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Cutaneous endometriosis is defined by the presence of endometrial glands and/or stroma in skin and represents less than 1% of all ectopic endometrium. Cutaneous endometriosis is classified as primary and secondary. Primary cutaneous endometriosis appears without a prior surgical history and secondary cutaneous endometriosis mostly occurs at surgical scar tissue after abdominal operations. The most widely accepted pathogenesis of secondary endometriosis is the iatrogenic implantation of endometrial cells after surgery, such as laparoscopic procedures. However, the pathogenesis of primary endometriosis is still unknown. Umbilical endometriosis is composed only 0.4% to 4.0% of all endometriosis, however, umbilicus is the most common site of primary cutaneous endometriosis. A 38-year-old women presented with solitary 2.5×2.0-cm-sized purple to brown colored painful nodule on the umbilicus since 2 years ago. The patient had no history of surgical procedures. The skin lesion became swollen with spontaneous bleeding during menstruation. The skin lesion was diagnosed as a keloid at private hospital and has been treated with lesional injection of steroid for several times but there was no improvement. Imaging studies showed an enhancing umbilical mass without connection to internal organs. Biopsy specimen showed the several dilated glandular structures in dermis. They were surrounded by endometrial-type stroma and perivascular infiltration of lymphocytes. The patient was diagnosed as primary cutaneous endometriosis and skin lesion was removed by complete wide excision without recurrence. We report an interesting and rare case of primary umbilical endometriosis mistaken for a keloid and review the literatures.

These results showed significantly high Th17 cytokines in both lesion and serum in AA patients, which may highlight a functional role of these cytokines in the pathogenesis of AA.

BackgroundAlopecia areata is marked by autoimmune assault on the hair follicle resulting in hair loss. T helper 17 cell subset has important roles in protecting the host against extracellular pathogens, however, also promotes inflammatory pathology in autoimmune disease, and it expresses both interleukin (IL)-17A and IL-17F, which can signal via the IL-17 receptor A.ObjectiveTo investigate the significance of IL17A and IL17RA gene polymorphisms in the susceptibility to alopecia areata.MethodsWe conducted case-control association study of 238 alopecia areata patients and 270 matched healthy controls. Allele frequency of total 2 single nucleotide polymorphims in the IL17A gene and 4 single nucleotide polymorphims in the IL17RA gene were studied. The statistical analyses were performed according to onset age, the presence of familyhistory, clinical subtypes, and presence of nail involvement or body hair involvement.ResultsOne single nucleotide polymorphim (rs879577) of IL17RA gene showed significant difference between alopecia areata patients group and controls group (p= 0.0288). One single nucleotide polymorphim (rs4819554) of IL17RA gene showed significant difference between the early onset and late onset alopecia areata (p=0.0421).ConclusionIL17RA gene polymorphism might contribute to the increased susceptibility to alopecia areata in Korean population, and IL17RA gene polymorphism may be associated with onset age.

Ceramides are the main lipids in the stratum corneum and are generated during cellular stress and apoptosis by de novo synthesis or by the action of sphingomyelinase. In addition, they are lipid second messengers produced by sphingolipid metabolism and trigger important cell responses, including protein kinase C-alpha (PKC-α) activation and the stimulation of signal transduction pathways with apoptosis and stress-activated protein kinases (SAPK), such as c-jun N-terminal kinase (JNK). Thus, ceramides have anti-proliferative and apoptotic effects. This study measured the changes in the levels of epidermal ceramides and ceramide-related apoptotic signaling molecules in psoriasis patients. Samples from lesional and non-lesional epidermis were obtained from psoriasis patients. Total ceramides were fractionated using thin-layer chromatography, and the levels of PKC-α and JNK expression were measured using Western blot analysis with specific antibodies. The ceramide level was reduced significantly, and this was associated with the downregulation of apoptotic signaling molecules, such as PKC-α and JNK, in the lesional epidermis of psoriasis patients. These results suggest that the decreased level of ceramides downregulates the apoptotic pathway, leading to epidermal proliferation in psoriasis.