we report that the reaction of aminobenzolamide with arylsulfonyl isocyanates affords a series of new arylsulfonylureido derivatives which were subsequently used as ligands (in the form of conjugate bases, as sulfonamide anions) for the preparation of metal complexes containing Ag(I) and Zn(II). All the new compounds proved to be very potent inhibitors of CA (isozymes I, II and IV). The newly synthesized complexes, unlike the free ligands, also act as effective antifungal agents against several Aspergillus and Candida spp., some of them showing activities comparable to ketoconazole, with minimum inhibitory concentrations in the range of 1.8-5 microg/mL. The mechanism of antifungal action of these complexes seem to be unconnected with inhibition of lanosterol-14-alpha-demethylase, since the levels of sterols assessed in the fungi cultures were equal in the absence or in the presence of the tested compounds. Probably the new complexes act as inhibitors of phosphomannose isomerase, a key enzyme in the biosynthesis of yeast cell walls.

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Mycetomas are endemic to northwest Africa. Most frequently located in the foot, they are seldom seen in the orbit. The color of the grains provides a clue as to the etiology. Black-grain mycetomas are always fungal and are treated surgically--essentially like cancer--as the persistence of a single grain will cause a recurrence.

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Prasugrel and clopidogrel inhibit platelet aggregation through active metabolite formation. Prasugrel's active metabolite (R-138727) is formed primarily by cytochrome P450 (CYP) 3A and CYP2B6, with roles for CYP2C9 and CYP2C19. Clopidogrel's activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6. In a randomized crossover study, healthy subjects received a loading dose (LD) of prasugrel (60 mg) or clopidogrel (300 mg), followed by five daily maintenance doses (MDs) (15 and 75 mg, respectively) with or without the potent CYP3A inhibitor ketoconazole (400 mg/day). Subjects had a 2-week washout between periods. Ketoconazole decreased R-138727 and clopidogrel active metabolite Cmax (maximum plasma concentration) 34-61% after prasugrel and clopidogrel dosing. Ketoconazole did not affect R-138727 exposure or prasugrel's inhibition of platelet aggregation (IPA). Ketoconazole decreased clopidogrel's active metabolite AUC0-24 (area under the concentration-time curve to 24 h postdose) 22% (LD) to 29% (MD) and reduced IPA 28% (LD) to 33% (MD). We conclude that CYP3A4 and CYP3A5 inhibition by ketoconazole affects formation of clopidogrel's but not prasugrel's active metabolite. The decreased formation of clopidogrel's active metabolite is associated with reduced IPA.

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A panel of 637 isolates of Candida albicans that had been typed by multilocus sequence typing (MLST) and tested for susceptibility to amphotericin B, caspofungin, fluconazole, flucytosine, itraconazole, ketoconazole, miconazole, terbinafine and voriconazole was the material for a statistical analysis of possible associations between antifungal susceptibility and other properties. For terbinafine and flucytosine, the greatest proportion of low-susceptibility isolates, judged by two resistance breakpoints, was found in MLST clade 1 and among isolates homozygous at the MAT locus, although only three isolates showed cross-resistance to the two agents. Most instances of low susceptibility to azoles, flucytosine and terbinafine were among oropharyngeal isolates from HIV-positive individuals. Statistically significant correlations were found between terbinafine and azole minimal inhibitory concentrations (MICs), while correlations between flucytosine MICs and azole MICs were less strong. It is concluded that a common regulatory mechanism may operate to generate resistance to the two classes of agent that inhibit ergosterol biosynthesis, terbinafine and the azoles, but that flucytosine resistance, although still commonly associated with MAT homozygosity, is differently regulated.

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Infant exposure to ketoconazole in human milk was calculated to be 0.4% on average (maximum 1.4%) of those expected from therapeutic doses given directly to infants. Potential risk of adverse reactions from this low exposure level seem to be outweighed by the benefits of breast-feeding.

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In 1985, available drugs to cure deep mycosis are in fact limited to amphotericin B (Fungizone), 5-fluorocytosine (Ancotil) and ketoconazole (Nizoral). Potassium iodide is not much utilized. In diffuse aspergillosis and meningitic cryptococcosis, Fungizone by I.V. injection remains the high-grade antifungal drug--Ancotil is not actually used anymore in mono-therapy, but associated either with Fungizone in cryptococcosis and diffuse aspergillosis, or with Nizoral in systemic candidosis--Nizoral, which does not diffuse in C.S.F. and has a limited efficiency in immunosuppressive patients, is recommended in systemic candidosis and tropical deep mycosis, particularly histoplasmosis, blastomycosis, entomophtoromycosis, as well as in candidosis and diffuse aspergillosis prophylaxis in people at high risk. New antimycosis drugs are under studies: itraconazole efficient against aspergillus and fluconazole, which diffuses in C.S.F. and has a long time action.

