Derm Dx: Asymptomatic hyper- and hypopigmented macules and patches - Clinical Advisor

Derm Dx: Asymptomatic hyper- and hypopigmented macules and patches

Slideshow

  • Tinea Versicolor 1_0112 Derm Dx 3

  • Tinea Versicolor 2_0112 Derm Dx 3

  • Tinea Versicolor 3_0112 Derm Dx 3

  • Tinea Versicolor 4_0112 Derm Dx 3

A 27-year-old Hispanic male presents with brown patches on his trunk and abdomen that have been present for three years.

Although the patches are present all year long, they are significantly more noticeable in the summer. The patient denies pain or itch, but is quite embarrassed by the appearance. Physical exam is significant for reddish-brown, well-demarcated patches on the central chest and central back with very subtle overlying scale.

Another patient, a 21-year-old black male, presents with a similar complaint of a two-month history of patches on his neck and chest. He also denies pain or itch. On exam the patient has well-demarcated, slightly scaly, violaceous, hypopigmented and hyperpigmented macules coalescing into plaques on his neck and anterior trunk. Both patients are otherwise healthy with no significant past medical history. What are your diagnoses?

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Tinea versicolor is a very common, benign, superficial fungal infection caused by lipophilic yeast of the genus Malassezia. There are seven Malassezia subspecies, with the most common tinea versicolor causing species being Malassezia globosa (50% to 60%) and Malassezia sympodialis...

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Tinea versicolor is a very common, benign, superficial fungal infection caused by lipophilic yeast of the genus Malassezia. There are seven Malassezia subspecies, with the most common tinea versicolor causing species being Malassezia globosa (50% to 60%) and Malassezia sympodialis (3% to 59%). 

Malassezia yeasts are found on all individuals as a part of the normal skin flora. However, in certain individuals the yeast transforms into the mycelial or hyphal form, leading to tinea versicolor. Exactly what causes the transformation from the yeast to the mycelial form is unkown, but factors that may influence the transformation include genetic susceptibility, use of oral contraceptives, hyperhidrosis, immunocompromised state and malnutrition. Keep in mind that tinea versicolor is exceedingly common in the general population with rates ranging from 1% to 50%, and frequently no specific susceptibility factors that can be identified in individual patients.1, 2, 3

Because the Malassezia species require lipids to thrive, tinea versicolor is most commonly found on seborrheic, or lipid-rich, body areas. Common sites are the chest, abdomen, back and neck. Tinea versicolor on the face is most common in children.

Lesions consist of scaly hyper and/or hypopigmented macules that coalesce into patches. Hyperpigmented lesions may have a pink, tan, brown, violaceous, gray or black hue. Patients sometimes report worsening in summer months or during exposure to a hot and humid climate.1, 2, 3

Diagnosis

Tinea versicolor diagnosis can be made based on typical physical exam findings and clinical history. A useful test is the potassium hydroxide preparation, in which scale from the lesions is scraped onto a glass slide and incubated with 10% to 15% potassium hydroxide. When examined under the microscope, specimens positive for tinea versicolor will with have the appearance of spaghetti and meatballs (or more accurately, ziti and meatballs), which represent hyphae and spores. 1, 2, 3                     

Treatment

Although there are multiple effective oral and topical therapies for tinea versicolor, patients should be counseled that relapse is very common. Therefore, monthly prophylactic topical or oral therapy may be required after the initial infection has cleared.

Additionally, patients should be counseled that any pigmentary alteration, especially hypopigmentation, might take months to resolve even after the infection has cleared. Persistent dyspigmentation may not represent a treatment failure.1, 2, 3

Practical topical therapies include:

  • Selenium sulfide shampoo or lotion applied for 10 minutes and then rinsed off, once daily for a week. A single overnight application may be equally effective and can be repeated once a month to prevent recurrence. 
  • A single application of ketonconazole shampoo applied for five minutes and then rinsed off. This can be repeated monthly for prophylaxis.
  • Terbinafine, butenifine or ketoconazole creams applied twice daily for 7 days.1, 2, 3

In practice, we find that many patients fail topical therapy. Oral therapy is generally well tolerated and highly effective. Additionally, oral therapy may be preferred in patients with widespread lesions or simply due to shear convenience. 

Practical oral regimens include:

  • Ketoconazole in 400 mg doses repeated at monthly intervals.
  • Itraconazole 200 mg once a day for 7 days, followed by prophylactic treatment with itraconazole 200 mg twice a day for one day a month. A 400 mg single-dose of itraconazole may be equally as effective and can be repeated monthly for prophylaxis. 
  • Fluconazole 400mg once or 300mg once a week for two weeks. A single 400 mg or 300 mg monthly dose can prescribed for prophylaxis. 1, 2, 3

Adam Rees, MD, is a graduate of the University of California Los Angeles School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine in Houston.

References

1. Bolognia J, Jorizzo JL and Rapini RP. “Chapter 76: Fungal Diseases.” Dermatology. St. Louis, Mo.: Mosby/Elsevier; 2008.
2. James WD, Berger TJ, Elston DM et al. “Chapter 15: Diseases resulting from fungi and yeasts.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunders Elsevier; 2006.

3. Gupta AK, Batra R, Bluhm R et al. “Pityriasis Versicolor.” Dermatologic Clinics..2003: 413-429.

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