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PubMed2004

Relation of sweat chloride concentration to severity of lung disease in cystic fibrosis.

In cystic fibrosis (CF), sweat chloride concentration has been proposed as an index of CFTR function for testing systemic drugs designed to activate mutant CFTR. This suggestion arises from the assumption that greater residual CFTR function should lead to a lower sweat chloride concentration, as well as protection against severe lung disease. This logic gives rise to the hypothesis that the lower the sweat chloride concentration, the less severe the lung disease. In order to test this hypothesis, we studied 230 patients homozygous for the DeltaF508 allele, and 34 patients with at least one allele associated with pancreatic sufficiency, born since January 1, 1955, who have pulmonary function data and sweat chloride concentrations recorded in our CF center database, and no culture positive for B. cepacia. We calculated a severity index for pulmonary disease, using an approach which takes into account all available pulmonary function data as well as the patient's current age and survival status. Patients with alleles associated with pancreatic sufficiency had significantly better survival (P = 0.0083), lower sweat chloride concentration (81.4 +/- 23.8 vs. 103.2 +/- 14.2 mEq/l, P < 0.0001), slower rate of decline of FEV(1) % predicted (-0.75 +/- 0.34 vs. -2.34 +/- 0.17% predicted per year), and a better severity index than patients homozygous for the DeltaF508 allele (median 73rd percentile vs. median 55th percentile, P = 0.0004). However, the sweat chloride concentration did not correlate with the severity index, either in the population as a whole, or in the population of patients with alleles associated with pancreatic sufficiency, who are thought to have some residual CFTR function. These data suggest that, by itself, sweat chloride concentration does not necessarily predict a milder pulmonary course in patients with cystic fibrosis.

Adolescent↗

PubMed1995

Production of sweat gland cholinergic differentiation factor depends on innervation.

Sympathetic neurons innervating sweat glands undergo a target-directed developmental switch in neurotransmitter properties. Using cultured sympathetic neurons as a bioassay for cholinergic differentiation factors, we and others found that extracts containing soluble proteins from developing and adult footpads caused the same changes in transmitter properties in sympathetic neurons in vitro that the target does in vivo. In the present studies, using footpads from Tabby mutant mice that lack sweat glands, we found that the presence of sweat glands is correlated with the presence of cholinergic differentiation activity in footpad extracts. We examined the conditions necessary for secretion of differentiation activity from primary cultures of sweat gland cells. Surprisingly, sweat gland cells cultured alone do not produce or secrete cholinergic differentiation activity. When grown in the presence of sympathetic neurons, however, gland cells induce cholinergic function, increase vasoactive intestinal peptide content, and reduce catecholamine production in the neurons. Medium conditioned by sweat gland/neuron cocultures has a similar effect on the transmitter properties of cultured sympathetic neurons, indicating that the target influence on phenotype is mediated by a secreted factor(s). The innervation-dependence of cholinergic differentiation factor production provides evidence that reciprocal interactions between neurons and sweat glands are necessary for acquisition of the mature transmitter phenotype.

Amino Acid Sequence↗

PubMed1998

Target-dependent development of the vesicular acetylcholine transporter in rodent sweat gland innervation.

Descriptive studies have delineated a developmental change in neurotransmitter phenotype from noradrenergic to cholinergic in the sympathetic innervation of sweat glands in rodent footpads. Transplantation and culture experiments provide evidence that interactions with the target tissue induce this change. Recent studies with an antiserum that recognizes the vesicular acetylcholine transporter (VAChT) suggest, however, that the development of cholinergic function in sympathetic neurons, including those that innervate sweat glands, occurs prior to and does not require target contact. To clarify these apparently contradictory findings, we directly compared the appearance of VAChT immunoreactivity in the sympathetic neurons that innervate sweat glands with the time that axons contact this target. We find that VAChT immunoreactivity is not detectable in either the axons or cell bodies of sweat gland neurons until several days after target innervation. Before and during VAChT acquisition, the developing sweat gland innervation contains vesicular stores of catecholamines. An analysis of mutant mice that lack sweat glands was undertaken to determine whether VAChT expression requires target interactions and revealed that VAChT does not appear in the absence of glands. These findings, together with previous studies, confirm the target dependence of cholinergic function in the sympathetic neurons that innervate sweat glands.

