Sweat gland (eccrine, apocrine, apoeccrine) carcinomas are exceedingly rare, arise most frequently in the skin of the head and neck or the extremities, and manifest as painless papules or nodules that grow slowly. From: Clinical Radiation
Oncology (Fourth Edition), 2016
Krzysztof Kobielak, ... Yvonne Leung, in
Translational Regenerative Medicine, 2015 Sweat glands are coiled
tubular structures vital for regulating human body temperature. Humans have three different types of sweat glands: eccrine, apocrine, and apoeccrine. Eccrine sweat glands are abundantly distributed all over the skin and mainly secrete water and electrolytes through the surface of the skin. Apocrine glands secrete oily substances containing lipids, proteins, and steroids through hair canals and are found only in skin containing hair (restricted
to the armpits, mammary, anal, and genital areas) [189,190]. Rather than responding to temperature, apocrine glands often respond to emotional stimuli including anxiety and fear. Under these circumstances, sweating is often observed in the armpits, palms, and soles of the feet [191–193]. For decades it was believed that these are the only two types of sweat glands. In 1987, however, apoeccrine glands were identified in areas of apocrine glands but secreted watery fluids
similar to eccrine glands [194]. Unlike humans, animals such as dogs and mice have sweat glands only in their paws because they have evolved a different method of thermoregulation, namely panting. In these animals, sweat glands are present in the paws to provide friction for running and climbing. For the purposes of this chapter, we focus only on eccrine sweat glands, referring to them hereafter as “sweat glands.” In humans, roughly 1.6 to
5 million sweat glands are found in the skin, and the amount varies between individuals as well as anatomic sites [195]. The region with greatest sweat gland density is the palms and soles of the feet, which contain 600–700 sweat glands/cm2 [195]. The primary function of sweat glands is to keep the core body temperature at approximately 37 °C by releasing sweat in a hot environment or during physical activity [189,195]. Sweat
glands are innervated by neurons, so the process of sweating is controlled by the central nervous system. Thermosensitive neurons in the brain can detect the internal body temperature and external skin temperature, instructing sweat glands to respond accordingly to maintain a constant core body temperature [189,195]. When an increase in temperature is detected, sweat is induced to cool the skin, and internal body temperature decreases when the sweat evaporates from the surface of
the skin. Therefore, sweat glands are essential in keeping the body temperature constant. A core body temperature higher than 40 °C can result in protein denaturation and apoptosis [189]. Physically, it can lead to hyperthermia, commonly known as heat exhaustion or heat stroke, which can be fatal. Sweat is a dilute electrolyte solution composed of 99% water, sodium chloride, potassium, bicarbonate, calcium, magnesium, lactate, ammonia, and
urea [196]. During sweating, some of the ions are reabsorbed through Na+/K+ ATPases on the membrane of the sweat duct [189,195]. In addition to Na+/K+ pumps, chloride channels also are found in sweat glands. Sweat glands consist of a coiled acinar secretory structure in the dermis and a straight duct that connects this acinar structure to the surface of the epidermis (Figure
4). This acinar secretory coil contains a basal layer composed of two distinct cell types, clear cells and myoepithelial cells, as well as a luminal layer composed of dark cells [5] (Figure 4). These dark cells secrete glycoproteins that can be identified with periodic acid Schiff (PAS) staining. In the basal layer, clear cells are rich in mitochondria and contain basolateral infoldings where water and ions are secreted. This sweat subsequently travels through
small intercellular canals to reach the lumen and through the sweat duct to be secreted at the skin surface [5]. Myoepithelial cells are located at the periphery of sweat glands and are believed to provide support for the sweat gland structure (Figure 4). Sweat gland disorders range from
excessive sweating (hyperhidrosis) and decreased sweating (hypohidrosis) to no sweating (anhidrosis). While hyperhidrosis is generally not a serious condition, anhidrosis can lead to death from hyperthermia. Patients with hypohidrosis or anhidrosis often display symptoms of heat intolerance that may lead to fatigue, weakness, dizziness, and difficulty breathing. Hyperhidrosis most commonly affects the armpits, palms, and soles of the feet [197]. Depending on its severity,
hyperhidrosis can be treated with topical aluminum salts or anticholinergic oral medications [198]. Hypohidrosis and anhidrosis are commonly caused by obstruction of sweat pores and ducts, as seen in patients with psoriasis, dermatitis, sclerosis, and miliaria. Some patients with miliaria, also known as a sweat rash, feel a stinging sensation in the affected areas caused by sweat retention from the ductal occlusion [198]. In some
