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Tinea Cruris Medication

  • Author: Michael Wiederkehr, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Nov 18, 2015
 

Medication Summary

To achieve the best results, particularly with follicular or extensive tinea cruris, the authors often recommend a combination of topical and systemic therapy.[9]

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Antifungal agents

Class Summary

The 2 classes of antifungal medications used most commonly to treat tinea cruris are the azoles and the allylamines. Azoles inhibit the enzyme lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol, which is an important component of the fungal cell wall. Membrane damage results in permeability problems and renders the fungus unable to reproduce. Allylamines inhibit squalene epoxidase, which is an enzyme that converts squalene to ergosterol, resulting in the accumulation of toxic levels of squalene in the cell and in cell death. Examples of both classes of antifungal agents are available for topical and systemic administration. Some data suggest that fungistatic azoles can be as effective as fungicidal allylamines.[10] Both may have depot effects in the stratum corneum.[11]

Studies have found terbinafine to be effective and well tolerated in children.[12] Terbinafine 1% emulsion gel was found to be more effective than ketoconazole 2% cream in the treatment of tinea cruris.[13]

There may be some advantage to giving itraconazole with whole milk to increase absorption.[14]

Haloprogin is an agent for use in the treatment of tinea cruris. It is prescription only and is available in 1% cream and solution/spray. It is not available in the United States.

Terbinafine (Lamisil)

 

Terbinafine is a synthetic allylamine derivative, which inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi that results in a deficiency of ergosterol, causing fungal cell death. It is a widely studied and effective topical or oral antifungal. The topical form is available without a  prescription. Some clinicians reserve this drug for more widespread/resistant infections because of its broad coverage and increased cost. Studies have found this medication to be effective and well tolerated in children.

Butenafine (Mentax)

 

Butenafine is a potent antifungal related to the allylamines. It damages fungal cell membranes, causing fungal cell growth to arrest. It is available in 1% cream only.

Clotrimazole topical (Lotrimin, Mycelex)

 

Clotrimazole topical is often the first-line drug used in the treatment of tinea cruris. It is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells. Reevaluate the diagnosis if no clinical improvement after is seen after 4 weeks. It is available without a prescription in 1% cream, solution/spray, and lotion.

Miconazole (Micatin, Monistat-Derm)

 

Miconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak, resulting in fungal cell death. It is available without a prescription, and 2% cream, solution/spray, lotion, and powder forms are available. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.

Ketoconazole topical (Nizoral)

 

Ketoconazole topical comes as 2% cream. It is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

Econazole topical (Ecoza)

 

Econazole is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. It disrupts fungal cell wall permeability, causing fungal cell death.

Luliconazole (Luzu)

 

Luliconazole is available as a 1% topical cream administered once daily for 1 week. It is an imidazole antifungal that alters the fungal cell membrane by interacting with 14-alpha demethylase (an enzyme necessary for conversion of lanosterol to ergosterol). It is indicated for tinea corporis.

Naftifine (Naftin)

 

Naftifine is a broad-spectrum antifungal agent and synthetic allylamine derivative; it may decrease the synthesis of ergosterol, which, in turn, inhibits fungal cell growth. It is available in 1% cream or solution. If no clinical improvement is seen after 4 weeks, reevaluate the patient.

Oxiconazole (Oxistat)

 

Oxiconazole is a broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. It is available in 1% cream or lotion.

Tolnaftate (Tinactin)

 

Tolnaftate is a nonprescription medication used in the treatment of tinea cruris. It is available in 1% cream, solution/spray, and powder.

Ciclopirox (Loprox)

 

Ciclopirox is a synthetic broad-spectrum antifungal agent. It interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells. It is available by prescription only in 1% cream and lotion.

Itraconazole (Sporanox)

 

Itraconazole has fungistatic activity. It is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P450–dependent synthesis of ergosterol, a vital component of fungal cell membranes. It is a widely used and well-studied oral antifungal that can be used in the treatment of tinea cruris. Studies have shown that it is tolerated better than griseofulvin. Best results are noted 2-3 weeks after the end of treatment.

Sulconazole (Exelderm)

 

Sulconazole is a broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. It is available as 1% cream or solution.

Griseofulvin (Fulvicin-U/F, Grifulvin-V)

 

Griseofulvin has fungistatic activity. Fungal cell division is impaired by interfering with microtubules. It binds to keratin precursor cells. Keratin gradually is replaced by noninfected tissue, which is highly resistant to fungal invasions. It is less effective than itraconazole in the treatment of tinea cruris.

