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Immunohistochemical identification of epithelial membrane antigen in sweat gland tumors by the use of a monoclonal antibody.

A total of 78 cases of adnexal tumors of the skin were examined with the use of monoclonal antibody against epithelial membrane antigen (EMA). The EMA reaction was confined to luminal surfaces and lateral borders of sweat glands, both eccrine and apocrine, being usually absent in ductal segments. Neoplastic lesions of all the adenomatous tumours and mixed tumours of sweat glands showed specifically positive EMA staining of luminal surfaces and lateral borders of tubular, duct-like, and cystic structures. However, solid foci of those tumours were negative for EMA. Tumours of ductal origin, e.g. syringomas and poromas, exhibited positive EMA staining in their plasma membrane, although normal intact keratinocytes did not stain for EMA. Immunohistochemical distribution of EMA in skin adnexal tumours was classified into two types: one in which the luminal surfaces and lateral outer borders were positive, similar to that of the normal secretory coil, and the other in which the plasma membrane of neoplastic cells of ductal origin was positive.

Adenoma, Sweat Gland↗

Cluster headache: on the mechanism behind attack-related sweating.

Eighteen cluster headache patients were studied using body heating or exercise tests; all but two of them were also studied with a pilocarpine test (0.1 mg/kg body wt, s.c.). Evaporimeter measurements were made on both sides of the forehead under standard conditions in a thermo room. Heat- and exercise-induced sweating was clearly less pronounced on the symptomatic side than on the non-symptomatic side of the forehead, and was significantly different compared to controls. Pilocarpine on the other hand induced a clearly more pronounced response on the symptomatic side than on the non-symptomatic side, which was also statistically significantly higher than in the control group. These findings suggest a supersensitivity of the sweat glands to pilocarpine on the symptomatic side of the forehead in most cases of cluster headache.

Adult↗

Sweat gland carcinoma ex eccrine spiradenoma.

We herein report two cases of sweat gland carcinoma that arose in association with eccrine spiradenoma. These lesions presented as enlarging masses that previously had been stable for many years. One produced widespread metastasis and death 5 months after diagnosis. Immunohistochemical studies demonstrated an antigenic relationship between the benign and malignant components of sweat gland carcinoma ex eccrine spiradenoma, but ultrastructural analyses showed a paucity of specialized differentiation. This neoplasm appears to display a range of microscopic appearances and has proven fatal in 20% of reported cases.

Adenocarcinoma↗

Proliferation of eccrine sweat ducts associated with heterotopic neural tissue (nasal glioma).

The term "nasal glioma" refers to the presence of heterotopic neural tissue, mainly glial in nature, at or near the root of the nose. We describe a case in which all three components of neural tissue, that is, leptomeninges, glia, and neurons, were present, associated with sweat-duct hyperplasia. Proliferation of sweat ducts is a reactive process in some benign and malignant neoplasms, hamartomas, and cysts. This is the first documented case of hyperplasia of eccrine ductal epithelium induced by nasal glioma.

Brain↗

Sweat gland carcinoma: a clinicopathologic analysis of an expanded series in a single institution.

Primary adenocarcinoma of sweat glands is a rare tumor; approximately 220 cases have been reported in the last 30 years. We reviewed the charts of patients with primary diagnosis of this tumor treated at the Mayo Clinic between 1935 and 1995. We included only cases with initial histology slides available for re-examination. Tumors were classified into five recognizable histologic patterns (solid, ductal, mucinous, microcystic adnexal, and adenocystic carcinoma) and graded by the Broder system. Statistical analysis consisted of Kaplan-Meier product limit method and Cox multiple regression test. In total, 55 patients were identified, and age ranged from 13 to 85 years (mean 59 years). Thirty-six patients (65 percent) presented to the Mayo Clinic for initial treatment; all except one had disease limited to the primary site. Microcystic adnexal carcinoma was the most frequent type, and more than 50 percent were grade 2 tumors. Among these 36 patients, 4 had some type of recurrence. Patients who developed metastasis had a high-grade tumor in the initial biopsy. Nineteen patients were referred with recurrence; 13 had local recurrence, 4 had regional diseases, and 2 had distant metastases. The histologic distribution showed 47 percent solid tumors, and 37 percent of them were grade 3. Multiple regression analysis did not show a difference in recurrence or survival when gender, age, tumor location, or histologic pattern was evaluated. In addition, there was no difference in the outcome between wide surgical resection and micrographic surgery. The only predictive factor for distant metastases and/or death (p < 0.003) was histologic grade. Overall 10-year survival rate was 86 and 60 percent for primary and referred patients, respectively. We conclude that histologic diagnosis of sweat gland carcinoma must be complemented by clinical examination to evaluate metastases. Clinical behavior depends on the histologic type of tumor, degree of differentiation, and clinical stage. On recurrence, the likelihood of further recurrences and mortality increases dramatically. Aggressive initial local ablation with tumor-free margins is recommended. In high-grade tumors, prophylactic regional lymph node dissection may further characterize tumor aggressiveness and may justify adjuvant radiotherapy as part of the primary treatment.

