Pediatric Dermatology Consult - November 2015

Tinea versicolor

Tinea versicolor – also called pityriasis versicolor – is a benign superficial fungal skin infection caused by Malassezia. It presents as well-demarcated, oval, finely scaling macules, patches, or thin plaques, which can be hypopigmented, hyperpigmented, or erythematous.^1,2,3 . The name, tinea versicolor, highlights the variability in the color of lesions.⁴

Scale may be minimal, but becomes more noticeable when lesions are scraped, which is called the “evoked scale sign.”⁵ The lesions may be asymptomatic or slightly pruritic.¹ Lesions range in size from several millimeters to several centimeters and may coalesce.6 They are most commonly found on the chest, back, upper arms, and neck,^2,7 but in children the face may be affected.^1,3,8 Hypopigmented lesions may be most noticeable during the summer when the surrounding uninvolved skin darkens with sun exposure.9 Tinea versicolor is not contagious, but pigmentary changes may cause cosmetic concerns, and the condition may persist for years if not treated.^2,4

Malassezia is a dimorphic fungus that is part of the normal skin flora in its yeast form, but if Malassezia converts to its hyphal form, it is able penetrate the stratum corneum and cause the tinea versicolor rash.^1,10 The reason for the conversion from yeast to hyphal form is not fully understood.¹¹Malassezia is lipophilic, so it thrives when sebum production is high, which is why tinea versicolor most commonly develops in adolescence or young adulthood, although it may be seen in younger children and older adults.¹² Genetic predisposition, warm and humid environments, oily skin, use of oily creams, use of corticosteroids, hyperhidrosis, physical activity, malnutrition, immunosuppression, and exposure to sunlight increase susceptibility.^1,13,14

Tinea versicolor is most commonly caused by Malassezia globosa and Malassezia furfur.^13,15,16 Hypopigmentation may be caused by Malassezia’s production of azelaic acid, which inhibits the dopa-tyrosinase reaction that is part of melanin synthesis.^15,17,18 Hyperpigmentation may result from inflammation.^15,18 The evoked scale sign results from the production of keratinase, which disrupts the stratum corneum.⁵

Tinea versicolor often can be diagnosed by its characteristic clinical appearance and may fluoresce golden under a Wood’s ultraviolet lamp.¹⁹ Diagnosis can be confirmed by microscopic examination of skin scrapings treated with potassium hydroxide (KOH), which will have a “spaghetti and meatball” appearance, with the hyphae resembling spaghetti and spores resembling meatballs.¹ For young children, removing scale with transparent tape can be a good alternative to scraping skin with a blade.^2,19

Differential diagnosis

Postinflammatory pigment changes, both hypo and hyper, usually lack scale, may be anywhere on the body, and should have the same distribution as some original inflammation.

Pityriasis alba presents with hypopigmented patches, typically on the face, and has a more subtle “blotchy” appearance, without discrete oval patches. Pityriasis rosea may appear similar to tinea versicolor with erythema and scale, but it typically begins with a single, large herald patch, and scale is primarily at the outer border of the lesions.¹

Tinea corporis (“ringworm”), which is caused by a dermatophyte, is more distinctly ring shaped with a scaly, vesicular, papular, or pustular border and there is often a clear center that may not scale when scraped.^5,9 It is much more commonly localized, except in immunosuppressed patients or if mistreated with topical corticosteroids. Vitiligo lesions are completely depigmented, rather than just hypopigmented, and lack scale.¹ Psoriasis scale is thicker and is visible without any provocation.  

Treatment

First-line treatments for tinea versicolor include ketoconazole shampoo, selenium sulfide lotion or shampoo, and zinc pyrithione shampoo, which are left on for 5-10 minutes before rinsing.^1,20 Any of these treatments is a fine first choice, as all are effective, and there are no robust data establishing the superiority of any single treatment.20 The typical treatment duration is 1-4 weeks.¹ Longer treatment durations yield better cure rates.20 Ketoconazole and selenium sulfide also are available in foam formulations.11 Shampoo and foam formulations have the benefit of easily covering a large affected area.

