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AUTHOR AND EDITOR INFORMATION

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Author: Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School

Robert A Schwartz is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Coauthor(s): Santiago A Centurion, MD, Staff Physician, Department of Dermatology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey

Editors: Shyam Verma, MBBS, DVD, FAAD, Adjunct Clinical Assistant Professor, Department of Dermatology, University of Virginia, State University of New York at Stonybrook, Penn State University; Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center; Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center

Author and Editor Disclosure

Synonyms and related keywords: EDP, ashy dermatosis, dermatosis cenicienta, erythema chronicum figuratum melanodermicum, lichen planus

INTRODUCTION

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Background

C. Oswaldo Ramirez of San Salvador, El Salvador, first described erythema dyschromicum perstans (EDP) in 1957.1 He called the patients with this eruption Los cenicientos, meaning the ashen ones. The Spanish term cenicienta also means Cinderella because of this folklore character's close association with ashes from sitting at home alone by the fireplace. Later, EDP was called dermatosis ceniciento, meaning ashy dermatosis, because of its ashy bluish gray color. The term EDP is credited to Marion B. Sulzberger, who suggested it when examining Convit's2 patients in Caracas. Sulzberger's comment, in discussion of another paper, is as follows:

... the narrow red border (which is often hard to find), represents the active lesions. This is why I suggested a name which contains the term "erythema" and which also suggests the variety and persistence of the final dyschromias.

The descriptive term ashy dermatosis was also used as a designation for their coloration. In South America, another name, erythema chronicum figuratum melanodermicum, is also used.

EDP (ashy dermatosis) is a distinct and somewhat controversial cutaneous eruption that may be best regarded as a form of lichen planus or lichen planus actinicus (see Lichen Planus).3, 4, 5

Pathophysiology

The etiology of EDP is unknown, but many consider EDP to be a variant of lichen planus actinicus. A variety of predisposing factors have been cited. These include ingestion of ammonium nitrite, an intestinal parasitosis caused by nematodes (whipworm infection, control of which produced EDP remission), orally administered radiographic contrast media, and, possibly, an occupationally associated cobalt allergy in a plumber. One case may be particularly revealing, that of a 13-year-old rural northern European truant who repeatedly ingested small amounts of a fertilizer, ammonium nitrate, to induce EDP and avoid school. Chlorothalonil exposure among banana farm workers is another possible cause of EDP.6

An abnormality in cell-mediated immunity might play a role. However, substantial immune dysfunction is limited at present to 1 report of an HIV-seropositive 41-year-old homosexual of Chinese lineage with EDP.7, 8

HLA-DR association with the genetic susceptibility to develop ashy dermatosis in Mexican Mestizo patients was analyzed, the results of which were reported by Correa in 2007.9 The most frequent allele was HLA-DR4 (65%), an impressive association because, in controls, it was seen in only 23%. Thus, although many factors may be involved, an important genetic susceptibility appears to be conferred by genes located within the major histocompatibility complex region.

Frequency

International

EDP is most common in Latin America and Asia; most of the cases occur in El Salvador where the first case was identified. Cases in Europe have also been described.

Mortality/Morbidity

EDP has a benign outcome, with most complaints relating to cosmetic issues.

Race

Darker-skinned individuals seem to be affected more often than lighter-skinned individuals. It is a rare disorder of pigmentation that is most common in Hispanic patients.10 Unlike adult patients, who are most commonly of Hispanic origin, children with EDP are usually white.11

Sex

Both sexes are affected, but women are affected more often than men.

Age

The age range affected is wide, both in Latin America and around the world. EDP has been observed in children aged 1 year and adults aged 80 years. For example, a 6-year-old British girl and 4 Finnish children aged 8-12 years were described, as were many older patients. An early report had a series of 5 patients; 3 males aged 11-36 years and 2 women.

The Medscape Pediatric Dermatology Resource Center may be of interest.


CLINICAL

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History

EDP has a slow onset and is unlikely to resolve spontaneously.10 The clinical course of childhood (prepubertal) may differ from that of adults; EDP may be more likely to resolve within 2-3 years.

  • EDP is an asymptomatic eruption of oval, polycyclic, or irregularly shaped, gray-blue hyperpigmented macules on the trunk, the arms, the face, and the neck.
  • It begins as ash-colored macules, sometimes with an erythematous or elevated border (see Media File 1).
  • No systemic symptoms or associations exist.

Physical

  • EDP has asymptomatic, gray-blue hyperpigmented patches of variable shape and size and an elevated erythematous border in the early stages (see Media File 2).
  • The eruption is symmetrically distributed on the face, the trunk, and the upper extremities. The oral cavity and the genitals are spared.

Causes

The etiology of EDP remains unknown.

  • It has been associated with ingestion of ammonium nitrate and whipworm infestation, but a specific etiology has not been established in any instance.
  • The geographical distribution of the disease has led some authors to suggest environmental factors, but all attempts to find these pollutants have failed.


