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At least 667 records · Page 37Linked to original sources

PubMed1984

Facial sweating in Horner's syndrome.

The distribution of sweating on the face was studied in 31 patients with Horner's syndrome. In patients whose lesion was known to be distal to the bifurcation of the common carotid artery impairment of sweating was confined to the medial aspect of the forehead and side of the nose. In more proximal lesions loss of sweating involved the whole of one side of the face. Facial sweating was normal in 6 patients with avulsion injuries of the brachial plexus and in 2 patients with a lateral medullary syndrome. These findings suggest that the pattern of sweating in Horner's syndrome may be useful in some patients in localizing the site of the lesion.

Adult↗

PubMed1988

Sweating and cardiovascular responses of aged men to heat exposure.

In this study, 6 older and 10 younger Japanese men were exposed, while sitting, to 40 degrees C and 40% relative humidity for up to 130 min. All participants were heat unacclimatized. Physiological measurements included sweat responses, esophageal and skin temperatures, nonevaporative heat exchange, heart rate, cardiac output, blood pressure, forearm blood flow, and metabolic heat production. There was no significant difference in sweat rate or in onset of sweating between the older and younger men; however, esophageal temperature at the onset of sweating was greater in the older men. Changes in skin temperature, nonevaporative heat exchange, metabolic heat production, heart rate, and cardiac output were the same during heat exposure in both age groups. However, forearm blood flow before and after exposure to heat was significantly lower in the elderly group. These data suggest that the greater health risk posed to resting, yet healthy, aged men by hot environments is not a consequence of inadequate sweating but could be associated with retardation of the vasodilation reflex, which can prevent effective transfer of the body heat to its shell, thus resulting in greater heat storage.

Adult↗

PubMed2001

Ectodysplasin-A1 is sufficient to rescue both hair growth and sweat glands in Tabby mice.

Mutations in the human ectodysplasin-A (EDA) are responsible for the most common form of the ectodermal dysplasia and the defective orthologous gene in mice produces the tabby phenotype, suggesting its vital role in the development of hair, sweat glands and teeth. Among several EDA splice isoforms, the most common and the longest EDA splice isoforms, EDA-A1 and EDA-A2, differing by only two amino acids, activate NF-kappaB-promoted transcription by binding to distinct receptors, EDAR and XEDAR. The extent to which any particular isoform is sufficient for the formation of hair, sweat glands or teeth has remained unclear. Here we report that transgenic expression of the mouse EDA-A1 isoform in tabby (EDA-less) males rescued development of several skin appendages. The transgenic tabby mice showed almost complete restoration of hair growth, dermal ridges, sweat glands and molars. The number of hair follicles in the transgenic mice is the same as in wild-type; though the development of follicles and associated glands varies from indistinguishable from wild-type to smaller and/or only partially formed. These results suggest that the other EDA isoforms may not be absolutely required for skin appendage formation, but consistent with distinctive temporal and spatial expression of the EDA-A2 isoform, are likely required for appropriate timing and completeness of development. Our data provide the first direct physiological evidence that EDA-A1 is a key regulator of hair follicle and sweat gland initiation; its soluble ligand form could aid in deriving therapeutic reagents for conditions affecting hair and sweat gland formation.

Animals↗

PubMed1996

Detection of methamphetamine in sweat by EIA and GC-MS.

Sweat was collected with the PharmChekTM sweat patch and drugs were eluted from the collection pad of the patch. A solid phase, enzyme immunoassay using microtiter plates was modified for analysis of methamphetamine in sweat. After methamphetamine administration, sweat contains primarily parent methamphetamine. The immunoassay was determined to have crossreactivity relative to 100% for the methamphetamine (MA) calibrators; to 144% for methylenedioxymethamphetamine (MDMA); to 30% for d-amphetamine; to 21% for methylenedioxyamphetamine (MDA); and to 8% for I-methamphetamine. The optimum cutoff concentration for this modified assay was determined by receiver operating characteristic analysis to be 10 ng/mL amphetamine equivalents. At this cutoff concentration the assay had a diagnostic sensitivity of 84.5% and a diagnostic specificity of 93.2% versus gas chromatography-mass spectrometry (GC-MS). The positive predictive value at a prevalence of 50% was 86%. The intra-assay precision at 10 ng/mL was 9.9% (coefficient of variation, CV) and the interassay CV was 13%. Analysis of spiked patches at plus or minus 25 and 50% around the cutoff gave a percent positive threshold of approximately 50% at a cutoff of 10 ng/mL and a 95% confidence level for a positive result by the EIA between 15 and 20 ng/mL. Of 18 potential adulterants that might be injected into or under the patch, two (tile cleaner and cough syrup) caused a false-positive response by immunoassay. All results were confirmed by GC-MS. The clinical sensitivity and specificity of the overall analysis system (sweat collection and analysis) were 85 and 100%, respectively, using known methamphetamine dosing of volunteers (10, 20, and 25 mg) as the reference standard.

