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Differences in composition of sweat induced by thermal exposure and by running exercise.

To determine the differences in sweat composition between sweat induced by thermal stress alone and that induced by physical exercise, seven young healthy men first sat in a hot room and then performed running exercise. A 20-minute stay in a climate chamber at 40 degrees C resulted in a 5% reduction in body weight. The same body weight loss was induced by running exercise. Both sodium and chloride concentrations were much lower in the sweat induced by thermal exposure than that induced by the running exercise (p less than 0.01), while urea nitrogen and creatinine concentrations were significantly higher after thermal exposure than after the running exercise (p less than 0.01). Potassium concentrations did not differ significantly with either procedure. These findings suggest that sweat composition varies with the kind of induction and that more salt seems to be lost through exercise-induced sweating than by just sitting in a hot environment.

Adult↗

Lymphatic mapping and sentinel lymph node biopsy in the detection of early metastasis from sweat gland carcinoma.

BACKGROUND: Several subtypes of sweat gland carcinoma have been found to demonstrate a propensity to metastasize systemically and to regional lymph nodes. The predictive value and benefit of sentinel lymph node (SLN) biopsy have been established in numerous other malignancies, but to the authors' knowledge there is little literature published to date regarding the use of SLN biopsy in patients with sweat gland carcinoma. In the current study, the authors demonstrated the utility of SLN biopsy in detecting subclinical metastases of sweat gland carcinoma, which may result in early treatment. METHODS: The authors identified five patients with malignant eccrine tumors in whom SLN biopsy was performed at the study institution. Clinical and histopathologic data were reviewed. RESULTS: The five study cases included two cases of aggressive digital papillary adenocarcinoma (both occurring on upper extremity digits), two cases of hidradenocarcinoma (occurring on the knee and foot, respectively), and an eccrine carcinoma (occurring on the scalp). In each biopsy-established case, there was no clinical evidence of metastatic disease, and a wide local excision or amputation was performed with concurrent SLN biopsy. Four of 18 SLNs in 3 of the 5 patients (60%) were found to be positive for metastatic carcinoma, as identified in hematoxylin and eosin stains and/or cytokeratin immunohistochemical stains. All three lymph node-positive patients subsequently underwent regional lymphadenectomy and were found to have no evidence of additional metastases. CONCLUSIONS: The results of the current study demonstrate that SLN biopsy detects subclinical metastases from sweat gland carcinomas to regional lymph nodes. SLN mapping and biopsy at the time of resection can provide useful information with which to guide early treatment. Further studies are necessary to determine whether this procedure results in a survival benefit in patients with sweat gland carcinomas.

Adenoma, Sweat Gland↗

Reinnervation of sweat glands in the mouse: axonal regeneration versus collateral sprouting.

The capacity of sudomotor axons to reinnervate sweat glands by regeneration after freezing was compared with their capacity to reinnervate by the mechanism of collateral sprouting. Two groups of mice were prepared in the same manner, with a single exception. All nerves to the hind paw were cut and tied to prevent regrowth. The exception, the lateral plantar nerve, was left intact in one group and frozen at the ankle in the other group. Reinnervation of sweat glands in the paw was charted frequently for 10 weeks using a silastic mold method. We found that sudomotor axons regenerating from the frozen nerve functionally reinnervated sweat glands of the paw sooner, beginning at 15 days postoperation, and at a higher rate than reinnervation from the collateral branching intact nerve, that began at about 25 days. Full recovery occurred by 41 days in most animals of both groups. We also found that stimulation of sweating by pilocarpine activated more sweat glands during the reinnervation period than stimulation by heating the mice, suggesting that the newly regenerating sudomotor axons have a high threshold.

Animals↗

Renin-like (angiotensinogenase) activity in sweat of patients with cystic fibrosis and controls.

