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If the above diagnoses are inconclusive or if a treatment regimen has already been started, a biopsy of the affected skin (i.e. Spray tub and bathroom floor with disinfectant after each use to help prevent reinfection and infection of other household members. Wash feet, particularly between the toes, with soap and dry thoroughly after bathing or showering. If you have experienced an infection previously, you may want to treat your feet and shoes with over-the-counter drugs.
Dry feet well after showering, paying particular attention to the web space between the toes. Try to limit the amount that your feet sweat by wearing open-toed shoes or well-ventilated shoes, such as lightweight mesh running shoes. After any physical activity shower with a soap that has both an antibacterial and anti-fungal agent in it. Some patients present with esophageal candidiasis as a first presentation of systemic candidiasis. This program is funded through Health Resources and Services Administration, US Department of Health and Human Services.
A 43-year-old HIV-infected woman presents to the clinic with oral candidiasis that is clinically not responding to fluconazole (Diflucan) 200 mg PO once daily. Which of the following is true regarding fluconazole-resistant oral candidiasis in HIV-infected patients? The most important risk factor identified for the development of fluconazole-resistant oropharyngeal candidiasis is the use of trimethoprim-sulfamethoxazole (Bactrim, Septra) for longer than 60 days.IncorrectAlthough some antimicrobials increase the risk of patients developing oral candidiasis, there are no data to suggest trimethoprim-sulfamethoxazole use is directly related to the development of fluconazole-resistant candidiasis.
Fluconazole resistance in Candida species occurs primarily through an increase production in cell wall precursors.IncorrectThe mechanism of action of fluconazole involves decreasing the synthesis of ergosterol, the key component of the fungal cell membrane.
More than 95% of Candida albicans isolates from patients with fluconazole-refractory oropharyngeal candidiasis show resistance to itraconazole (Sporanox). Major identified risk factors for the development of fluconazole-resistant candidiasis include low CD4 cell count and cumulative fluconazole use.CorrectThe most important risk factors identified related to the development of fluconazole-resistant candidiasis include low CD4 cell count, greater number of fluconazole-treated episodes, and longer median duration of fluconazole therapy.
Figure 1Figure 1 - Fungal Ergosterol BiosynthesisFungal cell membrane synthesis is a multi-step process that involves the conversion of lanosterol to ergosterol. Figure 2Figure 2 - Mechanism of Action of FluconazoleFluconazole exerts its effect by selectively inhibiting the fungal cytochrome P-450 enzyme 14 alpha-demethylase. Figure 3Figure 3 - Fluconazole-Resistant Candidiasis, Mechanism of Action: Altered Binding SiteCandidaspecies have adapted several mechanisms of fluconazole resistance. Figure 4Figure 4 - Fluconazole-Resistant Candidiasis, Mechanism of Action: Efflux PumpsCandida species have adapted several mechanisms of fluconazole resistance.
Figure 5Figure 5 - Treatment of Fluconazole-Refractory Oropharyngeal and Esophageal CandidiasisImage A.
During the 1980s and 1990s, numerous reports emerged describing the development of refractory oropharyngeal candidiasis in AIDS patients following prolonged exposure to fluconazole (Diflucan).[1] The emergence of fluconazole-resistant candidiasis in HIV-infected persons correlated with the widespread use of fluconazole for oropharyngeal candidiasis during this time period.
Ergosterol is the predominant sterol in the fungal membrane and it serves as a bioregulator of fungal membrane fluidity and integrity.[8] The synthesis of ergosterol requires multiple steps and multiple enzymes (Figure 1). In 2012, the Subcommittee for Antifungal Testing of the Clinical Laboratory Standards Institute (CLSI) defined breakpoints for antifungal agents active against Candida species. Micafungin sodium is an echinocandin that is FDA approved for the treatment of candidemia, acute disseminated candidiasis, candida peritonitis and abscesses, and esophageal Candidiasis; prophylaxis of Candida Infections in Patients Undergoing Hematopoietic Stem Cell Transplantation. There is limited information regarding Off-Label Guideline-Supported Use of Micafungin sodium in adult patients.