Adenocarcinoma↗

Malignant eccrine tumor--a case report and a classification of tumors of eccrine sweat apparatus.

A case of malignant eccrine tumor and its histological findings were reported. In this case, we considered basal cell carcinoma or malignant melanoma clinically; however, the histological features matched those of malignant eccrine tumor. It has been said that it is very difficult to determine the origin of tumors of sweat apparatus; to contribute to this ongoing dialogue, the classification of tumors of eccrine sweat apparatus was also discussed.

Adult↗

Expression of differentiation antigens in benign sweat gland tumours.

Fifty benign sweat gland tumours were studied for the expression of carcinoembryonic antigen (CEA) and apocrine epithelial antigen (AEA), using immunohistochemical methods. CEA was found in thirty-two and AEA in thirty-three neoplasms. Both antigens were located in the epithelium of the luminal structures and in the intraluminar material and CEA was occasionally found also in proliferating cells. Co-expression of CEA and AEA occurred frequently in cases of syringoma, syringocystadenoma papilliferum, hidradenoma papilliferum, eccrine spiradenoma and clear cell hidradenoma. AEA was seen also in tumours showing eccrine differentiation, even though it is not present in normal eccrine sweat ducts.

Antigens, Neoplasm↗

Presence and distribution of carcinoembryonic antigen and lectin-binding sites in benign apocrine sweat gland tumours.

The presence and distribution of carcinoembryonic antigen (CEA) and lectin-binding sites in benign apocrine sweat gland tumours was investigated using immunoperoxidase and immunofluorescent techniques respectively. CEA was present in apocrine hidrocystoma, hidradenoma papilliferum, and syringocystadenoma papilliferum. The distribution pattern of CEA was indistinguishable in each of the three types of tumour. The distribution of lectin-binding sites was similar in all cases of a given type of neoplasm, and the staining patterns were similar but not identical in hidradenoma papilliferum and syringocystadenoma papilliferum. However, the distribution of lectin-binding sites in apocrine hidrocystoma was different. These results could be useful in elucidating the nature of the cells of origin of benign apocrine sweat gland tumours and providing a basis for their classification.

Adenoma, Sweat Gland↗

Electrical field stimulation of isolated primate sweat glands.

An in vitro method is described for inducing secretion in isolated monkey eccrine sweat glands by means of electrical field stimulation (EFS). Ultrastructural analyses of these glands revealed unmyelinated nerve fibres surrounding the secretory coils. Numerous small clear vesicles, characteristic of cholinergic nerve terminals, were observed, along with a few which were large and dense-cored. EFS elicited an immediate secretory response which ceased abruptly upon termination of the current. The response was inhibited in a dose-dependent manner by atropine (IC50 1.5 X 10(-9) mol/l). Although most glands were completely inhibited by atropine, a minor atropine insensitive component was operative in some preparations. Physostigmine (10(-6) mol/l) potentiated the response to subthreshold EFS. Lidocaine (3 X 10(-4) mol/l) completely and reversibly blocked EFS but had no effect on methacholine (10(-6) mol/l) induced secretion. These results confirm that eccrine sweat gland activation is predominantly via cholinergic pathways and that EFS of isolated glands may be a useful model to study the control of secretory function in normal and diseased states.

Animals↗

Sweat-gland necrosis after beta-adrenergic antagonist treatment in a patient with pheochromocytoma.

We describe the dermatological consequences of treatment with a beta-adrenergic antagonist, atenolol, in a patient with pheochromocytoma. There were acral skin lesions, histologically characterized by epidermal and sweat-gland necrosis. It is believed that the combined action of severe local ischaemia and profuse sweating produced these lesions, which resembled histologically the changes found in patients comatose as the result of carbon monoxide or drug poisoning. The importance of such lesions in diagnosis is discussed.

Adrenal Gland Neoplasms↗

Effects of topically-applied antiperspirant on sweat gland function.

In subjects exposed to a hot environment, short-term topical pretreatment with aluminium zirconium tetrachlorhydrate delayed the onset of visible sweating although it failed to prevent the response. The delay was considered most probably to be due to the occlusive action, in the duct within the upper epidermis, of aluminium-containing conglomerates, which disappear after continuous sweating. However, microanalytical evidence indicated that ionic transport within the fundus secretory cells was also modified.

Administration, Topical↗

Sclerosing-sweat-duct (microcystic adnexal) carcinoma--a tumor from a single eccrine origin.

A patient with a sclerosing-sweat-duct carcinoma of the upper lip is reported. Histologically the tumour showed solid islands and strands of squamous cells and sparse small ductal structures, some of them containing central cores of dense eosinophilic keratin. All this was embedded in a sclerotic stroma. These features, in addition to positive immunoreactivity for carcinoembryonic antigen (CEA) in the lumina of small ducts, and the presence of S-100 protein-positive cells in some cords and ducts, are consistent with the notion that this tumour exhibits differentiation toward eccrine sweat structures.