Alternatively, terbinafine cream can be applied twice daily for a week or ketoconazole cream can be applied twice daily for 1-4 weeks.^1,21 It is advisable to treat the whole trunk, neck, arms, and legs down to the knees, even if only a small area is involved.^14,22 Antifungal treatments are well tolerated, with skin irritation and contact allergy being the most common adverse effects.1 Selenium sulfide has a strong odor.1

Hypopigmentation and hyperpigmentation can persist for months after the active infection has resolved and do not necessarily indicate a treatment failure.^2,20 However, because Malassezia is a part of the normal skin flora, recurrence is common, occurring in 60%-80% of patients within 2 years.¹⁴ Recurrence or persistence of an active infection can be proven by a positive KOH scrape test. If a first treatment fails, a different first-line topical medication should be tried.1 Referral to a dermatologist is recommended if the eruption is unresponsive to two treatments.1

Oral antifungals such as itraconazole, fluconazole, and pramiconazole are effective for tinea versicolor, but have more adverse effects than topicals and interact with other medications because of their inhibition of the cytochrome P450 system, so they are used only for refractory or widespread disease.^1,11 In 2013, the Food and Drug Administration issued a black box warning against oral ketoconazole due its ability to cause life-threatening hepatotoxicity and adrenal insufficiency^1,23,24; it should not be used to treat tinea versicolor. Topical ketoconazole is safe and remains a first-line treatment for tinea versicolor, as discussed above.24 Oral terbinafine is not effective for tinea versicolor despite its efficacy as a topical treatment.¹¹

Patients with recurrent tinea versicolor can try preventive therapy with ketoconazole shampoo, zinc pyrithione shampoo, or selenium sulfide lotion or shampoo one to four times per month.1 Oral antifungals also are effective for prevention of recurrence, but should be used only if the condition is refractory to topical prophylaxis.^20,25 It is important to remember that hypopigmentation and hyperpigmentation may persist for months after resolution of active infection; absence of hyphae on skin scraping prepared with KOH confirms absence of active disease.^15,16 

References

1. BMJ. 2015;350:h1394. doi:10.1136/bmj.h1394.
2. Lancet. 2004 Sep 25-Oct 1;364(9440):1173-82.
3. Pediatr Dermatol. 1991;8(1):9-12.
4. J Eur Acad Dermatol Venereol. 2002;16(1):19-33.
5. Arch Dermatol. 2009;145(9):1078.
6. Vitiligo and other disorders of pigmentation, in: “Dermatology,” Vol 1. 3rd ed. (Philadelphia: Elsevier Saunders, 2012, pp.1041-2.)
7. Am J Clin Dermatol. 2000 Mar-Apr;1(2):75-80.
8. Mycoses. 1995;38(5-6):227-8.
9. “Skin Disorders Due to Fungi,” in: Hurwitz Clinical Pediatric Dermatology 4th ed. (Philadelphia: Saunders, 2011, pp. 396-403).
10. Infect Control Hosp Epidemiol. 2002 Apr;23(4):212-6.
11. Expert Opin Pharmacother. 2014 Aug;15(12):1707-13.
12. Clin Microbiol Rev. 2002 Jan;15(1):21-57.
13. Clin Dermatol. 2010 Mar 4;28(2):185-9.
14. J Am Acad Dermatol. 1994 Sep;31(3 Pt 2):S18-20.
15. Int J Dermatol. 2014 Feb;53(2):137-41
16. Mycopathologia. 2006 Dec;162(6):373-6.
17. J Invest Dermatol. 1978 Sep;71(3):205-8.
18. Int J Dermatol. 1992 Apr;31(4):253-6.
19. Pediatr Dermatol. 2000 Jan-Feb;17(1):68-9.
20. Arch Dermatol. 2010 Oct;146(10):1132-40.
21. Dermatology (Basel). 1997;194(1):22-4. doi:10.1159/000246179.
22. Red Book Plus: 2009 Report of the Committee on Infectious Disease.
23. http://www.fda.gov/Drugs/DrugSafety/ucm362415.htm    
24. J Cutan Med Surg. 2015 Jul-Aug;19(4):352-7.
25. Arch Dermatol. 2002 Jan;138(1):69-73.

Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego and professor of dermatology and pediatrics at the University of California, San Diego. Ms. Haddock is a medical student at the University of California, San Diego, and a research associate at the hospital. Dr. Eichenfield and Ms. Haddock said they have no relevant financial disclosures.

