Medical scientists from around the world reported on their progress in studies funded by the National Rosacea Society (NRS) to uncover potential causes and other key aspects of the disorder during the fifth annual rosacea research workshop, held in conjunction with the annual meeting of the Society for Investigative Dermatology. The NRS conducts the workshop to promote interest in studying rosacea and to share new information from ongoing studies.
"Some researchers are now looking more deeply into areas where they have had successful results in their initial studies, and others are striking out into new frontiers that have not been investigated before," said Dr. Michael Detmar, associate professor of dermatology at Harvard Medical School and a member of the Society's medical advisory board. "This steadily growing understanding of rosacea should yield important advances in its effective treatment, as well as its potential prevention or cure."
Dr. Youwen Zhou, assistant professor of dermatology, University of British Columbia, and his colleagues are seeking to discover the genetic pathways or individual genes that are related to rosacea. In a study with 14 rosacea skin samples and six normal skin samples, Dr. Zhou and colleagues used a gene scanner to identify 21,000 unique genes for the study, roughly 56 to 60 percent of the total number of genes in the human genome.
Dr. Zhou presented early results showing differences between several genes in normal and rosacea affected skin. He will test the genes in further research.
Another investigator, Dr. Richard Gallo, chief of dermatology, University of California, San Diego, and colleagues concluded that a natural substance that is part of the body's innate immune system appears to have a role in producing the papules (bumps) and pustules (pimples) of rosacea.
He noted that the body produces peptides to defend itself from viruses, fungi and bacteria, and speculates that certain peptides known as cathelicidins may be triggered too easily in rosacea patients. The level of the protective cathelicidins was 200 percent to 300 percent higher in rosacea patients, he found. While many types of bacteria may trigger the formation of cathelicidins, he said, they appear to be particularly sensitive to the bacterium Helicobacter pylori, which has been linked with rosacea in some studies.
The researchers have also noticed that while the peptide is inactive when it is first made on the skin surface, enzymes in sweat cause it to become active. They concluded that cathelicidins may stimulate the production of bumps and pimples in rosacea, possibly in connection with H. pylori and other bacterial triggers.
In a study by Dr. Diane Thiboutot, associate professor of dermatology at Pennsylvania State University, and colleagues of the moisture level, elasticity, skin thickness, extent of photodamage and other characteristics of rosacea skin, investigators found rosacea patients had thicker facial skin than normal subjects, which might be a result of edema (swelling). However, the researchers found no significant difference in skin water loss and elasticity between the 20 rosacea patients and 20 subjects without rosacea.
Their questionnaire revealed that rosacea patients, who are often affected by sun exposure, were more likely to keep the upper body covered from the sun while doing outdoor work and were less likely to have had sunburns that required medical attention. Despite their apparently reduced sun exposure, however, those with rosacea had more visible blood vessels and blood vessels with a larger diameter.
Vascular endothelial growth factor (VEGF), a regulator of blood vessel growth that may be associated with sun exposure, was highly expressed in the sebaceous glands of the rosacea patients, Dr. Thiboutot said. She noted that previous research has found VEGF may be involved in the formation of visible blood vessels in rosacea, and that rosacea patients may therefore be especially sensitive to sunlight.
In an ongoing study, researchers demonstrated that neuropeptides -- substances produced by nerves or other cells in the skin -- and ultraviolet B (UVB) radiation (found in sunlight) appear to induce the expression of VEGF. Dr. Richard Granstein, chairman of dermatology at Cornell University, reported that small amounts of UVB, the type of sunlight that causes sunburn, appear to increase VEGF expression in endothelial cells -- that is, cells that line blood vessels.
In addition, UVB caused an increase in interleukin 8, which plays a role in inflammation. The peptide somatostatin, however, had an inhibiting effect on interleukin and on VEGF production in certain skin cells known as keratinocytes. The relationship to rosacea is still being explored.
Dr. Granstein and his colleagues are now examining the role of adenosine triphosphate (ATP), a substance that serves as an energy source inside cells and is then released by damaged or dying cells, providing what may be a danger signal. They plan to look at this substance under a variety of different conditions and in different concentrations to determine its potential role in rosacea.
Dr. Kevin Kavanagh of the National University of Ireland-Maynooth presented final results of a study that found a potential link between the inflammation of subtype 2 (papulopustular) rosacea and bacteria associated with microscopic mites known as Demodex. These results were reported in the spring 2004 issue of Rosacea Review.