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PubMed1975

Effects of adrenergic stimulating and blocking agents on the eccrine sweat secretion in atopic dermatitis and psoriasis.

Quantitative measurements of eccrine sweat secretion following stimulation with adrenaline and terbutaline sulphate, a beta-stimulator, have been performed in patients with atopic dermatitis and psoriasis by means of the electrolytic water analyzer, "Meeco". Seasonal variations were demonstrated, the values being lower in the late autumn. The response to adrenaline could be blocked by phentolamine, an alpha-inhibitor, while propranolol, a beta inhibitor, had no effect.--The response to terbutaline was blocked by atropine and partly by practolol, a beta-inhibitor. Terbutaline induced a larger sweat response than isoprenaline, another beta-stimulator. A beta-receptor mechanism, in some way related to cholinergic receptors, is suggested.

Adrenergic Agonists↗
PubMed1986

Direct demonstration of high transepithelial chloride-conductance in normal human sweat duct which is absent in cystic fibrosis.

The transepithelial electrical potential difference (Vt) and the transepithelial resistance (Rt) were measured across individual microdissected sweat ducts obtained from biopsies of the scapular region of normal human volunteers and of a Cystic Fibrosis (CF) patient. During luminal and contraluminal perfusion with NaCl Ringer solution Vt and Rt were -10.7 +/- 1.1 (mV, lumen negative) and 10.9 +/- 1.7 (omega X cm2). Bilateral substitution of Cl- by gluconate increased Vt and Rt to -42.7 +/- 5.1 (mV) and 98.0 +/- 12.0 (omega X cm2), respectively. Luminal application of amiloride (10(-4) mol/l) collapsed Vt and increased Rt to 11.4 +/- 1.7 and 159.7 +/- 12.0 omega X cm2 in Cl- and gluconate Ringer respectively. These data indicate that 90% of the total transepithelial conductance is attributed to Cl- and 5% to Na+ while the remaining 5% is unaccounted for at present. In CF ducts Vt and Rt were high already in Cl- Ringer solution (-78.9 +/- 9.9 mV and 91.2 +/- 15.6 omega X cm2) and did not change significantly after replacement of Cl- by gluconate. The data demonstrate that normal human sweat duct epithelium, despite its ability to generate high electric and osmotic gradients, is a low resistance epithelium, probably because of a high Cl(-)-permeability of its cell membranes. In addition, the data demonstrate that this Cl(-)-conductance is missing in CF, in conformation of what has been postulated previously from simple potential measurements.

Adult↗
PubMed1987

Cutaneous blood flow and local sweating after systemic atropine administration.

Localized cutaneous vasodilation (flush) is seen following systemic atropine administration. To verify calculated enhanced dry heat loss with actual changes in cutaneous blood flow, four men were studied in both control and atropine (0.025 mg.kg-1; im) experiments (Ta = 30 degrees C, Tdp = 7 degrees C) during moderate exercise (55% VO2 peak). Esophageal temperature (Tes) and arm sweating (ms) by local dewpoint were measured continously. Skin (forearm) blood flow (FBF) was measured twice each minute by venous occlusion plethysmography. Injection of atropine (2 mg) caused an increased sensitivity (+85%, p less than 0.01) in FBF to Tes with no change in the vasodilator threshold. An elevated Tes onset (0.3 degrees C, p less than 0.05) for sweating occurred with no change in the sensitivity of ms to Tes (-27%, p less than 0.20). No elevation in either forearm or Tsk occurred before the onset of vasodilation, however, both mean skin (Tsk) and local arm temperatures were higher in the atropine experiments after 15 min of exercise. Systemic atropine resulted in higher cutaneous vasodilation at the same core temperature with the local skin temperature following passively. The effect of systemic atropine in stimulation of increased cutaneous vasodilation is suggested to result by a combination of central and local responses which may be mediated through the release of vasoactive sustances.

Adult↗
PubMed1995

Seasonal variation in sweating responses of older and younger men.

