Arsenical Keratosis Clinical Presentation

  • Author: from Memorial Sloan-Kettering - Chih-Shan Jason Chen, MD, PhD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Oct 28, 2010
 

History

Arsenical keratoses, skin hyperpigmentation, and several types of skin cancers, including basal cell carcinoma, squamous cell carcinoma, and Merkel cell carcinoma,[20] are skin lesions characteristic of long-term arsenic exposure. A long latency period (years to decades) occurs before the development of these cutaneous lesions. A study in West Bengal, India, has shown an average latency for skin lesions was 23 years from first exposure to arsenic.[18, 21] Chronic arsenic exposure usually does not cause symptoms, and the skin lesions are usually the first sign to manifest clinically.

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Physical

Arsenical keratoses are usually multiple and typically occur at sites of friction and trauma, especially on the palms and the soles. Keratoses usually manifest as small, punctate, nontender, horny, hard, yellowish, often symmetric, cornlike papules. The diameter of the papule ranges from 0.2-1 cm.

A mild form of the arsenic keratoses may manifest as diffuse thickening or small (< 2 mm) keratoses with sand paper–like texture. Moderate-sized lesions (2-5 mm) may coalesce into larger (>5 mm) verrucous papules or plaques. These lesions are most frequently seen on the thenar and lateral borders of the palms; the base and lateral aspect of the digits; the soles, heels, and toes of the feet, as demonstrated in the image below. Keratoses may also develop on the dorsum of the hands, the arms, and the legs.

Arsenical keratosis on the sole of a carpenter. Arsenical keratosis on the sole of a carpenter.

Another type of arsenical keratosis seen in most patients with arsenical cancers manifests as scaly erythematous or pigmented patches on unexposed body areas.

Mee lines (transverse white bands) on the fingernails are seen in acute and chronic arsenic toxicity.

Other skin manifestations of chronic arsenic toxicity include hyperpigmented and hypopigmented macules on the torso and limbs. The pigmented lesions often present as finely freckled or raindroplike macules distributed bilaterally symmetrically. Diffuse hyperpigmented patches in the intertriginous, genital, and acral areas may be an early sign of chronic arsenic toxicity.

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Causes

A dose-response relationship exists between the amount of arsenic exposure and the frequency of various skin lesions. However, several studies have shown skin lesions that have developed in persons exposed to arsenic at concentrations of less than 50 μg/L. A detail investigation has found that arsenic exposures of greater than 100 μg/L, even 200 μg/L, are the cause of the characteristic skin lesions.[21] Three main categories of sources from which patients might have been exposed to arsenic include medicinal, drinking water (environmental), and occupational hazards.

Medicinal arsenic

Inorganic arsenic has been used in medicine for at least 2500 years, particularly since the 18th century, when it was used to treat a great variety of illnesses (eg, acne, diarrhea, gastric ulcer, asthma, malaria, lupus, psoriasis, neurodermatitis, eczema, rheumatism). During the 19th and early 20th centuries, the most popular preparation in the Western world was called Fowler solution, which contained 1% potassium arsenite. In Asia, Chinese proprietary herbal medicine has been the mainstay of remedies for thousands of years and is still popular in that area; it is also available in the United States. Some of these traditional Chinese medicines have been reported to contain high levels of arsenic.[22, 23, 24]

Drinking water

Studies from endemic areas have found that arsenic-contaminated water (mainly well water) is the source of exposure. Cases of arsenic-induced toxicity have been reported in some endemic areas of Chile, Taiwan, India,[25] Bangladesh, and Mexico. An area on the southwest coast of Taiwan has been referred to as the endemic area of Blackfoot disease (a chronic peripheral vascular disease that may progress into gangrenous changes of the lower extremities). The same area also shows a high prevalence of skin cancer. Both conditions are dose related to high arsenic levels in artesian well water that local residents consume daily. In a Taiwanese study, Morales et al[26] reported the lifetime risk of death is 1 in 100 from consuming 50 μg/L of arsenic in drinking water.

Occupational hazards

Legge reported skin manifestations and lung cancer in sheep dip workers exposed to arsenic as early as 1902. Other reports showed arsenic carcinogenesis in smelter workers, pesticide workers, glass manufacturers, and miners. Burning plywood may cause arsenic-containing fumes to be inhaled. High-tech industries use gallium arsenide to produce semiconductor computer chips.

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Contributor Information and Disclosures
Author

from Memorial Sloan-Kettering - Chih-Shan Jason Chen, MD, PhD  Associate Attending, Dermatology Service, Memorial Sloan-Kettering Cancer Center; Director, Dermatologic Surgery and Mohs Micrographic Surgery Unit, MSK Skin Cancer Center; Chief, Dermatologic Surgery, Northport Veterans Affairs Medical Center

from Memorial Sloan-Kettering - Chih-Shan Jason Chen, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American Society for Dermatologic Surgery, Association of Professors of Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Specialty Editor Board

Daniel J Hogan, MD  Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association

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

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.

Lester F Libow, MD  Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association

Disclosure: Nothing to disclose.

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

Catherine M 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, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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