DIFFERENTIALS

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Addison Disease
Contact Dermatitis, Allergic
Hemochromatosis
Leprosy
Lichen Planus

Other Problems to be Considered

  • Lichen planus pigmentosus
  • Lichen planus–like drug eruption12: See Drug Eruptions. 
  • Atrophic lichen planus
  • Tuberculoid leprosy
  • Pinta: See Pinta.
  • Idiopathic eruptive macular pigmentation (IEMP): This is a rare disease that can be distinguished by different clinical appearance of the macules: gray with an erythematous border and possibly confluent in EDP, versus brownish and nonconfluent in IEMP.13


WORKUP

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Lab Studies

  • All cases, to date, have resulted in negative laboratory study results, which include the following:
    • Bacterial, viral, and mycologic cultures
    • Erythrocyte sedimentation rate
    • Glucose studies
    • Liver function test
    • Urinalysis

Imaging Studies

  • Radiographic studies have not shown abnormalities.

Histologic Findings

The biopsy specimen is obtained as much to rule out other diagnoses as to confirm that of EDP because the EDP histologic pattern is relatively nonspecific. One should attempt to obtain a biopsy sample of the border of an active macule, which usually demonstrates mild basal cell layer vacuolar degeneration overlying an upper dermis with a mild perivascular mononuclear cell infiltrate and increased melanophages.

Distinguishing ashy dermatosis from lichen planus pigmentosus (LPP) is not always easy. A Mexican study of 20 patients with EDP and 11 with LPP provided clear clinical delineation between the 2 often histologically indistinguishable disorders.14 LPP has pruritic brownish black macules or patches, with no active border, on the face and the flexor folds. EDP does not involve mucosal surfaces, where LPP does. In favor of EDP being either a subset of idiopathic lichen planus or a lichenoid drug eruption are reports of LP and EDP occurring in the same patient, the clinical resemblance of EDP to atrophic LP, and similar histologic patterns with immunofluorescence in both EDP and LPP.

The border of an active EDP lesion and the border of an LPP lesion often both show hyperkeratosis, a thinned epidermis, hydropic degeneration of the basal layer, pigment incontinence, and a perivascular lymphohistiocytic infiltrate (see Media Files 3-4). Colloid bodies are occasionally seen in both.

Immunopathologic study of EDP shows immune-associated (Ia) antigen expression in keratinocytes and strong OKT 4 and OKT 6 staining of Langerhans cells. It also shows dermal infiltration by T lymphocytes of both helper-inducer and suppressor-cytotoxic phenotypes, a pattern commonly seen with lichen planus. CD36 expression is evident in the viable upper epidermis on lesional keratinocytes, which may imply a delayed hypersensitivity reaction. Beneath, in the dermis, the cellular infiltrate has been found to express CD69 and the cytotoxic cell marker CD94. In addition, as with lichen planus, the colloid bodies stained immunoglobulin G positive.


TREATMENT

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Medical Care

Many therapeutic options are available, but few have been effective, except for clofazimine. In one series of 8 patients, 7 had a good or excellent response to clofazimine administered either 100 mg every other day to patients weighing less than 40 kg or 100 mg every day to patients weighing more than 40 kg. This medication was continued for 3 months, then reduced to 200 mg/wk and 400 mg/wk, respectively. The one remaining patient had only a marginal response. One study found some improvement in early cases, but no cures were reported. This medication seems to have a valuable effect on the inflammatory phase of EDP.

Clofazimine is a lipophilic rhimophenazine dye with both antimicrobial and anti-inflammatory properties originally developed to treat tuberculosis. Although its mechanism of action is unclear, it seems to exert its main effect upon neutrophils and monocytes in a variety of ways, such as stimulating phagocytosis and release of lysosomal enzymes.15

Clofazimine is administered orally, with improved bioavailability when taken with food. It concentrates in lipid-rich tissues, including the reticuloendothelial system, the intestine, the breasts, and the liver. Its half-life is 70 days. Isoniazid increases its serum levels and enhances its urinary excretion. Its most common adverse effects are in the skin, the gut, and the eye. It gives a temporary orange discoloration of the skin and the eye (ie, cornea, conjunctivae); it also may produce ichthyosis. Its most serious adverse effect is crystal deposition in the gut that produces a potentially fatal enteropathy. This rare complication is associated with months of high-dose (>100 mg/d) therapy. Nausea and diarrhea are more common. Splenic infarction and eosinophilic enteritis are also rare adverse effects.

Many other therapeutic modalities have been attempted, none with satisfactory results. These include ultraviolet exposure, ultraviolet avoidance, antibiotics, antihistamines, griseofulvin, chemical peels, antibiotics, corticosteroids, vitamins, isoniazid, chloroquine, and psychotherapy.

A patient from Turkey was described to have responded remarkably well to treatment with dapsone.16


MEDICATION

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The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Leprostatics

Have both antimicrobial properties and anti-inflammatory properties. They were originally developed to treat tuberculosis.

