Cutaneous lupus erythematosus (LE) encompasses a group of skin disorders that can present with several clinical presentations like chronic cutaneous lupus erythematosus (that includes localized and generalized discoid LE , hypertrophic LE, tumid LE, and lupus panniculitis), subacute cutaneous LE and acute LE. The etiology of LE is presently unknown, but it is thought both genetic and environmental factors play a role in its development. Among environmental factors involved in LE the most well known are sunlight and several drugs. Previous studies have suggested that smoking might be another factor involved in the pathogenesis of LE.

In a recent study published in the September issue of the Archives of Dermatology, a group of dermatologist from 3 different hospitals in France has studied prospectively the relationship of cigarette smoking and alcohol consumption as risk factors for developing cutaneous LE comparing a series of patients with a control group. 108 patients with LE and 216 controls were included in the study. Of the LE patients there were 48.1% of DLE or disseminated DLE, 24.1% of subacute LE, and 15.7% of acute LE, 6.5% of tumid LE, and 5.6% of SLE with no specific cutaneous lesions. 73.1% of the LE patients were smokers while only 49.5% of the controls smoked (P<.001). There was no difference in alcohol consumption between LE patients and controls. Patients who met ACR criteria for SLE smoked less than those who did not, and those with SLE smoked much less (average 5.5 pack-years), than those who did not met ACR criteria for SLE (average 16 pack-years). In addition, patients who had circulating anti-nDNA were less frequently smokers. Globally, patients with LE with only cutaneous involvement, who did not met ACR criteria for SLE, and had no anti-nDNA antibodies were those who smoked most. On the other hand, those patients who ACR criteria for SLE and had anti-nDNA antibodies were those who smoked the least (compared with other LE patients, and even with controls).

These data suggest that cigarette smoking is strongly associated with cutaneous manifestations of lupus erythematosus. The authors hypothesize that smoking can trigger lupus erythematosus through some of its toxic substances (some may also be contained in drugs known to be associated with lupus erythematosus), a possible phototoxic potential, and/or its effects on the immunologic system. (more…)

Two recent separate studies that have been published on-line in the journal Nature Genetics have identified new genetic risk factors for male-pattern baldness. Both studies have found similar results, and they found that there is a susceptibility locus for male-pattern baldness at chromosome 20p11. These studies add a new candidate gene for androgenetic alopecia. Previous studies had shown that variants in the androgen receptor gene on the X chromosome were associated with androgenetic alopecia. These investigators found that the combination of both gene variants (the one on chromosome X and the new one found in chromosome 20) were present in 1 out of 7 caucasian men, and that this increased seven-fold their risk of having androgenetic alopecia.

The gene on chromosome 20p11 has not been identified but it is probable that it harbors an androgen-independent pathway in androgenetic alopecia that may be the target of future therapies. (more…)

Atopic dermatitis (AD) or atopic eczema is a chronic inflammatory condition that usually begins in childhood. The prevalence of AD has been rising in all industrialized countries during the last decades and it currently affects 10 to 20% of children. Although there is a genetic basis for AD, the underlying causes remain unknown.

In a recent study published in the Archives of Disease in Childhood, a group of Swedish investigators have found that introducing fish in the diet of babies before they are nine months old may cut their risk of developing AD.

The investigators followed the children from a cohort of 8176 families, who were sent a questionnaire about diet and home environment when the children were six months of age. These families were then sent another questionnaire when the child was twelve months of age. 4941 families completed the two questionnaires. The prevalence of eczema was13% at six months, and 20% at twelve month.

Genetic factors were found to be the most important risk factor for developing eczema, as having either the mother or a sibling with eczema doubled the risk of a child to develop eczema. Breast feeding, the age at which dairy products were introduced, and the presence of a furry pet in the home had no detectable influence on eczema. Interestingly, the introduction of fish into the diet before nine months diminished the risk of developing eczema by 25 percent compared with children who never ate it. There was no link with the amount of fish or type of fish. Although one explanation might be that fish is rich in omega-3 fatty acids, the investigators found no differences between children who ate white fish, and those who ate other types of fish richer in omega-3. (more…)

In a recent study published in the Journal of the National Cancer Institute a group of researchers from several centres in the United States have found that a previous history of nonmelanoma skin cancer (NMSC) doubles the risk of another cancer like lung, colon or breast cancer. The authors performed a prospective cohort study using the CLUE II cohort, in Washington County, Maryland, United States. They compared a group of persons with no personal history of NMSC (n = 18405) with a group who had pathologically confirmed NMSC in the past (n = 769) during a 16-year follow-up period. They found that patients with NMSC there was an incidence of cancer of 293.5 per 10 000 person-years, while this incidence was only of 77.8 per 10 000 person-years in those with no history of NMSC. The risk was higher among younger individuals, and it was observed for both basal and squamous cell carcinomas. Site-specific analyses yielded associations that were much stronger for melanoma (RR = 7.94); and similar for lung (RR = 1.92), colorectal (RR = 1.78), and breast (RR = 1.64) cancers; and somewhat weaker for prostate cancer (RR = 1.27).

Therefore NMSC may be a clinical marker of cancer risk. This may be due to an inadequate ability to repair DNA, or alternatively, ultraviolet radiation exposure that causes NMSC may induce some degree of immunosuppression resulting in an increased risk for internal cancers, as well as of NMSC. (more…)