A. Studies have shown that psoriatic plaques and adjacent normal skin usually have the same type of bacteria, but the number of bacteria per square millimeter is higher in the psoriatic plaques. This, in itself, is usually not an increased risk for secondary infections.
Risk is increased when skin and/or plaques or guttate pustules are colonized by the highly invasive Staphylococcus aureus, a species of bacteria capable of causing serious skin and systemic infections.
Risk for secondary infections may also be increased by hard scratching that abrades the skin and opens it to bacterial invasion. Hard scratching should be avoided for this reason, and also because abrasion of the skin can be a trigger for formation of new psoriatic lesions.
A skin hygiene program recommended by a dermatologist is usually adequate to keep bacterial populations in check. Specific anti-bacterial measures may be prescribed by a dermatologist when such measures are warranted.
Symptoms of secondary infection are redness of skin around a psoriatic lesion or increased redness of the lesion, increased warmth in the skin and/or pus in the skin in the area of a lesion. Fever, malaise and light-headedness can be symptoms of more serious, systemic infection.
A. The immunologic dysfunctions that are a major predisposing factor in psoriasis are believed to be the same in all persons regardless of skin color. The patterns of genetic inheritability for the predisposing factors may vary in different groups.
The pigmentation of skin is controlled by hormonal processes that are unrelated to the immune and inflammatory processes that underlie psoriasis. It is interesting to note that all humans, regardless of skin color, have about the same number of melanocytes (pigment-containing cells) at any given site on the skin. Variations in skin color are due to differences in hormonal regulation of pigment formation within the melanocytes, and transfer of the pigment from melanocytes to keratinocytes (the cells that make up the majority of the outer layer of skin). A principal hormone in the regulation of human skin color is melanocyte-stimulating hormone (MSH).
The incidence of psoriasis is much lower in dark-skinned West Africans and African-Americans than in light-skinned people of European ancestry. Incidence is also low in Japanese and Eskimos, and is extremely low to non-existent in Native Americans in both North and South America. The reasons for this epidemiologic disparity are not known, but are believed to involve genetic, geographic and environmental factors.
The treatment of psoriasis in African-Americans is largely the same as treatment in light-skinned patients. An adjustment is therapy is made in the use of photochemotherapy (PUVA) and phototherapy . In PUVA, both the chemical photosensitizer and the ultraviolet dose are adjusted for skin type and pigmentation.
A. Parakeratosis is a word you may have come across when you read about psoriasis, especially plaque-type psoriasis. It is a term that describes the process by which psoriatic skin continuously forms and scales off.
In normal skin, the outer layer, made up mostly of cells called keratinocytes, is replaced every 27 to 28 days with newly formed keratinocytes. The replacement usually occurs without a person noticing it; if it takes place unusually quickly or in unusual amounts, we may notice flakes and scales on our skin, clothing, bedding, etc.
In psoriasis, the process of keratinocyte production is sped up. New keratinocytes are formed and moved upward to the skin surface faster than they can be incorporated into skin. Some are moved upward so fast that they are not yet mature cells. The keratinocytes accumulate and are scaled off. Parakeratosis is the word used to describe the entire process.
Psoriatic plaque has other features also, including inflammatory cells and dilated small blood vessels that contribute to both the appearance and the symptoms of a psoriatic lesion.