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Tinea Nigra Medication

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD  more...
 
Updated: Jun 22, 2016
 

Medication Summary

Because tinea nigra is caused by a superficial fungal infection of the skin, topical medicines designed to eradicate the dermatomycosis are used, including topical butenafine.[26]

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Dermatologic agents

Class Summary

These agents are used to treat tinea nigra because of their action on the skin. They may either aid in the removal of excessive keratin in hyperkeratotic skin disorders or increase epithelial cell turnover. These agents are used in conjunction with fungicidal or fungistatic medications.

Salicylic acid topical (Compound W, Salactic Film, Sal-Plant, Panscol)

 

Salicylic acid topical causes desquamation of the horny layer of skin by dissolving intercellular cement substance, while not affecting structure of viable epidermis. Hydrate the skin and enhance the effects of medication; soak the affected area in warm water for 5 minutes prior to use; remove any loose tissue with a brush, washcloth, or emery board, and dry thoroughly. Improvement should occur in 1-2 weeks.

Tretinoin topical (Avita, Retin-A)

 

Topical tretinoin decreases the cohesiveness of follicular epithelial cells and stimulates their mitotic activity, resulting in quicker turnover of the epithelial layer.

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Topical imidazoles

Class Summary

These medications are broad-spectrum antifungals that are commonly used in the treatment of tinea pedis, but they are also effective in the treatment of tinea nigra.

Clotrimazole (Lotrimin, Mycelex, Femizole-7)

 

Clotrimazole 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 is see after 4 weeks.

Ketoconazole topical (Nizoral)

 

Ketoconazole is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Miconazole (Micatin, Femizol-M)

 

Miconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. It increases membrane permeability, causing nutrients to leak out and resulting in fungal cell death.

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Topical pyridones

Class Summary

Topical pyridones are broad-spectrum agents with antidermatophyte, antibacterial, and anticandidal activity.

Ciclopirox (Loprox)

 

Ciclopirox interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.

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Topical allylamines

Class Summary

These drugs are effective in treating a variety of fungal infections. Because they have demonstrated potent activity against dermatophytes, they are often used in recalcitrant infections.

Terbinafine topical (Lamisil)

 

Terbinafine is an allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi. This effect results in a deficiency in ergosterol in the fungal cell wall, causing fungal cell death.

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Fungistatic agents

Class Summary

These medications do not kill the fungus, but rather, they prevent their growth and replication.

Undecylenic acid & derivatives (Blis-To-Sol powder, Caldesene, Cruex)

 

These are fungistatic. They are indicated for superficial dermal fungal infections.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

George Kihiczak, MD Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital

George Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Medical Society of New Jersey

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Neil Shear, MD Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada

Neil Shear, MD is a member of the following medical societies: Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Vinay Arya, MD, to the development and writing of this article.

References
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Tinea nigra, evident as a painless cluster of brown-to-black macules. Courtesy of Dr. Peter Santalucia.
Tinea nigra, showing hyperkeratosis and mild acanthosis. A scant amount of perivascular lymphocytic infiltrate may be found in the papillary and subpapillary layers of the dermis (hematoxylin and eosin stain). Courtesy of Thomas N. Helm, MD.
Tinea nigra, with histologic section demonstrating periodic acid-Schiff–positive septate hyphae within the stratum corneum. Courtesy of Thomas N. Helm, MD.
 
 
 
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