Using bioassay method (rat blood pressure technique) as well as the radioimmunoassay, renin-like activity (RLA) was measured in eccrine sweat of patients with cystic fibrosis of the pancreas (CF) and of controls. Sweat-formation was induced by pilocarpine-iontophoresis or by local injection of carbamylcholine (Doryl). RLA-values between O (not measurable) and 460 ng/ml.h were measured. With increasing sweat flow-rate a tendency to lower RLA-values was detected. No significant difference was observed between CF and controls. From the observation that RLA of sweat is up to 30 times higher than that of plasma, it is concluded that RLA is probably released not from plasma but from the sweat glands themselves, where it is stored or synthesized.

Adolescent↗

Mechanisms of underdeveloped sweating responses in prepubertal boys.

To approach the mechanisms underlying the underdeveloped sweating responses of prepubertal boys, 8 boys (7-11 years old) and 11 men (21-25 years old) were exposed to a standard heat stress for 60 min. The test consisted of placing the subjects' lower legs into a 42 degrees C water bath while they sat in otherwise constant environmental conditions (ambient temperature 25 degrees C and 45% relative humidity). Rectal (T[re]) and skin temperatures, local sweating rates (mSW: on the chest, back, forearm and thigh) and the frequency of sweating expulsions (fSW: as an indicator of central sudomotor activity) were measured during the test. During the passive heating, no group differences were observed for the increase in T(re), mean skin temperature and metabolic heat production. However, mean body temperature (Tb) during heating was significantly higher for the boys (P < 0.001) because of a higher baseline T(re). The boys had lower mSW on the chest (P < 0.004) and thigh (P < 0.001) during the latter half of the 60-min exposure compared to the young men, although a similar mSW was observed between the groups during the first half of the test. The group difference of mSW on the back was similar to that of the chest and thigh, but the difference was not significant (P = 0.10). In contrast, the boys had a greater mSW on the forearm throughout the heating (P < 0.03). The slope of the mSW vs fSW relationship was significantly lower for the chest and thigh in the boys compared to the men (P < 0.05), and the same tendency was observed for the back (but was not significant, P = 0.10). In contrast, no difference was observed between the groups for the slope of mSW vs fSW for the forearm. Furthermore, a lower sweat output per gland was also observed on the chest, back, and thigh in the boys (P < 0.01), but not on the forearm. No group difference was observed for the slope of the fSW vs Tb relationship. These results suggest that the lower mSW observed in the prepubertal boys were due possibly to underdeveloped peripheral mechanisms, including the sweat glands and their surrounding tissues, rather than to an underdeveloped central drive activity related to sudomotor function. Regional differences may well exist in any underdeveloped peripheral mechanism associated with maturation.

Adult↗

Failure to produce axon reflex-sweating in the volar skin of Japanese monkey (Macaca fuscata) and crab-eating monkey (Macaca irus).

The functional properties of the sweat glands and their innervation in the volar skin of three Japanese monkeys and two crab-eating monkeys were investigated. The sweat glands responded to both cholinomimetic and adrenomimetic agents, the former being highly predominant in the sudorific effect. Spontaneous emotional sweating was strongly or completely inhibited by atropine at 10(-8)-10(-7) g/ml, but not by dihydroergotamine at 10(-5)-10(-4) g/ml. Axon reflex sweating could not be produced by nicotine at 10(-5)-10(-4) g/ml in all of primates tested. The nerve fibers surrounding the sweat glands were histochemically confirmed to contain both acetyl- and butyrylcholinesterase.

Acetylcholine↗

Somatotopic arrangement of sudomotor axon reflex sweating in humans.

BACKGROUND: Impaired sweating may be one of the first symptoms in neuropathies, and therefore the evaluation of sweating might facilitate their early detection. Sudomotor axon reflexes can be quantified by two different methods: quantitative sudomotor axon reflex testing (QSART) measures the amount of local sweating, whereas staining with the iodine starch reaction assesses the extension of the sudomotor axon reflex area. The aim of our study was to compare both tests at three different sites on the leg: foot, lower leg and thigh. METHODS: QSART and iodine starch staining after iontophoretic stimulation with acetylcholine were performed on 15 male volunteers (mean age: 25; range 24-27 years) on the left resp. the right leg during a single session. RESULTS: QSART response, measured as area under the curve (AUC), was maximal at the lower leg (911 AUC), smaller at the dorsum of the foot (585 AUC) and even smaller at the thigh (480 AUC). The difference between lower leg and thigh was significant (p < 0.02). The sudomotor axon reflex area was also biggest on the lower leg (39 cm(2)) followed by the foot dorsum (28 cm(2)), and then the thigh (16 cm(2)). The differences between lower leg and thigh as well as between lower leg and foot were significant (p < 0.01, resp. p < 0.04). The size of the sudomotor axon reflex areas and QSART responses were correlated (p < 0.01). CONCLUSIONS: QSART and sudomotor axon reflex areas had similar somatotopic arrangements in human skin. The bigger the axon reflex area was the stronger the QSART response was. This indicates that the size of the innervation territories of sudomotor fibres covaries with the amount of local sweat production. The latter is a surrogate for increased sweat gland density or capacity in skin areas of dense sudomotor innervation.

