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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:
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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.

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.


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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The disposition of ketoconazole was characterized in the rat over a wide dose/concentration range. Bolus dose (0.03-10 mg/kg) studies indicate that plasma concentration-time profiles for ketoconazole are not superimposable when dose normalized because of nonlinearities occurring in both volume of distribution and clearance. The volume of distribution decreases from 3 to less than 1 L/kg, while the plasma clearance decreases 10-fold from 25 mL/min/kg as the dose is escalated. From these results, infusion rates were calculated to maintain the plasma concentrations achieved with particular bolus doses. The curvilinear relationship between steady-state plasma concentration (0.015-8.3 mg/L) and ketoconazole infusion rate (0.021-2.45 mg/hr/kg) was analyzed in terms of Michaelis-Menten kinetics. A Vmax of 3.2 mg/hr/kg and Km of 2.1 mg/L were obtained by nonlinear regression analysis. At the end of the ketoconazole infusion, liver, adrenals and kidneys were removed and assayed for ketoconazole. Tissue-to-plasma partition coefficients for the liver and adrenals showed a marked dependence upon steady-state plasma concentration. Both parameters (liver, 22; and adrenals, 53) showed a decrease of approximately 10-fold as the plasma concentrations were increased. In contrast, the kidney:plasma partition coefficient (1.8), blood:plasma concentration ratio (0.6), and plasma binding (96%) of ketoconazole did not show a concentration dependence over the range studied. It is concluded that the liver is an important determinant of ketoconazole's volume of distribution and that saturation of this process accounts largely for the reduction in volume of distribution with increasing dose.(ABSTRACT TRUNCATED AT 250 WORDS)

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To improve our understanding of the prescribing and patient-monitoring practices of physicians prescribing medications with a BBW to patients age >or=65 years in an ambulatory care setting.

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Two experimental approaches were used: (i) blockade of CYP3A4 metabolism by coadministration of ketoconazole to increase the plasma concentrations of the parent compound in the conscious guinea-pig, and (ii) administration of the compound directly into the coronary circulation of the anaesthetised dog in order to circumvent first-pass metabolism.

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With the availability of more number of antifungal agents in recent years, drugs other than saturated solution of potassium iodide (SSKI) are being increasingly used to treat sporotrichosis. It was therefore considered pertinent to evaluate in vitro antifungal susceptibility pattern of Sporothrix schenckii strains isolated at three centers in India against five commonly used antifungal agents.

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The effect of several imidazole containing drugs including keto on human adrenal 17 alpha-hydroxylase, 17,20-lyase, 21-hydroxylase, 11 beta-hydroxylase and 3 beta-hydroxysteroid dehydrogenase-isomerase (3 beta-HSD-I) activities was studied in vitro. The order of decreasing inhibitory potency as determined from ID50 values for both 17 alpha-hydroxylase (ID50 values ranged from 1.13-4.17 mumol/l) and 17,20-lyase (0.57-1.95 mumol/l) activities was: bifon greater than clot greater than keto greater than micon greater than econ greater than isocon greater than tiocon. Using [3H]progesterone (5.50-12.25 mumol/l) as the substrate for the 21-hydroxylase activity the order of decreasing inhibitory potency was: clot greater than bifon greater than isocon greater than micon greater than tiocon greater than econ greater than tiocon greater than keto. For the 11 beta-hydroxylation of [3H]deoxycortisol (1.48-2.34 mumol/l) the order of decreasing inhibitory potency was keto greater than bifon greater than clot greater than micon greater than econ greater than isocon greater than tiocon. The cytochrome P-450 dependent enzyme most sensitive to inhibition was 17,20-lyase and the least sensitive was 21-hydroxylase whereas the imidazole drugs were without effect on the cytochrome P-450 independent 3 beta-HSD-I activity. In agreement with previous results a common structural feature of the imidazole drugs having an inhibitory effect was the presence of aromatic rings on the N-1 substituent of the imidazole ring.

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Seborrhoeic dermatitis is a common entity that conventionally is difficult to treat. Recently, topical ketoconazole has been proven successful. To determine if other azoles, and in particular the more modern ones, are also helpful in this condition, a double-blind multicentre randomized controlled trial was performed in patients suffering from seborrhoeic dermatitis involving individuals 16 years and older without human immunodeficiency virus (HIV) infection. One hundred patients were enrolled and treated according to a random plan with either bifonazole 1% cream or the corresponding vehicle once daily for 4 weeks. All patients were evaluated at the beginning of the study, as well as after 2 and 4 weeks, i.e. the treatment period proper, and after 6 weeks of follow-up. Clinical evaluation was based on scores of 0-3 for the following parameters: erythema, papules, infiltration, scaling, itch. In addition, mycological evaluation was performed using adequate contact plates for quantitative determination of Malassezia furfur. In the end, 92 patients were at least partially evaluable. In general, the verum preparation tended to be more efficacious, e.g. the score for erythema amounted to 0.75 after 4 weeks as compared with 0.88 in the control group, the baseline values being 2.18 and 2.04 respectively. With itch, the corresponding figures were 0.17 and 0.33 as compared with 1.42 and 1.38 before treatment. While in statistical terms there was significant difference in these parameters, such a difference was demonstrated by clinical judgement at follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

