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Confluent and reticulated papillomatosis (CRP) is a skin disorder which seems to arise due to dysregulation of skin cell turnover. The etiology has been studied for several decades.
Initial suspicion fell upon the presence of Malassezia furfur, a yeast organism, which was thought to induce an abnormal host immune response, precipitating the eruption. The organism is not always seen on skin scrapings for fungi, however. The lack of response to antifungal therapy also led to this theory being dropped.
In 2005, a new actinomycete was isolated from the skin scrapings of a patient with CRP. This confirmed the etiological theory that ascribed the condition to a bacterial infection. This was later cultured and named Dietzia papillomatosis. It is an aerobe, and Gram-positive, but non-acid fast and non-alcohol fast. This new species has been considered the primary pathogen in the causation of CRP since then.
Another interesting approach has been to investigate the connection of CRP with endocrine disease. Many patients with this disease have had diabetes and/or obesity, both of which involve insulin resistance. In support of this idea, much improvement in the metabolic condition has occurred with weight loss and good control of blood glucose levels, and this has led to alleviation of CRP as well. Furthermore, worsening of control is associated with poor lesion control as well. It is thought that high insulin levels in blood lead to increased binding to insulin-like growth factor 1 and a host of other growth factors, including epidermal growth factor and fibroblast growth factor receptor. This binding causes proliferation of epidermal cells with decreased rates of apoptosis. Polycystic ovarian disease and hyperthyroidism have also been seen in some patients with CRP. However, this cannot account for the large number of patients with no metabolic derangement.
Another putative exposure was to ultraviolet light. It was hypothesized that this stimulated temporary epidermal hyperplasia with melanin synthesis, but this has not been experimentally proved. Amyloidosis of the skin has also been proposed as an etiological agent.
While most cases of CRP are sporadic, some familial cases have been reported. There seems to have been an increased level of keratin production within the granulosum cell layer of the epidermis. This is traced to K16 activation, a gene that is linked to other keratin disorders such as palmoplantar keratoderma. Another patient with CRP was found to have partial tetrasomy, or four copies, of the 15q chromosome, a genetic defect that has been found to play a role in dyspigmentation of the skin.
Reviewed by Afsaneh Khetrapal BSc (Hons)