There is limited information regarding Off-Label Guideline-Supported Use of Micafungin sodium in pediatric patients. Micafungin sodium is contraindicated in persons with known hypersensitivity to micafungin, any component of micafungin sodium, or other echinocandins. Isolated cases of serious hypersensitivity (anaphylaxis and anaphylactoid) reactions (including shock) have been reported in patients receiving micafungin sodium. Acute intravascular hemolysis and hemoglobinuria was seen in a healthy volunteer during infusion of micafungin sodium (200 mg) and oral prednisolone (20 mg). Laboratory abnormalities in liver function tests have been seen in healthy volunteers and patients treated with micafungin sodium.
Elevations in BUN and creatinine, and isolated cases of significant renal impairment or acute renal failure have been reported in patients who received micafungin sodium. A double-blind study was conducted in a total of 882 patients scheduled to undergo an autologous or allogeneic hematopoietic stem cell transplant. All adult patients who received micafungin sodium (382) or fluconazole (409) experienced at least one adverse reaction during the study. The overall safety of micafungin sodium was assessed in 479 patients 3 days through 16 years of age who received at least one dose of micafungin sodium in 11 separate clinical studies.
Of the 479 pediatric patients, 264 (55%) were male, 319 (67%) were Caucasians, with the following age distribution: 116 (24%) less than 2 years, 108 (23%) between 2 and 5 years, 140 (29%) between 6 years and 11 years, and 115 (24%) between 12 and 16 years of age.
The selected treatment-emergent adverse reactions, those occurring in 15% or more of the patients and more frequently in a micafungin sodium group, for all micafungin sodium pediatric studies and for the two comparative studies (candidemia and prophylaxis) described above are shown in TABLE 6. The following adverse reactions have been identified during the post-approval use of micafungin sodium for injection. A total of 14 clinical drug-drug interaction studies were conducted in healthy volunteers to evaluate the potential for interaction between micafungin sodium and amphotericin B, mycophenolate mofetil, cyclosporine, tacrolimus, prednisolone, sirolimus, nifedipine, fluconazole, itraconazole, voriconazole, ritonavir, and rifampin.
There was no effect of a single dose or multiple doses of micafungin sodium on mycophenolate mofetil, cyclosporine, tacrolimus, prednisolone, fluconazole, and voriconazole pharmacokinetics. Sirolimus AUC was increased by 21% with no effect on Cmax in the presence of steady-state micafungin sodium compared with sirolimus alone. Patients receiving sirolimus, nifedipine or itraconazole in combination with micafungin sodium should be monitored for sirolimus, nifedipine or itraconazole toxicity and the sirolimus, nifedipine or itraconazole dosage should be reduced if necessary. Micafungin is neither a substrate nor an inhibitor of P-glycoprotein and, therefore, would not be expected to alter P-glycoprotein-mediated drug transport activity.
When pregnant rabbits were given 4 times the recommended human dose, there were increased abortion and visceral abnormalities including abnormal lobation of the lung, levocardia, retrocaval ureter, anomalous right subclavian artery, and dilatation of the ureter. There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Micafungin sodium in women who are pregnant. Safety and effectiveness in pediatric patients younger than 4 months of age have not been established. Safety and effectiveness of micafungin sodium in pediatric patients 4 months of age and older have been demonstrated based on the evidence from adequate and well-controlled studies in adult and pediatric patients and additional pediatric pharmacokinetic and safety data. A total of 418 subjects in clinical studies of micafungin sodium were 65 years of age and older, and 124 subjects were 75 years of age and older. The exposure and disposition of a 50 mg micafungin sodium dose administered as a single 1-hour infusion to 10 healthy subjects aged 66-78 years were not significantly different from those in 10 healthy subjects aged 20-24 years. Dose adjustment of micafungin sodium is not required in patients with mild, moderate, or severe hepatic impairment. There is no FDA guidance one the use of Micafungin sodium in patients who are immunocompromised. There is limited information regarding the compatibility of Micafungin sodium and IV administrations. Micafungin inhibits the synthesis of 1, 3-beta-D-glucan, an essential component of fungal cell walls, which is not present in mammalian cells. There is limited information regarding Micafungin sodium Pharmacodynamics in the drug label. Steady-state pharmacokinetic parameters in relevant patient populations after repeated daily administration are presented in TABLE 7.
