Thousands of darker-skinned people (Fitzpatrick types III-VI) around the world have a variety of possibly interrelated acquired macular dermal hyperpigmentation disorders of unknown etiology, including ashy dermatosis (AD), lichen planus pigmentosus (LPP)/lichen dyschromicum perstans, erythema dyschromicum perstans (EDP), and idiopathic eruptive macular pigmentation. Although many people also include Riehl melanosis within the aforementioned acquired pigmentary disorders, international pigmentary consensus meetings reported in 2018 have determined that Riehl melanosis is better classified as a separate entity because the clinical presentation slightly differs and it is hypothesized to arise as a result of contact dermatitis.[1]
It was in the spring of 1917, during World War I, when Riehl first 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.[2, 3] The hyperpigmentation was also noted on the thorax, but it was less pronounced in this region and primarily consisted of small follicular-based pigmented macules. Subtle hyperpigmentation was also identified on the hands, forearms, and intertriginous regions.[3] 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.[3, 4, 5] Histologically, the lesions were marked by a dense inflammatory cell infiltrate in the superficial dermis admixed with melanophages.[3, 4]
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.[2, 3, 4, 5] Concomitant with the end of the war, no further cases were identified; thereby, supporting his hypothesis.[3] 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.[3, 4]
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.[6]
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.[4] 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.[3]
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).[7] Subsequently in 1973, Nakayama introduced the term pigmented cosmetic contact dermatitis for cases that were ascribed to the use of certain cosmetics.
To date, the etiology of Riehl melanosis remains controversial, and although the majority of experts believe it is synonymous with pigmented contact dermatitis, some authors insist that this is an erroneous assumption because the cases reported by Riehl appear to have been related to nutritional alterations that arose during World War I, with no further case reports noted after the war ended, and thereby insist that Riehl melanosis should be classified as a distinct entity.[2, 3, 4, 5] Pigmented contact dermatitis, on the other hand, is caused by an allergic contact dermatitis to a variety of topical and airborne allergens or a lichenoid immune reaction that may be caused by intrinsic or extrinsic factors.[8, 9]
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.[10, 11] 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.[5] Furthermore, Imokawa and Kawai have provided clinical evidence that various allergens implicated in allergic contact dermatitis can stimulate melanogenesis.[12]
A variety of contact allergens have been implicated in pigmented contact dermatitis, as described below.[4, 5, 13] 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.[5, 14, 15]
Textile allergens are as follows:
Cosmetic allergens are as follows[17] :
Fragrance allergens are as follows:
Miscellaneous allergens are as follows:
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.[5, 21] 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.[5]
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.[29]
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.
Although the hyperpigmentation has a tendency to lighten over time and with avoidance of the eliciting agent, some pigmentation may persist.
Because ultraviolet light has been implicated as a contributing factor in some cases of pigmented contact dermatitis, sun avoidance and sunblock usage are prudent. See Sunscreens and Photoprotection for detailed information.
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,[3] 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.[3, 5, 13]
Several case reports published in 2017 describe patients who presented with pigmented contact dermatitis secondary to balsam of Peru and/or fragrances that was associated with reversible alopecia if the trigger was identified early and removed.[23, 24]
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.[5] 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.[3, 5]
The most prominent findings on dermatoscopy and confocal microscopy are pseudonetworks, gray dots/granules, basal layer liquefaction, and pigment incontinence.[30, 31]
Perform closed patch testing with the standard series, cosmetic series, fragrance series, and patient's personal products.
Photo-patch testing may also be warranted.
Provocative use test or repeated open application test (ROAT) is performed when closed patch testing results are equivocal or negative. The concentration of the allergen (eg, preservatives, fragrances) may be too low in the cosmetic series to produce a positive reaction on the back.[5]
Skin biopsy typically is not required unless there is an unusual clinical presentation.
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.
Complete avoidance of the suspected allergen is necessary, and removal of these agents often leads to gradual improvement.
Consider use allergen-free apparel, soaps, and cosmetics
Cosmetic camouflage makeup may be used if the cosmetic disability is distressing to the patient.
Vigilant sun-protection is essential.
Topical treatments are similar to those used to treat melasma and include hydroquinone, retinoids, and azelaic acid. In addition, light chemical peels such as glycolic acid can also be considered.
Other options include intense pulsed-light therapy, Q-switched Nd:YAG lasers, and other lasers with wavelengths that specifically target the hyperpigmentation.[8, 35, 36]
A small study from 2018 used a combination of oral tranexamic acid and a glycyrrhizin compound for 3 months, followed by another 3 months of oral tranexamic acid alone, with marked improvement of the hyperpigmentation in the majority of patients; however, because this study only consisted of 10 patients, further research is needed.[37]
Another small pilot study used a combination of therapies to include low-fluence, 1064-nm, Q-switched Nd:YAG laser, hydroquinone cream, and oral tranexamic acid, with the majority of patients experiencing significant improvement and a few patients having almost complete clearing.[38]
Topical treatments similar to those used to treat melasma may hasten the resolution of the hyperpigmentation, including 2-5% hydroquinone and tretinoin, either on their own or in combination, and azelaic acid.[32]
In addition, pilot studies have shown oral tranexamic acid and compounded glycyrrhizin may also be of benefit.[38, 37]
Lastly, chemical peels and various lasers are alternative treatment options to be used on their own or in combination with the above medical therapies.[32, 38, 37]