Calibration↗

PubMed1997

Qualitative detection of opiates in sweat by EIA and GC-MS.

Sweat was collected with the PharmChek sweat patch, and drugs were eluted from the collection pad of the patch. A solid-phase enzyme immunoassay (EIA) using microtiter plates was modified for the analysis of opiates in sweat. After opiate administration, sweat contains primarily parent opiate (heroin, codeine) and lipophilic metabolites (6-monoacetylmorphine [6-MAM]). The immunoassay was determined to have a cross-reactivity with codeine of 588%, with hydrocodone of 143%, with diacetylmorphine of 28%, and with 6-MAM of 30% relative to 100% for the morphine calibrators. The optimum cutoff concentration for this modified assay was determined by receiver operator characteristic analysis using 215 patches from 95 subjects to be 10 ng/mL morphine equivalents. At this cutoff concentration the assay had a diagnostic sensitivity of 86.9% and a diagnostic specificity of 92.8% versus gas chromatography-mass spectrometry (GC-MS), which was the reference method. The positive predictive value at a prevalence of 50% was 86%. The intra-assay precision at 10 ng/mL was 7.8%, and the interassay coefficient of variation (CV) was 39%. Analysis of spiked patches around the cutoff gave a percent positive threshold of approximately 50% between 10 and 15 ng/mL and a 95% confidence level for a positive result by the EIA between 20 and 25 ng/mL. Eighteen possible adulterants that could be injected into or under the patch were studied. Two (tile cleaner and detergent) can cause false-positive responses in the immunoassay. Two adulterants reduced response to spiked drug (Visine eye drops and Ben Gay ointment), which could cause a false-negative response. All results were confirmed by GC-MS. The clinical sensitivity and specificity for detecting drug use by analyzing sweat collected from human subjects following known doses of codeine (0, 30, and 60 mg orally) or heroin (20 mg intravenously) were 76 and 100%, respectively.

Calibration↗

PubMedDate not supplied

Excretion of MBDB and BDB in urine, saliva, and sweat following single oral administration.

A procedure based on gas chromatography-mass spectrometry (GC-MS) for the simultaneous identification of N-methyl-1-(3,4-methylenedioxyphenyl)-2-butanamine (MBDB) and its desmethylated metabolite 3,4-(methylenedioxyphenyl)-2-butanamine (BDB) in urine, saliva, and sweat specimens is presented. For urine and saliva, the method involved the alkaline extraction of a 1-mL specimen (MDEA-d5 internal standard) into ethyl acetate followed by derivatization with heptafluorobutyric anhydride. Sweat specimens, which were collected by a sweat patch, were tested after methanolic elution. The procedure was used to study the excretion of MBDB and BDB in urine, saliva, and sweat after single oral administration of 100 mg of MBDB to one subject. Urine tested positive for 36 h with a peak concentration at 4 h. Immunoassays were positive for 24 and 4 h using FPIA and EMIT, respectively. Peak saliva concentration was observed at 2 h. MBDB and BDB were detected in saliva during the first 17 h. Finally, both compounds were excreted into sweat with a constant increase in concentration during the first 36 h followed by a decrease for the remaining time. In all the biological specimens that were tested, MBDB was present in higher concentrations than its metabolite.

3,4-Methylenedioxyamphetamine↗

PubMed1995

Alfentanil slightly increases the sweating threshold and markedly reduces the vasoconstriction and shivering thresholds.

