Light spots on the back - Clinical Advisor

Light spots on the back

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Case #1

An 18-year-old man of Mediterranean descent comes in for evaluation of the skin across his upper back and neck, which he says has lost its normal color; a friend initially noticed this while they were surfing earlier in the summer. Although he has no associated symptoms, he is very worried about what is happening to his skin, as well as his appearance, because his fellow surfers tease him about the color change. He has no remarkable past medical history. Physical examination reveals coalescent, hypopigmented, scaly macules with minimal erythema, symmetrically distributed over his upper back. 

Case #2 

A 27-year-old African American woman presents with color changes that she noted on her lower back while showering 1 week ago. She says nothing is different in her bathing regimen and reports no recent travel, outdoor activities, illness, or underlying medical conditions. Although asymptomatic, she thought she had a fungal infection; however, topical antifungal creams have failed to improve the rash. Physical examination reveals nonscaly, hypopigmented, symmetrically distributed macules convalescing into patches over the midline of the lower back.

Case #1 Tinea versicolor (TV), also known as pityriasis versicolor, is an innocuous superficial skin infection caused by the commensal yeast Malassezia. Well known to clinicians in lower-latitude regions of the United States, the prevalence of TV is estimated to be...

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Case #1 

Tinea versicolor (TV), also known as pityriasis versicolor, is an innocuous superficial skin infection caused by the commensal yeast Malassezia. Well known to clinicians in lower-latitude regions of the United States, the prevalence of TV is estimated to be as high as 50% in tropical regions such as West Samoa and as low as 11.1% in northern areas such as Sweden.1

In 1801, TV was identified as a distinct dermatologic entity; 45 years later, a yeast was discovered as its cause.2 The exact genus was debated until 1963, when both Malassezia and Pityrosporum were found to have identical antigens and turned out to be the same organism.2 Although it has been traditionally taught that M furfur is the most common causative organism, molecular studies recently revealed M globosa to be the most common isolate.3

Malassezia resides in the outermost layer of the epidermis, the stratum corneum, where it breaks down host lipids to synthesize its own cell wall. This cell wall provides mechanical stability, a structure for keratinocyte adherence, and a defense mechanism against host immune attacks.4 Ubiquitously present, Malassezia is part of the natural human flora; excessive overgrowth is required for the development of TV. This becomes possible when the host provides excessive lipids via sebaceous secretions and/or the host immune system cannot suppress the growth, and it is promoted by a warm, humid environment.

Individuals with oily skin or immune deficiency have a predilection to develop TV. Thus, postpubescent young adults with hormonally active sebaceous glands are the most commonly affected age group. Transplant patients who take chronic immunosuppressive medications are also commonly affected. TV is most apparent in hot, humid weather due to increased sweat production and normal tanning of unaffected skin, which emphasizes the color changes. Other predisposing factors include pregnancy, use of oral contraceptives, and malnutrition. There is no predilection for race or sex.1

Sun-exposed areas of the upper back and neck are most commonly affected. Classically, TV develops with hypopigmented, confetti-like, scaly macules with a subtle erythematous rim; however, some cases are inversely hyperpigmented. Pigment variability is likely due to a combination of pigmentary effects specific to the causative Malassezia species, as well as host immune responses4; scale represents fungal overgrowth and the inflammatory response. Although the eruption is sometimes mildly pruritic, patients are more often concerned with the esthetic effects.