cases, controlling the temperature and humidity of the environment to reduce sweating can relieve the obstruction. Hypohidrosis and anhidrosis may also be caused by dysfunctional sweat glands, as in Fabry’s disease of systemic sclerosis or absent sweat glands in anhidrotic ectodermal dysplasia [198,199]. Anhidrotic ectodermal dysplasia is a dermatological disorder that affects multiple skin appendages, including sweat glands [200]. It is caused by a mutation in the
ED1 gene-encoding ectodysplasin-A (EDA) ligand, its EDA receptor, or EDARDD adaptor protein, and can be life threatening for children because of their inability to sweat [201–203]. Hypohidrosis may also result from injuries caused by burns, irradiation, and trauma that damage sweat glands. In general, all these conditions vary in severity and can either be localized to a specific region of the body or more globally affect a patient. Hyperhidrosis,
hypohidrosis, or anhidrosis may often be associated with more serious underlying diseases and processes. For instance, people undergoing anxiety, menopause, or drug withdrawal often experience excessive sweating. Because sweat glands are innervated by neurons, diseases affecting the central nervous system (such as Parkinson’s disease) or spinal cord often cause abnormal sweating [204,205]. During wound healing, HF SCs can migrate up to the epidermis to help re-epithelialize the skin [11]. Although human skin contains both HFs and sweat glands in most regions of the body, certain areas such as the palms and soles only contain sweat glands and do not have any hair. Thus, there is great interest in the ability of sweat glands to participate in epidermal wound healing, especially in areas lacking HFs. The first experiment
to test their epidermal regenerative potential was performed by Miller et al. [206], who generated wounds on porcine skin, which is very similar to human skin. Deep wounds were generated to remove HFs along with the epidermis, and because sweat glands reside deeper in the dermis, they occasional remained. Interestingly, although shallow wounds containing HFs healed faster, the deep wounds also re-epithelialized in the absence of HFs. This newly formed skin over the deep
wounds was distinctly different from the surrounding skin and did not contain any HFs [206]. Thus, one possible explanation was that cells from the remaining sweat glands migrated up to re-epithelialize the epidermis in the absence of HFs. In an independent study, a skin graft generated from human sweat gland cells formed a fully stratified epidermis when transplanted onto the back of an immunocompromised rat [207]. Furthermore, sweat gland cells have been shown to
contribute to wound healing of human skin [208]. Taken together, these reports suggest that sweat gland cells also have the potential to differentiate into cells of the epidermis and contribute to wound healing after injury. However, which sweat gland cells have this potential and whether they are the SCs that maintain the normal homeostasis of this appendage remain unclear. Lu et al. [17] recently reported the presence of unipotent SCs in adult sweat glands located in the basal and luminal layers. Upon injury, the unipotent sweat gland SCs located in the luminal and basal layers of the glandular region become activated to replenish their respective layers and therefore restore sweat function. Similar to the quiescent
characteristic of HF SCs in the bulge, myoepithelial sweat gland cells localized in the acinar basal layer are also slow-cycling LRCs that have the potential to regenerate skin under favorable conditions [17,18]. Interestingly, however, these cells of the acinar (glandular) region do not respond to shallow epidermal scrape wounds. Instead, sweat duct cells become activated to re-epithelialize the epidermis in conjunction with surrounding basal layer epidermal SCs. These sweat
duct cells were likely activated over the glandular cells because of their close proximity to the wound and epidermis, serving as a first line of defense. It was speculated that deeper wounds may subsequently activate the sweat gland SCs of the glandular region. Indeed, recent transplantation studies have demonstrated that basal layer sweat gland cells, including slow-cycling myoepithelial sweat gland SCs, can contribute and differentiate into the various layers of the stratified epidermis in
addition to the de novo formation of sweat glands, further highlighting their SC characteristics [17,18] (Figure 4). Moreover, its fate is partially influenced by the surrounding environment. For example, transplantation of these sweat gland myoepithelial cells into cleared mammary fat pads of lactating mice results in the formation of mammary gland-like structures in addition to sweat glands [17]. Although