Acetylcholine↗

Evaluation of direct and axon reflex sweating in the mouse.

The nicotinic axon reflex-mediated sudomotor response was studied in mice and rats by recording the impressions of sweat droplets made in silicone molds after local injection of nicotine, and compared with sweating induced by acetylcholine and pilocarpine. Nicotine failed to activate mouse plantar sweat glands at any of the concentrations used (from 3 x 10(-6) to 3 x 10(-1) M). On the contrary, both acetylcholine and pilocarpine produced a dose-dependent increase in the number of secreting sweat glands. The location of sweat glands reactive to pilocarpine and acetylcholine was similar and restricted to the pads near the site of injection. We conclude that the sudomotor axon reflex response mediated by nicotinic receptors is not present in the mouse and the rat.

Acetylcholine↗

Dermcidin: a novel human antibiotic peptide secreted by sweat glands.

Antimicrobial peptides are an important component of the innate response in many species. Here we describe the isolation of the gene Dermcidin, which encodes an antimicrobial peptide that has a broad spectrum of activity and no homology to other known antimicrobial peptides. This protein was specifically and constitutively expressed in the sweat glands, secreted into the sweat and transported to the epidermal surface. In sweat, a proteolytically processed 47-amino acid peptide was generated that showed antimicrobial activity in response to a variety of pathogenic microorganisms. The activity of the peptide was maintained over a broad pH range and in high salt concentrations that resembled the conditions in human sweat. This indicated that sweat plays a role in the regulation of human skin flora through the presence of an antimicrobial peptide. This peptide may help limit infection by potential pathogens in the first few hours following bacterial colonization.

Amino Acid Sequence↗

Biomarkers of inflammation in sweat after myocardial infarction.

ST-elevation myocardial infarction (STEMI) triggers a significant inflammatory response. Sweat may offer a novel, non-invasive medium for monitoring inflammation. In this prospective study, we characterized the inflammatory signatures in plasma and sweat collected from the skin surface of two patient groups: (1) 18 STEMI patients immediately following percutaneous coronary intervention (exposure) and (2) six patients who underwent outpatient angiography without subsequent intervention (control). Levels of 92 biomarkers were measured using a high-throughput proteomic assay and reassessed after 4-6&#xa0;weeks in STEMI patients. Adjusting for patient group, sweat biomarkers did not show significant changes over time. In plasma, hepatocyte growth factor and interleukin-6 showed a significant decrease from the acute phase to follow-up, adjusted for patient group. STAM binding protein was significantly higher in the sweat of STEMI patients compared to controls, adjusted for time effects. While sweat was less sensitive than plasma for detecting biomarker levels in the setting of STEMI, its longitudinal analysis via wearable sensors holds promise for detecting specific markers.Trial registration: The trial is registered on www.clinicaltrials.gov with the trial registration number NCT05843006.

Aged↗

Disorders of sweating.

