Riehl Melanosis



During World War I, in the spring of 1917, Riehl identified approximately 17 patients who had striking dark-brown to grayish-brown facial pigmentation that was most pronounced on the lateral aspects of the face and neck and primarily concentrated on the forehead, ears, temple, and zygomatic regions.[1, 2] Pigmentation was also noted on the thorax, but it was less pronounced and primarily consisted of small follicular-based pigmented macules. Subtle hyperpigmentation was also identified on the hands, forearms, and intertriginous regions.[2] All patients were white and from Vienna, and all had no evidence of an underlying illness. The patients varied in age and sex. In addition to the hyperpigmentation, erythematous macules and papules were also identified.[2, 3, 4] Histologically, the lesions were marked by a dense inflammatory cell infiltrate in the superficial dermis admixed with melanophages.[2, 3]

Although Riehl was unable to identify the cause of the eruption, he speculated that the hyperpigmentation occurred because of some nutritional alteration that he attributed to wartime conditions.[1, 2, 3, 4] Concomitant with the end of the war, no further cases were identified; thereby, supporting his hypothesis.[2] Subsequently in World War II, a similar eruption surfaced in approximately 165 people in France, again associated with the scarce food supplies and disappearing with the end of the war; however, this latter situation differed from that seen in World War I in that the majority of cases were reported in women.[2, 3]

Later, Hoffmann and Habermann described a condition referred to as melanodermatitis toxica that was hypothesized to be a form of contact dermatitis associated with the use of certain oils and hydrocarbons. Although these authors emphasized the clinical similarities between Riehl melanosis and melanodermatitis toxica, Riehl could not accept that the melanosis that he described was due to a local chemical irritant and felt that the conditions were separate entities. The role of nutrition as a possible cause of this unusual melanosis was further addressed in a paper by Findlay, who described several cases of Riehl melanosis in the Bantu people in South Africa; however, no further reports in the literature linked Riehl melanosis to nutritional deficiencies.[5]

Subsequent to the great wars, the majority of cases of Riehl melanosis described in the literature differ from the cases originally described by Riehl. In 1950, Minami and Noma described a pigmented dermatitis in Asian women unrelated to the war and named the condition melanosis faciei feminae.[3] The etiology of this latter pigmentation was unknown for many years, until 2 studies from Argentina in the late 1940s and 1950s described facial pigmentation similar to Riehl melanosis that was subsequently attributed to the use of cosmetics. In the first study, patch testing identified aniline dye (orange II) present in facial powder as the cause of the pigmented contact dermatitis, whereas the second study emphasized that photosensitizing may play an addition role in the pigmentation.[2]

In 1970, Osmundsen subsequently reported 7 patients who had a similar bizarre hyperpigmentation that occurred as a result of contact dermatitis to an optical whitener, Tinopal CH 3566, in washing powder and called the condition pigmented contact dermatitis (PCD).[6] Subsequently in 1973, Nakayama introduced the term pigmented cosmetic contact dermatitis for cases that were ascribed to the use of certain cosmetics.

Although the majority of the literature suggests that Riehl melanosis is synonymous with pigmented contact dermatitis, this is an erroneous assumption because the cases reported by Riehl appear to be a distinct entity related to nutritional alterations that occurred in World War I, with no further case reports noted after the war ended. Pigmented contact dermatitis, on the other hand, is caused by an allergic contact dermatitis to a variety of topical and airborne allergens. Because of this, the remainder of the article focuses on pigmented contact dermatitis.[2, 3, 4]


The hyperpigmentation in pigmented contact dermatitis is postulated to be caused by frequent and repeated contact with small amounts of sensitizing allergens primarily in cosmetic and textile materials. Nakayama hypothesized that allergens used in commercial products were too low in concentration to produce typical eczematous dermatitis, but rather accumulation of these allergens resulted allergic contact dermatitis, a type IV cytolytic reaction.[7, 8] This later reaction is characterized by vacuolar degeneration of the basal layer of the epidermis associated with pigment incontinence in the superficial dermis. The melanin pigment is slowly engulfed by macrophages; therefore, resolution of the hyperpigmentation is a prolonged process. Because most cases of pigmented contact dermatitis occur in patients with a darker completion, one hypothesis is that various pigment-genetic interactions contribute to the development of this condition.[4] Furthermore, Imokawa and Kawai have provided clinicalevidence that various allergens implicated in allergic contact dermatitis can stimulate melanogenesis.[9]



United States

The incidence is not known. Most cases are reported outside of the United States, with a large proportion of cases reported in Japan.