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Serum lactate dehydrogenase (LDH) isoenzyme activity was analyzed in cetaceans. Animals that were treated by i.m. injection and others that received azole therapy had distinctly different LDH isoenzyme profiles. A third distinctive pattern was occasionally observed in clinically normal animals with elevations in total transaminase and LDH activity levels. DH isoenzyme activity patterns were not affected by mild or moderate hemolysis, refrigeration after 24 hr, or freezing for 24 hr with subsequent thawing. However, severe hemolysis produced artifactual changes similar to those observed in individuals that received injections but of a lesser magnitude. DH isoenzyme activity patterns may provide useful corroboration of other clinical findings when diagnostic modalities are limited, especially to differentiate nonspecific enzyme elevation from nonpathologic elevations in serum enzyme concentrations due to i.m. injections or azole therapy.

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Guinea pigs and athymic nude (RNU/RNU) rats were used to assess the efficacy of three orally administered antifungal agents--Tolciclate, Tolnaftate, and Ketoconazole--against Trichophyton mentagrophytes dermatophytosis. All three antifungal agents inhibited the test strain of T. mentagrophytes in vitro. Antifungal agents were tested in intervention (oral therapy started 5 days after challenge) or prophylaxis (oral therapy started 5 days before challenge) protocols. Oral treatment of dermatophytosis on guinea pig skin demonstrated that Tolciclate and Tolnaftate alleviated clinical symptoms and shortened the duration of the dermatophytosis, in comparison to nontreated controls. Assessment of antifungal efficacy in the guinea pig model was time consuming (30-35 days) and variability in the duration and severity of clinical symptoms on guinea pig skin was common. Oral therapy of chronically infected athymic rats demonstrated that Tolciclate, Tolnaftate, and ketoconazole were effective antifungal agents in vivo. Obvious improvement in clinical symptoms of dermatophytosis (i.e. less erythema and fewer lesions) was evident with all three antifungal agents within 10 days of starting oral therapy. By day 20, athymic rats that were treated with either Tolciclate or Ketoconazole showed marked clinical improvement of the chronic dermatophytosis. Chronically infected athymic rats, which lack thymus matured T-cells, are a promising new model to evaluate the efficacy of antifungal agents by culture, histology, and visual observations of clinical symptoms.

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At doses similar to those used for clinical treatment, voriconazole showed lower antifungal activity in experimental rat paracoccidioidomycosis than that obtained with itraconazole and sulfamethoxazole-trimethoprim.

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nizoral cream generic 2015-02-10

The concurrent administration of ketoconazole and donepezil produces no change in ketoconazole plasma concentrations, but a statistically significant change in donepezil plasma concentrations. These observed changes, which are smaller than those produced by ketoconazole for other agents sharing the CYP-3A4 pathway, are most likely the result of donepezil also being metabolized by CYP-2D6, as well Cardura Cost as its slow rate of clearance from plasma.

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The aim of this study was to develop tocol derivatives of chitosan able (i) to self-assemble in the gastrointestinal tract and (ii) to enhance the solubility of poorly soluble drugs. Among the derivatives synthesized, tocopherol succinate glycol chitosan (GC-TOS) conjugates spontaneously formed micelles in Imdur Er Generic aqueous solution with a critical micelle concentration of 2 μg mL(-1). AFM and TEM analysis showed that spherical micelles were formed. The GC-TOS increased water solubility of 2 model class II drugs. GC-TOS loading efficiency was 2.4% (w/w) for ketoconazole and 0.14% (w/w) for itraconazole, respectively. GC-TOS was non-cytotoxic at concentrations up to 10 mg mL(-1). A 3.4-fold increase of the apparent permeation coefficient of ketoconazole across a Caco-2 cell monolayer was demonstrated. Tocol polymer conjugates may be promising vehicles for the oral delivery of poorly soluble drugs.

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We present a case of transient band-like corneal deposit, a novel complication of Cymbalta Generic Discount fluocinonide and ketoconazole exposure.

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Fifteen cases of CS were collected (eleven cases of Cushing disease, two cases of ectopic secretion of ACTH, one case of adrenal adenoma, and one case of adrenal carcinoma). The clinical characteristics as well as laboratory data of patients with AH Feldene Generic Name and the response to therapy were studied.