Acetylcholine↗

PubMed1981

Cyclic AMP accumulation in the beta adrenergic mechanism of eccrine sweat secretion.

Tissue cyclic 3'5'-AMP (cAMP) concentrations were measured after stimulation of isolated monkey palm eccrine sweat glands with various stimulants of sweat secretion. The cellular cAMP levels increased curvilinearly with time of incubation to reach a steady state after 5 min of incubation with isoproterenol. Theophylline more than doubled the isoproterenol-induced cAMP accumulation, whereas theophylline alone increased the basal cAMP level to a minor extent. Phenylephrine failed to stimulate cAMP accumulation. There was no increase in the cAMP level after stimulation with methacholine. A calcium ionophore, A23187, also failed to stimulate cAMP accumulation. Since isoproterenol, theophylline (or isobutylmethylxanthine), and dibutyryl cAMP all induced eccrine sweat secretion in isolated, cannulated sweat glands to varying degrees in vitro, cAMP is probably involved in the beta adrenergic mechanism of sweat induction. The isoproterenol-induced cAMP accumulation was not inhibited by removal of Ca2+ from the incubation medium for as long as 30 min. The striking similarity between the eccrine sweat gland and the salivary glands in the roles that Ca2+ and cAMP play in stimulus secretion coupling indicates that the eccrine sweat gland will serve as another useful model system for the study of the mechanisms of exocrine secretion.

Animals↗

PubMed1994

Modulatory effects of calcitonin gene-related peptide and substance P on human cholinergic sweat secretion.

Immunoreactivity to various peptides has been demonstrated in nerve terminals around the sweat glands, suggesting a regulatory function for these peptides on sweating. The present study evaluated the calcitonin-gene related peptide and substance P related regulation of sweating in man. Both calcitonin-gene related peptide and substance P, when administered alone, failed to cause sweat secretion, whereas sweating induced by methacholine chloride alone was four times greater when administered with calcitonin-gene related peptide and suppressed by 70% when administered with substance P. The degree of calcitonin-gene related peptide dependent augmentation and substance P dependent suppression of the methacholine chloride induced sweating was dependent on the concentration of calcitonin-gene related peptide and substance P. These findings suggest that calcitonin-gene related peptide enhances cholinergic sweating and substance P inhibits it.

Adult↗

PubMed1994

Demonstration of sweat allergy in cholinergic urticaria.

Twenty patients with cholinergic urticaria, 11 sex- and age-unmatched patients with acute or chronic urticaria and 20 sex- and age-matched non-atopic control subjects were skin tested with autologous sweat. All cholinergic urticaria patients showed positive immediate-type skin reactions at 2(0)-2(9) dilutions of sweat (geometric mean of maximal positive dilutions +/- S.D. was 2(4.6 +/- 2.6), while in acute and chronic urticaria only three patients showed positive reactions at low dilutions (two 2(0) and one 2(1)) and none of 20 controls showed positive reactions. Prausnitz-Küstner (P-K) tests performed with the serum and sweat from six patients were all positive at 2(3)-2(8) dilutions. Percent histamine release from peripheral leukocytes of five patients challenged with the standard sweat samples was significantly higher than in five control subjects. Histamine release from leukocytes of the patient on sweat challenging was abandoned by acid treatment of leukocytes. Leukocytes, from a healthy subject sensitized with the patient's serum, released histamine on sweat challenging. These results seem to indicate that cholinergic urticaria patients have a type I allergy to their own sweat.

Adolescent↗

PubMed1994

Comparison of 16-androstene steroid concentrations in sterile apocrine sweat and axillary secretions: interconversions of 16-androstenes by the axillary microflora--a mechanism for axillary odour production in man?