unpurified, transplantation of sweat gland cells together with newborn dermal fibroblasts has shown that they are able to form HFs [18]. Taken together, recent reports of sweat gland SCs have shown their ability to differentiate into various components of the skin, including the epidermis, sweat gland or even mammary gland and HF, highlighting its potential in regenerative wound healing of the skin.Skin and Skin Appendage Regeneration
IV Sweat Gland
Structure and Function
Sweat Gland Disorders
Sweat Glands in Wound Healing
Sweat Gland Stem Cells and Their Multipotency in
Regeneration of the Epidermis, Sweat Glands, and Hair Follicles
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The Epithelial Stem Cell Niche in Skin
Géraldine Guasch, in Biology and Engineering of Stem Cell Niches, 2017
2.4 Stem Cells in the Sweat Gland
Sweat glands are eccrine glands which excrete directly to the surface of the interfollicular epidermis. They develop over most of the human body at approximately 5 months of fetal gestation in human and in mouse, sweat buds emerge just before birth (embryonic day E17.5). Sweat glands have a coiled tubular structure and are crucial for thermoregulation (Fig. 9.5). This coiled tubular structure represents the secretory part of the gland and contains an outer basal layer of myoepithelial cells (that expresses K5, K14, smooth muscle actin, and integrins α6 and β1) and an inner layer of luminal cells (positive for K8, K18, and K19). Sweat glands do undergo little renewal compared to other glands and until recently it was unclear if stem cells were present in this appendage.
Figure 9.5. Compartmentalization of the sweat gland.
The sweat gland can be divided into three distinct regions: the sweat gland that represents the coiled secretory part located deeper in the skin, the sweat duct, and the epidermal duct or acrosyringium that give rise to the surface pore. The secretory part of the sweat gland contains myoepithelial and luminal cells. Sma, smooth muscle actin; α6hi or α6med, integrin α6 with high or medium level of expression; β1hi or β1med, integrin β1 with high or medium level of expression; K14hi or K14low, keratin 14 expression at high or low level.
Using the K5-TetVP16 x TRE-H2BGFP mouse model13 and pulse-chase studies as described previously (Section 2.2.1), three types of adult unipotent progenitors within the sweat gland and its duct have been identified.70 Each of these three populations derive from a common multipotent K14+ sweat bud progenitor that can differentiate into myoepithelial cells, form the suprabasal layer of luminal cells, and respond distinctly to different types of skin injuries. Ductal progenitors can respond to a wound injury but the luminal and myoepithelial cells from the gland compartment cannot. These populations vary also in their plasticity potential when placed in foreign environments. Ductal and myoepithelial progenitors, but not luminal cells, can make functional sweat glands when placed into the mammary fat pads of nonlactating recipients and can only generate epidermis when transplanted into the backskin. This highlights the importance of the microenvironment on the cell fate specification of stem cells from sweat duct and sweat gland.
Both normal development of eccrine sweat glands and hypohidrotic ectodermal dysplasia (deficiency of sweat glands and other ectodermal appendages) have been associated with cellular signaling through ectodysplasin A (EDA), the EDA receptor (EDAR), and the Wnt pathway.71 As both sebaceous and sweat glands are found in the epidermis where their activities can have a profound effect on tissue homeostasis, they share a similar tissue microenvironment that may regulate their development and regulation. It is likely that there is molecular cross talk between these appendages and the surrounding dermal tissue.
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Cutaneous Autonomic Innervation
Christopher H. Gibbons, Roy Freeman, in Primer on the Autonomic Nervous System (Third Edition), 2012
Sweat Glands
Sweat glands are tubular structures located within the deeper dermal tissue that contain a rich network of capillaries and nerve fibers. The investigation of sweat gland innervation began simultaneously to the initial studies of cutaneous epidermal nociceptive C-fibers using skin biopsies [1]. Recently, the widespread availability of skin biopsies for evaluation of intra-epidermal sensory nerve fiber density combined with scientific advances in quantitative immunohistochemistry staining of specific neuronal subtypes have extended the utility of studies of sudomotor innervation [2]. Clinical skin biopsies can be stained with the pan-axonal marker protein gene product (PGP) 9.5 and imaged by light microscopy to highlight the nerve fibers that surround the sweat gland tubules [2,3]. The nerve fibers that surround sweat gland tubules are primarily sympathetic cholinergic (Fig. 85.2A,C), although some sympathetic adrenergic and sensory fibers are present (Fig. 85.2D). In addition to a dense network of nerve fibers, there are also a large number of capillaries within sweat glands that have separate innervation (Fig. 85.2B).
