Poromas or poroid tumors are a group of rare, benign cutaneous neoplasms derived from the terminal eccrine or apocrine sweat gland duct. There are four poroma variants with overlapping features: dermal duct tumor (DDT), eccrine poroma, hidroacanthoma simplex, and poroid hidradenoma, of which DDT is the least common. Clinically, the variants have a nonspecific appearance and present as solitary dome-shaped papules, plaques, or nodules. They can be indistinguishable from each other and a multitude of differential diagnoses, necessitating a better understanding of the characteristics that make the diagnosis of poroid neoplasms. However, there remains a paucity of information on these lesions, especially DDTs, given their infrequent occurrence. Herein, we review the literature on DDTs with an emphasis on epidemiology, pathogenesis, clinical features, diagnosis, and management.
Acrospiromas are a broad class of benign skin adnexal tumors of acrosyringial differentiation. A group of benign growths derived from cells of the terminal eccrine or apocrine sweat gland duct, known as poromas or poroid tumors, fall within this class [1]. There are several types of poromas: dermal duct tumors (DDT), eccrine poromas, hidroacanthoma simplex, and poroid hidradenomas [1]. Each is differentiated by histopathological features such as lineage (eccrine/apocrine) and location of the poroid cells in relation to the epidermis [2]. It is estimated that sweat gland tumors account for approximately 1% of all primary skin lesion cases, of which eccrine and apocrine poromas are believed to account for approximately 10% [3]. However, there remains a paucity of information on poromas, especially DDTs, given their infrequent occurrence.
2. Discussion
DDTs are predominantly located within the dermis and thus are also known as intradermal or dermal eccrine poromas [2]. They are composed of a mixture of three types of cells: poroid, cuticular, and clear cells [2]. These features are key in differentiating DDTs from other poroma variants. However, all of these variants have features that can overlap.
3. Epidemiology
While the exact incidence of poromas is unknown, several studies have revealed specific epidemiological data. One single center study reviewed approximately 1,741,379 epithelial skin tumor biopsies over 17 years and noted the occurrence of 101 poromas (0.0058%) [4]. Another single center study examining 18,653 biopsy specimens processed over 15 years revealed 25 poroid neoplasms (0.134% of all pathology) [5]. The presence of all poroma variants except DDT was noted in this particular study. Across 3 studies examining 675 cases of poroid neoplasms, solitary DDT was the rarest variant, occurring only 22 times (3.3%) [5,6,7].
Poromas typically occur in the elderly population (mean age 65.1–66.6) with a slight predilection for males (male to female ratio: 1.13–1.52) [4,6]. Long-term radiation exposure has been associated with poroma formation in patients with chronic radiation dermatitis [8]. Poroma eruptions have also occurred during pregnancy and after bone marrow transplantation [9,10]. In addition, poromas may occur in patients with underlying skin conditions, including hypohidrotic ectodermal dysplasia, Bowen’s disease, and nevus sebaceus [8].
4. Pathogenesis
The exact pathogenesis of poroid neoplasms is unknown, although immunohistochemical studies have provided clues (Figure 1). Based on the ubiquitous expression of keratin K5 and K14 in poroid cells, it has been postulated that poromas are periductal sweat gland tumors derived from basal keratinocytes of the sweat duct ridge and the lower acrosyringium [6,11]. As basal keratinocytes differentiate and advance to the upper acrosyringium, cells express keratins K1 and K10, which are found within cuticular cells. Further supporting the basal keratinocyte origin is the lack of luminal duct keratins (K77) [6]. Basal keratinocytes of the sweat duct ridge constitute an outermost third layer of the dermal bilayered ductal structure, merging with the adjacent epidermis [6]. This third layer has a highly variable length, which could account for the various forms of poroid neoplasms, according to the initial site of tumor induction [6,11].
Figure 1. A simplified schematic of keratin expression in an eccrine sweat gland is shown [6,10]. The basal keratinocytes of the sweat duct ridge and lower intraepidermal acrosyringium are thought to give rise to poroid neoplasms based on the similarities in keratin expression [6,10]. K5 and K14 expression is ubiquitous throughout poromas, while K1 and K10 are found in focal aggregates. K77 is restricted to normal luminal cells embedded within the tumors.
More recently, YAP1 gene fusions have been implicated in the tumorigenesis of poroid neoplasms. The exact role of YAP1 in poromas has not been elucidated; however, results from 2 studies revealed certain fusions (YAP1-NUTM1 or YAP1-MAML2) were present in 113/146 (77.4%) poromas [12,13]. However, only 3 DDTs were studied, with a 2/3 (66.7%) rate of expression. While more extensive studies are needed, its presence may serve as a diagnostic aid in uncertain cases.
