Degranulation and shrinkage of dark cells in eccrine glands and elevated serum carcinoembryonic antigen in patients with acquired idiopathic generalized anhidrosis. (20th July 2017)

• Record Type: Journal Article
• Authors: Sano, K.; Asahina, M.; Uehara, T.; Matsumoto, K.; Araki, N.; Okuyama, R.
• Is Part Of: Journal of the European Academy of Dermatology and Venereology. Volume 31:Number 12(2017)
• Page Start: 2097
• Page End: 2103
• Publication Date: 2017-07-20
• Subjects: Dermatology -- Periodicals; Sexually transmitted diseases -- Periodicals; 616.5
• DOI: 10.1111/jdv.14443
• Languages: English
• ISSNs: 0926-9959

Abstract

Abstract: Background: Acquired idiopathic generalized anhidrosis (AIGA) is characterized by anhidrosis/hypohidrosis without other autonomic and neurological dysfunctions. Pathologically, AIGA is considered to usually present no significant morphological alterations in eccrine glands, the secretory portion which consists of clear cells, dark cells, and myoepithelial cells. AIGA patients recently have been reported to show high serum concentrations of carcinoembryonic antigen (CEA). Objective: Our aim is to reveal morphological abnormalities of dark cells and investigate their relationship with serum CEA. Methods: We performed comparative analysis of eccrine glands between sweat‐preserved and non‐sweating skin in four AIGA patients. Serum CEA concentrations in 22 cases with AIGA were measured with healthy volunteers. Furthermore, we semiquantitatively investigated dermcidin, FoxA1 and CEA expression in eccrine glands of 12 cases with AIGA and 5 cases with non‐AIGA. Results: Marked degranulation and shrinkage of dark cells consistently occurred in AIGA. Furthermore, high serum CEA concentrations were found in 14 of 22 AIGA patients (over 60%), but serum CEA levels were not correlated with CEA expression in eccrine glands. Dermcidin expression in dark cells apparently decreased in AIGA patients, severely in those with high serum CEA and moderately in those with low serum CEA, while well‐preserved expression was found in non‐AIGA subjects. Conclusion: Our study suggests morphological damage and molecular dysregulation of dark cells, leading to impairment of their functions in AIGA patients. Severely damaged dark cells correspond to high serum CEA. Accordingly, these pathological changes in eccrine dark cells may be involved in anhidrosis/hypohidrosis of AIGA.