The differential diagnosis for TV is extensive and includes vitiligo, postinflammatory hypopigmentation (or hyperpigmentation), pityriasis alba, hypomelanosis of Ito, discoid lupus erythematosus, secondary syphilis, progressive macular hypomelanosis (PMH), tinea corporis, seborrheic dermatitis, and mycosis fungoides. Clinical subtleties may help the provider distinguish TV from many of these other entities. For example, vitiligo presents with depigmentation, not hypopigmentation, produces white hairs in the affected areas, and does not have scale. Postinflammatory hypopigmentation is usually preceded by an inflammatory and/or symptomatic process. Pityriasis alba is more commonly seen in children, is often on the face, and is associated with atopy. Mycosis fungoides, a type of cutaneous T-cell lymphoma, can mimic many eruptions. However, it is more common in sun-protected areas, such as across the hips and buttocks, fails to respond to typical treatments for TV, and ultimately requires a biopsy for diagnosis. If any of these clinical parameters are present, patients should be referred to a dermatologist. The dermatophyte causing tinea corporis can be identified by culture or distinct characteristics upon the examination of skin scrapings prepared with potassium hydroxide. Clinical clues to aid in the diagnosis of TV include age, humid climate, oily skin, scale, a prior history of a similar rash, as well as exacerbation in the summer months with resolution in the winter. Laboratory studies can be used to confirm the diagnosis.

The Wood’s lamp may be a useful bedside diagnostic tool. Although the sensitivity is suboptimal, Wood’s lamp fluorescence of TV should reveal a diffuse yellow-white or copper-orange sheen or a folliculocentric bluish-white fluorescence.5

A better diagnostic test is microscopic examination of skin scrapings after preparation with potassium hydroxide (KOH). Although they are taught as a straightforward procedure, KOH preparations can be challenging; however, if one develops technical expertise, many fungal diagnoses can be made at the bedside. To perform this test, the area must first be wiped with alcohol; scale should be gently scraped with a number 15 blade and placed on a glass microscope slide. The examiner should then apply 1 to 2 drops of a 10% to 20% KOH solution, cover it with a coverslip, and view it under 10× to 40× magnification to reveal the classic “spaghetti” (hyphae) and “meatballs” (spores) findings of TV; if a dermatophyte is the cause, as in tinea corporis, branching, septate hyphae will be seen instead. Chemicals such as Chicago Sky Blue and chlorazole black are added to some commercially available KOH products to increase diagnostic accuracy because these chemicals adhere to and stain the fungal wall, thereby improving visualization.6 Routine fungal cultures will yield false-negative results for TV because standard media does not contain the nutrients necessary to grow the lipophilic Malassezia. On biopsy, histologically, hyphae and spores in the stratum corneum are seen, sometimes with mild epidermal or dermal inflammation.7

Patients diagnosed with TV should be educated that Malassezia is not contagious because it is part of the normal flora and that the color change is caused, in part, by the body’s reaction to the yeast. Therefore, there will be a delay in resolution of the color change despite effective therapy. Because epidermal regeneration requires 4 weeks, it may take up to 1 month for the skin to return to normal color. Continued treatment should be encouraged to assure complete resolution, as results are not immediate. The treatment course is 4 weeks. In 60% to 80% of patients, the condition recurs within 2 years; patients should be educated to anticipate this.7

Topical antifungal treatments were recently proven to be equally as effective as oral azoles.8 Although the duration of topical treatment may result in suboptimal patient compliance, the safety profile of topical therapy may outweigh this limitiation.8,9 Topical treatments contain antifungal agents such as selenium sulfide, zinc pyrithione, an azole, or an allylamine. Shampoos containing selenium sulfide or zinc pyrithione should be applied to affected areas for 10 minutes daily before washing off; topical azoles or allylamines should be applied twice daily.

Although highly effective, oral azole and allylamine medications are more expensive, are associated with hepatotoxicity, and have numerous drug-drug interactions through inhibition of the cytochrome P450 system. Systemic therapy should be used only in special occasions, such as extensive disease or when topical therapy is not practical in an otherwise healthy patient.8,9

Preventive treatments are theoretical; some authors suggest that monthly use of topical agents or shampoos may be beneficial.9 If the rash persists after 4 weeks of compliant treatment, an alternative diagnosis should be considered.

In our case, the patient was treated with 1% terbinafine cream; resolution was noted after 3 weeks of therapy. He continues to surf with his friends who stopped teasing him once they discovered his rash was not contagious.

