eMedicine Specialties > Dermatology > Diseases of Pigmentation

Idiopathic Guttate Hypomelanosis

Author: Stephen W White, MD, Clinical Assistant Professor, Department of Dermatology, George Washington University Hospital; Chief, Sub-section of Dermatology, Suburban Hospital
Coauthor(s): Christopher R Gorman, MD, Bethesda Dermatology, Private Practice; Assistant Clinical Professor, George Washington University School of Medicine and Health Sciences; Staff Dermatologist, Walter Reed Army Medical Center
Contributor Information and Disclosures

Updated: Jun 30, 2010

Introduction

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, dermabrasioncryotherapy, 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.

Clinical

History

Typically, idiopathic guttate hypomelanosis develops first on the legs of fair-skinned women in early adult life. Later, it may spread to other sun-exposed areas, such as the arms and the upper part of the back. The face is inexplicably not involved early in idiopathic guttate hypomelanosis. A familial tendency to develop idiopathic guttate hypomelanosis has been noted.5

Physical

Idiopathic guttate hypomelanosis consists of discrete, angular or circular macules that are 1-3 mm in diameter. However, lesions may measure up to 10 mm in diameter. These lighter-than-normal skin macules are off white, hypopigmented, or achromic. They are often noted first on the anterior aspects of the legs. Later, they appear on the forearms. The distribution seems to be photo related, except for the face, which is affected later than the limbs.

Causes

The exact cause of idiopathic guttate hypomelanosis is not agreed upon; however, it is hypothesized that ultraviolet light plays an important role.6

More on Idiopathic Guttate Hypomelanosis

Overview: Idiopathic Guttate Hypomelanosis
Differential Diagnoses & Workup: Idiopathic Guttate Hypomelanosis
Treatment & Medication: Idiopathic Guttate Hypomelanosis
Follow-up: Idiopathic Guttate Hypomelanosis
References

References

  1. 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].

  2. Ortonne JP, Perrot H. Idiopathic guttate hypomelanosis. Ultrastructural study. Arch Dermatol. Jun 1980;116(6):664-8. [Medline].

  3. 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].

  4. 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].

  5. 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].

  6. 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].

  7. Asawanonda P, Sutthipong T, Prejawai N. Pimecrolimus for idiopathic guttate hypomelanosis. J Drugs Dermatol. Mar 2010;9(3):238-9. [Medline].

  8. 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].

  9. 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].

Further Reading

Keywords

idiopathic guttate hypomelanosis, IGH, hypomelanosis of Cummins and Cottel, hypomelanosis guttata idiopathica, leukodermia lenticular disseminata, leukopathia guttata et reticularis symmetrica idiopathic guttate, macular hypopigmentation of the legs of women, senile depigmented spots, symmetric progressive leukopathy of the extremities

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, Walter Reed Army Medical Center
Christopher R Gorman, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University 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.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-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.

CME Editor

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

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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