Figure 85.2. Sweat glands. In (A), a sweat gland (green) with accompanying innervation is seen. The red/gold nerve fibers are stained by from PGP 9.5, a pan-axonal marker, showing the innervation around the sweat gland. In (B), the vascular system through a typical skin biopsy is shown. The blood vessels (shown in green) are stained by the endothelial marker CD31. The sweat gland tubules are shown as a faint green, and are much larger than the blood vessels. The nerve fibers, shown in red, are stained with the pan-axonal marker PGP 9.5. In (C), the sympathetic cholinergic innervation (green) stained with vasoactive intestinal peptide is seen. In (D), the same sweat gland as (C) is shown, but the fibers are stained with tyrosine hydroxylase, a sympathetic adrenergic marker. Note that very little of the total innervation of the sweat gland has adrenergic innervation. White scale bars at the bottom of each image indicate 100 μm.
The complexity of sweat gland innervation limits the utility of descriptive and semi-quantitative methods for determining sudomotor density [3,4]. More recent studies have described both an unbiased stereologic and a rapid automated method for quantitation of sudomotor density [2,3]. Both techniques can differentiate groups of patients with diabetic neuropathy from healthy control subjects. The automated approach is much faster, but has larger confidence intervals, thereby reducing the utility in individual patients, but proving of value in larger group studies where time constraints may play a factor. Thus far, quantitation of sudomotor nerve fibers has been limited to healthy control subjects and patients with diabetes. Sudomotor fiber density correlates with both neurophysiologic sweat testing and questionnaire responses about sweat output.
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TERATOMAS, DERMOIDS, AND OTHER SOFT TISSUE TUMORS
Jean-Martin Laberge MD, ... Kenneth Shaw MD, in Ashcraft's Pediatric Surgery (Fifth Edition), 2010
Sweat Gland Lesions
Sweat gland pathology results from disorders of the sebaceous, apocrine, or eccrine adnexal structures of the skin. One series reported that only 1.7% of pediatric skin biopsy specimens showed these lesions.206 Hidradenomas originate from the ductal portion of the sweat gland and are seen as multiple small flesh-colored papules on the face, neck, and upper chest during puberty and adolescence. Two subtypes are of interest: the eruptive form results in many lesions in a short period, whereas the clear cell variant causes solitary and occasionally painful lesions.206 Sweat gland carcinomas are uncommon and are rarely differentiated enough to subtype confidently.206 They may be locally aggressive and metastasize to the local lymph nodes. Treatment primarily involves resection with individualized adjuvant therapy.
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Diabetes and the Nervous System
Gigi Ebenezer, Michael Polydefkis, in Handbook of Clinical Neurology, 2014
Cutaneous autonomic nerve fiber innervation in diabetes
Both sweat glands and piloerector muscles innervated by autonomic fibers are loose complex structures in the dermis without a well-defined anatomic boundary. Though functional testing of sudomotor fibers is well established few attempts have been made to quantify the autonomic fibers. Morphometric analysis of sweat gland innervation has shown significant loss of sudomotor fibers in diabetic neuropathy and the linear loss of fibers correlated with Neuropathy Impairment Score in the Lower Limb (NIS-LL) (Gibbons et al., 2010; Luo et al., 2012).
In a detailed stereology-based morphometric analysis of 71 healthy subjects (unpublished) the sweat gland nerve fiber (SGNF) innervation was greater in females and showed a length-dependent innervation, the thigh area showing higher innervation (17.9 ± 0.55 in m/mm3) than the distal leg (12.4 ± 0.3.1 in m/mm3). The SGNF innervation pattern has not been identified to progressively decline with aging. The SGNF innervation was reduced significantly among diabetes mellitus patients with poor glycemic control (HbA1c > 8.5%) compared to patients with better glycemic control (HbA1c < 6%) (Fig. 19.5).