Drug NameClofazimine (Lamprene)
DescriptionLipophilic rhimophenazine dye with antimicrobial and anti-inflammatory properties originally developed to treat tuberculosis. Inhibits mycobacterial growth, binds preferentially to mycobacterial DNA. Has antimicrobial properties, but mechanism of action unknown.
Although its mechanism of action is unclear, it seems to exert its main effect upon neutrophils and monocytes in a variety of ways (eg, stimulating phagocytosis and release of lysosomal enzymes).
Adult Dose<40 kg: 100 mg PO qod; continue for 3 mo then reduce to 200 mg/wk
>40 kg: 100 mg PO qd; continue for 3 mo then reduce to 400 mg/wk
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsDapsone may inhibit anti-inflammatory activity; avoid concurrent administration of clofazimine with aluminum-magnesium-containing antacids due to decreased absorption; concurrent use of phenytoin and clofazimine may result in reduced phenytoin efficacy; concurrent administration of small quantities of orange juice with clofazimine may result in modest reduction of clofazimine relative bioavailability
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMost noticeable adverse effect is skin discoloration (red to purple-black), which fades slowly on withdrawal; secretions discolored; urine becomes red; ichthyosis of shins and forearms may be prominent
Adverse effects include liver disease, stomach or intestinal disease, and skin problems (instruct patients to inform health care provider as soon as possible if symptoms develop); bleeding in the digestive system (symptoms may include blood in stools, black tarry stools, vomiting blood, and vomit that looks like coffee grounds); intestinal obstruction (symptoms may include abdominal pain and cramping, vomiting blood, abdominal distention, and diarrhea); liver damage (symptoms may include abdominal pain for more than a few days, dark urine, fatigue, general discomfort, uneasiness or ill feeling [malaise], loss of appetite, pale or clay-colored stools, and yellow eyes or skin); doses >100 mg/d should only be given for as short a period as possible and only under close medical supervision
Severe abdominal symptoms with rare reports of splenic infarction, bowel obstruction, and GI bleeding; autopsy reveals crystalline deposits of clofazimine in tissues, including intestinal mucosa, spleen, liver, and mesenteric lymph nodes

Drug NameDapsone (Avlosulfon)
DescriptionBactericidal and bacteriostatic against mycobacteria; mechanism of action is similar to that of sulfonamides, in which competitive antagonists of PABA prevent formation of folic acid, inhibiting bacterial growth
Adult Dose50-300 mg PO qd
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; known G-6-PD deficiency
InteractionsMay inhibit anti-inflammatory effects of clofazimine; hematologic reactions may increase with folic acid antagonists, eg, pyrimethamine (monitor for agranulocytosis during second and third months of therapy); probenecid increases toxicity; trimethoprim with dapsone may increase toxicity of both drugs; because of increased renal clearance, levels may significantly decrease when administered concurrently with rifampin
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsAssociated with a variety of systemic toxicities, including agranulocytosis, anemia, methemoglobinemia, hepatitis, and neuropathy; patients may experience headache and/or GI distress on initiation of therapy; perform weekly blood counts (first mo), then monthly WBC counts (6 mo), then semiannual WBC counts; discontinue if a significant reduction in platelets, leukocytes, or hematopoiesis occurs; caution in methemoglobin reductase deficiency, G-6-PD deficiency, or hemoglobin M because of high risk for hemolysis and Heinz body formation; caution in patients exposed to other agents or conditions (eg, infection, diabetic ketosis) capable of producing hemolysis; peripheral neuropathy can occur (rare); phototoxicity may occur when exposed to UV light; pancreatitis may occur; various forms of renal complications including acute renal failure, acute tubular necrosis, and oliguria have occurred with dapsone use


FOLLOW-UP

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Complications

  • No significant complications have been described.
  • See Medical Care for complications associated with clofazimine therapy.

Prognosis

  • EDP may persist for years.


MULTIMEDIA

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Media file 1:  Ash-colored, partially confluent, macular lesions over the patient's back. Reprint with permission from Cutis 1986; 37: 42-44.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo

Media file 2:  Close-up photograph shows ash-colored macular lesions and lack of an inflammatory border. Reprint with permission from Cutis 1986; 37: 42-44.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo

Media file 3:  Photomicrograph of a lesion on the patient's back shows slight basilar vacuolar change, extensive pigment incontinence, dilatation of dermal lymphatics, and lack of inflammation (hematoxylin & eosin, original magnification X24.8). Reprint with permission from Cutis 1986; 37: 42-44.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo

Media file 4:  Higher-power photograph shows slight vacuolar basilar change, marked dilatation of intradermal lymphatics, incontinence of melanin pigment, and lack of inflammation (hematoxylin & eosin, original magnification X238). Reprint with permission from Cutis 1986; 37: 42-44.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Photo


REFERENCES

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Erythema Dyschromicum Perstans excerpt

Article Last Updated: May 20, 2008