Idiopathic Guttate Hypomelanosis

Author: Stephen W White, MD; Chief Editor: William D James, MD more...

Updated: Aug 29, 2011

What would you like to print?

Background
Pathophysiology
Epidemiology
Show All

Background

Idiopathic guttate hypomelanosis (IGH) is an acquired, benign leukoderma of unknown etiology. Idiopathic guttate hypomelanosis is most commonly a complaint of middle-aged, light-skinned women, but it is increasingly seen in both sexes and older dark-skinned people with a history of long-term sun exposure.

Idiopathic guttate hypomelanosis is a benign condition. The cause is not known, but it appears to be related to the effect of the sun on melanocytes, which makes them effete.

A variety of therapeutic methods, including topical steroids, topical retinoids, dermabrasion, cryotherapy, and minigrafting, have been used for idiopathic guttate hypomelanosis with variable success.^[1]

Pathophysiology

Because pigmentation of the skin is due to an integration of melanocyte and keratinocyte function, an acquired defect of the epidermal melanin unit results in the observed hypopigmentation in idiopathic guttate hypomelanosis patients. Significantly fewer dopa oxidase-positive, KIT⁺, and melanocytes are seen in the lesions.^{[2, 3]}In 1967, Hamada and Saito found a 50% reduction in melanocytes.

Frequency

United States

Idiopathic guttate hypomelanosis is a very common condition to the point of being almost universal in elderly fair-skinned individuals. In 2002, a case control study of 47 renal transplant patients demonstrated a significant positive association between HLA-DQ3 and the development of idiopathic guttate hypomelanosis and a significant negative association between HLA-DR8 and the development of idiopathic guttate hypomelanosis.^[4]

International

Idiopathic guttate hypomelanosis is most common in countries with fair-skinned populations having a high degree of sun exposure.

Mortality/Morbidity

Idiopathic guttate hypomelanosis is cosmetic alone, albeit, it is indicative of cumulative sun exposure.

Race

Idiopathic guttate hypomelanosis affects fair-skinned people at a younger age.

Sex

Idiopathic guttate hypomelanosis is seen far more frequently in women, beginning around the age of 30 years. However, with increasing age and sun exposure, it is found almost equally in elderly men and women. Why idiopathic guttate hypomelanosis occurs earlier in young women than in young men is unknown.

Age

Idiopathic guttate hypomelanosis is related to the lack of pigmentary protection from the sun and sun exposure rather than to age. Fair-skinned women develop this condition first; later, with increasing age and exposure to sun, both sexes seem to be equally affected.

Proceed to Clinical Presentation

Contributor Information and Disclosures

Author

Stephen W White, MD Clinical Assistant Professor, Department of Dermatology, George Washington University Hospital; Chief, Sub-section of Dermatology, Suburban Hospital

Stephen W White, MD is a member of the following medical societies: American Academy of Dermatology, International Society of Dermatology, Society for Investigative Dermatology, and Society for Pediatric Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher R Gorman, MD Bethesda Dermatology, Private Practice; Assistant Clinical Professor, George Washington University School of Medicine and Health Sciences; Staff Dermatologist, National Naval Medical Center

Christopher R Gorman, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel Mark Siegel, MD, MS Director, Procedural Dermatology Fellowship Program, Clinical Professor of Dermatology, Department of Dermatology, State University of New York Downstate

Daniel Mark Siegel, MD, MS is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American College of Physician Executives, American Society for Dermatologic Surgery, American Society for MOHS Surgery, and International Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System

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

Disclosure: Elsevier Royalty Other

References

Ploysangam T, Dee-Ananlap S, Suvanprakorn P. Treatment of idiopathic guttate hypomelanosis with liquid nitrogen: light and electron microscopic studies. J Am Acad Dermatol. Oct 1990;23(4 Pt 1):681-4. [Medline].
Ortonne JP, Perrot H. Idiopathic guttate hypomelanosis. Ultrastructural study. Arch Dermatol. Jun 1980;116(6):664-8. [Medline].
Wallace ML, Grichnik JM, Prieto VG, Shea CR. Numbers and differentiation status of melanocytes in idiopathic guttate hypomelanosis. J Cutan Pathol. Aug 1998;25(7):375-9. [Medline].
Arrunategui A, Trujillo RA, Marulanda MP, et al. HLA-DQ3 is associated with idiopathic guttate hypomelanosis, whereas HLA-DR8 is not, in a group of renal transplant patients. Int J Dermatol. Nov 2002;41(11):744-7. [Medline].
Falabella R, Escobar C, Giraldo N, et al. On the pathogenesis of idiopathic guttate hypomelanosis. J Am Acad Dermatol. Jan 1987;16(1 Pt 1):35-44. [Medline].
Kaya TI, Yazici AC, Tursen U, Ikizoglu G. Idiopathic guttate hypomelanosis: idiopathic or ultraviolet induced?. Photodermatol Photoimmunol Photomed. Oct 2005;21(5):270-1. [Medline].
Asawanonda P, Sutthipong T, Prejawai N. Pimecrolimus for idiopathic guttate hypomelanosis. J Drugs Dermatol. Mar 2010;9(3):238-9. [Medline].
Pagnoni A, Kligman AM, Sadiq I, Stoudemayer T. Hypopigmented macules of photodamaged skin and their treatment with topical tretinoin. Acta Derm Venereol. Jul 1999;79(4):305-10. [Medline].
Friedland R, David M, Feinmesser M, Fenig-Nakar S, Hodak E. Idiopathic guttate hypomelanosis-like lesions in patients with mycosis fungoides: a new adverse effect of phototherapy. J Eur Acad Dermatol Venereol. Feb 17 2010;[Medline].

View Table List

Read more about Idiopathic Guttate Hypomelanosis on Medscape