Fig. 19.5. Sweat gland innervation in controls and diabetic patients. The innervation of sweat glands with PGP 9.5 fibers is significantly decreased (#,* p < 0.0001) among diabetes mellitus (DM) subjects at the distal thigh (A) and distal leg (B). Sweat gland innervation progressively reduced among DM subjects with poor glycemic control (HbA1c > 8.5%) compared to DM subjects with excellent control (HbA1c < 6%).
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Autonomic Nervous System
Ningshan Wang, Christopher H. Gibbons, in Handbook of Clinical Neurology, 2013
Sweat glands
Sweat glands are located 3–5 mm below the epidermal layer, and are made up of sweat gland tubules that are intertwined with capillaries and nerve fibers (Fig. 30.3A–C). (Gibbons et al., 2009, 2010a). Many tools used to assess the integrity of the peripheral autonomic nervous system investigate the sympathetic cholinergic, or sudomotor, response. The quantitative sudomotor axon reflex test (QSART) has become a widely used and reliable marker of peripheral autonomic and peripheral nerve dysfunction (Low et al., 1983). A number of other measures of sudomotor function have been developed, such as quantitative direct and indirect sweat testing (Gibbons et al., 2008), the dynamic sweat test (Provitera et al., 2010), and silicone impressions (Vilches and Navarro, 2002). Such widespread investigation of sudomotor function is, in part, secondary to reports that peripheral sudomotor dysfunction may be the most sensitive finding in patients with distal small fiber neuropathy (Low et al., 2006).
Fig. 30.3. Cutaneous innervation. Various dermal structures are shown, with their specific autonomic innervation highlighted. (A–C) A sweat gland. In (A), the green stain is CD31, an endothelial marker that is highlighting the blood vessels; there is also some background stain picked up by the sweat glands tubules. In (B), the red stain is from PGP 9.5, a panaxonal marker, showing the innervation around the sweat gland. In (C), the merged picture highlighting both the innervation and the vasculature is shown. (D–F) A sweat gland. In (D), the blue stain is CD31 (blood vessels) while the green stain is vasoactive intestinal peptide (VIP, stains for sympathetic cholinergic fibers). In (E), the blue stain is CD31 (blood vessels) while the red stain is tyrosine hydroxylase (TH, stains for sympathetic adrenergic fibers). (F) Shows the merged picture with sympathetic adrenergic and cholinergic fibers seen surrounding a sweat gland and accompanying blood vessels. (G–I) Cutaneous blood vessels. In (G), the red stain is CD31 (blood vessels), the green is PGP 9.5 (all nerve fibers). In (H), the red stain is CD31 highlighting the dermal capillaries at a magnified view. In (I), the innervation (PGP 9.5) is shown with the accompanying blood vessels. (J–L) Arrector pilorum muscle. In (J), the sympathetic adrenergic fibers (stained with TH) are shown in an arrector pili muscle. In (K), the sympathetic cholinergic innervation (stained with VIP) is shown, and is much less than the sympathetic adrenergic innervation. In (L), the merged image showing both cholinergic and adrenergic innervation within an arrector pili muscle is shown. White scale bars at the bottom of each image indicate 100 μm.
Although structural investigation of sudomotor fibers has existed for a number of years (Kennedy et al., 1994), recent advances in methodology and the widespread use of skin biopsies have resulted in a number of recent publications on the subject (Gibbons et al., 2009). Clinical skin biopsies stained with the panaxonal marker PGP 9.5, imaged by light microscopy, can highlight the network of innervation surrounding sweat glands, and may be reduced in diseases affecting the peripheral nervous system (Gibbons et al., 2009, 2010a). Despite the clinical utility of a panaxonal marker, such as PGP 9.5, it cannot differentiate sensory and autonomic nerve fiber subtypes. Sweat glands contain primarily sympathetic cholinergic innervation, although some sympathetic adrenergic fibers are noted as well (Fig. 30.3D–F). There are also dense networks of capillaries within sweat glands that are accompanied by their own innervation (Fig. 30.3A–C). The use of multiple immunoflorescent stains that can identify nerve fiber subtypes with confocal imaging may play an increasing role in diagnosing specific diseases and defining disease severity.