Eight older (60-65 years) and six younger (20-25 years) men were exposed to a standard heat stress for 60 min in summer, autumn, winter, and spring. The test consisted of placing the lower legs and feet in a 42 degrees C water bath while sitting in constant environmental conditions (30 degrees C and 45% relative humidity). The increase of rectal temperature (delta Tre) was significantly greater (P < 0.05) in autumn, winter, and spring than in summer for the older group, but significantly greater only in winter than in summer for the younger group (P < 0.05). The delta Tre was greater for the older group in all seasons, but of significance only in autumn and spring (P < 0.01). There were no significant season-related differences for metabolic heat production (M) and mean skin temperature (Tsk) during the heat test in the respective groups, although the M and Tsk were lower for the older group in all seasons (P < 0.01). In the older group total body sweating rate (msw) divided by delta Tre (total msw/delta Tre) decreased from summer to winter (P < 0.02) and did not differ between winter and spring, whereas total msw/delta Tre in the younger group increased in spring after decreasing from autumn to winter (P < 0.03). The variations of the value, local sweating rate on the back and thigh divided by delta Tre (back msw/delta Tre and thigh msw/delta Tre), were similar to those of the total msw/delta Tre in each group, except for back msw/delta Tre in the younger group, which did not increase from winter to spring.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1981

Eccrine sweat glands are not innervated in hereditary sensory neuropathy type IV. An electron-microscopic study.

The ultrastructural study of a skin biopsy in a patient afflicted with hereditary sensory neuropathy type IV (congenital insensitivity to pain with anhidrosis) did not reveal any unmyelinated axons or axonal terminals around eccrine sweat glands but only processes, partially covered by a basement membrane and therefore resembling Schwann cell processes. The absence of such unmyelinated axons in close proximity to eccrine sweat glands where they normally occur appears to be the morphological equivalent to the anhidrosis and also corresponds to the deficiency of unmyelinated axons in the sural nerve of the same patient, as previously reported.

Basement Membrane↗
PubMedDate not supplied

The distribution of substance P-, CGRP-, galanin- and ANP-like immunoreactive nerves in human sweat glands.

The distribution in immunoreactivities towards atrial natriuretic peptide, calcitonin gene-related peptide, galanin and substance P were demonstrated in human skin at the light and electron microscopic levels. Nerves immunoreactive to the first three of these peptides were found around eccrine sweat glands, whereas only a few positively-labelled nerve fibres could be seen around apocrine glands. At the ultrastructural level, immunoreactivity to the neuropeptides was localized in the large dense-cored vesicles of the nerve terminals. No immunoreactivity to substance P could be detected around sweat glands. In addition to these findings, the four types of immunoreactivity were seen in the thick preterminal nerve bundles.

Atrial Natriuretic Factor↗
PubMed1977

Pharmacology and function of the myoepithelial cell in the eccrine sweat gland.

Both acetylcholine and a Ca-ionophore, A23187, are comparatively strong stimulants of eccrine sweat secretion in vitro. Nevertheless, the contraction of the secretory coil was seen only after stimulation with acetylcholine but not with alpha or beta adrenergic drugs or with A23187. It was thus inferred that the myoepithelial contraction may not be playing an indispensable role in the overall process of eccrine sweat secretion.

Acetylcholine↗
PubMed1985

Urea excretion in sweat during short-term efforts of high intensity.

The sweat urea excretion during different types of short-term efforts of high intensity was examined in well trained competitors. It has been found that considerable amounts of urea were excreted in the sweat during each exercise test investigated. It is concluded that the purine nucleotide cycle was the source of ammonia for the increased urea formation during the efforts.

Adolescent↗
PubMed1993

A simple clinical staging system that predicts progression to AIDS using CD4 count, oral thrush, and night sweats.

OBJECTIVE: To develop a simple clinical staging system based on CD4 count and clinical variables that predicts progression to AIDS in HIV-infected non-AIDS patients. DESIGN: Retrospective cohort study. SETTING: A primary care outpatient clinic for HIV-infected patients at a VA Medical Center. PATIENTS: One hundred seventy-six HIV-infected non-AIDS patients seen at the Houston VA Special Medicine Clinic between January 1986 and December 1990 and followed for a mean of 22 months. Fifty-four patients (31%) progressed to AIDS during follow-up. MEASUREMENTS: The medical records were reviewed, and data corresponding to the initial (baseline) clinic visit and subsequent six-month visits were extracted. MAIN RESULTS: "Predictive" baseline variables (i.e., those associated with progression to AIDS) were first identified and then examined in Cox proportional hazards modeling. In the final model, CD4 category, oral thrush, and night sweats made significant independent contributions. A three-stage prognostic system was constructed by assigning points to the three variables: CD4 > 500 cells/mm3 = 0; 500 > or = CD4 > or = 200 = 1; CD4 < 200 = 2; presence of oral thrush = 1; presence of night sweats = 1. Stages were assigned as follows: stage I = 0 points, stage II = 1-2 points, and stage III = 3-4 points. The proportions of patients who progressed to AIDS were: stage I, 6/39 (15%); stage II, 31/106 (29%); and stage III, 17/31 (55%). CONCLUSIONS: These results demonstrate that simple, clinically sensible prognostic staging systems that predict progression to AIDS can be constructed using CD4 count and clinical variables.