The concentrations of five 16-androstene steroids were determined, by a GC-MS method, in freshly-produced apocrine sweat (adrenaline-induced), in 8 men and 2 women. The ranges of concentrations (nmol/microliter) in apocrine sweat were: 5 alpha-androst-16-en-3-one (5 alpha-A), 0.1-2.0 and 4,16-androstadien-3-one (androstadienone), 0-1.9, 5,16-Androstadien-3 beta-ol (androstadienol) was also found in 5 of the subjects (range 0.05-1.05). 5 alpha-Androst-16-en-3 alpha- or 3 beta-ols [3 alpha (beta)-androstenols] were only found in small amounts (< 0.1 nmol/microliters) in a few subjects. In the second study, prior to apocrine sweat collection (adrenaline injection), the axillary skin of 6 of the male subjects was washed with diethyl ether on an adjacent site of the axillary vault. The concentrations of 16-androstenes were compared in the ethereal extracts and apocrine sweat. The former contained detectable levels (pmol/cm2) of androstadienone (17.9 +/- 2.4), 3 alpha-androstenol (6.9 +/- 3.7), 3 beta-androstenol (1.8 +/- 1.0) and androstadienol (1.9 +/- 0.5) (means +/- SEM) in all 6 subjects. All but 1 subject also had 5 alpha-androstenone, the mean value for the others being 2.5 +/- 0.6. The axillary skin levels of 3 alpha- and 3 beta-androstenols, androstadienol and, in 3 subjects, androstadienone exceeded those in the apocrine sweat obtained from the same subjects, whereas levels of 5 alpha-androstenone in the skin extracts were all lower than in apocrine sweat samples, when related to the corresponding areas of skin sampled. The metabolism of 16-androstenes was studied in vitro in the presence of two aerobic coryneform bacteria, previously shown to metabolize testosterone as well as being capable of producing odour from extracts of axillary sweat in an odour-generation test. Although both coryneforms caused complex metabolic reactions and were capable of oxidation or reduction at C-3 and C-4, the overall direction favoured reduction. For example, large quantities of the more odorous 5 alpha-androstenone and 3 alpha-androstenol were formed from androstadienol and androstadienone. In contrast, strains of corynebacteria, unable to produce odour and incapable of metabolizing testosterone, were also unable to metabolize 16-androstenes.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinomycetales↗

PubMed2006

Endoscopic thoracic sympathectomy for severe hyperhidrosis: impact of restrictive denervation on compensatory sweating.

BACKGROUND: Compensatory sweating is noted frequently after sympathectomy and may be difficult to control in some patients. This prospective trial was projected to measure the impact of limited denervation on compensatory sweating while performing endoscopic thoracic sympathectomy. METHODS: One hundred seventy-eight patients (127 female and 51 male) with severe primary hyperhidrosis unsuccessfully treated by conservative means entered the study. Group A was treated with sympathectomy from T2 to T4. In group B sympathectomy was performed from T3 to T5. Physical condition was measured after 1, 6, and 24 months by means of the SF-36 Health Survey Test. RESULTS: Evaluation rate was 94.9%. Horner's syndrome was not detected, recurrence rate was 0.6%, and rate of persistent pneumothorax was 2.3%. Compensatory sweating was reported with 17.1% in group A and diminished to 4.9% in group B. Gustatory sweating was comparable in both groups (4.3% versus 4.9%). Satisfaction rate was 97% in patients with palmar hyperhidrosis, 95% for axillary hyperhidrosis, and 87% for facial hyperhidrosis. Discomfort originating from compensatory sweating was less than symptoms from primary hyperhidrosis 24 months after endoscopic thoracic sympathectomy in more than 90%. Only 7.1% of the entire group was not satisfied. CONCLUSIONS: Our study demonstrates that limiting denervation beyond T2 ganglion offers good clinical results in axillary as well as palmar hyperhidrosis and may reduce the risk for compensatory sweating. In women, reduction was as high as 75% and in men, near 50%. Our impression is that severe compensatory sweating and the majority of stellate ganglion lesions occur as a result of starting sympathectomy at level T2.

Adult↗

PubMed2005

Effects of exercise intensity, posture, pressure on the back and ambient temperature on palmar sweating responses due to handgrip exercises in humans.

