eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Erythema Dyschromicum Perstans

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Santiago A Centurion, MD, Staff Physician, Department of Dermatology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey

Updated: Aug 31, 2009

Introduction

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, erythema dyschromicum perstans was called dermatosis ceniciento, meaning ashy dermatosis, because of its ashy bluish gray color. The term erythema dyschromicum perstans 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.

Erythema dyschromicum perstans (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 erythema dyschromicum perstans is unknown, but many consider erythema dyschromicum perstans 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 erythema dyschromicum perstans 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 erythema dyschromicum perstans and avoid school. Chlorothalonil exposure among banana farm workers is another possible cause of erythema dyschromicum perstans.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 erythema dyschromicum perstans.^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

Erythema dyschromicum perstans 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, including in Italy.¹⁰

Mortality/Morbidity

Erythema dyschromicum perstans 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.¹¹ Unlike adult patients, who are most commonly of Hispanic origin, children with erythema dyschromicum perstans are usually white.¹²

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. Erythema dyschromicum perstans 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.

Clinical

History

Erythema dyschromicum perstans has a slow onset and is unlikely to resolve spontaneously.¹¹ The clinical course of childhood (prepubertal) may differ from that of adults; erythema dyschromicum perstans may be more likely to resolve within 2-3 years. A proposed clinical classification has been devised, dividing ashy dermatoses from erythema dyschromicum perstans with the former lacking erythematous borders, and having a third category for simulators such as lichen planus variants, and medication-induced melanodermas.¹³

• Erythema dyschromicum perstans 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.

Ash-colored, partially confluent, macular lesions over the patient's back. Reprint with permission from Cutis 1986; 37: 42-44.

Physical

Erythema dyschromicum perstans 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.

Close-up photograph shows ash-colored macular lesions and lack of an inflammatory border. Reprint with permission from Cutis 1986; 37: 42-44.

Causes

The etiology of erythema dyschromicum perstans 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 erythema dyschromicum perstans has led some authors to suggest environmental factors, but all attempts to find these pollutants have failed.

Differential Diagnoses

Addison Disease
Contact Dermatitis, Allergic
Hemochromatosis
Leprosy
Lichen Planus

Other Problems to Be Considered

• Lichen planus pigmentosus
• Lichen planus–like drug eruption¹⁴
• Atrophic lichen planus
• Tuberculoid leprosy
• 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 erythema dyschromicum perstans, versus brownish and nonconfluent in IEMP.¹⁵
• Drug reaction: Ashy dermatosis–like pigmentation has been described attributed to ethambutol.¹⁶

Workup

Laboratory Studies

• All cases of erythema dyschromicum perstans (EDP), 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 in erythema dyschromicum perstans patients have not shown abnormalities.

Histologic Findings

The biopsy specimen is obtained as much to rule out other diagnoses as to confirm that of erythema dyschromicum perstans because the erythema dyschromicum perstans 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 erythema dyschromicum perstans and 11 with LPP provided clear clinical delineation between the 2 often histologically indistinguishable disorders.¹⁷ LPP has pruritic brownish black macules or patches, with no active border, on the face and the flexor folds. Erythema dyschromicum perstans does not involve mucosal surfaces, where LPP does. In favor of erythema dyschromicum perstans being either a subset of idiopathic lichen planus or a lichenoid drug eruption are reports of lichen planus and erythema dyschromicum perstans occurring in the same patient, the clinical resemblance of erythema dyschromicum perstans to atrophic lichen planus, and similar histologic patterns with immunofluorescence in both erythema dyschromicum perstans and LPP.

The border of an active erythema dyschromicum perstans 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.

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.

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.

Treatment

Medical Care

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.¹⁸

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.¹⁹

Medication

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

Leprostatics

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

Clofazimine (Lamprene)

Lipophilic 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).

Dosing

Adult

<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

Not established

Interactions

Dapsone 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

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Most 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

Dapsone (Avlosulfon)

Bactericidal 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

Dosing

Adult

50-300 mg PO qd

Pediatric

Not established

Interactions

May 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

Contraindications

Documented hypersensitivity; known G-6-PD deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated 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

Complications

• No significant complications have been described in erythema dyschromicum perstans (EDP).
• See Medical Care for complications associated with clofazimine therapy.

Prognosis

• Erythema dyschromicum perstans may persist for years.

Multimedia

Media file 1: Ash-colored, partially confluent, macular lesions over the patient's back. Reprint with permission from Cutis 1986; 37: 42-44.

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.

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.

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.

References

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15. Volz A, Metze D, Bohm M, Bruckner-Tuderman L, Nashan D. Idiopathic eruptive macular pigmentation in a 7-year-old girl: case report and discussion of differences from erythema dyschromicum perstans. Br J Dermatol. Oct 2007;157(4):839-40. [Medline].

16. Srivastava N, Solanki LS, Chand S, Garbyal RS, Singh S. Ashy dermatosis-like pigmentation due to ethambutol. Indian J Dermatol Venereol Leprol. May-Jun 2008;74(3):281-2. [Medline].

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Keywords

erythema dyschromicum perstans, EDP, ashy dermatosis, dermatosis cenicienta, erythema chronicum figuratum melanodermicum, lichen planus

Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Santiago A Centurion, MD, Staff Physician, Department of Dermatology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey
Santiago A Centurion, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

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
Shyam Verma, MBBS, DVD, FAAD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting; Medicis Honoraria Consulting; Celgene Honoraria Consulting

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

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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