AIDS-Related Opportunistic Infections↗
PubMed1985

Culture of sweat gland epithelial cells from normal individuals and patients with cystic fibrosis.

Recent electrophysiological and pharmacological studies have confirmed previous clinical evidence that the gene defect in cystic fibrosis is strongly expressed in the sweat gland. This has provided a major impetus to efforts to culture the cells of this tissue in order to provide a source of experimental material for molecular studies. Toward this end, eccrine sweat glands were isolated from collagenase treated skin specimens and the secretory coil and the reabsorptive duct separated. Segments of each portion of the gland were transferred to a plastic or collagen substrate and covered with serum-containing or serum-free defined growth media. Epithelial cell outgrowth took place in both media but fibroblast overgrowth occurred in the presence of serum at concentrations as low as 1%. In serum-free medium both secretory and reabsorptive cells formed tightly joined epithelial sheets, first as monolayers and later as multilayers consisting of at least six cell layers. Growth continued for approximately fifteen generations each of about two and a half days. Remarkably large domes or hemicysts with diameters as great as two cm were formed, apparently attesting to the retention of the capacity of the cells to actively transport ions and water. Ultrastructurally, cells which grew out from the secretory coil resembled the fluid secreting clear cells; neither dark cells nor myoepithelial cells were propagated.

Cell Division↗
PubMed1989

Human sweat duct cells in primary culture. Basic bioelectric properties of cultures derived from normals and patients with cystic fibrosis.

Human sweat duct cells from the coiled reabsorptive segment have been cultured successfully, free from fibroblasts, in a low serum, hormone-supplemented medium, Ham's F12. The cultured cells exhibited a typical epithelial cobblestone pattern, and microvilli-covered luminal cells were seen joined together with typical junctional complexes. In cultures derived from normals and patients with cystic fibrosis (CF), growth and morphologic characteristics were indistinguishable. When grown on a membranous support, and mounted in an Ussing chamber, vectorial electroconductive ion-transport could be identified. The epithelial preparations produced active mucosa to serosa-directed sodium flux via amiloride-sensitive, apical sodium channels and ouabain-sensitive sodium pumps located in the basolateral membrane, which also contained a potassium shunt. These findings are consistent with a polarized epithelium with properties similar to the intact organ. High transepithelial resistance and increased amiloride sensitivity were typical for cells derived from CF, indicating that principal normal as well as pathologic properties of the sweat duct are preserved in culture.

Adolescent↗
PubMed1986

Treatment of metastatic sweat gland carcinoma by a four drug combination chemotherapy: response in two cases.

Two patients with metastatic sweat gland carcinoma were treated with a combination chemotherapy consisting of adriamycin, cyclophosphamide, vincristine and bleomycin. In one patient, a complete remission of two years' duration, and in the other a partial remission (4 + months) were achieved. A review of the literature about chemotherapy in metastatic sweat gland carcinoma is given.

Adenocarcinoma↗
PubMed2006

The use of botulinum toxins to treat hyperhidrosis and gustatory sweating syndrome.

Hyperhidrosis is a chronic condition characterized by excessive sweating. Recent studies report that it affects approximately 2.8% of the population and typically begins during adolescence. Gustatory sweating usually occurs after parotid gland injury or surgery, and both disorders can be debilitating for those who are affected. Both diseases respond very well to botulinum toxin therapy and this article will review the use of botulinum toxins, including the serotypes used, dosing, and complications.

Animals↗
PubMed2001

[Sweat gland carcinoma in the axillary area. A case report and review of the literature].

The sweat gland carcinoma is a rare tumor, representing in approximately 1% of primary skin lesions. In the literature 220 cases of sweat gland carcinomas have been presented over the last three decades. The medium age is 57 years, with an equal male-to-female distribution. Topographically, the tumor is located at the lower limbs (32.9%), the upper extremities (28%), and the head (26%). Involvement of the trunk is rare. Diagnosis can be complicated as the carcinoma is a rare entity, with no correlation of its histologic classification and biologic presentation. This can only implicate the difficulties in treatment.