BACKGROUND: Hypothermia is common in surgical patients and victims of major trauma; it also results from environmental exposure and drug abuse. In most cases, hypothermia results largely from drug-induced inhibition of normal thermoregulatory control. Although opioids are given to a variety of patients, the thermoregulatory effects of opioids in humans remain unknown. Accordingly, the hypothesis that opioid administration impairs thermoregulatory control was tested. METHODS: Eight volunteers were studied, each on 3 days: (1) a target total plasma alfentanil concentration of 100 ng/ml, (2) control (no drug), and (3) a target alfentanil concentration of 300 ng/ml. Each day, skin and core temperatures were increased sufficiently to provoke sweating. Temperatures subsequently were reduced to elicit peripheral vasoconstriction and shivering. Mathematical compensations were made for changes in skin temperature using the established linear cutaneous contributions to control of sweating (10%) and to vasoconstriction and shivering (20%). From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C) and unbound plasma alfentanil concentrations, the individual concentration-response relationship was determined. The concentration-response relationship for all the volunteers was determined similarly using total alfentanil concentrations. RESULTS: In terms of unbound concentration, alfentanil increased the sweating threshold (slope = 0.021 +/- 0.016 degrees C.ng-1.ml; r2 = 0.92 +/- 0.06). Alfentanil also significantly decreased the vasoconstriction (slope = -0.075 +/- 0.067 degrees C.ng-1.ml; r2 = 0.92 +/- 0.07) and shivering thresholds (slope = -0.063 +/- -0.037 degrees C.ng-1.ml; r2 = 0.98 +/- 0.04). In terms of total alfentanil concentration (degrees C.ng-1.ml), the sweating threshold increased according to the equation: threshold (degrees C) = 0.0014[alfentanil] + 37.2 (r2 = 0.33). In contrast, alfentanil produced a linear decrease in the core temperature, triggering vasoconstriction: threshold (degrees C) = -0.0049[alfentanil] + 36.7 (r2 = 0.64). Similarly, alfentanil linearly decreased the shivering threshold: threshold (degrees C) = -0.0057[alfentanil] + 35.9 (r2 = 0.70). CONCLUSIONS: The observed pattern of thermoregulatory impairment is similar to that produced by most general anesthetics: a slight increase in the sweating threshold and a substantial, linear decrease in the vasoconstriction and shivering thresholds.

Adult↗

PubMed1998

Up-to-date report of botulinum toxin type A treatment in patients with gustatory sweating (Frey's syndrome).

Several therapeutic approaches exist to treat gustatory sweating (Frey's syndrome) following parotidectomy. Because of the lack of effective treatment, a new therapeutic modality using botulinum toxin injections was presented previously by our group. The duration of the demonstrated positive effect was essentially unknown so far. Based on our experiences using this technique since December 1993, the purpose of this clinical investigation was to make an up-to-date report and demonstrate the duration of effect of BOTOX injections in patients with severe gustatory sweating. Nineteen patients with severe gustatory sweating have been treated with BOTOX by intracutaneous injections into the affected skin areas. The maximal follow-up time was 33 months. The results were obtained by interviews and controls using Minor's starch iodine test. In all treated cases (n = 19 patients, 22 treated sides) gustatory sweating ceased completely within 2 days. Side effects were absent. In 12 patients gustatory sweating reappeared. The mean duration of effect was 17.3 months (subjective personal communication of 18 patients). Findings show that intracutaneous injection of BOTOX is a highly effective, safe, and minimally invasive treatment of Frey's syndrome with long-lasting therapeutic effect.

Adolescent↗

PubMed2002

Comparison of sweat loss estimates for women during prolonged high-intensity running.