Email to [email protected].

Tinea versicolor

Tinea versicolor – also called pityriasis versicolor – is a benign superficial fungal skin infection caused by Malassezia. It presents as well-demarcated, oval, finely scaling macules, patches, or thin plaques, which can be hypopigmented, hyperpigmented, or erythematous.^1,2,3 . The name, tinea versicolor, highlights the variability in the color of lesions.⁴

Scale may be minimal, but becomes more noticeable when lesions are scraped, which is called the “evoked scale sign.”⁵ The lesions may be asymptomatic or slightly pruritic.¹ Lesions range in size from several millimeters to several centimeters and may coalesce.6 They are most commonly found on the chest, back, upper arms, and neck,^2,7 but in children the face may be affected.^1,3,8 Hypopigmented lesions may be most noticeable during the summer when the surrounding uninvolved skin darkens with sun exposure.9 Tinea versicolor is not contagious, but pigmentary changes may cause cosmetic concerns, and the condition may persist for years if not treated.^2,4

Malassezia is a dimorphic fungus that is part of the normal skin flora in its yeast form, but if Malassezia converts to its hyphal form, it is able penetrate the stratum corneum and cause the tinea versicolor rash.^1,10 The reason for the conversion from yeast to hyphal form is not fully understood.¹¹Malassezia is lipophilic, so it thrives when sebum production is high, which is why tinea versicolor most commonly develops in adolescence or young adulthood, although it may be seen in younger children and older adults.¹² Genetic predisposition, warm and humid environments, oily skin, use of oily creams, use of corticosteroids, hyperhidrosis, physical activity, malnutrition, immunosuppression, and exposure to sunlight increase susceptibility.^1,13,14

Tinea versicolor is most commonly caused by Malassezia globosa and Malassezia furfur.^13,15,16 Hypopigmentation may be caused by Malassezia’s production of azelaic acid, which inhibits the dopa-tyrosinase reaction that is part of melanin synthesis.^15,17,18 Hyperpigmentation may result from inflammation.^15,18 The evoked scale sign results from the production of keratinase, which disrupts the stratum corneum.⁵

Tinea versicolor often can be diagnosed by its characteristic clinical appearance and may fluoresce golden under a Wood’s ultraviolet lamp.¹⁹ Diagnosis can be confirmed by microscopic examination of skin scrapings treated with potassium hydroxide (KOH), which will have a “spaghetti and meatball” appearance, with the hyphae resembling spaghetti and spores resembling meatballs.¹ For young children, removing scale with transparent tape can be a good alternative to scraping skin with a blade.^2,19

Differential diagnosis

Postinflammatory pigment changes, both hypo and hyper, usually lack scale, may be anywhere on the body, and should have the same distribution as some original inflammation.

Pityriasis alba presents with hypopigmented patches, typically on the face, and has a more subtle “blotchy” appearance, without discrete oval patches. Pityriasis rosea may appear similar to tinea versicolor with erythema and scale, but it typically begins with a single, large herald patch, and scale is primarily at the outer border of the lesions.¹

Tinea corporis (“ringworm”), which is caused by a dermatophyte, is more distinctly ring shaped with a scaly, vesicular, papular, or pustular border and there is often a clear center that may not scale when scraped.^5,9 It is much more commonly localized, except in immunosuppressed patients or if mistreated with topical corticosteroids. Vitiligo lesions are completely depigmented, rather than just hypopigmented, and lack scale.¹ Psoriasis scale is thicker and is visible without any provocation.  

Treatment

First-line treatments for tinea versicolor include ketoconazole shampoo, selenium sulfide lotion or shampoo, and zinc pyrithione shampoo, which are left on for 5-10 minutes before rinsing.^1,20 Any of these treatments is a fine first choice, as all are effective, and there are no robust data establishing the superiority of any single treatment.20 The typical treatment duration is 1-4 weeks.¹ Longer treatment durations yield better cure rates.20 Ketoconazole and selenium sulfide also are available in foam formulations.11 Shampoo and foam formulations have the benefit of easily covering a large affected area.