Case #2 

Progressive macular hypomelanosis (PMH) is a newly described, poorly understood, and largely underdiagnosed dermatologic condition.10 It was first described in 1983 by Guillet et al.11 on dark-skinned young women as a “bizarre,” hypopigmented macular rash that did not respond to antifungal therapy. Over the next two decades, numerous reports surfaced describing the same condition by other names, including Creole dyschromia, nummular and confluent hypomelanosis of the trunk, cutis trunci variata, and idiopathic multiple large macule melanosis. As with tinea versicolor (TV), PMH is an innocuous condition that may be cosmetically distressing to the individual affected.

The cause of PMH was unknown until 2001, when Westerhof et al. observed a curious red fluorescence at the base of hair follicles using a Wood’s lamp; red, glowing dots were present within lesional skin and were notably absent on unaffected skin.12,13 Knowing that Propionibacterium acnes, the bacteria associated with acne vulgaris, fluoresces red under Wood’s light due its coproporphyrin molecules, Westerhof thought this was the causative organism. Data from other investigators supported his hypothesis.14 However, in 2010, Westerhof reported the results from molecular analyses of organisms cultured from PMH and suggested that a novel species of Propionibacterium was likely instrumental in this new condition.13 Exactly how Propionibacterium causes PMH remains speculative; the leading theory is that this organism secretes an unidentified factor that, in some way, interferes with melanogenesis.10,12-14

One can surmise a possible pathogenesis from the clinical findings. Because Propionibacterium bacteria reside within pilosebaceous units, the hypothetical factor associated with skin lightening may diffuse radially from the ducts into the surrounding tissue, causing hypopigmented macules around each affected hair follicle, identified as glowing red by Wood’s light.13 These macules are more prevalent in the midline of the torso due to the higher concentration of sebaceous glands and typically coalesce into larger patches. This is a key clinical feature of PMH that suggests a functional role for glandular activity, because it corresponds to the anatomic sites noted to sweat more during exertion. PMH is asymptomatic and clinically lacks scale, erythema, or other secondary changes.

The prevalence of PMH is unknown. Researchers in the Netherlands report PMH to be more common than either TV or pityriasis alba, suggesting that PMH is generally more common than it is recognized.10 Although controversial, current literature suggests a slight predominance in women.10,15 The increased reporting in dark-skinned individuals may simply reflect heightened recognition because the adjacent darker normal skin highlights the lighter affected skin. Most patients are young adults and no person older than age 50 years has been diagnosed with PMH, suggesting disease regression over time.15 Hence, the term “progressive” may be somewhat inaccurate, although Guillet et al.11 initially reported that the disease worsened over a 4-year period before regressing. The lack of an association with acne vulgaris may support causation by a newly discovered Propionibacterium species.12,13

Diagnosis of PMH requires a high index of suspicion. To the untrained eye, PMH and TV can appear indistinguishable. Both consist of asymptomatic, hypopigmented macules coalescing over the back, more often in young adults during the summer months. However, some clinical features can provide clues; PMH does not have scale or an erythematous rim, which are characteristic of TV. However, one should suspect the diagnosis of PMH in cases of presumed—but unconfirmed—TV that fail an appropriate course of antifungal medication.

As previously described, hypopigmented macules on the trunk can be caused by other conditions, including pityriasis alba, leprosy, mycosis fungoides, hypomelanosis of Ito, and postinflammatory hypopigmentation.

Use of Wood’s lamp can help distinguish PMH from TV, as well as from several other similar conditions, but proper Wood’s lamp technique is crucial. The examination room should be completely dark, and the investigator should allow 1 minute for the lamp to warm and 3 minutes for his or her eyes to acclimate. The skin of interest should be cleaned with an alcohol wipe to remove any soap or lotion residue that may fluoresce.5 When illuminating the skin with Wood’s light, the investigator should compare lesional to nonlesional skin, noting the specific characteristics. If the diagnosis remains in question, other studies can help ensure a proper diagnosis.

