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Nizoral (Ketoconazole)

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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.


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.


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.


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.


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.

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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.


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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Reboxetine, at systemic exposures approximately twice the recommended dose, did not significantly affect cardiac repolarization in healthy subjects. Use of QT versus RR relationship in the drug-free state to correct QT for heart rate in the drug-treated state may provide an acceptable alternative to classic correction equations.

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Prior to the development of ketoconazole, the treatment of systemic histoplasmosis and blastomycosis was limited to AMB. The convenience of oral dosing, combined with avoidance of the significant toxicities associated with AMB, make ketoconazole an attractive alternative for the treatment of selected forms of histoplasmosis and blastomycosis. Although high-dose (800 mg/day) ketoconazole is generally more effective than low-dose (400 mg/day), therapy should be initiated at the lower dose due to significantly more adverse effects at higher doses; the daily dose should be increased in patients with progressive disease. Caution should be exercised when ketoconazole is used to treat patients with GU tract disease and in patients with naturally occurring or pharmacologically induced achlorhydria. Thus, AMB remains the drug of choice for difficult to treat cases of histoplasmosis and blastomycosis; however, recent studies have established ketoconazole as the drug of choice in immunocompetent patients with non-life-threatening, non-meningeal H capsulatum and B dermatitidis disease.

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A case of fungal keratitis caused by Scopulariopsis brevicaulis following a penetrating eye injury is described. Treatment with antifungal agents and keratoplasty resulted in a favourable outcome.

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We report the effects of ketoconazole and the bistriazole ICI 195,739 acting alone or in combination with the allylamine terbinafine (Lamisil) on murine models of Chagas' disease. Mice infected with 10(5) Trypanosoma (Schizotrypanum) cruzi blood trypomastigotes and treated orally with 30 mg of ketoconazole per kg of body weight per day for 7 days, starting at 24 h postinoculation, had 100% survival after 35 days, while controls (untreated) or animals that received 15 mg of ketoconazole or 100 mg of terbinafine per kg/day by the same route had 0% survival after the same period of time. However, all mice receiving the combination of 15 mg of ketoconazole plus 100 mg of terbinafine per kg/day survived for 35 days after infection; it was shown that the survival of the animals treated with this combination was statistically greater than that obtained with either drug acting alone and was indistinguishable from that observed with the high doses of ketoconazole, indicating a synergistic action of the drugs in vivo. However, most animals that survived after the 7-day treatments were not cured, as indicated by a delayed but persistent parasitemia. When the treatment was extended to 14 days, 100% survival was obtained 10 weeks after inoculation for mice treated with 30 mg of ketoconazole per kg/day and the combination of 15 mg of ketoconazole per kg/day plus 100 mg of terbinafine per kg/day, while two-thirds of the mice treated with 15 mg of ketoconazole per kg/day alone were alive after the 14-day treatment; controls or animals that received 100 mg of terbinafine per kg/day did not survive after 25 days. Parasitemia in all surviving mice was negative after 55 days but parasitological cure, as assessed by subinoculation of organs in naive animals, was predominant only in animals that received the combined drug treatment. We also investigated the bistriazole ICI 195,739 and found, as reported previously, that just 1 mg of the compound per kg/day administered orally for 5 days was enough to protect most mice from death 30 days after inoculation, but no parasitological cures were observed. However, in the protocol used in the present study, the protective activity of ICI 195,739 at suboptimal doses (0.5 mg/kg/day) could be enhanced when it was used in combination with terbinafine at doses of the allylamine that by themselves induced no significant protection. Survival of the mice was inversely correlated with the levels of parasitemia in all cases. Extension of the treatment period with the triazole to 15 days at 1 mg/kg/day afforded definitive protection against death, with parasitological cure being achieved in 50% of mice at 10 weeks postinoculation, but no enhancement of its activity at suboptimal doses was observed when it was used in combination with terbinafine during this extended observation period. Taken together, these results supports the proposition that ketoconazole used in combination with terbinafine could be useful in the treatment of humans with Chagas' disease because it can promote parasitological cure without the need to resort to the use of high levels of the azole, which is known to interfere with hepatic function and steroid synthesis in the host. They also support the conclusions of previous in vitro studies which suggested that the triazole ICI 195,739 blocks the proliferation of T. cruzi by a mechanism which differs from those of classical ergosterol biosynthesis inhibitors.

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Being endemic in India and Sri Lanka, rhinosporidiosis is not much known in Africa where only few cases have been reported for the last 20 years. It is a chronic mycosis striking electively two target zones: nasal and conjunctival mucosae. Many features are still unknown about this pathogenic agent which belongs to the group of phycomycetes. But it has never been yet possible to cultivate it nor to inoculate it to animals. It has a cyclic development, well described by Ashworth. Its treatment is both surgical and medical (fungicides).