PURPOSE: This study evaluated the error produced by four commonly used field estimates and two prediction equations of total body sweat loss. METHODS: Eight women distance runners were studied during a 30-km treadmill run (approximately 70% .VO(2max)) in a warm (30 degrees C T(db)) and a cool (14 degrees C T(db)) environment. Total sweat loss (TSL) was determined from changes in body mass corrected for fluid intake (FI), urine losses (UL), clothing (trapped sweat, TS), CO(2)-O(2) exchange (metabolic mass loss, MML), and respiratory water loss (RWL). TSL was compared with four estimates of sweat losses (often employed in the field) from body mass changes corrected for: a) FI only (F-1); b) FI and TS (F-2); c) FI and UL (F-3); or d) FI, TS, and UL (F-4). Two prediction equations were used also for comparison to TSL values. RESULTS: In the warm environment, F-1, F-3, and F-4 accurately estimated (0.2-6.9%; P > 0.05) TSL, whereas F-2 produced a large error (15.3%; P < 0.05). In the cool environment, all four estimates produced large errors (14-41%; P < 0.05). Both prediction equations markedly underestimated (20-22%) TSL in the warm environment and underestimated (41%) or overestimated (20%) TSL in the cool environment. CONCLUSION: TSL can be accurately estimated from changes in body mass using F-1, F-3, or F-4 methods in hot environments; however, none of the methods accurately estimated actual TSL values in a cool environment. Neither prediction equation provided accurate estimates of TSL in warm or cool conditions for women runners. These results illustrate the difficulty of accurately estimating and predicting sweat losses in the field.

Adult↗

PubMed1989

Distribution of a prolactinlike material in human eccrine sweat glands.

Because prolactin has been implicated in the transport of electrolytes in several mammalian tissues, we have looked for the presence of prolactin in human eccrine sweat glands where a primary isotonic secretion, rich in sodium chloride, is produced and subsequently modified by recovery of some sodium and chloride in excess of water. Sweat glands were microdissected from skin biopsies and then fixed overnight in phosphate-buffered 4% formaldehyde. The fixed tissue was dehydrated (to 95%) in ethanol and then embedded in glycol methacrylate. Sections were cut (5 microns) and immunostained with antihuman prolactin (NIDDK IC2) and the specifically-bound antibody was visualized using a biotinylated second antibody and Vector ABC reagents. Prolactinlike immunoreactivity was localized in the clear cells of the secretory coil and, to a much lesser extent, in the basal layer of duct cells. In many of the clear cells, the immunoreactive material appeared as a lateral strip and occasionally, in favorable sections, as a horseshoe of reaction product a few microns in from the apical and lateral membranes. In a subset of clear cells, with more euchromatic nuclei and a long, thin cellular profile, the immunostaining was more intense and was localized in a more juxtanuclear position. Controls for endogenous peroxidase, and those using normal serum or antihuman prolactin serum preabsorbed with purified human prolactin, gave no peroxidase localization in the tissue. These results are important because 1) they represent the first demonstration of prolactin or a prolactinlike substance in the sweat gland, 2) the prolactinlike material was localized to clear cells that are thought to be responsible for much of the fluid secretion, 3) the necessity for prolactin or pituitary extract in primary cultures of sweat gland epithelium is potentially explained, although not fully understood, and 4) it means that further studies concerned with the possible influence of prolactin on ion transport in the sweat gland are warranted.

Humans↗

PubMed1975

IgE in human eccrine sweat.

By the use of a sensitive and specific double antibody radioimmunoassay, immunoglobulin E was demonstrated in sweat from 6 of 11 healthy volunteers; the concentrations of IgE ranged from 1 to 3.9 ng/ml of sweat. Six of seven patients with dermatitis and elevated levels of serum IgE also had high IgE levels in sweat; the highest IgE value in sweat was 75.5 ng/ml and was noted in a patient with atopic dermatitis. Thus, all the main immunoglobulin classes can be demonstrated in eccrine sweat.

Adult↗

PubMed2004

Acute effects of dehydration on sweat composition in men during prolonged exercise in the heat.

