The treatment of leg ulcers is a common and sometimes difficult problem. They can be costly to treat and are associated with loss of working capacity and sometimes significant morbidity. In the western world, leg ulcers are most frequently caused by venous insufficiency, arterial insufficiency, neuropathy (usually diabetic), or a combination of these factors. The pathogenesis, clinical features, and management of these types of leg ulcers are emphasized in this review.

Humans↗

PubMed1991

Necrobiosis lipoidica.

Necrobiosis lipoidica has distinctive clinical and histopathologic features. Although theories abound, its cause and pathogenesis remain unknown. Despite many reports of effective treatments, a critical review of the literature suggests that none is uniformly effective.

Diagnosis, Differential↗

PubMed1991

Q-switched ruby laser irradiation of normal human skin. Histologic and ultrastructural findings.

The Q-switched ruby laser is used for treatment of tatoos. The effects of Q-switched ruby laser pulses on sun-exposed and sun-protected human skin, as well as senile lentigines, were investigated with clinical observation, light microscopy, and transmission electron microscopy. A pinpricklike sensation occurred at radiant exposures as low as 0.2 J/cm2. Immediate erythema, delayed edema, and immediate whitening occurred with increasing radiant exposure. The threshold for immediate whitening varied inversely with skin pigmentation, ranging from a mean of 1.4 J/cm2 in lentigines to 3.1 J/cm2 in sun-protected skin. Transmission electron microscopy showed immediate alteration of mature melanosomes and nuclei within keratinocytes and melanocytes, but stage I and II melanosomes were unaffected. Histologically, immediate injury was confined to the epidermis. There was minimal inflammatory response 1 day after exposure. After 1 week, subthreshold exposures induced hyperpigmentation, with epidermal hyperplasia and increased melanin staining noted histologically. At higher radiant exposures, hypopigmentation occurred with desquamation of a pigmented scale/crust. All sites returned to normal skin color and texture without scarring within 3 to 6 months. These observations suggest that the human skin response to selective photothermolysis of pigmented cells is similar to that reported in animal models, including low radiant exposure stimulation of melanogenesis and high radiant exposure lethal injury to pigmented epidermal cells.

Adult↗

PubMed1991

Cutaneous manifestations of human immunodeficiency virus infection. Part I.

The prevalence of dermatologic problems during the course of human immunodeficiency virus infection makes knowledge of these skin manifestations imperative to all practicing dermatologists. Detection of early infection is encouraged as effective therapy now exists both to delay the progression of human immunodeficiency virus-induced immunodeficiency and to prevent opportunistic infections. Skin manifestations of human immunodeficiency virus infection discussed in this article include the following groups: neoplastic, ie, Kaposi's sarcoma, lymphoma, and squamous cell carcinoma; infectious, ie, viral, bacterial, fungal, protozoal, and arthropod infestations; and a miscellaneous group including papulosquamous, papular, vascular, autoimmune, oral, and drug-related skin disorders.

Acquired Immunodeficiency Syndrome↗

PubMed1991