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Widespread and repeated use of fluconazole in the prophylaxis and therapy resulted in resistance among Candida strains. Investigation of the expression of efflux pump encoding genes was aimed in fluconazole-resistant and -susceptible C.albicans isolates in order to determine the role of this mechanism in fluconazole resistance. Five fluconazole-resistant, six -susceptible and four trailing effect showing susceptible C.albicans isolates were included in the study. The MIC values of fluconazole and other antifungal agents were determined by the microdilution method. The fluconazole MIC values of the fluconazole-resistant strains were also studied by E-test performed on yeast extract peptone dextrose agar with and without cyclosporin A. The expression levels of CDR1, CDR2 and MDR1 transcripts were determined by real-time PCR method. The expression of these genes was normalized with their ACT1 levels and compared with the fluconazole-susceptible C.albicans ATCC 14053 strain. It was detected that all strains were susceptible to amphotericin B and all except one strain were also susceptible to clotrimazole. Three out of five fluconazole-resistant strains and three out of four trailing effect showing susceptible strains were resistant to 5-flucytosine, and all except one susceptible strains were found as intermediate to 5-flucytosine. All except one fluconazole-resistant strains were determined as resistant to itraconazole and ketoconazole, and had miconazole MIC values of ≥ 64 µg/ml. All fluconazole-susceptible isolates were detected to be susceptible to ketoconazole and dose dependent susceptible to itraconazole. Fluconazole-resistant and -susceptible strains were determined as susceptible to voriconazole. Out of five fluconazole-resistant isolates, two strains overexpressed high levels and three strains overexpressed mild levels of CDR1/2; one strain overexpressed high levels and three strains overexpressed low levels of MDR1 in comparison to C.albicans ATCC 14053 control strain. It was observed that CDR1, CDR2 and MDR1 gene expression levels were mild in strains showing trailing effect except one which highly expressed MDR1, while susceptible isolates except three expressed efflux pump genes at low levels. It was determined that the expression levels of CDR1 and CDR2 genes for the same strain were in parallel for all isolates. It can be concluded that overexpression of efflux pump genes is an important mechanism of resistance in fluconazole-resistant C.albicans isolates.

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All patients received itraconazole for 3 months at a dose of 100 or 200 mg daily. Itraconazole levels of distal nail clippings were determined during a 6-month posttherapy period.

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Advanced prostate cancer remains dependent on androgens and signaling through the androgen receptor despite castrate levels of testosterone defined as testosterone levels <1.7 nmol/l. Ketoconazole, a nonspecific inhibitor of androgen synthesis, has been tested in clinical trials and showed clinical activity; however, high doses are needed which are associated with significant sides effects, mainly neurotoxicity, gastrointestinal intolerance, and liver toxicity. Abiraterone acetate is an irreversible inhibitor of two key enzymes of androgen synthesis, 17a-hydroxylase and 17,20-lyase, and has been tested in a randomized phase III study in patients with castration-resistant prostate cancer who progressed after chemotherapy. Abiraterone plus prednisone resulted in a significant overall survival benefit of 4.6 months compared to prednisone alone. Abiraterone was well tolerated, with mostly mild or moderate side effects consistent with secondary mineralocorticoid excess, namely fluid retention, hypokalemia, and hypertension. Abiraterone plus prednisone is considered a new standard therapy option for patients with castration-resistant prostate cancer who progressed after chemotherapy.

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Lenvatinib is an oral, multitargeted, tyrosine kinase inhibitor under clinical investigation in solid tumors. In vitro evidence indicates that lenvatinib metabolism may be modulated by ketoconazole, an inhibitor of CYP3A4 and p-glycoprotein.

