AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Eccrine spiradenoma (ES) usually manifests as a solitary, 1 cm in diameter, gray, pink, purple, red, or blue nodule on the upper half of the ventral side of the body. ES can be painful, often in paroxysms. Multiple ESs have been reported. Their initial elaboration is attributed to Kersting and Helwig.¹

ES is usually benign. It can occur in infancy but most commonly arises in persons aged 15-35 years. About 15 cases of linear/zosteriform/nevoid/blaschkoid multiple spiradenomas exist in the literature.^{2, 3} About 50 case reports of malignant ES (MES) exist in the literature. Dabska⁴ first described MES in 1972.

ES can occur in Brooke-Spiegler syndrome, which manifests with cylindromas, ES, and trichoepitheliomas. In this syndrome, lesions can have combined features of both cylindromas and ES.^{5, 6}

Pathophysiology

A defective tumor suppressor gene is believed to result in the development of ES. In Brooke-Spiegler syndrome, of which ESs are a manifestation, the defective gene is the CYLD gene on chromosome 9. Work remains to be performed on the genetic defect causing isolated and sporadic ESs.

The expression of p53 in MES seems to be increased.

The cells of origin of ES appear to have apocrine and trichoepitheliomatous differentiation, ie, they have complex hair follicle (folliculosebaceous apocrine) differentiation rather than eccrine differentiation.

In cases of linear/zosteriform/nevoid/blaschkoid multiple ESs, an abnormal clone arising during embryogenesis is postulated to produce the multiple abnormal cells that result in such ESs.

In a cytogenetic study, Dijkhuizen et al⁷ found an ES and 2 lymph node metastases, with a growth pattern and microscopic appearance typical for benign ES, a 46,XY-5,del(16)(q22),+mar(t(?;5)(?::5q13----5qter)) karyotype.

These similar genetic defects seem to support a relationship between the chromosomal abnormalities and the clinical malignant action of this benign-appearing neoplasm.

Frequency

ES is rare worldwide. MES is very rare worldwide.

Mortality/Morbidity

ES can be painful. The rate of malignant transformation is very low, and, sometimes, malignant transformation has been reported to develop spontaneously. The rate of metastasis is about 50% and can result in death.

Race

No racial link exists in ES.

Sex

No sexual predilection exists in ES or MES.

Age

• ES has been reported to arise in infancy but is rare.
• Most ESs arise in persons aged 15-35 years.
• MESs tend to develop after age 50 years. MES presents at an average age of 59 years (range, 21-92 y).

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

ES lesions tend to arise on the head; the neck; the trunk; and, less commonly, the arms followed by the legs. Lesions tend to be about 1 cm in diameter, and they remain stable in size.

The lesions are mostly solitary, but they can be multiple, giant, linear, blaschkoid, or grouped.

Mambo⁸ performed a clinical and pathologic study of 49 ESs occurring in 46 patients. While textbooks say ESs are painful, this was not reported in most patients. Pain, increased sensation, and/or tenderness were noted in only 23% of the 35 patients who had well-documented clinical histories. In 2 patients, the ES underwent malignant transformation but did not recur in the 35 patients who underwent surgical removal.

• MES can occur in long-standing lesions.⁹
• Granter et al¹⁰ reported clinicopathologic features of 12 cases.
• • In one study of approximately 10 patients, the male-to-female ratio of patients with ES was 1:1; most patients were in their 60s.
  • ES occurred most commonly on the trunk. The next most common regions were the extremities and the head and neck. The average size of the ES was 7.5 cm in diameter. According to the history, the ES had been present 7 months to 30 years before surgical removal. Only 1 patient had metastatic spread of the ES. In this patient, an apparent remission occurred with dissection of the lymph nodes.
  • When biopsy specimens were examined, areas of benign ES and MES coexisted, with more MES tissue usually present. The cancerous nature of MES was revealed by an increased mitotic rate, necrosis, nuclear atypia, pleomorphism, hyperchromasia, loss of nested and trabecular growth patterns, and an absence of a dual cell population.
  • MES with pulmonary metastasis has been reported.¹¹
  • Granter et al¹⁰ found 2 distinctive histologic patterns in MES (both with focal squamous differentiation). The first was an abrupt transition between a benign ES and a high-grade carcinoma component. The second was a contiguity between benign ES and MES. In the later case, the diagnosis was defined by an increased nuclear-to-cytoplasmic ratio, hyperchromasia, and marked mitotic activity.
• In MES of the breast, a long-standing cutaneous nodule begins to enlarge rapidly. The growth is often associated with an ulceration and a change in color.
• Kao et al¹² noted that ESs rarely (<1%) occur in infancy. ESs in infants differ from the conventional ESs by the presence of superficial dermal nodules. The nodules display a less distinct 2-cell pattern of immature adnexal epithelial cells. Ductule formation is rare. In infants and young adults, these tumors may be mistaken for mesenchymal neoplasms involving the skin and the subcutis.
• ESs can mimic other painful tumors, in particular angiolipomas, because of their similar color.
• Papular lesions of the proximal nail fold have been noted to be ESs.¹³
• Brooke-Spiegler syndrome with combined lesions containing cylindromatous, spiradenomatous, trichoblastomatous, and sebaceous differentiation have been reported.¹⁴
• ES has been noted to occur in the ears in several case reports,¹⁵ including that by Nadig et al¹⁶ from 2004. External auditory canal eccrine spiradenocarcinoma has also been noted.¹⁷