We have, by using newly developed ratemeters, attempted to examine the effects of exercise intensity, posture, pressure on the skin of the back, and ambient hyperthermic conditions (approximately 30 degrees C) on the 5-s handgrip exercise-mediated responses of active palmar sweating in humans. Thirty-five right-handed male (n=5) and female (n=30) volunteer students (20.2+/-1.3 years old) participated in the present study. Oral explanation of only the isometric handgrip exercise (IHG) caused a rapid and oscillatory response (pre-operational) of active palmar sweating in almost all subjects (10 of 14 subjects). Performing the IHG for 5-s caused a significant increase in active sweating rate (operation-mediated response) in both ipsi- and contra-lateral palmar surfaces of the thumbs of all subjects. The operation-mediated responses of active palmar sweating to the IHG were reproducible, resulting in no habituation. The increase of operation-mediated responses to the IHG was dependent upon exercise intensity (100-25% maximal voluntary contractions). The IHG-mediated ipsi- and contra-lateral responses of active palmar sweating were significantly decreased by changing the body posture from a seated to a supine position or by pressing the skin of the back. Ambient hyperthermic conditions (approximately 30 degrees C) for 60 min also resulted in a significant decrease in the back-pressure-dependent reduction of the operation-mediated responses of active palmar sweating to the IHG. In conclusion, in order to optimize the precision and reproducibility of clinical tests involving palmar sweating responses, it is important that subjects maintain a constant handgrip force and posture and that ambient temperature be kept under normothermic conditions.

Adult↗

PubMed2005

Sweat collection for testing in Canadian Cystic Fibrosis Centers, is it optimal?

OBJECTIVES: The goal of this study was to examine the ability of the current Canadian CF center network to conduct sweat testing, with a particular focus on testing in infants less than 3 months old. METHODS: Surveys were sent to the 37 CF centers in Canada supported by the Canadian CF Foundation, and results were interpreted with respect to their ability to obtain adequate sweat volumes in children less than 3 months and potential factors influencing these results. RESULTS: Ten centers that care for adult patients referred patients to their local pediatric CF center for sweat testing; the remaining 27 centers conducted sweat tests and 26 responded. Insufficient sweat volume results in children <3 months occurred in a median of 18.3% of tests. The corresponding proportion for the remaining population was 4.5% (P < 0.001). 15 of 19 centers had an incidence of >5% of insufficient tests in children <3 months of age, and 9 of 19 had an incidence of <20% in this age group. Six of 19 had an incidence of >5% of insufficient sweat volumes in older children and adults. CONCLUSIONS: Standardization of testing procedures is required to reduce the rates of insufficient sweat volumes in both infants less than 3 months old and children >3 months old. This will decrease the need for repeat testing and delay in diagnosis.

Adult↗

PubMed2005

Sweat testing infants detected by cystic fibrosis newborn screening.

OBJECTIVE: Describe and define limitations of early pilocarpine iontophoresis (sweat testing) for cystic fibrosis (CF) newborn screening (NBS). STUDY DESIGN: Population-based results from follow-up of CF NBS-positive newborns. RESULTS: Insufficient quantity of sweat is more likely if the sweat test is done too early, but testing is generally successful after 2 weeks of age. Sweat chloride levels drop over the first weeks of life. CF carriers have higher sweat chloride concentrations than non-carriers. CONCLUSIONS: Sweat testing can be performed effectively after 2 weeks of age for CF NBS-positive newborns. Earlier testing has a higher risk of insufficient sweat for completing testing.

Age Factors↗

PubMed1998

Changes in cholinergic responses of sweat glands during denervation and reinnervation.

Functional sudomotor responses have been studied in sweat glands reinnervated after sciatic nerve crush and partially denervated by cisplatin intoxication in the mouse. The sudomotor function mediated by the sciatic nerve was evaluated by silicone imprints on the plantar surface of the hindpaws. Five days after nerve crush, completely denervated sweat glands became unresponsive to cholinergic stimulation with pilocarpine. During the following weeks, the number of reinnervated, reactive sweat glands increased progressively to reach a maximum of 89% of preoperative control counts by 40 days after nerve crush. At this time, the mean volume of sweat secreted per gland was normal, but reinnervated glands showed a secretory activity abnormally sustained over time after pilocarpine stimulation and, on the other hand, had an increased resistance to the inhibition of secretion induced by atropine. The effects of cisplatin administration on sudomotor function were investigated in two groups of mice, one treated with high doses of cisplatin (10 mg/kg/week for 4 weeks) and another treated with low doses of cisplatin (5 mg/kg/week for 8 weeks). Cisplatin intoxication produced abnormal sudomotor responses indicative of denervation from cumulative doses of 10 mg/kg. The first abnormality found was a partial resistance of sweat glands to atropine, followed by a decrease in the sweat output per gland and finally a decline in the number of sweat glands activated by pilocarpine. These abnormalities in the sudomotor responses were more pronounced in mice treated with a high dose than in those with a lower dose regime.