Adenocarcinoma↗

The process of secretion in swine apocrine sweat glands.

The secretory process in swine apocrine sweat glands were studied by electron microscope. The sweat appeared to result from three different mechanisms: (a) fluid transport, probably involving a region of complex cellular interdigitations adjacent to the basement membrane, (b) exocytosis of vesicles, which in this species seem to be derived from the Golgi apparatus and finally (c) apocrine secretion.

Animals↗

Eccrine sweat gland carcinoma: an histologic and immunohistochemical study of 32 cases.

In an attempt to characterize the immunocytochemical attributes of eccrine sweat gland carcinoma, we studied 32 examples of this tumor with antibodies to epithelial membrane antigen (EMA), cytokeratin (CK), carcinoembryonic antigen, S100 protein, alpha-lactalbumin, salivary amylase, blood group isoantigens, beta-2-microglobulin, and Leu M1. All cases expressed EMA and CK, and 28 of 32 cases also displayed at least 2 of the 6 remaining antigens. No significant variations were noted in the immunophenotypes of histologic subtypes of eccrine carcinoma. These results provide an objective means of diagnostic separation between sweat gland carcinoma and other primary malignant cutaneous tumors. However, they do not appear to correlate with the degree of tumoral differentiation, and are of no assistance in the separation of benign and malignant sudoriferous neoplasms. The ability of immunocytochemical techniques to distinguish between primary malignant adnexal cutaneous tumors and metastases to the skin appears unlikely, but remains to be studied further. Also, the use of immunostaining panels is advised in the study of adnexal carcinomas, since no single determinant in isolation is specific for these neoplasms.

Adenocarcinoma↗

Immunohistochemical study of carbonic anhydrase in mixed tumours and adenomas of sweat and sebaceous glands.

Immunohistochemical distribution of carbonic anhydrase II (CA) in mixed tumours and adenomas of sweat gland origin and in sebaceous adenomas was demonstrated by the PAP method. Normal sweat glands, both eccrine and apocrine, clear cells of the secretory coils, and ductal epithelial cells all showed conspicuous staining for CA, and sebaceous glands were also positive. Mixed tumours of the skin indicated strongly positive staining for CA in the luminal cells of tubular and duct-like or cystic structures, while most of the other tumour cells were negative. In solid or massive foci, CA positive cells were found scattered among the cellular mass. Sebaceous adenomas were usually moderately positive for CA throughout the tumour.

Adenoma↗

Proliferation of eccrine sweat ducts associated with alopecia areata.

Proliferation of sweat ducts has been described as a reactive process in a variety of benign and malignant neoplasms and inflammatory conditions in the skin, including scarring alopecia. However, to our knowledge this phenomenon has not been observed in non-scarring alopecia. The following case documents such a proliferation arising in an alopecia consistent with alopecia areata. An 83-year-old female developed progressive, fairly well circumscribed patches of alopecia over a 2-3 year period. Unequivocal scarring was not present. Histopathological examination revealed non-scarring alopecia with miniaturized and telogen follicles and a proliferation of eccrine ductal structures in the reticular dermis. These ductal structures varied in size and degree of cystic dilatation and resembled a primary eccrine neoplasm, such as syringoma. Only minimal focal fibrosis was observed in association with the eccrine proliferation. In summary, this case indicates that eccrine sweat duct proliferation may occur in non-scarring alopecia and must be differentiated from a primary eccrine neoplasm.

Aged↗

Syringoma-like sweat duct proliferation in scalp alopecias.

We have reviewed a series of 585 scalp biopsies taken for histologic evaluation of hair loss and have looked for syringoma-like eccrine sweat duct proliferation. This feature was found in 6 specimens with scarring alopecia and one each with alopecia areata and female-pattern alopecia. Syringoma-like sweat duct proliferation appears to play no role in the etiology of hair loss.

Adenoma↗

Effects of season and lower ambient temperature on the structure of the sweat glands in anhidrotic horses.

Histological studies of the sweat glands of anhidrotic horses in the Hong Kong summer and under conditions of reduced thermal stress, both natural and controlled, were undertaken to determine if glandular regeneration occurs. Clinical data were collected for comparison with the histological results in each instance. Horses were assigned to one of three categories on the basis of the resulting change in the number of thin glandular profiles in a cooler environment. Group 1, which was classed as normal, had a low initial value, which was maintained. Group 2, typical of mild and moderately affected animals, had a high initial value, which fell markedly after as little as six weeks in the cool environment. Animals in Group 3, classed as severely affected, had a high initial value which remained high even after prolonged exposure to the cool environment. Light microscopical examination of the sweat glands in the heat, and after six weeks in a cool environment, provided a means of predicting the degree of anhidrotic severity and the potential for recovery in a cool climate. This was superior to clinical observation, although a diagnostic test based on glandular function is still required.

Animals↗