Micafungin pharmacokinetics in 229 pediatric patients 4 months through 16 years of age were characterized using population pharmacokinetics.
Micafungin is metabolized to M-1 (catechol form) by arylsulfatase, with further metabolism to M-2 (methoxy form) by catechol-O-methyltransferase. The excretion of radioactivity following a single intravenous dose of 14C-micafungin sodium for injection (25 mg) was evaluated in healthy volunteers. There has been no evidence of either psychological or physical dependence or withdrawal or rebound effects with micafungin sodium.


There have been reports of clinical failures in patients receiving micafungin sodium therapy due to the development of drug resistance. Hepatic carcinomas and adenomas were observed in a 6-month intravenous toxicology study with an 18-month recovery period of micafungin sodium in rats designed to assess the reversibility of hepatocellular lesions. Although the increase in carcinomas in the 6-month rat study did not reach statistical significance, the persistence of altered hepatocellular foci subsequent to micafungin sodium dosing, and the presence of adenomas and carcinomas in the recovery periods suggest a causal relationship between micafungin sodium, altered hepatocellular foci, and hepatic neoplasms. High doses of micafungin sodium (5 to 8 times the highest recommended human dose, based on AUC comparisons) have been associated with irreversible changes to the liver when administered for 3 or 6 months, and these changes may be indicative of pre-malignant processes. Two dose levels of micafungin sodium were evaluated in a randomized, double-blind study to determine the efficacy and safety versus caspofungin in patients with invasive candidiasis and candidemia. In two cases of ophthalmic involvement assessed as failures in the above table due to missing evaluation at the end of IV treatment with micafungin sodium, therapeutic success was documented during protocol-defined oral fluconazole therapy.
In two controlled trials involving 763 patients with esophageal candidiasis, 445 adults with endoscopically-proven candidiasis received micafungin sodium, and 318 received fluconazole for a median duration of 14 days (range 1-33 days). Relapse was assessed at 2 and 4 weeks post-treatment in patients with overall therapeutic cure at end of treatment. In this study, 459 of 518 (88.6%) patients had oropharyngeal candidiasis in addition to esophageal candidiasis at baseline. In a randomized, double-blind study, micafungin sodium (50 mg IV once daily) was compared to fluconazole (400 mg IV once daily) in 882 [adult (791) and pediatric (91)] patients undergoing an autologous or syngeneic (46%) or allogeneic (54%) stem cell transplant. Successful prophylaxis was defined as the absence of a proven, probable, or suspected systemic fungal infection through the end of therapy (usually 18 days), and the absence of a proven or probable systemic fungal infection through the end of the 4-week post-therapy period. The number of proven breakthrough Candida infections was 4 in the micafungin sodium and 2 in the fluconazole group. The efficacy of micafungin sodium against infections caused by fungi other than Candida has not been established.
There is limited information regarding Micafungin sodium Look-Alike Drug Names in the drug label.
Specimens for fungal culture and other relevant laboratory studies (serology, histopathology) should be obtained prior to therapy to isolate and identify causative organisms.
Microcrystalline cellulose, Anhydrous dibasic calcium phosphate, Povidone k30, Croscarmellose Sodium, FD&C red no.
The disease usually occurs in patients in immunocompromised states, including post-chemotherapy and in AIDS. Patients in whom esophageal candidiasis is suspected should receive a brief course of antifungal therapy with fluconazole. You may redistribute it, verbatim or modified, providing that you comply with the terms of the GFDL. Specifically, fluconazole blocks a step in the conversion of squalene to ergosterol by inhibiting the fungal cytochrome P-450 enzyme 14 alpha-demethylase. Fewer than 5% of patients with fluconazole-refractory oropharyngeal candidiasis will respond to itraconazole solution at a dose of 200 mg per day.IncorrectAvailable data suggest more than 50% of patients with fluconazole-refractory oropharyngeal candidiasis will respond to itraconazole solution given at a dose of 100 to 200 mg per day. Fluconazole resistance can involve an alteration in the target enzyme 14-alpha demethylase (change in binding site or over expression of the enzyme) or enhanced drug efflux caused by plasma membrane transporters.