AIM: To determine whether acute exercise-heat-induced dehydration affects sweat composition, eight males cycled for 2 h at 39.5 +/- 1.6% VO2peak on two separate occasions in a hot-humid environment (38.0 +/- 0.0 degrees C, 60.0 +/- 0.1% relative humidity). METHODS: During exercise, subjects ingested either no fluid (dehydration) or a 20 mmol L(-1) sodium chloride solution (euhydration). The volume of solution, calculated from whole-body sweat loss and determined in a familiarization trial, was ingested at 0 min and every 15 min thereafter. Venous blood was collected at 0, 60 and 120 min of exercise and sweat was aspirated from a patch located on the dominant forearm at 120 min. RESULTS: Following the 2-h cycling exercise, sweat [Na+] and [Cl-] was greater (P < 0.05) in the dehydration trial (Na+ 91.1 +/- 6.8 mmol L(-1); Cl- 73.3 +/- 3.5 mmol L(-1)) compared with the euhydration trial (Na+ 81.1 +/- 5.9 mmol L(-1); Cl- 68.5 +/- 3.3 mmol L(-1)). In addition, dehydration invoked a greater serum [Na+] (142.2 +/- 0.7 mmol L(-1); P < 0.05), [Cl-] (105.8 +/- 0.6 mmol L(-1); P < 0.05) and [K+] (5.27 +/- 0.2 mmol L(-1); P < 0.05) over the euhydration values for [Na+], [Cl-] and [K+], respectively (138.9 +/- 0.6, 102.9 +/- 0.5 and 4.88 +/- 0.1 mmol L(-1)). Plasma aldosterone was also significantly higher during exercise in the dehydration trial compared with the euhydration trial (53.8 +/- 3.8 vs. 40.0 +/- 4.3 ng dL(-1); P < 0.05). CONCLUSIONS: Acute exercise-heat stress without fluid replacement resulted in a greater sweat [Na+] and [Cl-] which was potentially related to greater extracellular fluid [Na+], plasma aldosterone or sympathetic nervous activity.

Adult↗

PubMed1994

Immunohistochemical demonstration of myoepithelial cells in sweat gland carcinomas.

Although myoepithelial cells are detectable in many benign sweat gland tumours, little is known about their role in sweat gland carcinomas. To specifically demonstrate myoepithelial cells, paraffin sections from 46 sweat gland carcinomas were stained, using a standard avidin-biotin-peroxidase complex method, with the monoclonal alpha-smooth muscle actin antibody 1A4. Myoepithelial cells were not found in adenoid cystic eccrine carcinoma (n = 2), malignant nodular hidradenoma (n = 2), porocarcinoma (n = 4), extramammary Paget's disease (n = 12), sclerosing sweat duct carcinoma (n = 4) or in adenosquamous-mucoepidermoid carcinoma (n = 1). In contrast, myoepithelial cells were demonstrated in two of eight apocrine adenocarcinomas, one of six mucinous eccrine carcinomas and two of seven eccrine adenocarcinomas. In all these tumours myoepithelial differentiation was found in peripheral cells of solid tumour islands, or in basal cells of tubular structures. However, in most areas of the tumours, myoepithelial layers were discontinuous. Cells in the centre of solid tumour nodules, and luminal cells of tubular structures, were negative for alpha-smooth muscle actin. In analogy to breast tumours, in which malignancy and invasiveness correlate with scattered or absent myoepithelial cells, we suggest that disrupted myoepithelial layers in sweat gland carcinomas may be interpreted as a loss of the invasion barrier.

Actins↗

PubMed1995

Normal sweat secretion rate in patients with alopecia areata.

We have examined sweat secretion rates in 22 patients with alopecia areata, and 22 age- and sex-matched controls. Mean sweat rate on the forearm in patients with alopecia areata was 20 mg/cm2 per h (95% confidence limits 15-25 mg/cm2 per h), and in controls was 24.1 mg/cm2 per h (95% confidence limits 19.1-29.1 mg/cm2 per h). Sweat secretion was higher in males than females in both the disease and control groups (27.8 mg/cm2 per h [95% confidence limits 21.3-34.3 mg/cm2 per h], compared with 18.08 mg/cm2 per h [95% confidence limits 14.63-21.6 mg/cm2]; P > 0.01). Our results confirm the previously reported sex difference in sweat secretion rate, and demonstrate that there is no statistically significant difference between patients with alopecia areata and controls. We discuss our results in the light of a previous report claiming that patients with alopecia areata have reduced rates of cholinergic-induced sweating.

Adult↗

PubMed2005

No compensatory sweating after botulinum toxin treatment of palmar hyperhidrosis.