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Cultured human epidermal keratinocytes were used as a model system for testing compounds with potential therapeutic effect against hyperproliferative skin disorders. We have investigated whether each test compound caused direct damage to the DNA or inhibited DNA repair and/or seminconservative replication of DNA, as well as its effect on the overall rate of protein synthesis and on expression of specific keratin genes. The following compounds were studied: (a) inhibitors of DNA polymerase alpha [aphidicolin and its derivative aphidicolin glycine], (b) inhibitors of topoisomerases [novobiocin, nalidixic acid, teniposide, etoposide, and 4'-(9-acridylamine) methanesulfon-m-anisidide], (c) modifiers of chromatin structure [sodium butyrate, 3-aminobenzamide, and nicotinamide], (d) inhibitors of calmodulin activation and protein kinase C [chlorpromazine and trifluoperazine]; and (e) drugs used in clinical dermatology [anthralin, fluocinolone acetonide, ketoconazole, and hydroxyurea]. The compounds were tested at concentrations at which they were known from the literature to be effective in their respective actions. Among the groups of compounds studied, the topoisomerase inhibitors were particularly interesting since they caused no detectable damage to DNA but exhibited maximal inhibitory effect on replication combined with minimal inhibition of DNA repair. In addition most of the topoisomerase inhibitors, particularly novobiocin, changed the pattern of gene expression by inhibiting the synthesis of certain keratins and inducing a Mr 67,000 protein in the prekeratin fraction. These properties combined with minimal systemic side effects may encourage the clinical exploration of some topoisomerase inhibitors for antiproliferative therapy of skin disorders.

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In docetaxel refractory mCRPC, the outcome of abiraterone treatment may be superior to ketoconazole.

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Fifty-one patients with nonmeningeal coccidioidomycosis were considered for treatment with intraconazole. Forty-nine patients who met study criteria were treated with itraconazole given orally in doses of 100 to 400 mg/day for periods up to 39 months. Of these patients, 12 had osteoarticular disease, 23 had chronic pulmonary disease, and 14 had skin or soft tissue disease. Clinical response was evaluated using a scoring system accounting for lesion number and size, symptoms, culture, and serologic titer. Remission was defined as reduction of the pretreatment score by 50% or more.

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An assessment was carried out in 59 women with proven vaginal candidosis to compare the efficacy and tolerance of itraconazole used in three different treatment regimens. Patients were allocated at random to receive a single oral dose of 200 mg itraconazole for 1, 2 or 3 days. They were reassessed 1 week and 4 weeks after treatment for remission of clinical signs and symptoms and repeat mycological investigations. All three regimens yielded successful clinical results, global evaluation at 4 weeks showing complete remission in 100% (5/5), 81.5% (25/27) and 92.3% (24/26) of patients, respectively. One patient (on 2-day treatment) required alternative treatment before the 4-week assessment. Minor gastric side-effects were reported by a few patients on the 2-day and 3-day treatment regimens; these resolved spontaneously.

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The in-vitro susceptibilities of 40 clinical isolates of Candida albicans to ketoconazole and fluconazole were determined and an attempt was made to correlate these data with the clinical responses of the patients from whom the strains were originally isolated to treatment with these agents. Of 40 patients with the acquired immunodeficiency syndrome (AIDS) with oropharyngeal and/or oesophageal candidosis, 21 received ketoconazole and 19 fluconazole. Susceptibility testing was performed by a microbroth dilution method with RPMI-2% glucose medium according to the recommendations of the National Committee for Clinical Laboratory Standards; growth inhibition was estimated spectrophotometrically and the MIC endpoint was defined in terms of the IC1/2. The MICs of 236 additional strains of C. albicans, which were also isolated from AIDS patients, were used to establish a susceptibility profile for this species. On the basis of the susceptibility test results and the clinical responses of the 40 patients, the following tentative breakpoints for ketoconazole and fluconazole are proposed: patients with infections caused by C. albicans strains with MICs of ketoconazole and fluconazole or < or = 0.001 and < or = 0.25 mg/L respectively would be expected to respond to treatment with these agents and isolates with MICs which meet these criteria are therefore classified as susceptible; patients with infections caused by strains with MICs of ketoconazole and fluconazole of > or = 0.06 and > or = 16.0 mg/L respectively would not be expected to respond to treatment with these agents and isolates with MICs which meet these criteria are therefore classified as resistant; the response of patients with infections caused by strains with MICs of ketoconazole and fluconazole of 0.003-0.03 and 0.5-8.0 mg/L respectively cannot be reliably predicted and isolates with MICs which fall within these ranges are therefore classified as being of indeterminate susceptibility. The present study demonstrates that the results of in-vitro susceptibility testing with RPMI-2% glucose broth correlate with the clinical response to therapy and can be used to facilitate optimal treatment in AIDS patients with oropharyngeal and/or oesophageal candidosis.