This illustration shows an alteration in the target enzyme 14 alpha-demethylase (change in binding site or over expression of the enzyme) or from enhanced drug efflux caused by plasma membrane transporters. Preferred and Alternative RegimensThis table is based on recommendations in: Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. During the 1980s and 1990s, the percentage of fluconazole-resistant Candida species ranged from approximately 5 to 33%.[1,2] In addition, following the widespread use of fluconazole, the proportion of C. Fluconazole exerts its action on the fungal membrane by inhibiting the fungal cytochrome P-450 enzyme 14 alpha-demethylase, thereby blocking the conversion of lanosterol to ergosterol (Figure 2).[6] The inhibitory action of fluconazole causes depletion of ergosterol which in turn alters the fungal membrane structure and function. In the largest trial involving itraconazole solution, 41 (55%) of 74 patients who failed fluconazole therapy (200 mg once daily) achieved a clinical response by day 28 when treated with itraconazole oral solution (100 mg bid), with 7 days as the median time to response.[19]The opportunistic infections guidelines do not provide a specific duration of therapy, but most experts would recommend at least 10 days of therapy for patients with fluconazole-refractory oropharyngeal candidiasis, with extension of the treatment course if the response is not complete at day 10. Diagnosis and treatment of oropharyngeal candidiasis in patients infected with HIV: a critical reassessment. Point prevalence, microbiology and fluconazole susceptibility patterns of yeast isolates colonizing the oral cavities of HIV-infected patients in the era of highly active antiretroviral therapy.
Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America.
Risk factors for fluconazole-resistant candidiasis in human immunodeficiency virus-infected patients. Infection due to fluconazole-resistant Candida in patients with AIDS: prevalence and microbiology.
Declining rates of oropharyngeal candidiasis and carriage of Candida albicans associated with trends toward reduced rates of carriage of fluconazole-resistant C. Antifungal agents: mode of action, mechanisms of resistance, and correlation of these mechanisms with bacterial resistance. Heterogeneous mechanisms of azole resistance in Candida albicans clinical isolates from an HIV-infected patient on continuous fluconazole therapy for oropharyngeal candidosis.
Molecular mechanisms of fluconazole resistance in Candida dubliniensis isolates from human immunodeficiency virus-infected patients with oropharyngeal candidiasis. Itraconazole solution: summary of pharmacokinetic features and review of activity in the treatment of fluconazole-resistant oral candidosis in HIV-infected persons.
Correlation of in vitro fluconazole resistance of Candida isolates in relation to therapy and symptoms of individuals seropositive for human immunodeficiency virus type 1.
Detection and significance of fluconazole resistance in oropharyngeal candidiasis in human immunodeficiency virus-infected patients. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Posaconazole for the treatment of azole-refractory oropharyngeal and esophageal candidiasis in subjects with HIV infection.
Itraconazole cyclodextrin solution for fluconazole-refractory oropharyngeal candidiasis in AIDS: correlation of clinical response with in vitro susceptibility. Treatment of fluconazole-refractory oropharyngeal candidiasis with itraconazole oral solution in HIV-positive patients. A randomized, double-blind, double-dummy, multicenter trial of voriconazole and fluconazole in the treatment of esophageal candidiasis in immunocompromised patients. A randomized double-blind study of caspofungin versus amphotericin for the treatment of candidal esophagitis. Efficacy of caspofungin in the treatment of esophageal candidiasis resistant to fluconazole. In vitro activities of voriconazole (UK-109,496) against fluconazole-susceptible and -resistant Candida albicans isolates from oral cavities of patients with human immunodeficiency virus infection.
Amphotericin B oral suspension for fluconazole-refractory oral candidiasis in persons with HIV infection. Clinical evaluation and microbiology of oropharyngeal infection due to fluconazole-resistant Candida in human immunodeficiency virus-infected patients. Validation of 24-hour fluconazole MIC readings versus the CLSI 48-hour broth microdilution reference method: results from a global Candida antifungal surveillance program.
WikiDoc is not a professional health care provider, nor is it a suitable replacement for a licensed healthcare provider. If these reactions occur, micafungin sodium infusion should be discontinued and appropriate treatment administered.