BACKGROUND: Primary focal hyperhidrosis is caused by excessive secretion by eccrine sweat glands, usually at the palms, soles and axillae. The underlying mechanism is unclear. In recent years botulinum toxin A has emerged as a useful treatment. Compensatory sweating, which is a major problem in many patients who have undergone transthoracic endoscopic sympathectomy for hyperhidrosis, has only rarely been reported after botulinum toxin. However, this potential side-effect of botulinum toxin treatment has not been systematically examined. OBJECTIVES: To investigate if treatment with botulinum toxin A in hyperhidrotic hands may cause compensatory sweating at other skin locations. METHODS: In 17 patients with a history of palmar hyperhidrosis repeated measurements of evaporation were made before and up to 6 months after treatment of the hands with botulinum toxin A. Recordings were made at 16 skin areas and compared with subjective estimates of sweating. RESULTS: Following treatment, palmar evaporation decreased markedly and then returned slowly towards pretreatment values, but was still significantly reduced 6 months after treatment. No significant increase of sweating was found after treatment in any nontreated skin area. CONCLUSIONS: Successful treatment of palmar hyperhidrosis with botulinum toxin does not evoke compensatory hyperhidrosis in nontreated skin territories.

Adolescent↗

PubMed1990

Characterization of soluble HLA molecules in sweat and quantitative HLA differences in serum of healthy individuals.

Soluble class I molecules were immunoprecipitated from human sweat and serum using the BB7.7 monoclonal antibody (mAb) coupled to immunomagnetic beads. Molecules were analysed biochemically on SDS-PAGE gels and finally by ID-isoelectric-focusing (IEF). Serum- and sweat-HLA IEF-band patterns of the same individual were fully identical, showing that HLA excreted in sweat possess polymorphic structures like those in serum. Quantitatively, we used a highly sensitive competitive enzyme-linked immunosorbent (ELISA) assay to determine soluble class I concentrations. The first group was that of non-HLA-A9 and -Bw62 sera, which were found to contain HLA levels with a mean concentration of 0.82 +/- 0.63 microgram/ml (n = 44). However, sera that were HLA-A23 or -24 (splits of HLA-A9) contained higher levels, with a mean of 3.2 +/- 0.94 microgram/ml (n = 20). Similarly, HLA-Bw62 individuals had a higher mean of 2.05 +/- 0.65 micrograms/ml (n = 10). The difference of the HLA-A9 group to the first group was statistically highly significant, P less than 0.0001, and that of the HLA-Bw62 to the first was also significant, P less than 0.004. Individuals who were both HLA-A9 and -Bw62 (n = 5) did not express significantly higher levels than those who only had one of these specificities. Sweat HLA levels had a mean of 0.42 +/- 0.4 microgram/ml (n = 10). These results show for the first time that soluble class I peptides are excreted in relatively high concentrations in sweat and possess polymorphic structures identical to those of serum HLA and that serum HLA levels are allotype dependent.

Female↗

PubMed1986

Saliva and sweat secretion in man during a one-hour calcium clamp.

The effect of a 1-h calcium infusion, directly regulated to obtain and maintain a predetermined blood calcium level ('calcium clamp'), on the composition of parotid saliva, mixed saliva, and sweat was determined in healthy volunteers. An increase in amylase content of the parotid saliva under hypercalcaemic conditions was observed, but the 'calcium clamp' had no effect on flow rate, total and ionized calcium, sodium, potassium, and phosphate levels as well as pH in parotid and mixed saliva. The sweat calcium concentration was negatively correlated with sweat rate, in contrast to sodium and chloride concentrations. Increasing serum calcium levels did not affect ionic composition of the sweat and sweat flow rate.

Adult↗

PubMed1973

The effect of pain on human sweating.

1. Attempts were made to induce emotional sweating in normal subjects by subjecting them to painful stimuli such as compression of pins on the forearm skin, immersion of the fingers in iced water, compression of the thoracic cage by rib calipers and ischaemic exercise of the forearm muscles.2. Changes in sweating were estimated by continuously monitoring the rate of total body weight loss.3. Of the painful stimuli used, only ischaemic forearm exercise significantly increased the rate of sweat secretion.4. Tasks in mental arithmetic caused much greater increases in sweat secretion than any of the pain stimuli except ischaemic pain.5. It is concluded that many varieties of pain, even when severe, do not induce sweating under laboratory conditions.

Body Weight↗