Acne is a ubiquitous affliction that can leave physical and emotional scars that can persist throughout the life of the affected individual. Recent studies have substantiated the psychological impact and support a causal, and at times reciprocal, link between acne and the emotional and functional status of the patient. The present article will examine the recent data substantiating the emotional and functional impact of acne on the affected individual. Criteria to identify high-risk patients are provided. High-risk patients are those at increased risk for psychological and functional impairment or self-injurious behavior.

Psoriasis does appear to cause significant psychosocial morbidity. Greater awareness by physicians and more comprehensive treatment addressing these psychosocial components may avert, or at least minimize, some of these negative sequelae.

Psoriasis is a chronic inflammatory hyperproliferative disease of the skin, scalp, nails, and joints. The physical symptoms of psoriasis include itching, irritation, burning/stinging, sensitivity, and pain. Patients also suffer psychological distress, especially as a result of stigmatization, self-consciousness, and embarrassment, which can in turn affect employment and social activities. Relatively high rates of depression are reported in patients with psoriasis. Inflammatory cytokines such as tumor necrosis factor alpha, interferon gamma, and other type 1 cytokines play an important role in the pathogenesis and comorbidities of psoriasis. Data from both animal and human studies suggest that these cytokines are linked to depression. Some psoriasis treatments have demonstrated improvements in symptoms of psoriasis as well as in measures of depression and health-related quality of life. Physicians managing patients with psoriasis must be aware of the psychological effects of psoriasis and need to use a multifaceted approach to managing this disease, focusing on both the physical and psychological aspects.

Central-nervous-system toxoplasmosis developed in 7 of 269 patients with the acquired immunodeficiency syndrome reported to the New York City Health Department through July 1982. Focal neurologic abnormalities, mass lesions on computed-tomographic brain scans, lymphocytic cerebrospinal fluid pleocytosis, and detectable IgG antibody to Toxoplasma gondii were common; but IgG titers of 1:1024 or more, IgM antibody to T. gondii, and positive open brain biopsies were uncommon. Serologic findings suggested that the disease resulted from recrudescent rather than primary infection. Four of five patients improved when treated with sulfonamides and pyrimethamine, but 2 had relapses. An aggressive diagnostic approach and sometimes even empiric therapy are warranted when central-nervous-system toxoplasmosis is suspected in a seropositive patient with the acquired immunodeficiency syndrome.

No abstract