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Methadone has become one of the most widely used drugs for opiate dependency treatment. This drug is extensively metabolized by the cytochrome P450 hepatic enzyme family in man, yielding an N-demethylated metabolite that cyclizes spontaneously into 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine. The specific forms of cytochrome P450 involved in this oxidative N-demethylation were examined in a panel of 20 human liver microsomal preparations previously characterized with respect to their P450 enzyme contents. Methadone was demethylated with an apparent Km of 545 +/- 258 microM (n = 3). The metabolic rates were 745 +/- 574 pmol/(min.mg of protein). This metabolic pathway was strongly correlated with estradiol 2-hydroxylation, testosterone 6 beta-hydroxylation, nifedipine oxidation, erythromycin N-demethylation, and toremifene N-demethylation, all of these monooxygenase activities being supported by P450 3A4. Furthermore, the total P450 3A content of liver microsomal samples, determined by immuno-quantification using a monoclonal anti-human P450 3A4 antibody, was correlated with methadone demethylation (r = 0.72; p < 0.003). Methadone metabolism was 60-72% inhibited either by three mechanism-based inhibitors of P450 3A4 (gestodene, TAO, and erythralosamine) or by four reversible inhibitors of P450 3A (ketoconazole, dihydroergotamine, quercetin, and diazepam with an apparent Ki of 50 microM) and by two nonspecific inhibitors (metyrapone and SKF-525A). Conversely, quinidine (inhibitor of P450 2D6), 7,8-benzoflavone (inhibitor of P450 1A), or sulfaphenazole (inhibitor of P450 2C) did not significantly inhibit, and may even have activated, methadone metabolism. Four heterologously expressed P450 proteins were able to catalyze the N-demethylation of methadone, namely, P450 2C8, P450 2C18, P450 2D6, and P450 3A4. However, referring to their relative liver content, it can be asserted that P450 3A4 is the major enzyme involved in the N-demethylation of methadone on average. Accordingly, caution should be advised in the clinical use of methadone when other drugs are also administered that induce or inhibit P450 3A4, such as rifampicin or diazepam, respectively.

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Leishmaniasis, which exists in both visceral and cutaneous forms, is currently treated with intramuscular antimony or intravenous amphotericin B. The primary unmet need is for oral therapy. Of the several drugs in clinical development, miltefosine is unique in being an oral agent with efficacy against both forms of the disease. Sitamaquine is an oral agent with substantial but not sufficient efficacy against visceral disease. Oral fluconazole has been shown to be more effective than placebo in one instance: for Leishmania major cutaneous disease from Saudi Arabia. Paromomycin is in widespread trial. Topical paromomycin formulations are being tested for cutaneous disease, and intramuscular paromomycin is in Phase III trial for Indian visceral disease. The most likely replacements for present therapy are oral miltefosine for many of the visceral and cutaneous syndromes, intramuscular paromomycin for visceral disease and topical paromomycin for some forms of cutaneous disease.

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Randomised trials of amphotericin B, fluconazole, ketoconazole, miconazole, or itraconazole compared with placebo or no treatment in cancer patients with neutropenia.

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After cardiac transplantation, ketoconazole greatly reduced the need for cyclosporine, resulting in substantial cost savings. Ketoconazole also reduced the rates of rejection and infection, without persistent toxic effects. We now use ketoconazole routinely in cardiac-transplant recipients.

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By principle both topical and systemic antifungals are available for oral candidosis. As therapeutic results have not yet reached an optimum these modalities deserve further consideration. This especially applies to bioavailability. As candidosis in general very often is a disease confined to other tissues than blood especially to cutaneous and mucosal surfaces, it is helpful to determine the drug level found at these sites. Both total and free drug levels should be looked at. The skin blistering techniques make this possible. In vitro simulation of the level profiles of various antifungals including in particular ketoconazole found in the skin can be simulated in vitro using Grasso's model. If this is done only a very limited candidacidal effect is to be seen. Taking this fact into account as well as a limited clinical efficacy of conventional treatment protocols it looks rewarding to use conventional antifungal drugs such as ketoconazole at comparatively high doses.

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Combination therapy with ketoconazole and calcitriol or EB 1089 may enhance antitumor activities of vitamin D compounds for prostate cancer and alleviate side effects of vitamin D deficiency that are likely associated with ketoconazole therapy.