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Ketoconazole (KZ) has been shown to inhibit testicular and adrenal steroidogenesis and is useful in the medical management of gonadotropin-independent precocious puberty, prostatic cancer, and Cushing's syndrome. To determine whether KZ similarly affects ovarian steroidogenesis, the authors examined its effect on the activity of the human ovarian 3 beta-hydroxysteroid dehydrogenase/isomerase (3 beta-HSD), 17-hydroxylase (17-OH), and aromatase (AR) in vitro. A dose-dependent decrease in the activities of 3 beta-HSD and 17-OH was observed with increasing amounts of KZ. With 10, 50, and 100-fold excess KZ, the activity of 3 beta-HSD decreased by 59% (P less than 0.001), 73% (P less than 0.005), and 85% (P less than 0.005), respectively. At equimolar concentrations with substrate (50 microM), KZ inhibited 17-OH by 70% (P less than 0.01). No significant effect on ovarian AR activity was observed, except at the highest concentration of KZ tested. The authors conclude that low concentrations of KZ profoundly inhibit the activity of human ovarian 3 beta-HSD and 17-OH in vitro. These observations suggest that KZ might be useful in the medical management of women with hyperandrogenism, but further experimentation and clinical trials will be necessary.

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In 2014, six active pharmaceutical ingredients were released on the German market for small animals. Those are the ektoparasiticide of the isoxazoline group afoxolaner (NexGard®) and fluralaner (Bravecto®) and the neonicotinoid dinotefuran (Vectra 3D, Vectra Felis), the antidiabetic protamine zinc insulin of human origin (ProZinc®), the antifungal agent ketoconazole (Fugazid®) as well as the cytostatic drug oclacitinib (Apoquel®). Two substances were authorized for an additional species. The antiparasiticide eprinomectin and the antibiotic clindamycin were also authorized for use in cats. In addition, two active pharmaceutical ingredients, which were approved 2014 for use in human medicine and are of potential interest to veterinary medicine, are discussed. These are the antihypertensive drug riociguat and the urological substance mirabegron.

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The high cost of tacrolimus is a major problem in Mexico. Ketoconazole increases tacrolimus bioavailability by inhibiting cytochrome P450 3A4 and glycoprotein-p.

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Concentrations of oral azoles in serum were compared in a single-dose pharmacologic study in mice. When hydroxypropyl-beta-cyclodextrin was used as a carrier and compared with a standard carrier, polyethylene glycol, drug concentrations determined by bioassay showed that the peak concentration and area under the concentration-time curve were greatly enhanced for itraconazole and saperconazole; moderately enhanced for ketoconazole; but negligibly affected for fluconazole, miconazole, and SCH 42427.

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Membrane-bound cytochrome P4503A4 (CYP3A4) is the major source of enzymatic drug metabolism. Although several structural models of CYP3A4 in various ligand complexes are available, none includes a lipid bilayer. Details of the effects of the membrane on protein dynamics and solvation, and access channels for ligands, remain uncertain. H/D exchange mass spectrometry (H/DXMS) with ligand free CYP3A4 containing a deletion of residues 3-12, compared to that of the full length wild type, in lipid nanodiscs afforded 91% sequence coverage. Deuterium exchange was fast in the F- and G-helices, HI loop, and C-terminal loop. In contrast, there is very low exchange in the F'- and G'-helices. The results are consistent with the overall membrane orientation of CYP3A4 suggested by published MD simulations and spectroscopic results, and the solvent accessibility of the F/G loop suggests that it is not deeply membrane-embedded. Addition of ketoconazole results in only modest, but global, changes in solvent accessibility. Interestingly, with ketoconazole bound some peptides become less solvent accessible or dynamic, including the F- and G-helices, but several peptides demonstrate modestly increased accessibility. Differential scanning calorimetry (DSC) of CYP3A4-nanodiscs suggests membrane-induced stabilization compared to that of aggregated CYP3A4 in buffer, and this stabilization is enhanced upon addition of the ligand ketoconazole. This ligand-induced stabilization is accompanied by a very large increase in ΔH for CYP3A4 denaturation in nanodiscs, possibly due to increased CYP3A4-membrane interactions. Together, the results suggest a distinct orientation of CYP3A4 on the lipid membrane, and they highlight likely solvent access channels, which are consistent with several MD simulations.

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Aspergillus terreus was isolated from a case of Keratomycosis. The patient, a 50 year old, female presented with a large corneal ulcer with hypopyon. The direct microscopic examination of the scrapings revealed hyaline, thin, septate and branched hyphae. In vitro some antimycotics (amphotericin B, 5-fluorocytosine, oxiconazole, amorolfine and ketoconazole) were tested against A. terreus by agar dilution method. Ketoconazole with MIC of 3 micrograms/ml after 7 days of incubation was most effective followed by oxiconazole (10 micrograms/ml). Experimental corneal ulcer was produced by injecting intralamellary 0.1 ml of the spore suspension containing 10 x 10(6) cfu/ml into the eyes of previously immunocompressed albino rabbits. Histopathologic examination showed infiltration and large destruction of the corneal stroma. Subconjunctival oxiconazole therapy exhibited complete cure. Based on our findings, a clinical evaluation of oxiconazole in human keratomycosis seems to be justified.