Animals↗

PubMed2003

Emotional sweating response in a patient with bilateral amygdala damage.

Sweat output on the palm or sole is distinct from thermoregulatory sweating and has been designated emotional sweating. The amygdala has been implicated in this phenomenon, but the role it plays remains unclear. We had the chance to evaluate emotional sweating in a 21-year-old female with bilateral restricted amygdala lesions caused by idiopathic subacute limbic encephalitis. At the peak of the illness, sweat responses in the palm were not evoked in this patient in conjunction with any sympathetic activation procedures, including deep inspiration, mental arithmetic, isotonic exercise, and tactile stimulation. After neurological improvement associated with diminution of amygdala lesions on the magnetic resonance imaging, normal sweat responses were incited. This indicates that the amygdala does play an important role in emotional sweating.

Adult↗

PubMed2003

Arithmetic calculation, deep inspiration or handgrip exercise-mediated pre-operational active palmar sweating responses in humans.

We examined the effects of repetitive mental stimulation such as arithmetic calculations with sequential subtraction or physical tasks such as handgrip exercise and deep breathing on active palmar sweating responses in humans. Thirty-three healthy, male and female volunteer students (20.4+/-2.1 years) participated in the present study. The responses of active palmar sweating were evaluated by using the newly developed ratemeter. The galvanic skin response (GSR) was also recorded in 10 out of 33 subjects. The oral explanation of the stimulation or tasks caused a rapid and wavy active palmar sweating response. The pre-operational responses of active palmar sweating to the stimulation or tasks were also observed by the GSR recording. The mental stimulation- and physical tasks-mediated pre-operational responses were significantly reduced by the trials. The mental stimulation or physical tasks also caused a rapid and oscillatory response of active palmar sweating during operation of the stimulation or tasks. The operation-mediated responses to physical tasks were observed ipsilaterally and contralaterally. The physical task-mediated responses were also reproducible, resulting in no habituation. In contrast, the operation-mediated responses to mental stimulation were reduced significantly by the trials, resulting in a marked habituation. The findings suggest that the mental stimulation- and physical tasks-mediated pre-operational responses of active palmar sweating obtained by using the newly developed ratemeter will make useful tests for evaluating neuronal activity of limbic system including amygdala, sympathetic sudomotor activity in the palmar skin and functional properties of the palmar sweat glands.

Adult↗

PubMedDate not supplied

Electrolyte loss in sweat and iodine deficiency in a hot environment.

The authors studied electrolyte loss from profuse sweating in soccer-team players and evaluated the relationship between this source of iodine loss and iodine deficiency. Thirteen male soccer-team players and 100 sedentary students from the same high school were evaluated for 8 d, during which the players were training. The authors analyzed 208 sweat samples to determine losses of iodine, sodium, potassium, and calcium in sweat. Excretion of urinary electrolytes by the subjects was also measured. The mean losses of iodine, sodium, potassium, and calcium in sweat following a 1-hr game were 52 microg, 1,896 mg, 248 mg, and 20 mg, respectively; the ratios of sweat loss to urinary daily loss of the four electrolytes were 0.75, 0.2, 1.88, and 0.92, respectively. Urinary iodine was significantly (p < .02) lower than the normal level of 50 microg/gm creatinine in 38.5% of the soccer players, compared with 2% of the sedentary students. Forty-six percent of the players had Grade I goiter, compared with a mere 1% of the sedentary students (p < .01). The results of the study suggest that loss of iodine through profuse sweating may lead to iodine deficiency, and loss of electrolytes through sweating may have a dietary significance for heat-stressed individuals or for individuals who perform heavy workloads.

