Argyria (ISV from Greek: αργύρος argyros silver + -ia) is a disease caused by the ingestion of elemental silver, silver dust or silver compounds. The most dramatic effect of argyria is that the skin is colored blue or bluish-grey. Argyria may be found as generalized argyria or local argyria. Argyrosis is the corresponding condition related to the eye. The condition is believed to be permanent. Most recent cases are due to the over consumption of home made colloidal silver as an alternative medicine.

Since at least the early part of the 20th century, doctors have known that silver or silver compounds can cause some areas of the skin and other body tissues to turn gray or blue-gray. Argyria occurs in people who eat or breathe in silver over a long period (several months to many years). A single exposure to a silver compound may also cause silver to be deposited in the skin and in other parts of the body; however, this is not known to be harmful. It is likely that many exposures to silver are necessary to develop argyria. Once argyria develops, it is believed to be permanent. However, the condition is thought to be only a "cosmetic problem". Most doctors and scientists believe that the discoloration of the skin seen in argyria is the most serious health effect of silver (in small doses).

Reports of cases of argyria suggest that gram amounts (from 2 to 4 grams) of silver or a silver compound taken in medication in small doses over several months may cause argyria in some humans. People who work in factories that manufacture silver can also breathe in silver or its compounds. In the past, some of these workers have become argyric. However, the level of silver in the air and the length of exposure that caused argyria in these workers is not known. It is also not known what level of silver causes breathing problems, lung and throat irritation, or stomach pain in people. Studies in rats show that drinking water containing very large amounts of silver (9.8 grams of silver per U.S. gallon water or 2.6 grams per liter) is likely to be life-threatening.

There is very little information about health effects following skin contact with silver compounds. Argyria that covers the entire body is not seen following skin contact with silver compounds, although the skin may change color where it touches the silver. However, many people who have used skin creams containing silver compounds such as silver nitrate and silver sulfadiazine have not reported health problems from the silver in the medicine. In one animal study, a strong solution of silver nitrate (81 milligrams silver nitrate per liter of water) applied to the skin of guinea pigs for 28 days did not cause the animals to die; however, it did cause the guinea pigs to stop gaining weight normally. It is not known if this would happen to people if they were exposed the same way.

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Lichen planus pigmentosus presenting as diffuse facial melanosis
From Journal of Drugs in Dermatology, 7/1/04 by M.R. Namazi

Abstract

Lichen planus pigmmentosus (LPP), an uncommon variant of lichen planus, has been characterized by hyperpigmented, dark brown macules in sun-exposed areas and flexural folds. In this paper, an unusual case of LPP showing diffuse darkening of the face without the presence of any lichenoid or macular lesion is presented.

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Case Report

A 49-year-old Iranian woman with skin type IV presented with an eight-year history of slowly progressive diffuse darkening of the total face (Figure 1). There was no history of a preceding skin inflammation, and the remaining parts of the skin, including the neck and mucous membranes, were free of lesions. The patient was otherwise healthy and was not taking any medication. The system review was unrevealing. Skin biopsy revealed vacuolar degeneration of the basal cell layer with scarce lymphohistiocytic lichenoid infiltrate, and prominent melanin incontinence extending to the deep dermis. The patient's condition was diagnosed as LPP.

[FIGURE 1 OMITTED]

Discussion

Lichen planus pigmentosus, an uncommon variant of lichen planus, has been characterized by hyperpigmented, dark brown macules in sun-exposed areas and flexural folds (12), without a sex predominance (3). It may or may not be associated with typical LP papules (4). The mucous membranes, palms and soles are usually not involved, but involvement of mucous membranes has been observed (4,5). Exacerbations and remissions during its course are common, and in some cases, are accompanied by itching (6).

This entity, originally reported from India (7), tends to occur in Latin Americans. Middle Easterns and other patients with darker pigmented skin (2). This variant of lichen planus bears significant similarity to ashy dermatosis or erythema dyschromicum perstans and may represent the phenotypic spectrum of lichenoid inflammation in darkly pigmented skin, with ethnic/genetic factors influencing the expression of disease. Erythema dyschromicum perstans may be strongly influenced by environmental agents as well (2).

Occupational dermatosis with hyperpigmentation, especially argyria and caloric melanosis, and drug-related dermatoses, such as fixed drug eruptions or the pigmentary reactions to carbamazepine are the most important differential diagnoses (3). The histopathologic picture of LPP shows an atrophic epidermis with vacuolar degeneration of the basal cell layer. In the dermis, a scarce lymphohistiocytic or lichenoid infiltrate and pigment incontinence with melanophages can be found (8). Lichen planus pigmmentosus has been reported in association with acrokeratosis of Bazex, (9) but whether LPP has a possible paraneoplastic relationship is unclear.

The cause of LPP is unknown. It seems that type hypersensitivity reactions play an important role in its pathogenesis, and the disorder frequently appears in patients on medications (3). The reported case was unusual as it presented with diffuse darkening of the facial skin rather than presenting with macular hyperpigmented lesions or even melasma-like hyperpigmentation.

References

1. Boyd AS, Nelder KH. Lichen planus. J Am Acad Dermatol 1991; 25:593.

2. Daoud MS, Pittelkow MR. Lichen planus. In: Freedberg IM. Eisen AZ. Nolff K. et al. editors. Dermatology in General Medicine. 5th ed. NewYork: McGraw-Hill; 1999:566.

3. Dominguez-Soto L. et al. Pigmentary problems in the tropics. Dermatol Clin 1994 Oct; 12(4):777-784.

4. Black MM. Lichen planus and lichenoid disorders. In: Champion RH, Burton JL, Burns DA, editors. Textbook of Dermatology. 6th ed. Oxford: Blackwell Science Ltd; 1988:1910.

5. Laskaris GC. et al. Lichen planus pigmentosus of the oral mucosa: a rare clinical variety. Dermatologica 1982; 162:61-63.

6. Bhutani LK. Bedi TR. Lichen planus pigmentosus. Dermatologica 1974; 149:43.

7. Weedon D. Strutten G. Skin Pathology. 1st ed. Edinburgh: Churchill-Livingstone; 1999:35.

8. Vega ME, et al. Ashy dermatosis and lichen planus pigmentosus: A clinicopathologic study of 31 cases. Int J dermatol 1992; 30:90.

9. Sassolas B, et al. Lichen planus pigmentosus associated with acrokeratosis of Bazex. Clin Exp Dermatol 1994; 19:70-73.

M R NAMAZI, MD

DERMATOLOGY DEPARTMENT, SHIRAZ UNIVERSITY OF MEDICAL SCIENCES, IRAN

ADDRESS FOR CORRESPONDENCE:

M R Namazi, MD

P.O. Box 71955-687

Shiraz, Iran

E-mail: namazi_mr@yahoo.com

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