Adenocarcinoma↗
PubMed2005

ENaC activity requires CFTR channel function independently of phosphorylation in sweat duct.

We previously showed that activation of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) Cl- conductance (gCFTR) supports parallel activation of amiloride-sensitive epithelial Na+ channel (ENaC) in the native human sweat duct. However, it is not clear whether phosphorylated CFTR, phosphorylated ENaC, or only Cl(-) -channel function is required for activation. We used basilaterally alpha-toxin-permeabilized human sweat ducts to test the hypothesis that ENaC activation depends only on Cl(-) -channel function and not on phosphorylation of either CFTR or ENaC. CFTR is classically activated by PKA plus millimolar ATP, but cytosolic glutamate activation of gCFTR is independent of ATP and phosphorylation. We show here that both phosphorylation-dependent (PKA) and phosphorylation-independent (glutamate) activation of CFTR Cl- channel function support gENaC activation. We tested whether cytosolic application of 5 mM ATP alone, phosphorylation by cAMP, cGMP, G-protein dependent kinases (all in the presence of 100 microM ATP), or glutamate could support ENaC activation in the absence of gCFTR. We found that none of these agonists activated gENaC by themselves when Cl- current (I(Cl-)) through CFTR was blocked by: 1) Cl- removal, 2) DIDS inhibition, 3) lowering the ATP concentration to 100 microM (instead of 5 mM required to support CFTR channel function), or 4) mutant CFTR (homozygous DeltaF508 CF ducts). However, Cl- gradients in the direction of absorption supported, while Cl- gradients in the direction of secretion prevented ENaC activation. We conclude that the interaction between CFTR and ENaC is dependent on activated I(Cl-) through CFTR in the direction of absorption (Cl- gradient from lumen to cell). But such activation of ENaC is independent of phosphorylation and ATP. However, reversing I(Cl-) through CFTR in the direction of secretion (Cl- gradient from cell to lumen) prevents ENaC activation even in the presence of I(Cl-) through CFTR.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2005

[Mucinous sweat gland carcinoma of a toe with metastasis to the maxilla. A case report].

Malignant tumors of the maxilla are rare. In addition to primary tumors metastatic disease has to be considered. Renal cell carcinomas, carcinomas of the breast, lung and adenocarcinomas are constituting the most frequent primary lesions for maxillary metastases. To the best of our knowledge, we present the first case of a mucinous sweat gland carcinoma metastasizing to the maxilla four years after primary diagnosis. Thirty-two months after resecting the hemimaxilla, there are no signs of local recurrence. Although skin tumors only rarely develop distant metastases, sweat gland carcinomas should be included in the differential diagnosis of tumors metastasizing to the maxilla.

Adenocarcinoma, Mucinous↗
PubMed1998

Codeine testing in sweat and saliva with the Drugwipe.

With the growing interest in drug testing within different sectors of society, there has become a need for drug assays that can be performed immediately at the site of specimen collection. Recently, Securetec (Ottobrunn, Germany) has introduced the Drugwipe, a non instrument-based, on-site immunodiagnostic assay for the detection of drugs on surfaces. Different tests are available for opiates, cocaine and cannabis. To document the applications of the Drugwipe "opiate" on human biological fluids, 60 mg codeine phosphate were orally administered to 6 subjects. First, sweat testing with the Drugwipe was studied. The wiping section of the kit was used to swab the forehead of the subjects for 10 s, at 1, 4, 9 and 24 h after codeine administration. At the same time, for each period, a sweat patch (Pharmchek, USA) was applied to the outer portion of the upper arm. Codeine was then quantified in the patch by GC/MS and the measured concentrations used as reference. In all subjects except one the Drugwipe tested positive for opiates, however with few false negative results. In the second part of the study, results of the Drugwipe were compared with those obtained by GC/MS for saliva. The tongue of the subjects was carefully wiped over a period 24 h, and at the same time a specimen of saliva collected. Although codeine could be detected using the Drugwipe, numerous false negative results were observed. Codeine tested positive by GC/MS but remained negative using the Drugwipe in several cases. This can be explained by a codeine concentration which was too low to show positive with the Drugwipe, interfering substances may be present in saliva or the sampling procedure is inadequate.

Adult↗