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The in vitro metabolism of ropinirole was investigated with the aim of identifying the cytochrome P450 enzymes responsible for its biotransformation. The pathways of metabolism after incubation of ropinirole with human liver microsomes were N-despropylation and hydroxylation. Enzyme kinetics demonstrated the involvement of at least two enzymes contributing to each pathway. A high affinity component with a K(M) of 5-87 microM and a low affinity component with a K(M) of approximately two orders of magnitude greater were evident. The high affinity component could be abolished by pre-incubation of the microsomes with furafylline. Additionally, incubation of ropinirole with microsomes derived from CYP1A2 transfected cells readily produced the N-despropyl and hydroxy metabolites. Some inhibition of ropinirole metabolism was also observed with ketoconazole, indicating a minor contribution by CYP3A. Multivariate correlation data were consistent with the involvement of the cytochrome P450 enzymes 1A2 and 3A in the metabolism of ropinirole. Thus, it could be concluded that the major P450 enzyme responsible for ropinirole metabolism at lower (clinically relevant) concentrations is CYP1A2 with a contribution from CYP3A, particularly at higher concentrations.

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Mycetoma is a variety of deep mycoses. The endemic centres are situated in the countries with tropic or subtropic climate. In diagnosis, the important place belongs to microbiological, histological and roentgenological investigations. Surgical treatment supposes the radical removal of a pathological focus in aiming at preservation of the weight-bearing surface of an extremity. In intact skin, the subcutaneous incision of the mycous infiltrate is performed. The extensive soft tissue defects, especially at the region of joints, require primary or secondary autodermoplasty. The medicamentous treatment of fungal mycetomas is ineffective. The positive effect of Ketocanazole (Nizoral) before the operation was noted.

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The evaluation of the response of patients with coccidioidomycosis to any therapeutic modality is a major challenge. A numerical scoring system was devised to quantitate separately the severity of disease on clinical presentation, the findings on chest film, bone scan, gallium scan, serology and skin test with coccidioidin and spherulin. The scoring system was used to evaluate the response to treatment with ketoconazole of seven patients with infiltrate pulmonary coccidioidomycosis; 20 patients with chronic cavitary coccidioidomycosis; and 40 patients with disseminated coccidioidomycosis. Dissemination included the soft tissue in 15, bone in 15, synovium in 11 and skin in 18. In all categories clinical severity scores improved dramatically. Radiographic scores showed similar improvement in cases of infiltrative pulmonary coccidioidomycosis but showed no change in cavitary coccidioidomycosis. Serology scores improved significantly (-2 or more) in one of seven infiltrative pulmonary cases, three of twenty chronic cavitary cases and twenty-three of forty disseminated cases. Among those with adequate mycology followup, cultures converted to negative in two of three infiltrative pulmonary coccidioidomycosis; seven of fourteen chronic cavitary coccidioidomycosis; and sixteen of twenty-two with disseminated disease. Unfortunately, when ketoconazole buy nizoral online was discontinued or interrupted, symptoms recurred in four of twenty (20 percent) with chronic cavitary and ten of forty (25 percent) of disseminated cases. The disease in two patients progressed while on ketonconazole. One of those developed meningitis.

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We report the cases of two adult buy nizoral online patients in whom fulminant hepatitis developed after 17 and 103 days of ketoconazole administration. Histologic administration showed massive, predominantly centrilobular necrosis. Clinical manifestations of hypersensitivity and eosinophilia were absent in both patients, which suggests that ketoconazole hepatotoxicity is not mediated through an immunoallergic mechanism.

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After 3 weeks of topical buy nizoral online treatment oxiconazole has revealed itself to be as efficient as ketoconazole, but it seems more rapidly efficient and better tolerated than ketoconazole.

nizoral pills medication 2017-08-01

Cytochrome P450 (CYP) 3A4 isoenzyme has been identified in vitro as the key buy nizoral online enzyme to metabolize desisobutyryl-ciclesonide (des-CIC), the pharmacologically active metabolite of the inhaled corticosteroid ciclesonide. This pharmacokinetic drug-drug interaction study was conducted to confirm this major metabolic pathway in vivo by using the strong CYP3A4 inhibitor ketoconazole, and to assess the effect of ketoconazole on the pharmacokinetics of ciclesonide and des-CIC.

nizoral drug 2016-01-02

Cilofungin, a lipopeptide antifungal agent, was tested for in vitro activity alone and in combination with ketoconazole, itraconazole, flucytosine and amphotericin B against 102 clinical isolates of Candida species. At 48 hours all isolates of Candida albicans, Candida tropicalis, Candida paratropicalis and Candida glabrata were inhibited by less than or equal to 5 meg/ buy nizoral online ml of cilofungin. In contrast, the MIC90 for Candida krusei was 10 mcg/ml and for Candida parapsilosis greater than 40 mcg/ml. The interaction of combinations of cilofungin with amphotericin B, itraconazole, ketoconazole and flucytosine was additive or indifferent at 48 hours for 100%, 88%, 78% and 70% of all Candida species isolates, respectively. Overall, cilofungin demonstrated good activity in vitro against most Candida species isolates.