5. Clinical Features
Clinically, poroma variants are typically indistinguishable. Moreover, poromas are often misdiagnosed as other skin neoplasms because their clinical presentations are nonspecific and variable [3]. In general, poromas present as solitary dome-shaped papules, plaques, or nodules [1]. They are usually slow growing and asymptomatic, although some patients may experience itching and pain [8]. Lesional color ranges from skin-toned to pink, red, white, or blue [8]. The surface may be smooth, verrucous, or ulcerated [14]. They may occur anywhere on the body, but are most commonly seen on acral, head, and neck surfaces [1,2]. Rarely, multiple poromas will develop, either in an acral or in a widespread distribution, a condition known as poromatosis [15].
Battistella et al. reviewed 19 cases of DDTs and revealed that lesions were most commonly described as small dermal nodules (50%), infiltrative dermal papules (40%), or pedunculated tumors (10%) [6] (Figure 2). Color ranged from pink to erythematous (69%), sometimes pigmented (25%), and rarely bluish (6%). Epidermal surface changes were only noted in one case of combined hidradenoma simplex and DTT, in which the lesion was verrucous [6]. No ulceration was noted. Pain was mentioned in 1 case [6]. The trunk was the most common lesion site 39%, followed by the upper limbs (28%), lower limbs (28%), and head/neck (1%) [6]. The location of 1 lesion was unknown. Lesion size was <1 cm in 69% of cases [6].
Figure 2. Dermal duct tumor: a small, purple-brown papule at the right superior nasolabial fold.
6. Differential Diagnosis
Differential diagnosis of DDTs includes all poroma variants (eccrine poroma, hidroacanthoma simplex, and hidradenomas) and other sweat gland tumors (Table 1). Other differentials include porocarcinoma, basal cell carcinoma, pyogenic granulomas, acrochordons, verrucae, soft fibroma, hemangioma, pigmented nevus, seborrheic keratosis, trichilemmoma, melanoma, Kaposi sarcoma, and other adnexal tumors [1]. Dermatoscopy can be utilized to narrow down the differential, but confirmation relies on histopathology.
Table 1. Differential diagnosis of sweat gland tumors with a focus on benign tumors with the exception of porocarcinoma.
Of the 19 DDTs reviewed by Battistella et al., the clinical diagnosis was most often dermatofibroma (33%), followed by dermal melanocytic nevus (28%), melanoma in pigmented cases (22%), and benign dermal tumors (neurofibroma, leiomyoma) (17%) [6].
7. Diagnosis
7.1. Dermatoscopy
While there are no specific reports reviewing dermatoscopic findings in DDTs, certain vascular patterns have been noted to aid in diagnosis of poromas. Polymorphic, glomerular, linear-irregular, leaf- and flower-like, and looped or hairpin variants are commonly seen [8]. While these patterns may be seen with other conditions, the leaf- and flower-like pattern appears to be relatively unique to the poromas [27]. Additional dermatoscopic features included the presence of vascular blush secondary to the vasodilatation and high vascular volume of these tumors, as well as structureless areas and white interlacing cords [1].
The predictive value of white interlacing areas around vessels, yellow structureless areas, milky-red globules, poorly visualized vessels, and branched vessels with rounded endings has been studied [28]. The presence of any of these 5 features was associated with poroma with a sensitivity and specificity of 62.8% and 82.0%, respectively [28].
7.2. Histology
Ultimately, differentiation occurs via histopathology. The principal finding in all forms of poroma is a circumscribed proliferation of compact cuboidal keratinocytes with small non-palisading monomorphous nuclei with scant eosinophilic cytoplasm (poroid cells) and larger squamous eosinophilic keratinocytes (cuticular cells) [15]. In some cases, poromas may display a clear cell change with small nuclei surrounded by a pale cytoplasm (clear cells). Poroid cells are smaller than those in the contiguous epidermis and tend to arrange themselves in cords and broad columns extending downward from the normal epidermis [29]. Some atypical features of malignant tumors can be observed in poroma, including a variable number of mitosing cells, highly vascularized stroma, and necrosis en masse [3,15].
The aggregates of poroid and cuticular cells in a poroma may show ductal or tubular formations; however, the degree of ductal differentiation may vary between each type [1]. Some poromas may have a multitude of ductal foci, whereas others may be more difficult to find [1]. In the latter case, immunostaining with carcinoembryonic antigen (CEA) can highlight the presence of both eccrine and apocrine ducts and thus aid in identification [15]. If the poroma displays more tubular foci lined by columnar cells with holocrine secretions, it is highly suggestive of an apocrine etiology [1].