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Cytochrome P450 3A is a drug-metabolising enzyme activity due to CYP3A4 and CYP3A5 gene products, that is involved in the inactivation of anticancer drugs. This study analyses the potential of cytochrome P450 3A enzyme in human colorectal cancer to impact anticancer therapy with drugs that are cytochrome P450 3A substrates. Enzyme activity, variability and properties, and the ability to inactivate paclitaxel (taxol) were analysed in human colorectal cancer and healthy colorectal epithelium. Cytochrome P450 3A enzyme activity is present in healthy and tumoral samples, with a nearly 10-fold interindividual variability. Nifedipine oxidation activity+/-s.d. for colorectal cancer microsomes was 67.8+/-36.6 pmol min(-1) mg(-1). The K(m) of the tumoral enzyme (42+/-8 microM) is similar to that in healthy colorectal epithelium (36+/-8 microM) and the human liver enzyme. Colorectal cancer microsomes metabolised the anticancer drug paclitaxel with a mean activity was 3.1+/-1.2 pmol min(-1) mg(-1). The main metabolic pathway is carried out by cytochrome P450 3A, and it is inhibited by the cytochrome P450 3A-specific inhibitor ketoconazole with a K(I) value of 31 nM. This study demonstrates the occurrence of cytochrome P450 3A-dependent metabolism in colorectal cancer tissue. The metabolic activity confers to cancer cells the ability to inactivate cytochrome P450 3A substrates and may modulate tumour sensitivity to anticancer drugs.

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An in vivo screening assay using intact adult male rats has been evaluated for its ability to detect four endocrine-active compounds (EACs) via oral (gavage) administration. The test compounds included the aromatase inhibitor fadrozole (FAD), the testosterone biosynthesis inhibitor ketoconazole (KETO), and the thyroid modulators phenobarbital (PB) and propylthiouracil (PTU). Three of the test compounds (KETO, PB, and PTU) have been previously evaluated in the 15-day intact male assay with compound administration via intraperitoneal injection (ip). For the current studies, male rats were dosed for 15 days via oral gavage and euthanized on the morning of test day 15. The endpoints evaluated included final body and organ weights (liver, thyroid gland, testes, epididymides, prostate, seminal vesicles with fluid, accessory sex gland unit [ASG]), serum hormone concentrations (testosterone [T], estradiol [E2], dihydrotestosterone [DHT], luteinizing hormone [LH,] follicle stimulating hormone [FSH], prolactin [PRL], T(3), T(4), thyroid stimulating hormone [TSH]), and histopathology of the testis, epididymis, and thyroid gland; positive results for each endpoint are described below. In addition, an evaluation of immune system endpoints (humoral immune function, spleen and thymus weights, and spleen cell number) was conducted on a subset of animals dosed with either KETO or PB. FAD and KETO decreased the weights for the androgen-dependent tissues and caused similar patterns of hormonal alterations (decreased serum T and DHT; increased serum FSH and/or LH). In addition, KETO caused spermatid retention. For FAD and KETO, effects on thyroid parameters were not indicative of thyroid toxicity. PB and PTU caused thyroid effects consistent with thyroid modulators (increased thyroid weight, decreased serum T(3) and T(4), increased serum TSH, thyroid follicular cell hypertrophy/hyperplasia, and colloid depletion). In addition, PB increased relative liver weight and altered reproductive hormone concentrations (decreased serum DHT, PRL, LH; increased serum E2). Orally administered KETO and PB did not alter the primary humoral immune response to sheep red blood cells (SRBC), although spleen weights were increased at the highest doses for both compounds. In the current study, all four test substances were identified as endocrine-active. The effects that were observed in the current study via oral (gavage) compound administration were similar to the responses that were observed by the ip route in previous studies for KETO, PB, and PTU. Overall, the sensitivity (i.e., the dose required to elicit similar magnitude responses) between the ip and oral routes of administration were similar for the three EACs that were examined by both routes of administration. This article, in addition to the > 20 compounds that have already been examined using the 15-day intact male assay, supports this assay as a viable screening assay for detecting EACs, and also illustrates that the ability to identify EACs using the intact male assay will be equivalent regardless of the route of compound administration.

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A 44-year-old woman with proven Acanthamoeba keratitis was successfully treated medically with resultant 6/9 vision. During the treatment, repeated attempts to titrate the patient off topical corticosteroids resulted in recurrent flare-up of inflammatory keratitis from which Acanthamoeba could not be recultured. It is suggested that steroid administration during the course of Acanthamoeba keratitis may need to be withdrawn extremely slowly to avoid the recurrence of what appears to be an immunological corneal reaction.

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Penicillium marneffei, a dimorphic fungus that is endemic in southeast Asia, causes deep-seated infection in humans and rodents. About 20 cases have been reported among the local populations of China, Thailand, and Hong Kong, and 35 cases have now been described in patients infected with the human immunodeficiency virus (HIV). We present a review of the literature and report two additional cases. Both immunocompromised and apparently immunocompetent hosts tend to develop disseminated, symptomatic infection. HIV-infected patients having travelled to southeast Asia and presenting with fever, skin lesions, hepatomegaly, adenopathies, or lung disease should be investigated for Penicillium marneffei infection. The diagnosis is based on the demonstration of the organism in clinical specimens. Treatment with amphotericin B or itraconazole is generally successful, but maintenance therapy is warranted for patients with an underlying immunodeficiency.

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Concomitant administration of loratadine and ketoconazole significantly increased the loratadine plasma concentrations (307%; 90% CI 205-428%) and DCL concentrations (73%; 62-85%) compared with administration of loratadine alone. Concomitant administration of loratadine and cimetidine significantly increased the loratadine plasma concentrations (103% increase; 70-142%) but not DCL concentrations (6% increase; 1-11%) compared with administration of loratadine alone. Cimetidine or ketoconazole plasma concentrations were unaffected by coadministration with loratadine. Despite increased concentrations of loratadine and DCL, there were no statistically significant differences for the primary electrocardiographic repolarization parameter (QTc) among any of the treatment groups. No other clinically relevant changes in the safety profile of loratadine were observed as assessed by electrocardiographic parameters (mean (90% CI) QTc changes: loratadine vs loratadine + ketoconazole = 3.6 ms (-2.2, 9.4); loratadine vs loratadine + cimetidine = 3.2 ms (-1.6, 7.9)), clinical laboratory tests, vital signs, and adverse events.