Alternatively, terbinafine cream can be applied twice daily for a week or ketoconazole cream can be applied twice daily for 1-4 weeks.^1,21 It is advisable to treat the whole trunk, neck, arms, and legs down to the knees, even if only a small area is involved.^14,22 Antifungal treatments are well tolerated, with skin irritation and contact allergy being the most common adverse effects.1 Selenium sulfide has a strong odor.1

Hypopigmentation and hyperpigmentation can persist for months after the active infection has resolved and do not necessarily indicate a treatment failure.^2,20 However, because Malassezia is a part of the normal skin flora, recurrence is common, occurring in 60%-80% of patients within 2 years.¹⁴ Recurrence or persistence of an active infection can be proven by a positive KOH scrape test. If a first treatment fails, a different first-line topical medication should be tried.1 Referral to a dermatologist is recommended if the eruption is unresponsive to two treatments.1

Oral antifungals such as itraconazole, fluconazole, and pramiconazole are effective for tinea versicolor, but have more adverse effects than topicals and interact with other medications because of their inhibition of the cytochrome P450 system, so they are used only for refractory or widespread disease.^1,11 In 2013, the Food and Drug Administration issued a black box warning against oral ketoconazole due its ability to cause life-threatening hepatotoxicity and adrenal insufficiency^1,23,24; it should not be used to treat tinea versicolor. Topical ketoconazole is safe and remains a first-line treatment for tinea versicolor, as discussed above.24 Oral terbinafine is not effective for tinea versicolor despite its efficacy as a topical treatment.¹¹

Patients with recurrent tinea versicolor can try preventive therapy with ketoconazole shampoo, zinc pyrithione shampoo, or selenium sulfide lotion or shampoo one to four times per month.1 Oral antifungals also are effective for prevention of recurrence, but should be used only if the condition is refractory to topical prophylaxis.^20,25 It is important to remember that hypopigmentation and hyperpigmentation may persist for months after resolution of active infection; absence of hyphae on skin scraping prepared with KOH confirms absence of active disease.^15,16 

References

1. BMJ. 2015;350:h1394. doi:10.1136/bmj.h1394.
2. Lancet. 2004 Sep 25-Oct 1;364(9440):1173-82.
3. Pediatr Dermatol. 1991;8(1):9-12.
4. J Eur Acad Dermatol Venereol. 2002;16(1):19-33.
5. Arch Dermatol. 2009;145(9):1078.
6. Vitiligo and other disorders of pigmentation, in: “Dermatology,” Vol 1. 3rd ed. (Philadelphia: Elsevier Saunders, 2012, pp.1041-2.)
7. Am J Clin Dermatol. 2000 Mar-Apr;1(2):75-80.
8. Mycoses. 1995;38(5-6):227-8.
9. “Skin Disorders Due to Fungi,” in: Hurwitz Clinical Pediatric Dermatology 4th ed. (Philadelphia: Saunders, 2011, pp. 396-403).
10. Infect Control Hosp Epidemiol. 2002 Apr;23(4):212-6.
11. Expert Opin Pharmacother. 2014 Aug;15(12):1707-13.
12. Clin Microbiol Rev. 2002 Jan;15(1):21-57.
13. Clin Dermatol. 2010 Mar 4;28(2):185-9.
14. J Am Acad Dermatol. 1994 Sep;31(3 Pt 2):S18-20.
15. Int J Dermatol. 2014 Feb;53(2):137-41
16. Mycopathologia. 2006 Dec;162(6):373-6.
17. J Invest Dermatol. 1978 Sep;71(3):205-8.
18. Int J Dermatol. 1992 Apr;31(4):253-6.
19. Pediatr Dermatol. 2000 Jan-Feb;17(1):68-9.
20. Arch Dermatol. 2010 Oct;146(10):1132-40.
21. Dermatology (Basel). 1997;194(1):22-4. doi:10.1159/000246179.
22. Red Book Plus: 2009 Report of the Committee on Infectious Disease.
23. http://www.fda.gov/Drugs/DrugSafety/ucm362415.htm    
24. J Cutan Med Surg. 2015 Jul-Aug;19(4):352-7.
25. Arch Dermatol. 2002 Jan;138(1):69-73.

Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego and professor of dermatology and pediatrics at the University of California, San Diego. Ms. Haddock is a medical student at the University of California, San Diego, and a research associate at the hospital. Dr. Eichenfield and Ms. Haddock said they have no relevant financial disclosures.

Email to [email protected].