Poroma variants are differentiated based on the predominant cell type present and the degree of epidermal/dermal involvement [2]. However, multiple variants can exist within the same lesion. DDTs are primarily confined to the superficial dermis and are composed of small solid and cystic nodular aggregates of poroid, cuticular, and clear cells (Figure 3, Figure 4 and Figure 5) [2]. Eccrine poromas are also composed of all three cell types, but are primarily located in the epidermis and superficial dermis. Hidroacanthoma simplex is mainly composed of poroid cells, less cuticular cells, and no clear cells [2]. It is confined to the epidermis. Poroid hidradenoma contains a mixture of all three cell types and is also confined to the dermis [2]. In contrast to DDT, poroid hidradenomas have large aggregates of solid and cystic components and extend deeper into the reticular dermis and even subcutis [2].
Figure 3. Well circumscribed, dermal-based, solid and cystic tumor with no connection to the overlying epidermis (H & E, 2×).
Figure 4. Higher magnification reveals small poriod cells with round to oval nuclei and scant cytoplasm. Ductal lumen formation is present (H & E, 10×).
Figure 5. Residual DDT on punch excision (from the transected spiecimen in Figure 3) (H & E, 10×).
The histopathologic diagnosis of DDT is rare due, in part, to the fact that some regard DDTs as poromas with a limited epidermal connection that has not been identified on the histologic sections examined or as hidradenomas that are smaller and more superficial [30]. As an example, Figure 3 may be regarded by some as representing a hidradenoma. This controversy in the histopathologic classification of poroid neoplasms without clear-cut evidence for the clinical significance of distinguishing these lesions from each other has given rise to the thinking that the poroma classification scheme may just be a matter of semantics [19]. This has led to some pathologists diagnosing these lesions under the overarching term as “acrospiroma” only without further classification.
8. Management
Superficial lesions may be treated with shaving or electrosurgical destruction [15]. Deeper lesions may be treated with simple excision [15]. As poromas are benign adnexal lesions, treatment is curative.
9. Complications
Malignant transformation risk is minimal; however, poromas may rarely evolve into porocarcinomas. The frequency of porocarcinoma is approximately 0.005–0.01% of all skin cancers [31]. It may present similarly to a benign poroma, as a firm, asymptomatic nodule, but it is typically more exophytic and ulcerative [1]. In the setting of a pre-existing poroma, malignant transformation may be identified clinically by recurrence, spontaneous bleeding, ulceration, sudden itching, pain, or rapid growth [32].
10. Conclusions
Poromas are a benign group of tumors derived from cells of the terminal eccrine or apocrine sweat gland duct with four variants: DDT, eccrine poroma, hidroacanthoma simplex, and poroid hidradenoma. DDT is the rarest and is differentiated from the other variants by its cellular composition, as well as its location in the dermis and small foci of solid or cystic components. However, these features may not always be clear cut and can overlap with other variants. Futhermore, all poroma variants can mimic many other dermatologic conditions. Therefore, it is essential to have a complete understanding of poromas to ensure proper diagnosis and treatment.
Author Contributions
Conceptualization and visualization, A.C.M. and S.K.T.; writing—original draft preparation, A.C.M., S.A., L.A.T.; writing—review and editing, A.C.M., S.A., L.A.T., P.G., A.S.J. and S.K.T. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
Not applicable.
Informed Consent Statement
Written informed consent has been obtained from the patient(s) to publish this paper.
Data Availability Statement
Not applicable.
Conflicts of Interest
The authors declare no conflict of interest.
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Androgenetic alopecia is a common form of hair loss in both men and women. In men, this condition is also known as male-pattern baldness. Hair is lost in a well-defined pattern, beginning above both temples. Over time, the hairline recedes to form a characteristic “M” shape. Hair also thins at the crown (near the top of the head), often progressing to partial or complete baldness.
The pattern of hair loss in women differs from male-pattern baldness. In women, the hair becomes thinner all over the head, and the hairline does not recede. Androgenetic alopecia in women rarely leads to total baldness.
Androgenetic alopecia in men has been associated with several other medical conditions including coronary heart disease and enlargement of theprostate. Additionally,prostate cancer, disorders of insulin resistance (such as diabetes and obesity), and high blood pressure (hypertension) have been related to androgenetic alopecia. In women, this form of hair loss is associated with an increased risk ofpolycystic ovary syndrome(PCOS). PCOS is characterized by a hormonal imbalance that can lead to irregular menstruation, acne, excess hair elsewhere on the body (hirsutism), and weight gain.