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This study was designed to investigate itraconazole nail kinetics in 39 patients with onychomycosis in relation to their therapeutic outcome.

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Epidemiological factors, lines of management, and follow-up results were recorded and statistically analyzed and there were regional variations in the prevalence, risk factors, and outcome in resistant corneal ulcers.

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This atudy was designed to evaluate the antifungal and cytotoxic activities of the Nannorrhops ritchiana (Mazari Palm) 80% methanol extract (NR-M) and its four crude extracts i.e., petroleum ether (NR-A), dichloromethane (NR-B), ethyl acetate (NR-C) and butanol (NR-D). The antifungal activity was determined by agar tube dilution method against nine fungal strains; Aspergillus flavus, Trichophyton longifusis, Trichophyton mentagrophytes, Aspergillus flavus and Microsporum canis were susceptible to the extracts with percentage inhibition of (70-80%). Extracts exhibited significant and good antifungal activity against various fungal strains. The results were deduced by comparing with those for miconazole, amphotericin B and ketoconazole as standard drugs. The fractions of methanolic extract were assayed for their brine shrimp cytotoxic activity. They exhibited low toxicity with LC50 values ranging from 285.7 to 4350.75 μg/mL at the concentration of obtained results warrant follow up through bioassay guided isolation of the active principles, future antiinfectious research.

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No statistically significant differences among treatments in mean dose-corrected pharmacokinetic parameters were observed, except that the dose-corrected area under the concentration-time curve from time zero to 12 hours and the peak plasma concentration were significantly increased on days 4 and 7 in the presence of ketoconazole. As expected, heart rate increased from baseline (approximately 8-11 beats/min) at > or =8 mg reboxetine daily. No statistically significant prolongation of QTc (Fridericia correction) occurred after any of the treatments. No relationships between DeltaQTc and plasma concentrations of reboxetine enantiomers were apparent. Similar results were obtained with Bazett's correction and two linear corrections that relied on exercise data generated before drug administration.

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Prostate carcinoma is linked to osteoblastic metastasis. We therefore investigated the value of bone-targeted consolidation therapy in selected patients with advanced androgen-independent carcinoma of the prostate.

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The in vitro susceptibilities of 183 clinical yeast isolates to sertaconazole (STZ) were compared to their susceptibilities to clotrimazole (CTZ), econazole (ECZ), ketoconazole (KTZ), miconazole (MNZ), fluconazole (FLZ), itraconazole (ITZ), tioconazole (TCZ), amphotericin B (AMB) and flucytosine (5FC) by using a commercial agar diffusion method. Strains were isolated from vaginal and other superficial clinical samples (18 species of Candida and five strains belonging to other yeast genera). Only one strain (0.5%) was resistant to STZ out of 87.4% of susceptible strains (n=160). The percentage of susceptible strains was higher than those obtained with the other agents evaluated and the percentage of resistant strains was lower than for most of the other antifungals. The pattern of susceptibility of C. albicans to STZ, TCZ, ITZ and CLZ was similar and superior to the pattern of susceptibility of this species to MNZ, ECZ, FLZ, 5FC and KTZ. C. dubliniensis was more susceptible to STZ, MNZ, MNZ, FLZ, ITZ, CLZ than to TCZ, ECZ, 5FC, AMB or KTZ. Ten susceptible strains to STZ were resistant to FLZ and one strain was resistant to ITZ. The overall antifungal activity of STZ in vitro against a wide range of clinically important yeasts from vaginal and cutaneous samples indicates the therapeutic potential of this agent for the treatment of infections caused by these fungi. However, the activity of STZ and the clinical value of in vitro data need to be verified in human clinical trials.

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nizoral 200mg tablets 2015-06-21

Dextromethorphan (DMO), a cough suppressing synthetic analog of codeine, undergoes parallel O-demethylation to dextrorphan (DOP), and N-demethylation to 3-methoxymorphinan (MEM), in humans. 3-hydroxymorphinan, a didemethylated metabolite, is formed secondarily. O-demethylation activity is well established as an index reaction for CYP2D6. However, this pathway appears to be mediated by at least two different enzymes in vitro. N-demethylation activity has recently been proposed to reflect CYP3A3/4 activity. We investigated both pathways in vitro with microsomal preparations from three human livers to assess the value of DMO as a probe drug for CYP2D6 and CYP3A3/4, DMO O-demethylation displayed a biphasic pattern with a high-affinity site reflecting CYP2D6 activity (mean Ki for quinidine, 0.1 +/- 0.13 microM). Kinetic parameters for the two O-demethylation mediating enzymes predict an average relative intrinsic clearance (Vmax/K(m) ratio) of 96% of total O-demethylation mediated via the high-affinity enzyme. Thus, in vitro data confirms the usefulness of DMO O-demethylation as an index reaction to monitor CYP2D6 activity. The Eadie-Hofstee plot of DMO N-demethylation was consistent with single-enzyme Michaelis-Menten kinetics (Vmax varying from 3.3 to 6.8 nmol mg-1 min-1, K(m) from 231 to 322 microM). However, ketoconazole, a CYP3A3/4 inhibitor, reduced N-demethylation only by 60% and had a mean Ki an order of magnitude higher (0.37 microM) compared to other pure CYP3A3/4 mediated reactions. Troleandomycin, a mechanism based CYP3A3/4 inhibitor, inhibited buy nizoral online MEM formation by an average maximum of 46%, with an IC50 varying from 1 to 2.6 microM. A polyclonal rat liver CYP3A1 antibody inhibited MEM formation only by approximately 50%. Diethyldithiocarbamate (DDC), a mechanism based CYP2E1 inhibitor, reduced MEM formation at concentrations up to 150 microM between 33 and 43%. Chemical inhibitors of CYP2d6 (quinidine), CYP1A1/2 (alpha-naphthoflavone), and CYP2C9 (sulfaphenazole), as well as a goat rat liver CYP2C11 polyclonal antibody (inhibitory against human CYP2C9 and CYP2C19), had minimal effect on MEM formation rate, thus excluding an involvement of any of these enzymes. DMO N-demethylation is only partly mediated by CYP3A3/4, and therefore is not a reliable index reaction for CYP3A3/4 activity either in vitro or probably in vivo.