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Handling, safety and practical applications for use of essential oils
Sue Clarke BSc (Hons) PhD, in Essential Chemistry for Aromatherapy (Second Edition), 2008
Sweat glands
Sweat glands are found throughout the skin but are more numerous in areas such as the soles of the feet, palms of the hand, armpits and groin. The body of the gland is made up of a coiled tube, surrounded by a good blood supply, and a duct, which opens onto the skin surface through a pore. Other glands open into the hair follicles after puberty. The important function of the sweat glands is to form the fluid sweat. The sweat is formed from the bloodstream, so in times of high sweat production the body's water intake and balance must be regulated. When liquid sweat changes to a vapour and evaporates from the skin surface, it takes heat away from the body. If the body is cold, the sweating mechanism is inhibited. Temperature regulation is controlled by a part of the brain called the hypothalamus responding to the core temperature of the blood.
AROMAFACT
Essential oils enter the body through the skin by the ducts of the sweat glands and the hair follicles. The permeability of the skin at various locations in the body can be linked to the number of available ducts acting as entry points. Sites such as the palms of the hands, soles of the feet, armpits, genitals, forehead and scalp are quite permeable to absorption of essential oils, while the limbs, buttocks, abdomen and trunk are relatively impermeable.
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Clinical Syndromes and Cardinal Features of Infectious Diseases: Approach to Diagnosis and Initial Management
John Browning, Moise Levy, in Principles and Practice of Pediatric Infectious Disease (Third Edition), 2008
Sweat Gland Abscess (Periporitis)
Sweat gland abscesses develop rarely in neonates, most often in association with malnutrition or debilitation.62 The infection has also been termed periporitis staphylogenes because of the almost uniform presence of S. aureus in the lesions. It appears that lesions of miliaria become infected secondarily, followed by extension of the infection into the sweat gland apparatus and, occasionally, into the adjacent subcutaneous tissue. Miliaria-like lesions, however, are not a constant feature. The 1- to 2-cm, round to oval nodular abscesses occur most commonly on the neck, occiput, back, and buttocks, and unlike furuncles and carbuncles of follicular origin, they are nontender, nonpointing, and cold. Constitutional symptoms can accompany numerous large abscesses, and lymphangitis or cellulitis occurs rarely. Therapy consists of control of factors such as skin occlusion or fever that predispose to miliaria, correction of malnutrition, local care of abscesses, and use of antistaphylococcal antibiotics. Healing occurs over several weeks, generally without scarring.
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Principles of Skin Grafts
Joyce C. Chen MD, Sonu A. Jain MD, in Plastic Surgery Secrets Plus (Second Edition), 2010
6 How do sweat glands affect skin grafts?
Apocrine sweat glands are concentrated in the axillae and groin. They become active at puberty, secrete continuously, and produce an odor due to bacterial decomposition. Eccrine sweat glands are found throughout the body except at mucocutaneous junctions and the nail beds. There are two types of eccrine glands: those located in the palms of the hand and soles of the feet and those located on the remainder of the body surface; the former respond to emotional and mental stress whereas the latter function in temperature regulation.
The sweat pattern of a skin graft follows that of its recipient site because sweat gland function is directed by sympathetic nerve fibers within the graft bed. Skin grafts initially lack the lubrication provided by the sweat glands because they are temporarily deinnervated. Therefore, lubricant creams should be applied to the graft until the glands are reinnervated.
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Cutaneous Carcinoma
Michael J. Veness, Julie Howle, in Clinical Radiation Oncology (Fourth Edition), 2016
Clinical Presentation and Pathology
Sweat gland (eccrine, apocrine, apoeccrine) carcinomas are exceedingly rare, arise most frequently in the skin of the head and neck or the extremities, and manifest as painless papules or nodules that grow slowly. This type of neoplasm is usually diagnosed in individuals 50 to 70 years of age.
Histologically, eccrine or sweat gland carcinomas may resemble carcinomas of the breast, bronchus, and kidney and are difficult to differentiate from cutaneous metastases. Many histologic variants are reported and include ductal eccrine carcinoma, mucinous eccrine carcinoma, porocarcinoma, syringoid eccrine carcinoma, clear cell carcinoma, and microcystic adnexal carcinoma (MAC).35
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