Frequency
Androgenetic alopecia is a frequent cause of hair loss in both men and women. This form of hair loss affects an estimated 50 million men and 30 million women in the United States. Androgenetic alopecia can start as early as a person’s teens and risk increases with age; more than 50 percent of men over age 50 have some degree of hair loss. In women, hair loss is most likely after menopause.
Causes
A variety of genetic and environmental factors likely play a role in causing androgenetic alopecia. Although researchers are studying risk factors that may contribute to this condition, most of these factors remain unknown. Researchers have determined that this form of hair loss is related to hormones called androgens, particularly an androgen called dihydrotestosterone. Androgens are important for normal male sexual development before birth and during puberty. Androgens also have other important functions in both males and females, such as regulating hair growth and sex drive.
Hair growth begins under the skin in structures calledfollicles. Each strand of hair normally grows for 2 to 6 years, goes into a resting phase for several months, and then falls out. The cycle starts over when the follicle begins growing a new hair. Increased levels of androgens in hair follicles can lead to a shorter cycle of hair growth and the growth of shorter and thinner strands of hair. Additionally, there is a delay in the growth of new hair to replace strands that are shed.
Although researchers suspect that several genes play a role in androgenetic alopecia, variations in only one gene,AR, have been confirmed in scientific studies. TheARgene provides instructions for making a protein called an androgen receptor. Androgen receptors allow the body to respond appropriately to dihydrotestosterone and other androgens. Studies suggest that variations in theARgene lead to increased activity of androgen receptors in hair follicles. It remains unclear, however, how these genetic changes increase the risk of hair loss in men and women with androgenetic alopecia.
Researchers continue to investigate the connection between androgenetic alopecia and other medical conditions, such as coronary heart disease and prostate cancer in men and polycystic ovary syndrome in women. They believe that some of these disorders may be associated with elevated androgen levels, which may help explain why they tend to occur with androgen-related hair loss. Other hormonal, environmental, and genetic factors that have not been identified also may be involved.
Learn more about the gene associated with Androgenetic alopecia
The inheritance pattern of androgenetic alopecia is unclear because many genetic and environmental factors are likely to be involved. This condition tends to cluster in families, however, and having a close relative with patterned hair loss appears to be a risk factor for developing the condition.
Androgenetic alopeciais a common form of hair loss in both men and women. In men, hair is usually lost in a well-defined pattern, beginning above both temples and is usually referred to asmale-pattern baldness. Over time, the hairline recedes to form a characteristic ‘M’ shape. Hair also thins near the top of the head, often progressing to partial or complete baldness. The pattern of hair loss in women differs from men (female pattern hair loss). In women, the hair becomes thinner all over the head, and the hairline does not recede. Androgenetic alopecia in women rarely leads to total baldness. A variety of genetic andenvironmental factorslikely play a role in causing this condition.Mutationsin theAR gene have also been associated with androgenetic alopecia.[1]
In addition tomale-pattern baldness, androgenetic alopecia in men has been associated with several other medical conditions includingcoronary heart disease andenlargement of the prostate. Additionally,prostate cancer, disorders of insulin resistance (such as diabetes and obesity), andhigh blood pressure(hypertension) have been related to androgenetic alopecia in men. In women, androgenetic alopecia is associated with an increased risk ofpolycystic ovary syndrome (PCOS), which is characterized by a hormonal imbalance that can lead to irregularmenstruation, acne, excess body hair (hirsutism), and weight gain.[1]
Last updated: 8/19/2011
This table lists symptoms that people with this disease may have. For most diseases, symptoms will vary from person to person. People with the same disease may not have all the symptoms listed. This information comes from a database called theHuman Phenotype Ontology (HPO). The HPO collects information on symptoms that have been described in medical resources. The HPO is updated regularly. Use the HPO ID to access more in-depth information about a symptom.
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HPO ID
Percent of people who have these symptoms is not available through HPO
Only 2 drugs currently have US Food and Drug Administration (FDA) approved indications for treatment of androgenetic alopecia:[2]
Minoxidil: Appears to lengthen the duration of the anagen phase (the active growth phase of hair follicles), and it may increase the blood supply to the follicle. Regrowth is better at the top of the head than in the front areas and is not noted for at least 4 months. It is used as a 2% or a 5% solution that rubs into the scalp and the 5% solution may work better. However, if the treatment is stopped the baldness returns. It works better in patients who just starting having the alopecia and who have small areas of hair loss.