If a biopsy is performed, the histologic findings of PMH include a paucity of epidermal melanin and a mild, perifollicular, lymphoid dermal infiltrate; a gram stain will demonstrate Propionibacterium, a gram-positive bacteria, within the pilosebaceous units.12,13

Successful treatment of PMH remains largely anecdotal. In theory, the goal is to inhibit sebum production, eliminate the causative bacteria, and stimulate melanin production. Suggested topical treatments include benzoyl peroxide and antibiotics such as clindamycin. Oral antibiotics may also be effective. Some studies report efficacy with phototherapy, but recurrence is common because phototherapy does not treat the presumed infectious cause.10,14,15 Low-dose isotretinoin may be successful, presumptively due to inhibition of sebum production.17 However, the patient and clinician must both be registered in the US Food and Drug Administration-regulated iPledge program, which monitors pregnancy risk in women.

The patient described in our case was effectively treated with a 2-month course of oral minocycline, 100 mg twice daily. She has not returned to the clinic for long-term follow-up.

 

Kyle Flores is a medical student and Julia R. Nunley, MD, is a professor of dermatology and program director of dermatology at the Medical College of Virginia Hospitals of Virginia Commonwealth University in Richmond.

 

References

  1. Muhammad M, Kamai M, Islam T, et al. A study to evaluate the safety and efficacy of oral fluconazole in the treatment of tinea versicolor. Mymensingh Med J. 2009;18(1):31-35.
  2. Negroni R. Historical aspects of dermatomycoses. Clin in Dermatol. 2010;28(2):125-132.
  3. Crespo Erchiga V, Delgado Florencio V. Malassezia species in skin diseases. Curr Opin Infect Dis. 2002;15(2):133-142.
  4. Hort W, Meyser P. Malassezia virulence determinants. Curr Opin Infect Dis. 2011;24(2):100-105.
  5. Asawanonda P, Taylor CR. Wood’s light in dermatology. Int J Dermatol. 1999;38(11):801-807.
  6. Lim SL, Lim CS. New contrast stain for the rapid diagnosis of pityriasis versicolor. Arch Dermatol. 2008;144(8):1058-1059.
  7. Faergemann J. Pityrosporum species as a cause of allergy and infection. Allergy. 1999;54(5):413-419.
  8. Gupta AK, Kogan N, Batra R. Pityriasis versicolor: A review of pharmacological treatment options. Expert Opin Pharmacother. 2005;6(2):165-178.Gupta AK, Lyons DC. Pityriasis versicolor: An update on pharmacological treatment options. Expert Opin Pharmacother. 2014;15(12):1707-1713.
  9. Relyveld GN, Menke HE, Westerhof W. Progressive macular hypomelanosis: An overview. Am J Clin Dermatol. 2007;8(1):13-19.
  10. Guillet G, Helanon R, Gauthier Y, et al. Progressive macular hypomelanosis of the trunk: Primary acquired hypopigmentation. J Cutan Pathol. 1988; 15(5):286-289.
  11. Westerhof W, Relyveld GN, Kingswijk MM, et al. Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis. Arch Dermatol. 2004;140(2):210-214.
  12. Relyveld GN, Westerhof W, Woudenberg J, et al. Progressive macular hypomelanosis is associated with a putative Propionibacterium species. J Inv Dermatol. 2010;130(4):1182-1184.
  13. Hassan A, El-Badawi MA, Abd-Rabbou FA, et al. Progressive macular hypomelanosis pathogenesis and treatment: A randomized clinical trial. Journal of Microscopy and Ultrastructure. 2014;2(4):205-216.
  14. Duarte I, Nina BI, Gordiano MC, et al. Progressive macular hypomelanosis: An epidemiological study and therapeutic response to phototherapy. An Bras Dermatol. 2010;85(5):621-624.
  15. Lo Schiavo A, Gambardella A, Caccavale S. The possible role of antiretroviral drugs in the pathogenesis of progressive macular hypomelanosis. Int J Dermatol. 2014;53(6):759-760.
  16. Kim YJ, Lee DY, Lee JY, Yoon TY. Progressive macular hypomelanosis showing excellent response to oral isotretinoin. J Dermatol. 2012;39(11):937-938. 
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