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Twenty patients who underwent hysterectomy received a single dose of 200 mg itraconazole at different moments before surgery. At the moment of surgery, a urine sample, blood sample and tissue samples of different organs of the female genital tract were collected. Blood levels and tissue levels of itraconazole were measured by means of an HPLC method. Itraconazole blood levels were lower than the corresponding tissue levels in the various organs of the female genital tract. This finding for itraconazole is different from findings with ketoconazole, indicating that itraconazole has a higher affinity for tissue than ketoconazole. Urine levels of itraconazole were virtually undetectable in all samples. None of the patients complained of side-effects, and blood biochemical parameters all remained within the normal limits. The premedication buy nizoral online with itraconazole had no effect whatsoever on the induction and maintenance of and recovery from the anaesthesia. No abnormal effects on ECG were observed.

nizoral drug 2017-04-19

Between April and May 2013, a national online 18 buy nizoral online -question survey was sent to major Italian radiotherapy centers.

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Thirty patients were treated. Five patients received carboplatin [AUC (6)] but experienced delayed thrombocytopenia. After a protocol amendment, 25 subsequent patients received carboplatin [AUC (5)]. Median age was 64 years. Median prostate-specific antigen (PSA) was 117 ng/mL. Fifty-three percent received prior ketoconazole and 10% had mitoxantrone. No dose-limiting toxicities were noted. Although maximal tolerated dose was not reached, docetaxel dose escalation was stopped at 43 mg/m2. Significant myelosuppression was not seen until the highest dose level, when seven and four patients experienced grade 3 buy nizoral online and 4 toxicities, respectively. Among all patients, PSA declines of > or =50% occurred in 63%. At the recommended phase II dose, PSA declines of > or =50% occurred in 75% (95% confidence interval, 43-95). Four of 14 (29%) patients with measurable disease had partial responses. Median survival was 14.6 months.

nizoral 100 mg 2016-09-06

Exploring caves is, without doubt, a very exciting adventure; however, it carries some dangers. Three of four travellers were admitted to hospital with lung changes after returning from Ecuador, successively. Epidemiological studies revealed that the travellers visited caves infested by bats, and had contact with bats buy nizoral online ' guano. They gave a history of fever, fatigue, myalgia, dry cough, and chest pain during the stay or just after returning from Ecuador. In two patients, symptoms persisted in mild nature. Chest X-ray films showed diffuse nodules (coin-like lesions) in the lungs in each case. Histoplasmosis was taken into consideration. Differential diagnosis included paragonimiasis, pulmonary tuberculosis, and pulmonary infection of other causes. Direct examination of sputum was negative. Cultures were negative. Final diagnosis was made on epidemiological histories, as well as typical radiological changes, and was supported by positive tests for antibodies to Histoplasma capsulatum. Immunodiffusion test (ID), complement fixation test (CFTs), and Western blot test were positive. In two cases antifungal treatment was established. Ketoconazole followed by Itraconazole were used. Persons who are going to explore caves should be equipped with anti-dusk masks to prevent pulmonary histoplasmosis. The threat of Histoplasma capsulatum infection in bat-inhabited caves should be emphasized to travellers and also to physicians.

nizoral 40 mg 2017-02-24

Besides the progesterone inducible steroid hydroxylase which catalyses the transformation of progesterone to 11alpha-hydroxyprogesterone the presence of another monooxygenase system in filamentous fungus Rhizopus nigricans (R. nigricans)--lanosterol demethylase was confirmed. Lanosterol demethylase was not inducible with progesterone. After subcellular fractionation both monooxygenase systems were found in microsomal fraction of fungus R. nigricans. To find out how to differentiate between the hydroxylase and demethylase systems the influence of inhibitors ketoconazole and metyrapone on both monooxygenase systems was studied. Both substances efficiently inhibited fungal steroid hydroxylase. Spectral studies used to characterize the interaction of inhibitors with cytochromes P450 showed that both inhibitors bind to induced fungal preparations whereas in noninduced fungal preparations interaction with P450 was found only buy nizoral online with ketoconazole. This indicated the difference in interaction of the two inhibitors on both monooxygenase systems present in fungus R. nigricans.