Tinea versicolor

Tinea versicolor – also called pityriasis versicolor – is a benign superficial fungal skin infection caused by Malassezia. It presents as well-demarcated, oval, finely scaling macules, patches, or thin plaques, which can be hypopigmented, hyperpigmented, or erythematous.^1,2,3 . The name, tinea versicolor, highlights the variability in the color of lesions.⁴

Scale may be minimal, but becomes more noticeable when lesions are scraped, which is called the “evoked scale sign.”⁵ The lesions may be asymptomatic or slightly pruritic.¹ Lesions range in size from several millimeters to several centimeters and may coalesce.6 They are most commonly found on the chest, back, upper arms, and neck,^2,7 but in children the face may be affected.^1,3,8 Hypopigmented lesions may be most noticeable during the summer when the surrounding uninvolved skin darkens with sun exposure.9 Tinea versicolor is not contagious, but pigmentary changes may cause cosmetic concerns, and the condition may persist for years if not treated.^2,4

Malassezia is a dimorphic fungus that is part of the normal skin flora in its yeast form, but if Malassezia converts to its hyphal form, it is able penetrate the stratum corneum and cause the tinea versicolor rash.^1,10 The reason for the conversion from yeast to hyphal form is not fully understood.¹¹Malassezia is lipophilic, so it thrives when sebum production is high, which is why tinea versicolor most commonly develops in adolescence or young adulthood, although it may be seen in younger children and older adults.¹² Genetic predisposition, warm and humid environments, oily skin, use of oily creams, use of corticosteroids, hyperhidrosis, physical activity, malnutrition, immunosuppression, and exposure to sunlight increase susceptibility.^1,13,14

Tinea versicolor is most commonly caused by Malassezia globosa and Malassezia furfur.^13,15,16 Hypopigmentation may be caused by Malassezia’s production of azelaic acid, which inhibits the dopa-tyrosinase reaction that is part of melanin synthesis.^15,17,18 Hyperpigmentation may result from inflammation.^15,18 The evoked scale sign results from the production of keratinase, which disrupts the stratum corneum.⁵

Tinea versicolor often can be diagnosed by its characteristic clinical appearance and may fluoresce golden under a Wood’s ultraviolet lamp.¹⁹ Diagnosis can be confirmed by microscopic examination of skin scrapings treated with potassium hydroxide (KOH), which will have a “spaghetti and meatball” appearance, with the hyphae resembling spaghetti and spores resembling meatballs.¹ For young children, removing scale with transparent tape can be a good alternative to scraping skin with a blade.^2,19

Differential diagnosis

Postinflammatory pigment changes, both hypo and hyper, usually lack scale, may be anywhere on the body, and should have the same distribution as some original inflammation.

Pityriasis alba presents with hypopigmented patches, typically on the face, and has a more subtle “blotchy” appearance, without discrete oval patches. Pityriasis rosea may appear similar to tinea versicolor with erythema and scale, but it typically begins with a single, large herald patch, and scale is primarily at the outer border of the lesions.¹

Tinea corporis (“ringworm”), which is caused by a dermatophyte, is more distinctly ring shaped with a scaly, vesicular, papular, or pustular border and there is often a clear center that may not scale when scraped.^5,9 It is much more commonly localized, except in immunosuppressed patients or if mistreated with topical corticosteroids. Vitiligo lesions are completely depigmented, rather than just hypopigmented, and lack scale.¹ Psoriasis scale is thicker and is visible without any provocation.  

Treatment

First-line treatments for tinea versicolor include ketoconazole shampoo, selenium sulfide lotion or shampoo, and zinc pyrithione shampoo, which are left on for 5-10 minutes before rinsing.^1,20 Any of these treatments is a fine first choice, as all are effective, and there are no robust data establishing the superiority of any single treatment.20 The typical treatment duration is 1-4 weeks.¹ Longer treatment durations yield better cure rates.20 Ketoconazole and selenium sulfide also are available in foam formulations.11 Shampoo and foam formulations have the benefit of easily covering a large affected area.