In some patients with serious underlying conditions who were receiving micafungin sodium along with multiple concomitant medications, clinical hepatic abnormalities have occurred, and isolated cases of significant hepatic impairment, hepatitis, and hepatic failure have been reported. Selected treatment-emergent adverse reactions, those occurring in 5% or more of the patients and more frequently in a micafungin sodium treatment group, are shown in TABLE 3. The following treatment-emergent adverse reactions in the micafungin sodium treated patients at least 16 years of age were notable: nausea (10% vs. Treatment-emergent adverse reactions resulting in discontinuation were reported in 17 (7%) micafungin sodium treated patients; and in 12 (5%) fluconazole treated patients. Treatment-emergent adverse reactions resulting in micafungin sodium discontinuation were reported in 15 (4%) adult patients; while those resulting in fluconazole discontinuation were reported in 32 (8%).
Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency.


In these studies, no interaction that altered the pharmacokinetics of micafungin sodium was observed.
Nifedipine AUC and Cmax were increased by 18% and 42%, respectively, in the presence of steady-state micafungin sodium compared with nifedipine alone. Animal reproduction studies in rabbits showed visceral abnormalities and increased abortion at 4 times the recommended human dose. No overall differences in safety and effectiveness were observed between these subjects and younger subjects. Higher doses (about twice the recommended clinical dose, based on body surface area comparisons) resulted in higher epididymis weights and reduced numbers of sperm cells.
The primary binding protein is albumin; however, micafungin, at therapeutically relevant concentrations, does not competitively displace bilirubin binding to albumin.
M-5 is formed by hydroxylation at the side chain (?-1 position) of micafungin catalyzed by cytochrome P450 (CYP) isozymes.
Some of these reports have identified specific mutations in the FKS protein component of the glucan synthase enzyme that are associated with higher MICs and breakthrough infection.
Rats administered micafungin sodium at the same dose for 6 months exhibited adenomas after a 12-month recovery period; after an 18-month recovery period, an increased incidence of adenomas was observed, and additionally, carcinomas were detected.
Whole-life carcinogenicity studies of micafungin sodium in animals have not been conducted, and it is not known whether the hepatic neoplasms observed in treated rats also occur in other species, or if there is a dose threshold for this effect. The efficacy of micafungin sodium was evaluated in less than 10 patients with Candida species other than C. Relapse was defined as a recurrence of clinical symptoms or endoscopic lesions (endoscopic grade greater than 0). Patients should be informed about the serious adverse effects of micafungin sodium including hypersensitivity reactions (anaphylaxis and anaphylactoid reactions including shock), hematological effects (acute intravascular hemolysis, hemolytic anemia and hemoglobinuria), hepatic effects (abnormal liver function tests, hepatic impairment, hepatitis or worsening hepatic failure) and renal effects (elevations in BUN and creatinine, renal impairment or acute renal failure). Therapy may be instituted before the results of the cultures and other laboratory studies are known; however, once these results become available, anti-infective therapy should be adjusted accordingly. However, it can also occur in patients with no predisposing risk factors, and is more likely to be asymptomatic in those patients.[1] It is also known as candidal esophagitis or monilial esophagitis.
If the infection resolves after treatment with fluconazole, then the diagnosis of esophageal candidiasis is made and no further investigation is needed. She is taking a 5-drug salvage antiretroviral therapy regimen, trimethoprim-sulfamethoxazole (Bactrim, Septra), azithromycin (Zithromax), and fluconazole. The net effect of the efflux pump is to decrease the intracellular concentration of fluconazole. The inhibition of 14 alpha-demethylase also results in the build-up of lanosterol and other ergosterol precursors. Isolated cases of significant hemolysis and hemolytic anemia have also been reported in patients treated with micafungin sodium. Patients who develop abnormal renal function tests during micafungin sodium therapy should be monitored for evidence of worsening renal function.
Selected adverse reactions, those reported in 15% or more of adult patients and more frequently on the micafungin sodium treatment arm, are shown in TABLE 5. Treatment-emergent adverse reactions resulting in micafungin sodium discontinuation were reported in 2 (4%) pediatric patients; while those resulting in AmBisome discontinuation were reported in 9 (16%). Three (7%) pediatric patients discontinued micafungin sodium due to adverse reaction; while one (2%) patient discontinued fluconazole.
Other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. The micafungin AUC was greater by 19% in Japanese subjects compared to blacks, due to smaller body weight.