nizoral shampoo review 2016-06-29

The tricyclic antidepressant, doxepin, is formulated as an irrational mixture of E (trans) and Z (cis) stereoisomers (85%: 15%). We examined the stereoselective metabolism of doxepin in vitro, with the use of human liver microsomes, recombinant CYP2D6 and gas chromatography-mass spectrometry. In human liver microsomes over the concentration range 5-1500 microM, the rate of Z-doxepin N-demethylation exceeded that of E-doxepin above 100 microM in two of three livers. Eadie-Hofstee plots were curvilinear indicating the involvement of several enzymes in N-demethylation. Coincubation of doxepin with 7,8-naphthoflavone and ketoconazole reduced the rates of N buy nizoral online -demethylation of E- and Z-doxepin by 30-50% and 40-60%, respectively, suggesting the involvement of CYP1A and CYP3A4, whilst quinidine had little effect on N-demethylation. In contrast, doxepin hydroxylation was exclusively stereo-specific; E-doxepin and E-N-desmethyldoxepin were hydroxylated with high affinity in liver microsomes and by recombinant CYP2D6 (Km in the range of 5-8 microM), but there was no evidence of Z-doxepin hydroxylation. In 'metabolic consumption' experiments with liver microsomes (having measurable CYP2D6 activity) and initial substrate concentration of 1 microM, the consumption of E-doxepin was greater (P < 0.05, n = 5) than that of Z-doxepin. Quinidine inhibited the consumption of E-doxepin but did not affect the consumption of Z-doxepin. With N-desmethyldoxepin, quinidine inhibited the consumption of E-N-desmethyl-doxepin whereas Z-N-desmethyldoxepin appeared to be a terminal oxidative metabolite. In summary, CYP2D6 is a major oxidative enzyme in doxepin metabolism; predominantly catalysing hydroxylation with an exclusive preference for the E-isomers. The relatively more rapid metabolism of E-isomeric forms, and the limited metabolic pathways for the Z-isomers may explain the apparent enrichment of Z-N-desmethyldoxepin that is observed in vivo.

nizoral generic shampoo 2017-09-29

Among the opportunistic infections in patients with leukemias systemic fungal infections contribute a major part if not the majority. This results from autopsy data and is supported clinically when using new criteria by imaging techniques, while microbiological documentation shows a low sensitivity in this situation. Those lessons require a change in strategy toward an earlier and empiric use of systemic antifungal drugs in the frequent infections appearing as fever of unknown origin. By its high systemic activity and low toxicity Fluconazole facilitates this approach. Amphotericin B with 5-Flucytosine remain as the most established standard. Liposomal Amphotericin B allowing higher dosage by lower toxicity appears effective as salvage treatment especially buy nizoral online in aspergillosis which also responds to Itraconazole available as oral formulation so far.

nizoral dandruff reviews 2017-01-01

The aquatic environment is challenged with complex mixtures of chemicals that may interact biochemically with each other in non-target aquatic organisms through a combination of actions, resulting in unpredictable mixture toxicity. This study focuses on the interactive effects of chemicals, including benzo(a)pyrene (BaP) and ketoconazole (KCZ), on 17β-estradiol (E2)-induced estrogenic responses in male goldfish (Carassius auratus). The possible interactions between BaP or KCZ and E2 were investigated on the expression of cytochromeP4501A (CYP1A, biotransformation enzyme) and on its corresponding catalytic activity 7-ethoxyresorufin-O-deethylase (EROD activity), as well as on the expression of CYP19 (steroidogenic enzyme) and E2 bioaccumulation in liver. Exposure to E2 caused a significant increase in estrogenic responses corresponding with the E2 bioaccumulation. When comparing results to the E2 exposure group, co-exposure to buy nizoral online BaP resulted in an increase in the cyp1a mRNA expression and its corresponding EROD activity and a marked decrease in the E2 bioaccumulation, but the expression of aromatase was not altered. Conversely, co-treatment with KCZ significantly suppressed the E2-modulated expression of metabolism and synthesis enzymes, which were accompanied by an increase in the E2 bioaccumulation. These data suggest that the modulation of E2-induced estrogenic responses by BaP and KCZ were correlated to the alterations of E2 bioaccumulation in goldfish, leading to a combination of changes in the capacity of biotransformation and steroidogenesis. The complex interactions between chemicals with different modes of actions highlight the need for caution in determining the safety of combined pollution in the aquatic environment.