The clinical spectrum of sweating disorders includes sudomotor excess and deficiency. Hyperhidrosis is characterized by sweating beyond that required to maintain a constant internal body temperature. Hypohidrosis and anhidrosis are distinguished by a reduced or absent ability to generate sweat for the purpose of evaporative heat dissipation. Whereas hyperhidrosis is usually benign, anhidrosis may predispose to hyperthermia. Either hyperhidrosis or anhidrosis may accompany a more serious underlying disorder. Correct diagnosis depends on determining the anatomical pattern of sweating and localizing the lesion within the autonomic nervous system. Sudomotor deficits may involve the frontal operculum, hypothalamus, brain stem, spinal cord, sympathetic chain ganglia, peripheral nerve, or eccrine sweat glands. Treatments for hyperhidrosis include topical aluminum chloride, oral anticholinergic agents, intradermal botulinum toxin for some localized syndromes, and thoracic ganglionic sympathotomy or sympathectomy for refractory palmar hyperhidrosis.

Animals↗

Treatment of gustatory sweating with low-dose botulinum toxin A: a case report.

UNLABELLED: Frey's syndrome, gustatory sweating in the preauricular area, is an unpleasant phenomenon occurring during meals after surgery on the parotid gland. Recently, botulinum toxin A (BTX) has been shown to reduce the symptoms, but the variation in the reported doses is large. OBJECTIVE: To quantify the effect of treatment with low-dose BTX in a case of Frey's syndrome over a period of 6 months. MATERIAL AND METHODS: A 56-year-old woman was treated with 10 U Botox given as 20 single, intracutaneous injections of 0.5 U, one for each cm(2), 3 years after resection of the parotid gland. Before treatment and repeatedly during the 6-month period, the sweating was rated subjectively on a 100-mm visual analog scale (VAS) and by a severity index, and objectively by assessment of the extent of the involved skin area using Minor's iodine-starch test, staining the area of sweating dark. RESULTS: The treatment decreased the involved area from 20 to 5 cm(2) and the VAS ratings from 98 to 8 mm. The index showed that treatment affected the sweating intensity, not the frequency. After the 6-month period the patient was still satisfied, but the involved skin area had increased; however, not entirely to pretreatment values. CONCLUSIONS: The effect of BTX injections for gustatory sweating obtained in this case was comparable to results reported using higher doses. Low doses of BTX can therefore be used in the treatment of Frey's syndrome, but studies to clarify the dose-response relationship, in terms of both time-course and obtained effect, are needed.

Botulinum Toxins, Type A↗

Heat--sweat--dehydration--rehydration: a praxis oriented approach.

In any situation where heat production as a result of physical exercise exceeds heat elimination from the body by radiation and convection, the body will depend on sweat secretion and evaporation for its thermoregulation. Sweat secretion will reach maximal levels at high energy expenditures in the heat but will be limited when exercising in the cold climate. Athletes and their coaches should understand some of the principles of thermoregulation in order to make an adequate decision about optimal fluid and carbohydrate replacement in a specific situation. In general it is advised that the carbohydrate content of rehydration drinks should be low (max 80 g l-1) when sweat loss is maximal, may be intermediate when both carbohydrate availability and moderate dehydration influence performance (up to 110 g l-1), and may be maximal (up to 160 g l-1) when the sweat loss is minimized and carbohydrate is the major determinant of the rate of fatigue development. Sodium should be added to rehydration drinks in order to maximize fluid and carbohydrate absorption. A range of electrolyte values for replacement of sweat induced losses, based on whole body wash down procedure is presented.

Body Temperature Regulation↗

Urea excretion in human sweat as a tracer for movement of water within the secreting gland.

Previous workers have found that the concentration of urea in human sweat exceeds the concentration of urea in plasma. This fact has been confirmed in the present work and extended by measurements of the concentrations of urea in the sweat and the corresponding concentrations of urea in the plasma over a range of 25- fold variation in the latter. An analysis of the data showed that the ratio of the concentration of urea in sweat to the concentration of urea in plasma, S/P, was independent of the plasma concentration, independent of the absolute flux of urea or water, and independent of the calculated energy expenditure. Two experiments showed that the concentration of urea in sweat followed a rising concentration in plasma with a time lag of approximately 5 minutes; this fact indicates that the accumulation of urea in sweat is a continuous process which is in operation during the observed discharge. These observations suggest that urea is carried into the gland in some precursor solution and subsequently raised to a higher concentration by the reabsorption from this solution of a constant fraction of the water.