Physical

• ESs are usually gray, pink, purple, red, or blue nodules about 1 cm in diameter.
• The lesions tend to occur on the scalp, the neck, and the upper part of the torso. About 5 cases have been reported on the eyelid.^{18, 19}
• ESs tend to be soft and are sometimes painful to palpation.
• MES tends to be larger than benign ES. MES tends to ulcerate.
• MES tends to preferentially involve the trunk and the extremities (92% of reported cases). The average size of MES at presentation is 3.9 cm (range, 0.5-15 cm) in diameter.
• Many MES lesions occur on the scalp.^{20, 21}
• MES has been reported to occur on a traumatized area.²²
• MES can result in lymph node, diffuse pulmonary or brain, and liver metastases (in order of occurrence).
• Chase et al²³ noted MES of the vulva, underlying that MES can occur in almost any location.

Causes

• ES seems to be caused by a defective tumor suppressor gene. In Brooke-Spiegler syndrome, a defect exists in the CYLD gene located on chromosome 9. The actual cause of solitary ES has yet to be defined.
• The cause of MES is unclear. The expression of TP53 seems to be increased in MES, but the significance of this observation is unclear.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Adenoid cystic carcinoma
Metaplastic breast carcinoma
Granular cell tumor
Neuroma
Angiolipoma
Endometrioma
Glomus tumor

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• In the case of MES, tissue has been tested to determine the presence of hormonal receptors.

Imaging Studies

• MRI, CT, and radiography can be used to assess the presence of metastatic foci in the case of MES.
• Han et al²⁴ noted MES distributed in several parts of a patient's body. On MRIs, the ESs manifested as multiple dispersive foci with clear circumferences in the skin and subcutis. The ESs demonstrated low-signal intensity on T1-weighted images and high-signal intensity on short tau inversion recovery images. Although the signal intensities of ESs were not characteristic of other benign tumors, MES should be in the differential diagnosis of the tumors of the skin and the subcutis.

Procedures

• A skin biopsy helps in establishing the diagnosis of these tumors. The best and really only treatment is surgical excision of these lesions one at a time.
• Fine-needle cytology of an ES of the breast can be performed to aid in diagnosis.²⁵

Histologic Findings

ESs consist of 1 or more large, sharply delineated, basophilic nodules in the dermis (cannon balls or big blue balls in the dermis). The nodules of ES are unattached to the epidermis and sometimes extend into the subcutis. The nodules consist of groups of cells in cords, islands, and/or sheets. A trabecular arrangement of cells can be present.

The 2 types of cells in the nodules of ES are small, dark, basaloid cells with hyperchromatic nuclei and cells with large, pale, vesicular, and ovoid nuclei. Pale cells tend to be at the center of the lesions. Ductlike structures can also be present at the center of the lesions. The lesions are peppered with lymphocytes. Strands of cells are positive for cytokeratin, and the lumina are positive for carcinoembryonic antigen.

Upon electron microscope examination, ESs consist of cellular sheets separated into lobules by strands of amorphous and fibrillar material. Examination reveals translucent polygonal or round cells with mitochondria, small vesicles, and sometimes glycogen granules, which are the dominant population of cells in ESs. Sparse, dark cells are also often noted. Lumina are not always noted, but, when present, they can have microvilli on the lining cells.

Jitsukawa et al²⁶ performed electron microscopic studies of ESs. Apposite morphologic aspects of the parenchyma were an adenoid cystic organization composed of epithelial, myoepithelial, and nonepithelial cell types; intracytoplasmic lumina were also present in epithelial cells. No evidence indicated that the parenchyma produced any type of secretion. The stroma ramified in and around the parenchyma, occupying extensive areas. The stroma formed tenuous septa of the loose connective tissue that contained embedded blood vessels and nerve fibers. Close examination revealed profiles of cystoid spaces resulting from stromal invagination into the parenchyma.

Meybehm and Fischer²⁷ noted that ESs and cylindromas express S-100 protein, ascribed to eccrine differentiation within their tubular and large, pale-staining cells. Tubular cells in both spiradenomas and cylindromas expressed human milk fat globulin and lysozyme, 2 markers associated with apocrine differentiation. In addition, antibodies to alpha–smooth muscle actin tightly mark the small basaloid cells of both spiradenomas and cylindromas.

Both spiradenomas and cylindromas demonstrate identical cytokeratin patterns. As with the sundry aspects of eccrine and apocrine units, the expression of keratins 7, 8, and 18 by spiradenomas and cylindromas demonstrates differentiation in the direction of a parentage from secretory tissue. On the other hand, the expression of keratin 14 in some of the neoplastic cells suggested ductal differentiation.

