Cutaneous blastomycosis.

We report on a patient with cutaneous blastomycosis and no evidence of systemic involvement. This diagnosis was made on the basis of clinical findings and confirmed by histologic examination and results of culture. The primary lesion in blastomycosis is almost always pulmonary. However, occasionally, as in our patient, the pulmonic focus resolves spontaneously before the patient presents. Disseminated lesions occur most often in the skin, followed by bone, genitourinary tract, and central nervous system. Our patient had an excellent response to ketoconazole without adverse effects.

Gender and dermatology.

Women are the primary focus of dermatologic care in the United States. The awareness of differences in cutaneous biology between the sexes is vital to appropriate diagnosis and treatment of patients. Although research directed at women's health has become a greater priority in recent years, there has been very little gender-specific research in dermatology. This paper reviews the available data pertaining to dissimilarities in male and female cutaneous biology.

Hirsutism: diagnosis and management.

The majority of women with hirsutism have the idiopathic variety characterized by normal circulating androgens. An index of suspicion should, however, be maintained for that subset of women whose hirsutism is indicative of a systemic hormonal aberration. The psychological consequences of this highly visible condition that can seriously impact quality of life substantiate the need for safer and more effective management options. The advent of a topical medication (eflornithine hydrochloride), devoid of systemic side effects, is one positive step toward this goal.

Therapy of sporotrichosis.

Sporotrichosis is a fungal infection caused by the dimorphic organism, Sporothrix schenkii. This etiologic agent typically gains entrance into the skin by traumatic implantation of infected soil or plant materials. The majority of cases are of the fixed cutaneous or lymphangitic cutaneous varieties, and less commonly, hematogenous dissemination to skin or viscera occurs. Untreated, the disease may spontaneously resolve or persist and gradually progress over time, its virulence being less than that of other dimorphic fungi. Potassium iodide remains a favored treatment for uncomplicated cutaneous disease. Amphotericin B, with its high toxicity, has historically been reserved for recalcitrant cutaneous or disseminated disease. Itraconazole, the newest triazole antifungal to become available in the United States, seems to be highly effective against Sporothrix schenkii without significant adverse effects and will likely become the first line therapy for all forms of this disease in the future.

Treatment of human papilloma virus in a 6-month-old infant with imiquimod 5% cream.

A healthy female infant was diagnosed with genital warts at six months of age. She was the product of an uncomplicated vaginal delivery to a mother who was diagnosed with genital warts during the pregnancy, but did not undergo any treatment. The infant's warts were clinically resolved following a three week course of 5% imiquimod cream, an immunomodulating agent that has been demonstrated to be a potent inducer of several cytokines promoting an antiviral cell-mediated immune response.

Androgen physiology and the cutaneous pilosebaceous unit.

Hormones play an important role in cutaneous physiology. The androgen hormones are of particular relevance in modulating hair growth and sebum production in the pilosebaceous unit, which is comprised of the hair follicle and sebaceous gland. Testosterone arising from the circulation is converted peripherally to its more potent, reduced form, dihydrotestosterone, by the enzyme 5 alpha-reductase. Dihydrotestosterone is primarily responsible for androgen receptor binding and exerting end-organ effects. The clinical sequelae of enhanced local androgen production include androgenetic alopecia, hirsutism, and acne. These disorders can be fraught with significant psychosocial ramifications because of their highly visible nature and impact on perceptions of masculinity and femininity.

Cutaneous photosensitivity diseases induced by exogenous agents.

Cutaneous photosensitivity diseases may be idiopathic, produced by endogenous photosensitizers, or associated with exogenous photosensitizers. Those caused by exogenous agents include phototoxicity, photoallergy, and the exacerbation or induction of systemic disorders in which photosensitivity is a prominent clinical manifestation. Phototoxic disorders have a high incidence, whereas photoallergic reactions are much less frequent. The action spectra for most phototoxins and photoallergens lie in the UVA range. Phototoxic and photoallergic reactions can be distinguished on the basis of pathogenesis, clinical characteristics, diagnosis, and management. Drugs capable of causing phototoxic reactions include psoralens, porphyrins, coal tar, antibiotics, and nonsteroidal antiinflammatory agents. Drugs capable of causing photoallergic reactions include topical antimicrobial agents, fragrances, sunscreens, nonsteroidal antiinflammatory agents, plants, and psychiatric medications. Drug-induced systemic diseases in which photosensitivity is a prominent component include drug-induced lupus erythematosus, porphyria, and pellagra.