Finasteride: It can only be used in men and is better for balding at the top of the head. If the treatment is stopped the baldness returns. It cannot be used in women who are still able to have children because it can result in ambiguous genitalia in male babies and it does not seem to be effective in women. The doses are about 1 mg daily by mouth.
Minoxidil use for several months can result in an eye condition known ascentral chorioretinopathy(aneye diseasethat lead to temporary visual impairment) , which can go back to normal after 1 months of not using the drug. Finasteride has no known side effects in men, according to several studies, but it cannot be used in women who are still trying to have children because it may produce fetal genital malformations.[2]
Every patient is unique and only the doctor can evaluate and determine the best treatment.
Some drugs that are not approved by the FDA but may be helpful are:[2][3]
Spironalactone: In women with androgenetic alopecia. Oral contraceptives: In women. Dutasteride: Is currently in study.
Topicallatanoprost0.1% is currently used to treatglaucomaand using it results in an increase of eyelashes. Some studies have shown that this medication could be useful for stimulating hair follicle activity and treating hair loss.
Follistatin, a humancellderived medication is also in study.
Also, low-level laser light therapy, a red light hairbrush–like device has shown some good results.
Surgical treatment of androgenetic alopecia has good cosmetic results. The main problem is covering the bald area with donor plugs (or follicles) sufficient in number to be effective. Micrografting produces a more natural appearance than the old technique of transplanting plugs.
It is important for the patients with androgenetic alopecia to be evaluated for treatable causes of “telogen effluvium” (diffuse hair shedding, often starting suddenly) likeanemiaor hypothyroidism, especially in patients who had a rapid progress of their disease or a sudden start of the disease. The following treatment options are recommended for women by some experts:[2]
Amoretti A, Laydner H, Bergfeld W. Androgenetic alopecia and risk of prostate cancer: a systematic review and meta-analysis. J Am Acad Dermatol. 2013 Jun;68(6):937-43. doi: 10.1016/j.jaad.2012.11.034. Epub 2013 Feb 8. Review.Citation on PubMed
Hillmer AM, Hanneken S, Ritzmann S, Becker T, Freudenberg J, Brockschmidt FF, Flaquer A, Freudenberg-Hua Y, Jamra RA, Metzen C, Heyn U, Schweiger N, Betz RC, Blaumeiser B, Hampe J, Schreiber S, Schulze TG, Hennies HC, Schumacher J, Propping P, Ruzicka T, Cichon S, Wienker TF, Kruse R, Nothen MM. Genetic variation in the human androgen receptor gene is the major determinant of common early-onset androgenetic alopecia. Am J Hum Genet. 2005 Jul;77(1):140-8. Epub 2005 May 18.Citation on PubMedorFree article on PubMed Central
Levy-Nissenbaum E, Bar-Natan M, Frydman M, Pras E. Confirmation of the association between male pattern baldness and the androgen receptor gene. Eur J Dermatol. 2005 Sep-Oct;15(5):339-40.Citation on PubMed
Quinn M, Shinkai K, Pasch L, Kuzmich L, Cedars M, Huddleston H. Prevalence of androgenic alopecia in patients with polycystic ovary syndrome and characterization of associated clinical and biochemical features. Fertil Steril. 2014 Apr;101(4):1129-34. doi: 10.1016/j.fertnstert.2014.01.003. Epub 2014 Feb 15.Citation on PubMed
Schweiger ES, Boychenko O, Bernstein RM. Update on the pathogenesis, genetics and medical treatment of patterned hair loss. J Drugs Dermatol. 2010 Nov;9(11):1412-9. Review.Citation on PubMed
Yazdan P. Update on the genetics of androgenetic alopecia, female pattern hair loss, and alopecia areata: implications for molecular diagnostic testing. Semin Cutan Med Surg. 2012 Dec;31(4):258-66. doi: 10.1016/j.sder.2012.08.003. Review. Retraction in: Semin Cutan Med Surg. 2015 Mar;34(1):48.Citation on PubMed
Zhuo FL, Xu W, Wang L, Wu Y, Xu ZL, Zhao JY. Androgen receptor gene polymorphisms and risk for androgenetic alopecia: a meta-analysis. Clin Exp Dermatol. 2012 Mar;37(2):104-11. doi: 10.1111/j.1365-2230.2011.04186.x. Epub 2011 Oct 10. Review.Citation on PubMed
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