nizoral generic name 2016-05-05

Surgery was the treatment of choice in all patients. Biochemical cure was achieved in 72.2% of patients. Nine patients developed in buy nizoral online the early postoperative period diabetes insipidus, which became in 2 patients only. Surprisingly, 3 patients with normal postoperative neurohypophyseal function later developed permanent diabetes insipidus. New hormone deficiencies occurred in 7 patients. Seventeen patients received ketoconazole before surgery (5 of them after surgery also), and 70% of them achieved normal urinary free cortisol levels. Three patients also received radiotherapy, and all of them were cured after a median follow-up of 85.5 months; they developed no tumors or other complications.

nizoral generic 2017-01-11

In a buy nizoral online double-blind study, 117 non-pregnant women with vaginal candidosis were treated for 3 days with 200 mg-tablets of ketoconazole taken once, twice or three times daily. The incidence of predisposing factors or of a recurrence history did not differ between treatment groups. Their male partners were randomly assigned to receive ketoconazole, 200 mg twice daily or placebo for 3 consecutive days. Cure and recurrence rates were not different in the three treatment groups, with or without simultaneous treatment of the male partner. Treatment of the sexual partner in the three dose-regimen-groups proved not to have influenced the therapeutic effect.

nizoral tab 2017-04-21

Following vitrectomy 9 of 20 patients (45%) achieved a visual acuity better than counting fingers at 3 m. No statistically significant difference was observed in anatomical and visual outcome between the steroid plus and steroid minus groups, though the number of patients with favourable visual outcome was buy nizoral online greater in the steroid plus group. Rate of clearance of inflammation was better in the steroid plus group (40 +/- 15.5 vs 55 +/- 8.6 days). All patients (6/20) with pre-operative vision better than counting fingers showed good anatomical and visual outcome in both groups.

nizoral pills buy 2016-08-27

Prevalence of non-AIDS-defining cancers (NADCs) has increased in the era of potent buy nizoral online antiretroviral treatments. Incidence rates of NADCs now exceed AIDS-defining cancers in HIV-positive patients. Treatment of NADCs may be complicated by interactions between antiretrovirals and chemotherapy mostly via inhibition or induction of CYP3A4. Erlotinib is used to treat non-small cell lung and pancreatic cancer and is primarily metabolized by CYP3A4 into multiple products including the active metabolite (OSI-420). Preclinical in vivo assessment was performed to gain a better understanding of CYP3A4-mediated interactions between antiretrovirals and erlotinib.

nizoral 40 mg 2017-12-22

Oxycodone is commonly used to treat severe pain in adults and children. It is extensively metabolized in the liver in adults, but the maturation of metabolism is not well understood. Our aim was to study the metabolism of oxycodone in cryopreserved human hepatocytes from different age groups (3 days, 2 and 5  months, 4  years, adult pool) and predict hepatic plasma clearance of oxycodone using these data. Oxycodone (0.1, 1, and 10 μM) was incubated with hepatocytes for 4 h buy nizoral online , and 1 μM oxycodone also with CYP3A inhibitor ketoconazole (1 μM). Oxycodone and noroxycodone concentrations were determined at several time points with liquid chromatography-mass spectrometry. In vitro clearance of oxycodone was used to predict hepatic plasma clearance, using the well-stirred model and published physiological parameters. Noroxycodone was the major metabolite in all batches and ketoconazole inhibited the metabolism markedly in most cases. A clear correlation between in vitro oxycodone clearance and CYP3A4 activity was observed. The predicted hepatic plasma clearances were typically much lower than the published median total plasma clearance from pharmacokinetic studies. The data suggests that there are no children-specific metabolites of oxycodone. Moreover, CYP3A activity seems to be the major determinant in metabolic clearance of oxycodone regardless of age group or individual variability in hepatocyte batches.