Alternatively, terbinafine cream can be applied twice daily for a week or ketoconazole cream can be applied twice daily for 1-4 weeks.^1,21 It is advisable to treat the whole trunk, neck, arms, and legs down to the knees, even if only a small area is involved.^14,22 Antifungal treatments are well tolerated, with skin irritation and contact allergy being the most common adverse effects.1 Selenium sulfide has a strong odor.1

Hypopigmentation and hyperpigmentation can persist for months after the active infection has resolved and do not necessarily indicate a treatment failure.^2,20 However, because Malassezia is a part of the normal skin flora, recurrence is common, occurring in 60%-80% of patients within 2 years.¹⁴ Recurrence or persistence of an active infection can be proven by a positive KOH scrape test. If a first treatment fails, a different first-line topical medication should be tried.1 Referral to a dermatologist is recommended if the eruption is unresponsive to two treatments.1

Oral antifungals such as itraconazole, fluconazole, and pramiconazole are effective for tinea versicolor, but have more adverse effects than topicals and interact with other medications because of their inhibition of the cytochrome P450 system, so they are used only for refractory or widespread disease.^1,11 In 2013, the Food and Drug Administration issued a black box warning against oral ketoconazole due its ability to cause life-threatening hepatotoxicity and adrenal insufficiency^1,23,24; it should not be used to treat tinea versicolor. Topical ketoconazole is safe and remains a first-line treatment for tinea versicolor, as discussed above.24 Oral terbinafine is not effective for tinea versicolor despite its efficacy as a topical treatment.¹¹

Patients with recurrent tinea versicolor can try preventive therapy with ketoconazole shampoo, zinc pyrithione shampoo, or selenium sulfide lotion or shampoo one to four times per month.1 Oral antifungals also are effective for prevention of recurrence, but should be used only if the condition is refractory to topical prophylaxis.^20,25 It is important to remember that hypopigmentation and hyperpigmentation may persist for months after resolution of active infection; absence of hyphae on skin scraping prepared with KOH confirms absence of active disease.^15,16 

References

1. BMJ. 2015;350:h1394. doi:10.1136/bmj.h1394.
2. Lancet. 2004 Sep 25-Oct 1;364(9440):1173-82.
3. Pediatr Dermatol. 1991;8(1):9-12.
4. J Eur Acad Dermatol Venereol. 2002;16(1):19-33.
5. Arch Dermatol. 2009;145(9):1078.
6. Vitiligo and other disorders of pigmentation, in: “Dermatology,” Vol 1. 3rd ed. (Philadelphia: Elsevier Saunders, 2012, pp.1041-2.)
7. Am J Clin Dermatol. 2000 Mar-Apr;1(2):75-80.
8. Mycoses. 1995;38(5-6):227-8.
9. “Skin Disorders Due to Fungi,” in: Hurwitz Clinical Pediatric Dermatology 4th ed. (Philadelphia: Saunders, 2011, pp. 396-403).
10. Infect Control Hosp Epidemiol. 2002 Apr;23(4):212-6.
11. Expert Opin Pharmacother. 2014 Aug;15(12):1707-13.
12. Clin Microbiol Rev. 2002 Jan;15(1):21-57.
13. Clin Dermatol. 2010 Mar 4;28(2):185-9.
14. J Am Acad Dermatol. 1994 Sep;31(3 Pt 2):S18-20.
15. Int J Dermatol. 2014 Feb;53(2):137-41
16. Mycopathologia. 2006 Dec;162(6):373-6.
17. J Invest Dermatol. 1978 Sep;71(3):205-8.
18. Int J Dermatol. 1992 Apr;31(4):253-6.
19. Pediatr Dermatol. 2000 Jan-Feb;17(1):68-9.
20. Arch Dermatol. 2010 Oct;146(10):1132-40.
21. Dermatology (Basel). 1997;194(1):22-4. doi:10.1159/000246179.
22. Red Book Plus: 2009 Report of the Committee on Infectious Disease.
23. http://www.fda.gov/Drugs/DrugSafety/ucm362415.htm    
24. J Cutan Med Surg. 2015 Jul-Aug;19(4):352-7.
25. Arch Dermatol. 2002 Jan;138(1):69-73.

Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital-San Diego and professor of dermatology and pediatrics at the University of California, San Diego. Ms. Haddock is a medical student at the University of California, San Diego, and a research associate at the hospital. Dr. Eichenfield and Ms. Haddock said they have no relevant financial disclosures.

Email to [email protected].