nizoral tabs 2015-03-10

Exposure to certain xenochemicals can alter the catalytic activity of the major drug-metabolizing enzyme, CYP3A4, either by enhancing expression of this cytochrome P450 or inhibiting its activity. Such alterations can result in adverse consequences stemming from drug-drug interactions. A simplified and reliable tool for detecting the ability of candidate drugs to alter CYP3A4 levels or inhibit catalytic activity was developed buy nizoral online by stable integration of human pregnane X receptor and a luciferase vector harboring the CYP3A4 enhancers. Treatment of stable transformants, namely DPX-2, with various concentrations of inducers including rifampicin, mifepristone, troglitazone, methoxychlor, and kava produced dose-dependent increases in luciferase expression (between 2- and 40-fold above dimethyl sulfoxide-treated cells). Northern blot analyses of CYP3A4 mRNA in DPX-2 cells exhibited a good correlation to results generated with the reporter gene assay (r(2) = 0.5, p < 0.01). Induction of CYP3A4 protein was examined by measuring catalytic activity with the CYP3A4 substrate, luciferin 6' benzyl ether (luciferin BE). Metabolism of luciferin BE by DPX-2 cells was enhanced 5.2-fold above dimethyl sulfoxide-treated cells by treatment with rifampicin. Constitutive androstane receptor-mediated regulation of CYP3A4 protein was addressed by measuring catalytic activity in a separate cell line over-expressing this receptor. Phenobarbital and dexamethasone produced 1.5- and 2.0-fold increases, respectively, above control in luciferin BE metabolism. To determine the utility of DPX-2 cells for identifying inhibitors of CYP3A4 catabolism, luciferin BE activity was measured in the presence of various concentrations of ketoconazole, erythromycin, or kava. These agents exhibited dose-dependent decreases in CYP3A4 activity with IC(50) values of 0.3 microM for ketoconazole, 108 microM for erythromycin, and 15.5 microg/ml for kava. Collectively, DPX-2 cells were used to identify xenobiotics that induce or inhibit CYP3A4 in a high throughput manner, demonstrating their applicability to early-stage drug development.

nizoral pills medication 2016-01-25

A 59-year-old man with prostatism, in otherwise good health, was treated with transurethral prostatectomy and ketoconazole. At microscopic examination of the prostatic tissue he had acute and chronic prostatitis with granulomatous lesions, in the center of which capsular-deficient cryptococcal organisms were demonstrated. The patient was well without evidence of systemic or local infection at 22 months. The buy nizoral online differential diagnosis of granulomatous prostatitis is discussed.

nizoral pills price 2015-02-21

Rivaroxaban did not interact with midazolam (CYP3A4 probe substrate). Exposure to rivaroxaban when co-administered with midazolam was slightly decreased by 11% (95% confidence interval [CI] -28%, 7%) compared with rivaroxaban alone. The following drugs moderately affected rivaroxaban exposure, but not to a clinically relevant extent: erythromycin (moderate CYP3A4/P-gp inhibitor; 34% increase [95% CI 23%, 46%]), clarithromycin (strong CYP3A4/moderate P-gp inhibitor; 54% increase [95% CI 44%, 64%]) and fluconazole (moderate CYP3A4, possible Bcrp [ABCG2] inhibitor; 42% increase [95% CI 29%, 56%]). A significant increase in rivaroxaban exposure was demonstrated buy nizoral online with the strong CYP3A4, P-gp/Bcrp (ABCG2) inhibitors (and potential CYP2J2 inhibitors) ketoconazole (158% increase [95% CI 136%, 182%] for a 400 mg once daily dose) and ritonavir (153% increase [95% CI 134%, 174%]).

nizoral t gel 2015-05-11

The therapeutic and endocrine effects of ketoconazole and liarozole in patients with disseminated prostatic cancer are discussed, including buy nizoral online data from the literature and personal experience.

nizoral london drugs 2015-12-19

The authors report on one case of histoplasmosis in a young girl aged of 12, showing about Paxil 60mg Tabs 200 ulcerous vegetative lesions distributed on her body. Several different therapies were used without success. Utilization of ketoconazole during 187 days lead to a very favourable course. But the patient, escaping from medical control, died 5 months later. Existence of an acquired immunodeficient was supposed.

nizoral shampoo reviews 2015-07-28

Co-administration of multiple dosages of 400 mg/day ketoconazole with a single 100 mg mirabegron oral controlled absorption system (OCAS) dose increased mirabegron maximum concentration (C(max)) and area under the curve extrapolated to infinity (AUC∞) to 145 % (90 % confidence interval [CI] 123-172 %] and 181 % (90 % CI 163-201 %), respectively. Co-administration of multiple dosages of 600 mg/day rifampicin with a single 100 mg mirabegron OCAS dose decreased mirabegron C max and AUC∞ to 65 % (90 % CI 50-86 %) and 56 % (90 % CI 49-65 %), respectively, without an effect on terminal elimination half-life (t(½)). The urinary excretion of mirabegron was increased by ketoconazole and decreased by rifampicin, reflecting the AUC changes, whereas renal clearance was not affected. Ketoconazole decreased mirabegron t ½ from 50.9 to 37.6 h suggesting that volume of distribution as well as first-pass effect decreased. Rifampicin did not affect mirabegron t ½, suggesting that it affects first pass through the intestinal wall or liver. Rifampicin greatly increased the ratio to parent drug of the presumed CYP-mediated mirabegron metabolites M8 and M15 by 777 and 646 %. Steady-state mirabegron pharmacokinetic parameters (50 and 100 mg mirabegron OCAS) were similar in 13 CYP2D6 poor, 40 intermediate, and 99 extensive metabolizers, whereas C max and AUC under the dosing interval τ of 24 h (AUCτ) were 30-47 % lower in 10 ultrarapid metabolizers. After administration of 160 mg mirabegron immediate release, C(max) was 14 % and AUC∞ 19 % higher in eight poor metabolizers than in eight extensive metabolizers (phenotyped Retrovir Dosing ) with similar t ½. All treatments were well tolerated.