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Contributor Information and Disclosures
Author

Michael Wiederkehr, MD Consulting Staff, Livingston Dermatology Associates; Consulting Staff, Comprehensive Dermatology and Laser Center

Michael Wiederkehr, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Gregory J Raugi, MD, PhD Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
  1. Foster KW, Ghannoum MA, Elewski BE. Epidemiologic surveillance of cutaneous fungal infection in the United States from 1999 to 2002. J Am Acad Dermatol. 2004 May. 50(5):748-52. [Medline].

  2. Sadri MF, Farnaghi F, Danesh-Pazhooh M, Shokoohi A. The frequency of tinea pedis in patients with tinea cruris in Tehran, Iran. Mycoses. 2000. 43(1-2):41-4. [Medline].

  3. Yehia MA, El-Ammawi TS, Al-Mazidi KM, Abu El-Ela MA, Al-Ajmi HS. The Spectrum of Fungal Infections with a Special Reference to Dermatophytoses in the Capital Area of Kuwait During 2000-2005: A Retrospective Analysis. Mycopathologia. 2009 Nov 17. [Medline].

  4. Patel GA, Wiederkehr M, Schwartz RA. Tinea cruris in children. Cutis. 2009 Sep. 84(3):133-7. [Medline].

  5. Silva-Tavares H, Alchorne MM, Fischman O. Tinea cruris epidemiology (São Paulo, Brazil). Mycopathologia. 2001. 149(3):147-9. [Medline].

  6. Koksal F, Er E, Samasti M. Causative agents of superficial mycoses in Istanbul, Turkey: retrospective study. Mycopathologia. 2009 Sep. 168(3):117-23. [Medline].

  7. Torok L, Tiszlavicz L, Somogyi T, Toth G, Tapai M. Perianal ulcer as a leading symptom of paediatric Langerhans' cell histiocytosis. Acta Derm Venereol. 2000 Jan-Feb. 80(1):49-51. [Medline].

  8. Chang CH, Young-Xu Y, Kurth T, Orav JE, Chan AK. The safety of oral antifungal treatments for superficial dermatophytosis and onychomycosis: a meta-analysis. Am J Med. 2007 Sep. 120(9):791-8. [Medline].

  9. Parish LC, Parish JL, Routh HB, Avakian E, Olayinka B, Pappert EJ, et al. A double-blind, randomized, vehicle-controlled study evaluating the efficacy and safety of naftifine 2% cream in tinea cruris. J Drugs Dermatol. 2011 Oct 1. 10(10):1142-7. [Medline].

  10. Choudhary S, Bisati S, Singh A, Koley S. Efficacy and Safety of Terbinafine Hydrochloride 1% Cream vs. Sertaconazole Nitrate 2% Cream in Tinea Corporis and Tinea Cruris: A Comparative Therapeutic Trial. Indian J Dermatol. 2013 Nov. 58(6):457-60. [Medline]. [Full Text].

  11. Plaum S, Verma A, Fleischer AB Jr, Olayinka B, Hardas B. Detection and relevance of naftifine hydrochloride in the stratum corneum up to four weeks following the last application of naftifine cream and gel, 2%. J Drugs Dermatol. 2013 Sep. 12(9):1004-8. [Medline].

  12. Bakos L, Brito AC, Castro LC, et al. Open clinical study of the efficacy and safety of terbinafine cream 1% in children with tinea corporis and tinea cruris. Pediatr Infect Dis J. 1997 Jun. 16(6):545-8. [Medline].

  13. Bonifaz A, Saul A. Comparative study between terbinafine 1% emulsion-gel versus ketoconazole 2% cream in tinea cruris and tinea corporis. Eur J Dermatol. 2000 Mar. 10(2):107-9. [Medline].

  14. Chen S, Ran Y, Dai Y, Lama J, Hu W, Zhang C. Administration of Oral Itraconazole Capsule with Whole Milk Shows Enhanced Efficacy As Supported by Scanning Electron Microscopy in a Child with Tinea Capitis Due to Microsporum canis. Pediatr Dermatol. 2015 Oct 8. [Medline].

 
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Tinea cruris.
Tinea cruris.
Tinea cruris.
Tinea cruris (hematoxylin and eosin stain).
Tinea cruris (periodic acid-Schiff stain, magnification X 20).
Tinea cruris (Gomori methenamine-silver stain, magnification X 20).
 
 
 
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