Tinea capitis: fluconazole in Trichophyton tonsurans infection.

Tinea capitis is the most common dermatophyte infection in children. Trichophyton tonsurans is the most common etiologic agent in the United States, and for more than four decades the standard therapy has been griseofulvin. The availability of newer, and often more effective, antifungal drugs creates the opportunity for choice and the ability to optimally tailor treatment for a particular patient. Fluconazole is an azole antifungal drug available in a pleasant, well-tolerated, liquid formulation ideal for the pediatric population. It has a good safety profile and is approved in the United States for use in children, although not for tinea capitis. We present five patients with tinea capitis successfully treated with fluconazole.

Expression of cytochrome P450 mRNAs in the colon and the rectum in normal human subjects.

The expression of mRNA for three isozymes of cytochrome P450, CYP1A1, 1A2 and 3A3, was examined in biopsied samples of colon and rectum from five healthy subjects. Using RT-PCR, it was possible to detect the three CYP mRNA species at both sites in all samples examined. The expression of each CYP mRNA was site-specific in that rectum had higher levels of CYP1A1 mRNA than colon, while colon had higher levels of CYP3A3 mRNA than in rectum. In contrast, there was no consistent trend in CYP1A2 mRNA expression between the two sites. Variability of alimentary CYP expression may contribute to individual differences in susceptibility to carcinogens and/or drugs.

Terminal hepatic failure in erythropoietic protoporphyria.

Erythropoietic protoporphyria is an inherited disorder characterized biochemically by a deficiency of ferrochelatase, the enzyme that catalyzes the incorporation of ferrous iron into protoporphyrin to form heme. We describe a patient who illustrates the unpredictability of the course of liver disease in erythropoietic protoporphyria. She remained stable for several years after her first evidence of liver function abnormalities. Then, in a period of weeks, hepatic failure developed and she died. Findings of serial liver biopsy specimens showed extensive hepatocellular degeneration and inflammation that appeared in a 10-day period. The factors that cause this rapid deterioration in hepatic function remain unknown. Reported cases of fatal hepatic failure in patients with erythropoietic protoporphyria are reviewed.

Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in North America.

In some, but not all countries, porphyria cutanea tarda (PCT) has been associated with chronic infection with the hepatitis C virus (HCV). Recently, PCT has also been associated with mutations in the HFE gene that are associated with HLA-linked hereditary hemochromatosis. Until now, few studies of these associations have been reported from North America. The aims of this study were: 1) to assess the prevalence of HCV infection and HFE mutations in North American patients with PCT; 2) to compare demographic and laboratory features between those who are HCV-positive and HCV-negative; and 3) to study urinary porphyrin excretions in American HCV-positive patients without clinically manifest PCT. Clinical and laboratory data, including tests for HCV and urinary porphyrins, were collected from 70 unselected patients with typical PCT. Urinary porphyrins were also measured in 110 non-PCT patients with chronic hepatitis C. Mutational analyses of the HFE gene were performed in 26 PCT patients. Thirty-nine of 70 (56%) of the PCT patients had evidence of HCV infection. Thirty-two of 39 PCT patients with HCV were men, all of whom used alcohol. In contrast, 22 of 31 PCT patients without HCV infection were women, 12 of whom had taken estrogens. The HCV-positive group was more likely to have used illicit intravenous drugs (45% vs. 0%; P = 0.01), to have had several (>4) sex partners (48% vs. 13%; P = 0.005), and less likely to have no known risk factors for HCV infection (33% vs. 78%; P = 0.004). Total urinary porphyrin excretion was the same in the two groups, but those with HCV infection had a significantly lower percentage of uroporphyrin and higher percentages of hepta-and hexa-carboxy porphyrins in urine. Sixteen of 110 (15%) HCV-positive subjects without PCT had increased urinary porphyrins, but, unlike PCT, these were mainly coproporphyrin. Forty-two percent of PCT patients carried the C282Y mutation of HFE (15% homozygous), and another 31% carried the H63D mutation (8% homozygous). Thus, 73% of PCT patients had one of these mutations. The prevalence of HCV infection (56%) and mutations in the HFE gene (73%) are high among North American patients with PCT. Alcohol and estrogen use are important additional risk factors. All PCT patients should be tested for HCV infection and for HFE gene mutations. Although HCV infection is a trigger for PCT, preclinical PCT is rare in chronic HCV hepatitis C in the United States.