No international statistics are available, but cases have been reported in France, Denmark, South America, Japan, India, and South Africa.


In general, pigmented contact dermatitis is most pronounced in darkly pigmented races.


Women appear to have a greater predilection for pigmented contact dermatitis.


Although it has been reported in a wide range of patients, the majority of cases appear to occur in young to middle-aged women.


Possible subtle signs of a preceding dermatitis include erythema, edema, and pruritus. Such symptoms are generally mild, if present.


Many cases are preceded by mild erythema, edema, and pruritus,[2] followed by a diffuse-to-reticulated pattern of hyperpigmentation. The pigmentation varies dependent upon the causal agent and can be brown, slate-gray, gray-brown, red-brown, or blue-brown.[2, 4, 10]

The site of pigmented contact dermatitis also depends on the allergen responsible. Pigmented cosmetic dermatitis more commonly involves the face, whereas pigmented contact dermatitis due to textiles more often involves the anterior thighs or the axilla, with sparing of the axillary vault.[4] Additionally, hyperpigmentation is most pronounced in individuals with darker complexions.

UV exposure may contribute to the hyperpigmentation in select cases, which is supported by the fact that some of the chemicals implicated are known photosensitizers, and, in these cases, the pigmentation appears to be most pronounced in sun-exposed areas.[2, 4]


A variety of contact allergens have been implicated in pigmented contact dermatitis, as described below.[3, 4, 10] Although the majority of cases occur because of direct contact with these allergens, a few cases secondary to contact with airborne allergens have been described.[4, 11, 12]

Cases of pigmented contact dermatitis have been reported in the Indian literature, and the most common allergen to be implicated is kumkum, a colored cosmetic used by Hindu women that is applied most often to the central forehead and along the hair line.[4, 18] Only commercially available red kumkum can sensitize and cause pigmented contact dermatitis. Components of kumkum include azo dyes, coal tar dyes, toludine red, erythrosine, lithal red calcium salt, fragrances, tumeric powder, groundnut oil, tragacanth gum, Cananga oil, and parabens.[4]

In addition to contact allergens, a Riehl melanosis–like eruption has been reported in Japanese women with Sjögren syndrome related to the development of anti-SSA (Ro) antibodies. The lesions are most pronounced on sun-exposed areas, primarily on the face, and the pigmentation typically resolves with the institution of ultraviolet protection. One hypothesis is that ultraviolet radiation induces expression of the SSA antigen on keratinocytes, which then becomes the target of circulating anti-SSA antibodies, resulting in an interface dermatitis and associated pigment incontinence.[24]

Laboratory Studies


Histologic Findings

Most biopsy results have shown interface dermatitis with vacuolar basal layer degeneration. The superficial dermis often contains a mild-to-moderate lymphohistiocytic infiltrate admixed with melanophages. Findings suggestive of spongiosis are lacking. Some biopsy specimens have shown mild atrophy of the dermis, but this is an inconsistent finding. Negative direct immunofluorescence study results help eliminate hyperpigmented lupus erythematosus from the differential diagnosis.

Medical Care


Medication Summary



Elizabeth K Satter, MD, MPH, Director of Dermatopathology, Naval Medical Center San Diego

Disclosure: Nothing to disclose.


Helena A Longin, MD, Resident Physician, Department of Dermatology, Naval Medical Center San Diego

Disclosure: Nothing to disclose.

Specialty Editors

John D Wilkinson, MD, MBBS, MRCS, FRCP, Chairman, Clinical Director, Department of Dermatology, Amersham Hospital and High Wycombe Hospital, UK

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

Disclosure: Nothing to disclose.

Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Disclosure: Nothing to disclose.

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference acknowledge the contributions of previous author, Mohsin Ali, MBBS, FRCP, MRCP, to the development and writing of this article.


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