Ishihara et al²⁸ have used a novel monoclonal antibody IKH-4, which stains the eccrine secretory coil but not the apocrine secretory segment. They saw positive staining in eccrine hidradenoma, eccrine poroma, ES, papillary eccrine adenoma, eccrine hidrocystoma, syringoma, eccrine carcinoma, and syringocystadenoma papilliferum (1 case). They noted negative staining in apocrine adenocarcinoma, hidradenoma papilliferum, erosive adenomatosis of the nipple, and primary and metastatic adenocarcinomas. IKH-4 antibody helped researchers differentiate eccrine neoplasms from apocrine neoplasms and eccrine carcinoma from metastatic adenocarcinomas.

Yasui et al²⁹ noted that DF3 (CA15-3) monoclonal antibody detects the 20–amino acid sequence of epithelial mucin. In normal skin, DF3 antibody reacts strongly and constantly with sebaceous and secretory parts of eccrine and apocrine sweat glands. DF3 stains ESs.

Saboorian et al³⁰ noted an interesting case of MES of the breast. Microscopically, the MES demonstrated the typical features of an ES, with areas of adenocarcinoma, squamous cell carcinoma, and sarcoma. The sarcomatous component consisted of rhabdomyosarcoma and osteosarcoma. Immunoperoxidase staining demonstrated p53 protein only in carcinomatous and sarcomatous cells.

Kurokawa et al³¹ found ESs co-expression of cytokeratin and smooth muscle actin, suggesting differentiation toward myoepithelial cells.

Ko et al³² noted a giant vascular ES that occurred in a 56-year-old Korean woman. They noted that the clinical differential diagnosis included an angiomatous lesion, a determination based on its florid vascularity and hemorrhagic manifestations. Immunohistochemical stainings demonstrated 3 types of cells, specifically (1) pale epithelial cells, (2) small basal cells, and (3) myoepithelial cells.

Ohtsuki et al³³ performed a detailed immunohistochemical analysis on ES tissue from a 40-year-old woman. Immunohistochemically, antibodies to cytokeratins (AE1/AE3, CAM5.2) and CK 5/6 stained diffusely positive in all tumor cells. The intermingled Langerhans cells did not stain diffusely positive. These Langerhans cells harbored interdigitated nuclei, and their cytoplasm was positive for S-100 protein and CD1a; additionally, their nuclei were occasionally positive for S-100 protein.
 
In these Langerhans cells, antibody-to-epithelial membrane antigen positively stained for the surface of both intracytoplasmic and true glandular lumina. With fine structural examination, Langerhans cells were noted among the tumor cells, extending fine irregular processes among the tumor cells. Birbeck granules manifested clearly within the cytoplasm of the Langerhans cells. Intracytoplasmic lumina with microvilli on their surfaces occurred in some tumor cells. In these examinations of ES, 15 Langerhans cells were seen per low-power field.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Radiation, hyperthermic limb perfusion chemotherapy, and chemotherapy are used in the treatment of MES. The mechanism for hyperthermic limb perfusion chemotherapy is uncertain, but some think that alterations of temperatures affect tumor cells more than healthy cells, which by analogy is like the increased sensitivity of cancer cells to radiation.

• Although ESs can be painful, they are not treated with medications.
• Sridhar et al³⁴ and Mirza et al³⁵ separately reported symptomatic improvement and shrinkage of MES with tamoxifen therapy in a patient with estrogen receptor–positive eccrine adenocarcinoma.

Surgical Care

The mainstay of treatment of ES and MES is surgical removal.

• If tumors are painful, ESs can be removed by surgical excision. The lesions do not tend to recur after surgery.
• Multiple ESs, such as those found in Brooke-Spiegler syndrome, were treated with a high-energy continuous wave carbon dioxide laser after debulking with bipolar scissors in one patient.³⁶ Debulking with bipolar scissors prior to laser therapy can be a beneficial technique in the surgical removal of large tumors.

Consultations

If MES is present, consult an oncologist, a radiation oncologist, and a radiologist.

Activity

Sometimes, pain can bother patients, but this pain should not affect their activities.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Management during the course of metastatic ES includes surgery, radiation therapy, hyperthermic limb perfusion chemotherapy, and chemotherapy, in particular tamoxifen.

Drug Category: Chemotherapy agents

These agents are used to block the growth of cells that have estrogen receptors.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Inpatient care is usually not necessary.

Further Outpatient Care

• Surgery is usually curative; therefore, further care is not needed.
• If MES occurs, the patient will need to follow up with oncologists, radiation oncologists, and radiologists.

Deterrence/Prevention

• Complete excision of lesions should be performed to ensure that they do not recur.

Complications

• Long-standing lesions of ES can turn into MES. The reason for this transformation is unclear.
• Hantash et al³⁷ noted de novo MES; thus, changing skin tumors should prompt apposite evaluation.

Prognosis

• Most ESs are benign and stable and do not require treatment.
• MES requires treatment, and it is metastatic in about 50% of cases. If metastatic and untreated, MES is fatal.

Patient Education

• Patients must understand that the lesions can be painful and that only surgery is curative.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to perform a biopsy on the lesions, especially for larger lesions that have ulcerated and turn out to be MES, is a pitfall.
• Failure to aggressively treat MES is a pitfall.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Feb 12, 2008