nizoral pill 2016-01-25

The aim of this study was to evaluate the effect of Lepidium meyenii (maca) in chemically and physically subfertile mice. After 35 days, the following groups of mice were evaluated: control, sham, chemical subfertility, chemical subfertility-maca-supplemented, physical subfertility, physical subfertility-maca-supplemented and maca-supplemented only. Motility (32.36% ± 5.34%) and sperm count (44.4 ± 5.37 × 10(6) /ml) in the chemically and physically subfertile mice (11.81% ± 4.06%, 17.34 ± 13.07 × 10(6) /ml) decreased compared to the Neurontin User Reviews control (75.53% ± 2.97% and 57.4 ± 19.6 10(6) /ml) and sham (53.5% ± 7.86% and 58.4 ± 14.10 10(6) /ml). Maca was able to reverse the deleterious effect of motility (76.36 ± 1.97) as well as sperm count (53.5 ± 9.18 × 10(6) /ml) on chemical subfertility. In contrast, maca did not reverse the effects of induced physical subfertility nor motility (18.78% ± 14.41%) or sperm count (20.17 ± 11.20 × 10(6) /ml). The percentage of sperm DNA fragmentation in the physically subfertile mice increased (11.1% ± 19.29%) compared to the control (0.84% ± 0.85%). However, in the physically subfertile group, maca decreased sperm DNA fragmentation (2.29% ± 2.30%) closer to the sham (1.04% ± 0.62%) and the control (0.84% ± 0.85%). The group supplemented only with maca showed 0.54% ± 0.50% of spermatozoa with DNA fragmentation. Yet, the differences observed were statistically not significant. In conclusion, it appears that maca activates the cytochrome P450 system after chemically induced subfertility. However, it does not reverse the low mitochondrial membrane potential in spermatozoa compromised in the physical subfertility group.

nizoral ketoconazole tablets 2016-11-16

Vitamin D receptor (VDR) agonists supporting human osteoblast (hOB) differentiation in the absence of bone resorption are attractive agents in a bone regenerative setting. One potential candidate fulfilling these roles is 24,25-dihydroxy vitamin D3 Serevent Inhaler Cost (24,25D). Over forty years ago it was reported that supraphysiological levels of 24,25D could stimulate intestinal calcium uptake and aid bone repair without causing bone calcium mobilisation. VDR agonists co-operate with certain growth factors to enhance hOB differentiation but whether 24,25D might act similarly in promoting cellular maturation has not been described. Given our discovery that lysophosphatidic acid (LPA) co-operated with VDR agonists to enhance hOB maturation, we co-treated MG63 hOBs with 24,25D and a phosphatase-resistant LPA analog. In isolation 24,25D inhibited proliferation and stimulated osteocalcin expression. When co-administered with the LPA analog there were synergistic increases in alkaline phosphatase (ALP). These are encouraging findings which may help realise the future application of 24,25D in promoting osseous repair.

nizoral generic 2017-03-28

After 8 days of simultaneous ketoconazole and St John's wort administration, CYP3A-mediated midazolam metabolism was strongly inhibited (81 % decrease in clearance). Following the induction of CYP3A with St John's wort (6.6-fold increase in clearance on day 8), a single dose of ketoconazole Pamelor Renal Dosing strongly inhibited midazolam metabolism to the same degree (82 % decrease in clearance in relation to baseline). An induction of midazolam metabolism was observed after discontinuation of both drugs in both study phases. These results apparently contradict the in vitro results where ketoconazole showed an inhibitory effect on the transcription of CYP3A genes.

nizoral buy online 2017-04-11

Vulvovaginitis is one of the main causes Plavix 20 Mg of premature membrane rupture.

nizoral cream generic 2015-04-22

There were 20 normal (NL) 120 Mg Evista men and 15 men with idiopathic hypogonadotropic hypogonadism (IHH) who completed the study.

dandruff nizoral reviews 2016-12-22

Copiamycin, a macrocyclic lactone antifungal antibiotic, was found to potentiate the antifungal effect of imidazole compounds, ketoconazole in particular. The potentiation of two nominally fungistatic agents in vitro was substantiated by a marked reduction of the minimum inhibitory and minimum fungicidal concentrations when the drugs were used in combination. The effectiveness of this synergistic combination was also demonstrated in experimental murine candidosis. Evidence is presented to suggest that this combined effect is due, at least in part, to the ionophoretic property of copiamycin. Whereas amphotericin B induces a marked increase in cellular permeability, this antibiotic does not possess the ionophoretic action of copiamycin, indicating that the enhancement of copiamycin activity and significant reduction of amphotericin B activity by ketoconazole pretreatment can be ascribed not only to changes in membrane permeability of the test organisms, but also to the different action mechanisms of copiamycin Luvox 150 Mg and amphotericin B. It is thus plausible that the strong synergism of copiamycin with imidazole compounds is related to the ionophoretic activity of the antibiotic. Further studies on the biochemical mechanism of this synergistic effect are being conducted together with an assessment of the clinical significance of this drug combination.

nizoral tablet treatment 2016-10-15

Two of our long term Norvasc Dosing efforts are to discover compounds with synergistic antifungal activity from metabolites of marine derived microbes and to optimize the production of the interesting compounds produced by microorganisms. In this respect, new applications or mechanisms of already known compounds with a high production yield could be continually identified. Surfactin is a well-known lipopeptide biosurfactant with a broad spectrum of antimicrobial and antiviral activity; however, there is less knowledge on surfactin's antifungal activity. In this study, we investigated the synergistic antifungal activity of C(15)-surfactin and the optimization of its production by the response surface method.