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Ketoconazole is an antifungal agent that, in high doses, inhibits testicular and adrenal steroid synthesis. The ability of ketoconazole to block steroid synthesis has prompted us to use it in the treatment of advanced prostatic carcinoma. This study was Hytrin Generic For designed to determine the site of steroid synthetic blockade that was induced by ketoconazole. Twelve patients with metastatic prostate carcinoma on long term high dose ketoconazole therapy were compared with 12 control volunteers. Values of serum progesterone, 17-hydroxyprogesterone, androstenedione, dehydroepiandrosterone sulphate, testosterone, and cortisol were measured in a baseline state and after Cosyntropin and human chorionic gonadotropin stimulation. Baseline data showed that serum levels of testosterone, androstenedione, and dehydroepiandrosterone sulphate were lower and that plasma progesterone, luteinizing hormone, and adrenocorticotropin were higher in the ketoconazole group. With Cosyntropin, plasma cortisol, androstenedione, and dehydroepiandrosterone sulphate increased only in the control group. With human chorionic gonadotropin, testosterone increased only in the control group. Basal 17-hydroxyprogesterone and progesterone rose after Cosyntropin only in the ketoconazole group. Following human chorionic gonadotropin, progesterone rose in the ketoconazole group but not in the control group. These results suggest that ketoconazole is a potent inhibitor of steroid synthesis. The major site of action appears to be in the inhibition of 17-20 desmolase. A moderate blockade of 17-hydroxylase may be present. There is a marked inhibition of 21- and/or 11-hydroxylase. The ability of ketoconazole to inhibit steroid synthesis should have therapeutic potential in the treatment of steroid dependent disease. Frequent high dose ketoconazole therapy can inhibit adrenal steroid synthesis, which can be important for patients undergoing stressful situations.

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Peripheral eosinophilia is an Ceftin Antibiotic Cost uncommon finding present in a relatively limited number of conditions in children. A minor eosinophilia often seen in premature neonates may in part be due to intubation. This case illustrates the potential danger of percutaneous application of drugs in newborn and infants as it has previously been pointed out way various chemicals. Any deterioration of the corneal layer such as observed in many dermatosis prompts an increase in the cutaneous permeability. Immaturity of the premature skin may have aiso played a role. Dermatologists should be aware of potential toxic topical ointments before prescribing them to very low weight babies.

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Fungal infections are among the major causes of morbidity in cancer patients. In order to optimize the treatment of such patients, it is critical to determine the type of fungus causing infection as well as its susceptibility to antifungals. This study was undertaken to the study resistance of Candida spp. isolated from blood cultures of cancer patients to ketoconazole (KET), fluconazole (FLU), amphotericin B (AmpB), and flucytosine (FCU). A modified NCCLS M 27-A method was used to evaluate the activity of the species. Of the 56 Candida albicans isolates, 7 (12.5%) were resistant to FLU (MIC > or = 64 microg/ml), 6 (10.7%) were resistant to KET (MIC > or = 64 microg/ml) and 3 (5.3%) were resistant to FCU (MIC > or = 32 microg/ml). One (14.3%) of 7 C. parapsilosis Luvox Generic isolates was resistant to FLU (MIC > or = 64 microg/ml). One (33.3%) of 3 C. tropicalis isolates was resistant to KET (MIC > or = 64 microg/ml). None of the C. guilliermondii or C. pelliculosa isolates was resistant to KET, FLU, AmpB, or FCU. Based on these results, AmpB is an effective antifungal agent that can be used against all Candida isolates.

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The incidence of CYP3A-mediated interaction potential was 47%, 22% and 11% for substrates, inhibitors and inducers, respectively. The basic models for precipitants gave conservative predictions with no false negatives, whilst the mechanistic static models provided reasonable quantitative predictions (2.3-3-fold error). Further analysis revealed that incorporating DDI at the level of the intestine was in most cases over-predicting interaction magnitude due to overestimates of the rate and extent of oral Flomax Cost absorption of the precipitant. Quantifying victim DDI potential was also demonstrated using fmCYP3A estimates from ketoconazole clinical DDI studies to predict the magnitude of interaction on co-administration with the CYP3A inducer, rifampicin (1.6-3.3 fold error).

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Dabigatran etexilate, an oral, reversible, competitive, and direct thrombin inhibitor, is an in vitro and in vivo substrate of P-glycoprotein (P-gp). Dabigatran etexilate was proposed as an in vivo probe Strattera Generic 2017 substrate for intestinal P-gp inhibition in a recent guidance on drug-drug interactions (DDI) from the European Medicines Agency (EMA) and the Food and Drug Administration (FDA). We conducted transcellular transport studies across Caco-2 cell monolayers with dabigatran etexilate in the presence of various P-gp inhibitors to examine how well in vitro IC50 data, in combination with mathematical equations provided by regulatory guidances, predict DDI likelihood. From a set of potential P-gp inhibitors, clarithromycin, cyclosporin A, itraconazole, ketoconazole, quinidine, and ritonavir inhibited P-gp-mediated transport of dabigatran etexilate over a concentration range that may hypothetically occur in the intestine. IC50 values of P-gp inhibitors for dabigatran etexilate transport were comparable to those of digoxin, a well established in vitro and in vivo P-gp substrate. However, IC50 values varied depending whether they were calculated from efflux ratios or permeability coefficients. Prediction of DDI likelihood of P-gp inhibitors using IC50 values, the hypothetical concentration of P-gp inhibitors, and the cut-off value recommended by both the FDA and EMA were in line with the DDI occurrence in clinical studies with dabigatran etexilate. However, it has to be kept in mind that validity of the cut-off criteria proposed by the FDA and EMA depends on in vitro experimental systems and the IC50-calculation methods that are employed, as IC50 values are substantially influenced by these factors.