Disease relevance of Eccrine Glands

• BACKGROUND: Anhidrosis of the distal lower limbs is a prominent feature of FAP type I. METHODS: Qualitative and morphometric study of amyloid deposition, eccrine glands, and their innervation in nine patients with FAP type I (duration of sensory symptoms, 8.4 +/- 3.9 years [mean +/- SD]; range, 3 to 15 years) and seven control subjects [1].
• BACKGROUND: Nodular hidradenoma is a rare adnexal tumor most likely arising from the eccrine gland [2].
• Two cases of coma-associated bulla with eccrine gland necrosis in patients without drug intoxication [3].
• One eccrine gland adenocarcinoma showed allelic loss of 17p and a Cys 176 Arg mutation in the p53 gene [4].
• Hypertrophic eccrine glands in eccrine angiomatous hamartoma produce gross cystic disease fluid protein 15 [5].

High impact information on Eccrine Glands

• In eccrine glands, MR immunoreactivity was present in the basal cells of excretory ducts, while 11 beta HSD2 immunoreactivity was localized in the luminal cells [6].
• In non-neoplastic skin, VLA-2 and VLA-3 were found in the basal layer, eccrine glands, and cells of the outer root sheath in which VLA-1 was detected [7].
• LL-37 was localized to both the eccrine gland and sweat ductal epithelial cells, whereas dermcidin, a previously described natural antibiotic in sweat, was expressed only in the gland itself [8].
• Immunohistochemistry revealed melanocortin 5 receptor immunoreactivity in the epithelium and appendages, including the sebaceous gland, eccrine glands, and apocrine glands, as well as low level expression in the interfollciular epidermis [9].
• Strong 15-lipoxygenase-2 immunostaining was also observed in secretory cells of apocrine and eccrine glands [10].

Biological context of Eccrine Glands

• These data indicate that plasma aldosterone concentrations decrease following heat acclimation; and eccrine gland responsiveness to aldosterone, as represented by sweat sodium reabsorption, may be augumented through exercise and heat acclimation [11].
• In vitro autoradiography of skin sections using 125I-labelled VIP and PHM, demonstrated binding sites on the membranes of eccrine gland secretory cells [12].
• While normal epidermis and other stratified squamous epithelia reacted strongly with antibodies specific for standard CD44 (CD44S) and CD44 isoforms containing exons v4, v6, and v9, the epithelium of eccrine glands was reactive, often in a polarized distribution, only with antibodies specific for CD44S and isoforms containing exon v9 [13].

Anatomical context of Eccrine Glands

• Antibody to androgen receptor also bound to the coil and ductal cells of eccrine glands, external root sheath of hair follicles, epithelium in the hair bulb, dermal papilla cells, and sebocytes [14].
• A polyclonal chicken antihuman antibody to the melanocortin 5 receptor localized to sebaceous glands, eccrine glands, hair follicles, and epidermis in human skin, rat skin, cultured human sebocytes, and rat preputial cells [15].
• Four of the 5 histochemical markers did recognize specific nonvascular, cutaneous elements: placental alkaline phosphatase stained smooth and striated muscle, cytokeratins 7 and 8 stained eccrine glands, and cytokeratin 17 stained pilosebaceous units [16].
• In normal eccrine and apocrine sweat glands, GCDFP-15, CU18, B72.3, and VU-1D9 staining was localized differently (intracellular, membranous, or intraluminal), whereas eccrine glands showed no B72.3 staining [17].
• After incubation with PNA, in eccrine glands the granules were the only structure labeled, whereas in apocrine glands the luminal side of the plasma membrane and cytoplasmic vesicles beneath it were the only structures labeled [18].

Associations of Eccrine Glands with chemical compounds

• Thus, the strongest 15-lipoxygenase-2 expression is in the androgen regulated secretory cells of sebaceous, apocrine, and eccrine glands [10].
• Effect of isotretinoin on eccrine gland function [19].
• Structural changes in axillary eccrine glands following long-term treatment with aluminium chloride hexahydrate solution [20].
• Following irradiation of the left-hind feet of mice, we measured the ability of the eccrine glands to secrete sweat following stimulation by pilocarpine [21].
• Immunohistochemical localization of cytokeratins in normal eccrine glands, with monoclonal antibodies in routinely processed, formalin-fixed, paraffin-embedded sections [22].

Gene context of Eccrine Glands

• No staining of iNOS or bNOS was observed in the eccrine gland [23].
• Co-expression of CEA-180, NCA-90, and BGP was consistent with differentiation towards the secretory part of eccrine glands or the transitional portion of proximal ducts [24].
• CEA and SP1 stained the secretory and duct-lining cells of normal eccrine glands [25].
• However, a differential expression of CEA and EMA was demonstrated in apocrine epithelia, mucous cells of eccrine glands, and sweat ducts [26].
• Amyloid deposition was observed around eccrine glands in seven of nine patients [1].

Analytical, diagnostic and therapeutic context of Eccrine Glands

• On electron microscopy, no focal destruction and degeneration of eccrine glands or ducts and of Schwann cell processes with or without nerve terminals or unmyelinated axons were observed in relation to adjacent amyloid deposition [1].

References