Adolescent↗

PubMed2000

Reliability of sweat-testing by the Macroduct collection method combined with conductivity analysis in comparison with the classic Gibson and Cooke technique.

UNLABELLED: This study was to ascertain the reliability of sweat-testing by the Macroduct collection method combined with conductivity analysis (MCS) compared with the Gibson and Cooke technique (GCT). Sweat stimulation by pilocarpine iontophoresis was identical for both procedures, sweat being collected for 30 min on a filter paper on one forearm and in the coil of the Macroduct collector on the other. Chloride, sodium and potassium concentrations were chemically analysed both on paper-eluted and tube-collected sweat; the latter was also analysed using a conductivity analyser. Chemical analyses were compared with conductivity analyses. This prospective study was carried out on 318 subjects with MCS (118 CFs, 200 controls) and on 305 of them with the GCT (113 CFs, 192 controls). The pilocarpine iontophoresis produced adequate sweat in 96.4% of collections with GCT and in 90.9% with the MCS. Sensitivity and specificity of the Macroduct/conductivity system were comparable to the GCT. No patient detected by the GCT technique was considered negative by conductivity, but one GCT positive was "borderline" with the MCS. Six non-CF subjects identified as negative by the GCT (3.3%) were in the borderline range with the MCS. CONCLUSION: Sweat-testing by the MCS has acceptable sensitivity and specificity when performed by trained CF sweat-testing technicians. Additional studies will be required to find out if these results can be confirmed in small clinics and hospitals where testing is done infrequently. Wherever the MCS is used all positive or borderline results should be confirmed by the GCT at a reference Cystic Fibrosis Center.

Adolescent↗

PubMedDate not supplied

Usefulness of sweat testing for the detection of MDMA after a single-dose administration.

Nine healthy male subjects and recreational users of 3,4-methylenedioxymethamphetamine (MDMA) participated in a study aimed to assess the usefulness of sweat testing for the detection of MDMA after a single 100-mg dose. Sweat was collected for up to 24 h with the PharmChek sweat patches from which drugs were eluted and then analyzed by immunoassay and gas chromatography-mass spectrometry using deuterated internal standards. The usefulness of a rapid onsite test, the Drugwipe immunochemical strip test, was also assessed. In the sweat patches, MDMA was detected as early as 1.5 h after consumption and peaked at 24 h. Intersubject variability was large; peak MDMA concentrations for the same dose varied in magnitude 30-fold. MDMA concentrations ranged between 3.2 and 1326.1 ng/patch. Only traces of the minor metabolite 3,4-methylenedioxyamphetamine were detected. In all subjects, the onsite test with the Drugwipe was positive at 1.5 h (peak time of MDMA plasma concentration). However, few false-negative results (18%) appeared in the first 6 h after administration. Both sweat patch testing and the onsite sweat strip test may find useful application for noninvasive monitoring of MDMA abuse in sweat.

3,4-Methylenedioxyamphetamine↗

PubMed1990

The validity of self-reported exercise-induced sweating as a measure of physical activity.

The validity of self-reported hours in which one engages in activities strenuous enough to produce sweating was assessed as a measure of physical activity. Respondents were 732 randomly selected adults between the ages of 25 and 65 years from the Boston, Massachusetts, metropolitan area who participated in a field trial of health risk appraisal instruments in 1987. A total of 68% of the men and 57% of the women in the sample were involved in sweat-inducing activities at least once per week. The correlation between the natural logarithm of reported sweat hours per week and energy expenditure measured by the Harvard Alumni Activity Survey was 0.39. Following a logarithmic transformation and adjustment for age and sex, sweat hours was significantly correlated with high density lipoprotein cholesterol (r = 0.11, p less than 0.05). However, these associations were not as strong as those found for the age- and sex-adjusted log of the Harvard Alumni Activity Survey score (r = 0.19 and r = -0.15 for high density lipoprotein cholesterol and body mass index (weight (kg)/height(m)2), respectively) and are considerably weaker than those reported in other studies using sweat episodes (days per week on which sweating occurred) as an indicator of physical activity. These results suggest that the utility of self-reported sweat hours may be limited to distinguishing active from inactive subjects in epidemiologic surveys.

Adult↗