nizoral shampoo reviews 2017-04-29

At high doses, ketoconazole blocks both testicular and adrenal androgen biosyntheses and partially inhibits the glucocorticoid production. To investigate the effects of this imidazole derivative on the mineralocorticoid biosynthesis, 7 male mongrel dogs received a single oral dose buy nizoral online of 15 mg/kg of ketoconazole or placebo, in a cross-over way. From 2 to 4 h after treatment, an iv infusion of angiotensin II (10 ng/kg per min) was performed. Ketoconazole treatment significantly blunted the aldosterone and cortisol increment, whereas 18-hydroxycorticosterone, corticosterone, 11-deoxycorticosterone (DOC), progesterone, and 17 alpha-hydroxyprogesterone rose to peak concentrations, respectively 2.5-, 6-, 8-, 2.5- and 1.5-fold higher than those observed after placebo administration. Plasma 11-deoxycortisol and renin activity levels remained similar in both groups. On the other hand, 2 X 2 groups of 10 male adult rats each were fed with a normal or a sodium-depleted diet. Of the two sets of groups, one was treated ip with ketoconazole (20 mg/kg twice a day), the other with vehicle solution. In animals on either diet, ketoconazole lowered 18-hydroxycorticosterone and aldosterone concentrations. Plasma DOC rose up to 25-fold in the salt-deprived animals. Serum Na+, Cl-, corticosterone and plasma renin activity remained unaffected by the treatment. These results show that high-dose ketoconazole treatment partially inhibits the biosynthesis of aldosterone by affecting the cytochrome P-45011 beta.(ABSTRACT TRUNCATED AT 250 WORDS)

nizoral dosage 2016-07-01

No significant adverse events were observed in volunteers during Phase I. In Phase II, 30 (63.83%) volunteers using essential oil and 18 (62.07%) using ketoconazole remained until the end of the study. We observed a predominance of lesions in disseminated form, with M. sympodialis detected as the predominant agent identified in cultures. After 40 days of treatment, the rate of mycological cure was buy nizoral online 60% (p <0.05) for the group treated with essential oil of C. citratus and over 80% (p <0.05) for the group treated with ketoconazole formulations.

nizoral brand 2016-01-28

In each of the 28 reports of antiglucocorticoid treatment of Cushing's syndrome, antidepressant effects were noted in some patients; the largest two series document a response rate of 70% to 73%. Full response, however, was at times erratic and delayed. Across the 11 studies of antiglucocorticoid treatment of major depression, some degree of antidepressant response was noted in 67% to 77% of patients. Aldactone Drug Interactions Antidepressant or antiobsessional effects of antiglucocorticoid augmentation of other psychotropic medications have also been noted in small studies of patients with treatment-resistant depression, obsessive-compulsive disorder, and schizoaffective disorder or schizophrenia.

nizoral tablet dosage 2017-04-14

Using a double-blind, controlled protocol, we assessed the comparative ability of antifungal preparations to suppress the expected delayed erythema response following in vivo human exposure to ultraviolet B Amaryl Overdose (UVB) irradiation generated by a solar stimulator.

nizoral 400 mg 2016-10-03

We randomly assigned 43 patients at the time of cardiac transplantation to receive ketoconazole (200 mg per day) (23 patients) or no ketoconazole (20 patients). The main end points were the Glucovance Tablet Technology dose of cyclosporine required and the incidence of cardiac rejection and infection.

nizoral pills dosage 2016-11-17

In this work we reported the synthesis and evaluation of anti-Toxoplasma gondii Zanaflex 5 Mg and antimicrobial activities in vitro of three new compound series obtained from ethyl(5-methyl-1-H-imidazole-4-carboxylate): acylthiosemicarbazide analogues 3a-d, 4-thiazolidinone analogues 4a-d and 1,3,4-thiadiazole analogues 5a-d. All synthesized compounds were characterized by IR, (1)H, (13)C NMR and HRMS. The majority of the tested compounds show excellent anti-T. gondii activity when compared to hydroxyurea and sulfadiazine. In addition it was also shown that most of the compounds in this study have a better performance against intracellular tachyzoites. The results for antimicrobial activity evaluation showed weak antibacterial and antifungal activities for all the tested molecules, when compared with the standard drugs (chloramphenicol and rifampicin for antibacterial activity; nistatin and ketoconazole for antifungal activity).

nizoral tabs 2015-04-06

Ketoconazole in high doses causes castrate levels of testosterone within twenty-four to forty-eight hours; therefore it is extremely useful in the initial medical treatment of patients with metastatic prostate cancer who need a prompt therapeutic response. Review of 17 patients who presented with severe radicular pain or acute paraparesis/paraplegia showed that there was frequent delay in urologic consultation, pathologic confirmation, and initiation of efficacious therapy. In fact, 5 of 12 patients (42%) who received radiation therapy prior to effective hormonal therapy suffered significant morbidity Zithromax Alcohol Drinken and mortality. The case is made for the use of ketoconazole for initial empirical therapy for these patients.