Blood↗

p53 protein in benign and malignant sweat gland tumors.

Mutation of the p53 gene and increased levels of p53 protein are among the most frequent alterations in human cancers. To date, very little is known about the mechanisms underlying the development of sweat gland carcinomas. In this study, we analyzed 43 benign and 39 malignant sweat gland tumors for p53 protein level using the antibody PAB1801. Nine (23%) of 39 sweat gland carcinomas were positive for p53 protein. Among these carcinomas, six of 12 cases of extramammary Paget's disease were positive using immunohistochemistry. No other correlation between tumor subtype and p53 reactivity was detected. Among 43 benign sweat gland tumors, only one case displayed staining for p53. We conclude that p53 protein plays a role in a subset of sweat gland tumors, especially in extramammary Paget's disease.

Adenocarcinoma↗

Transcutaneous chemical collection of caffeine in normal subjects: relationship to area under the plasma concentration-time curve and sweat production.

A novel transcutaneous chemical collection device (TCD) has been developed to study the phenomenon of outward transcutaneous chemical migration. The TCD is a Bandaid-like device containing an immobilized aqueous media and binding reservoir material to prevent back-transfer into the skin. This device, when placed against the skin, allows collection and quantitation of chemicals that diffuse directly through the skin from within the body. The relationship of the amount of drug collected in the TCD to the amount in the body available for collection (as represented by the area under the plasma-concentration time curve, AUC) and the effects of sweating, a potential confounding factor, on collection of drug in a TCD were studied, using caffeine as a model compound. TCD were placed on the skin of normal male volunteers. Twenty-four hours later subjects took caffeine by mouth. Blood samples were collected and TCD were removed at various times after drug intake and analyzed by HPLC for caffeine. Studies of the sweating effect were carried out in a similar manner, except that one arm of each subject was maintained at 40 degrees C to induce local sweating, the other arm acted as a non-sweating control. The amount of caffeine collected was linearly related to the AUC. Sweating seemed to have a large (40%) contribution to transdermal collection in the early period (5.5 h) of the study, but this difference was much less (14%) at longer collection times (10 h).

Adult↗

Long-term sweat collection using salt-impregnated pads.

To facilitate a study of the pharmacokinetics of drugs dissolved in sweat, a technique was devised for collecting sweat at a steady rate over an 8-day period. Three normal subjects each wore 4 absorbent pads applied to their skin under waterproof dressings for 8 days. The absorbent pads were either plain cotton or cotton impregnated with sodium chloride crystals. Each pad (3 cm x 3 cm) was applied to an area of skin (2 cm x 2 cm) defined by an adhesive template, and was removed daily, weighed, and replaced, to determine progressive uptake of sweat. Sweat uptake by plain cotton pads reached a plateau value within 2 to 3 days and did not significantly increase thereafter; in contrast, uptake by the salt-impregnated pads continued at a steady rate for the full 8 days of the study (mean rate 0.79 mg/cm2/hr, SD = 0.16, N = 6). This effect may be related to an osmotic gradient across the skin, but the physiologic mechanisms are not completely clear. This appears to be a convenient tool for the collection of sweat over long periods at a steady rate.

Humans↗

Immunohistochemical study of lysozyme in various benign sweat apparatus tumors.

We investigated the existence of lysozyme in various sweat apparatus tumors by adopting the avidin-biotin-peroxidase complex method. Positive reactions for lysozyme were found in four cases of apocrine cystadenoma, hidradenoma papilliferum, and an apocrine sweat apparatus benign tumor resembling "apocrine spiradenoma", all of which derive from apocrine sweat apparatus. On the other hand, in ten cases of syringoma, eccrine hidrocystoma, clear cell hidradenoma, eccrine spiradenoma, and eccrine poroma, which derive from eccrine sweat apparatus, no positive stainings for lysozyme were obtained. In four out of five cases of mixed tumor of the skin, the apocrine type exhibited positive results. Two cases of syringocystadenoma papilliferum were negative for lysozyme. The investigation of lysozyme in various sweat apparatus tumors is useful in determining the direction of differentiation in these tumors.

Adenoma, Sweat Gland↗