Porokeratosis is related to variable interaction of hereditary factors and additional exogenous factors. An autosomal dominant mode of inheritance with reduced penetrance has been established for porokeratosis of Mibelli, PPPD, and DSP. In genetically predisposed skin, additional factors are assumed to trigger the clinical manifestations. Irradiation with ultraviolet light, organ transplantation, bone marrow transplantation, chronic hepatic failure, renal failure and HIV infection are thought to be triggering factors.
In our patient, there was no family history of porokeratosis and no remarkable medical history except early gastric cancer. Furthermore, the skin lesions suddenly spread all over his body simultaneously with the diagnosis of gastric cancer. Therefore the DSP lesions seem to have occurred as a paraneoplastic phenomenon associated with gastric adenocarcinoma.
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Several cases with rapid extension of DSP have been reported in patients with chemotherapy and bone marrow transplantation, which are associated with immunosuppression. Moreover, DSP are often recognized after hematopoietic malignancies but there are few cases of development of DSP in patients with cancer of visceral organs. Lee et al reported DSP in a patient with cholangiocarcinoma and Takata et al reported hereditary non-polyposis colorectal cancer associated with DSP.
Gastric cancer is very common in Korea, being the leading cancer type accounting for 20.8% of all malignant neoplasms and the second leading cause of cancer deaths. Several risk factors are involved in the development of gastric cancer including diet, gastritis, intestinal metaplasia, and Helicobacter pylori infection. In addition, inactivation of the p53 gene may play an important role in gastric tumorigenesis by loss of suppression of cancer cells. A negative regulator of p53 function, mdm2, is also associated with molecular pathogenesis of gastric cancer. In porokeratosis, too, overexpression of p53, decreased mdm2, and dysregulated cell cycle are pathogeni- cally implicated.
Shumack et al reported that hyperproliferative state of keratinocytes in porokeratosis is influenced by inflammatory mononuclear infiltrate, composed of helper T cells and suppressor T cells, located beneath the epidermis. Soluble factors released by activated T cells may provide a mitotic stimulus for overlying keratinocytes. Gastric cancer cells have been reported to secrete several cytokines including transforming growth factor (TGF)- a, interleukin (IL)-6, and IL-8. Thus, we speculate that these cytokines secreted by gastric cancer cells may play a role in the proliferation of keratinocytes, leading to increase in size and number of DSP lesions.
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This case demonstrates the importance of thorough systemic work-up in patients with sudden appearance of DSP.