Even though micafungin is a substrate for and a weak inhibitor of CYP3A in vitro, hydroxylation by CYP3A is not a major pathway for micafungin metabolism in vivo. Fecal excretion is the major route of elimination (total radioactivity at 28 days was 71% of the administered dose).
A lower dose of micafungin sodium (equivalent to 5 times the human AUC) in the 6-month rat study resulted in a lower incidence of adenomas and carcinomas following 18 months recovery. There was no statistically significant difference in relapse rates at either 2 weeks or through 4 weeks post-treatment for patients in the micafungin sodium and fluconazole treatment groups, as shown in TABLE 13. The status of the patients’ underlying malignancy at the time of randomization was: 365 (41%) patients with active disease, 326 (37%) patients in remission, and 195 (22%) patients in relapse.
Duration of therapy was slightly longer in the pediatric patients who received micafungin sodium (median duration 22 days) compared to the adult patients who received micafungin sodium (median duration 18 days).
Patients should be instructed to inform their health care provider if they develop any unusual symptom, or if any known symptom persists or worsens.
In open noncomparative studies of relatively small numbers of patients, fluconazole tablets USP were also effective for the treatment of Candida urinary tract infections, peritonitis, and systemic Candida infections including candidemia, disseminated candidiasis, and pneumonia. Before prescribing fluconazole tablets USP for AIDS patients with cryptococcal meningitis, please see CLINICAL STUDIES section under package insert.
However, if the infection persists or if there are other factors involved which may warrant further investigation, then patient will undergo an esophagogastroduodenoscopy if it is safe to do so.
She has taken fluconazole on and off for 6 months for recurrent bouts of oropharyngeal candidiasis and the past 3 months she had taken fluconazole 200 mg PO once daily.
Fluconazole resistance results from an alteration in the target enzyme 14 alpha-demethylase (change in binding site or over expression of the enzyme) or enhanced drug efflux caused by plasma membrane transporters. Clinical failure refers to persistence or progression of oropharyngeal candidiasis despite antifungal therapy. The duration of micafungin dosing in these rat studies (3 or 6 months) exceeds the usual duration of micafungin sodium dosing in patients, which is typically less than 1 month for treatment of esophageal candidiasis, but dosing may exceed 1 month for Candida prophylaxis. Relapse included patients who died or were lost to follow-up, and those who received systemic antifungal therapy during the post-treatment period. The more common baseline underlying diseases in the 476 allogeneic transplant recipients were: chronic myelogenous leukemia (22%), acute myelogenous leukemia (21%), acute lymphocytic leukemia (13%), and non-Hodgkin’s lymphoma (13%). Patients should be instructed to inform their health care provider of any other medications they are currently taking with micafungin sodium, including over-the-counter medications. Studies comparing fluconazole tablets USP to amphotericin B in non-HIV infected patients have not been conducted.
Endoscopy often reveals classic diffuse raised plaques that characteristically can be removed from the mucosa by the endsocope. May 7, 2013.Figure 5Figure 5 - Treatment of Fluconazole-Refractory Oropharyngeal and Esophageal CandidiasisImage B. The selective action of fluconazole for fungal cell membranes occurs because human cells use cholesterol, not ergosterol, for the synthesis of cell membranes.
Patients were stratified by APACHE II score (20 or less or greater than 20) and by geographic region. Clinical cure was defined as complete resolution in clinical symptoms of esophageal candidiasis (dysphagia, odynophagia, and retrosternal pain). Transplant recipients who died or were lost to follow-up during the study were considered failures of prophylactic therapy. Brushing or biopsy of the plaques shows yeast and pseudohyphae by histology that are characteristic of Candida species. Rating Scheme for 2013 Opportunistic Infections GuidelinesSource: Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. The echinocandins have a mechanism of action distinct from the azoles: these agents inhibit fungal cell wall synthesis by blocking the production of 1,3-beta-D-glucan. Mycological eradication was determined by culture, and by histological or cytological evaluation of esophageal biopsy or brushings obtained endoscopically at the end of treatment. As shown in TABLE 12, endoscopic cure, clinical cure, overall therapeutic cure, and mycological eradication were comparable for patients in the micafungin sodium and fluconazole treatment groups.



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