nizoral dosage directions 2016-02-27

The study population comprised out-patients who had facial seborrhoeic dermatitis for at least 2 months Abilify Generic Cost , with moderate to severe erythema and desquamation at inclusion. The primary end-point was complete remission, defined as the disappearance of both erythema and desquamation. The non-inferiority of lithium was assessed on the 95% confidence interval (CI) of the difference between treatments.

nizoral reviews 2015-04-30

Idelalisib is a potent and selective phosphatidylinositol 3-kinase-δ inhibitor, which is a first-in-class agent to be approved for the treatment of relapsed chronic lymphocytic leukaemia, follicular B cell non-Hodgkin's lymphoma and small lymphocytic lymphoma. In dose-ranging studies, idelalisib exposure increased in a less than dose-proportional manner, likely because of solubility-limited absorption. The approved starting dose of 150 mg twice daily was supported by extensive exposure-response evaluations, with dose reduction to 100 mg twice daily being allowed for specific toxicities. Idelalisib may be administered without regard to food on the basis of the absence of clinically relevant food effects, and was accordingly dosed in primary efficacy/safety studies. Idelalisib is metabolized primarily via aldehyde oxidase (AO) and, to a lesser extent, via cytochrome P450 (CYP) 3A. Coadministration with the strong CYP3A inhibitor ketoconazole 400 mg once daily resulted in a ~79 % increase in the idelalisib area under the plasma concentration-time curve (AUC). Administration with the potent inducer rifampin resulted in a 75 % decrease in idelalisib exposure (AUC) and, as such, coadministration with strong inducers should be avoided. GS-563117 is an inactive primary circulating metabolite of idelalisib formed mainly via AO. Unlike idelalisib, GS-563117 is a mechanism-based inhibitor of CYP3A. Accordingly, idelalisib 150 mg twice-daily dosing increases the midazolam AUC 5.4-fold. Clinically, idelalisib is not an inhibitor of the transporters P-glycoprotein, breast cancer resistance protein, organic anion-transporting polypeptide (OATP) 1B1 or OAPT1B3. In a population pharmacokinetic model, no meaningful impact on idelalisib pharmacokinetics was noted for any of the covariates tested. Idelalisib exposure was ~60 % higher with moderate/severe hepatic impairment; no relevant changes were observed with severe renal impairment. This article reviews a comprehensive pharmacology programme, including drug-drug interaction studies and mechanistic and special population studies Reglan Generic Cost , which has allowed a thorough understanding of idelalisib clinical pharmacokinetics and their impact on clinical safety and efficacy.

nizoral medicine 2017-01-25

To investigate the effect of ketoconazole on acetaminophen Elavil 300 Mg (AAP)-induced hepatotoxicity in mice.

nizoral dandruff reviews 2015-11-02

The discovery of the antifungal activity of azole compounds represented an important therapeutic advance. Miconazole, ketoconazole, and fluconazole are currently commercially available, and itraconazole has undergone extensive clinical evaluation. Because of its limited activity and toxicity, miconazole has been replaced by newer agents. Ketoconazole has proven useful in therapy for superficial infections and invasive infections caused by the pathogenic fungi. Among its disadvantages are limited absorption in the absence of gastric acid and its potential for drug-drug interactions. Fluconazole is the only azole available as oral and intravenous preparations. Unlike other azoles, it is only minimally metabolized in the liver and largely excreted in the urine as active drug. It is more effective than ketoconazole against superficial candidal infections and is the drug of choice for maintenance therapy for cryptococcal meningitis in patients infected with Moduretic Pills human immunodeficiency virus. An advantage of itraconazole is its activity against aspergillosis. It is also active against many infections caused by pathogenic fungi. Other azole compounds are at varying stages of preclinical and clinical investigation.

nizoral 200mg tablets 2016-02-19

Lithium significantly improved seborrhoeic dermatitis symptoms in comparison with placebo. Objectives This randomized controlled trial was designed to show a non-inferiority of 15% (primary end-point) of lithium gluconate 8% ointment compared with ketoconazole 2% emulsion.

nizoral shampoo review 2017-09-20

The cytochrome P-450 enzyme system is involved in two major metabolic steps of the medullipin system: synthesis of medullipin I by the kidney and conversion of medullipin I to medullipin II by the liver as shown previously.

nizoral online 2017-08-13

The authors present a case study of a mentally healthy man who repeatedly experienced short-lived, obsessional-like suicidal ideas and images after ingestion of the anti-fungal drug ketoconazole. Ego-alien, suicidal ideas are an extremely rare form of adverse drug reaction. This is probably the first report of drug-induced ego-dystonic, mood incongruent suicidal ideas appearing in a fully conscious, healthy individual.