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One-step iodine starch method for direct visualization of sweating.

Despite recent progress in eccrine sweat gland physiology, simple, safe and reliable methods of visualizing local and generalized sweating are not available for clinicians and physiologists. We developed a simple one-step method for visualizing sweating that requires only soluble starch previously treated with iodine. When the powder is sprayed on the skin, sweat droplets are visualized as discrete dark purple dots. Since visualized dots are easily wiped off without staining the skin, sweating patterns can be obtained consecutively on the same skin site. The method is far superior to the classical Minor's method and is useful for clinical diagnosis of disorders of sweating and for visualization of the total body sweating for physiological studies. Two simple devices for spraying powder also have been presented.

Female↗

A finger sweat chloride test for the detection of a high-risk group of chronic pancreatitis.

OBJECTIVES: Mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene are associated with chronic pancreatitis in Caucasians. We developed a simple method for measuring finger sweat chloride concentration to test whether CFTR dysfunction underlies chronic pancreatitis in Japan where cystic fibrosis (CF) is rare. METHODS: We studied 25 patients with chronic (21 alcoholic and 4 idiopathic) pancreatitis and 25 healthy volunteers. Sweat chloride concentrations were measured by a finger sweat chloride test. We analyzed DNA for 20 common CFTR mutations in Europeans, 9 CF-causing mutations in Japanese, and 2 polymorphic loci, a poly-T tract and (TG) repeats, at intron 8. RESULTS: Thirteen patients (52%) had sweat chloride levels >60 mmol/L, a level consistent with CF, while only 4 (16%) healthy subjects exceeded this level. The 29 CF mutations and the 5T allele were detected in neither the patients nor controls. The (TG) 12 allele was common in both the patients (58%) and controls (48%). The (TG) 12/12 genotype was common in alcoholic pancreatitis (29%) compared with the (TG) 11/11 (10%). Patients with the (TG) 12/12 genotype had significantly higher sweat chloride concentrations than the controls. CONCLUSION: CFTR dysfunction as evidenced by a finger sweat chloride test is present in about half of Japanese patients with chronic pancreatitis, suggesting that this test may be useful for detecting the high-risk group. A higher proportion of the (TG) 12 allele may be a genetic background for elevated sweat chloride concentrations in Japanese patients.

Adult↗

Daily pattern of sweating and response to stress and exercise in patients with palmar hyperhidrosis.

BACKGROUND: Focal hyperhidrosis is an embarrassing condition that can have a significant negative impact on patient quality of life. It is characterized by excessive sweating affecting a variety of areas, including the palms. Little is known about the daily pattern of sweating in patients with palmar hyperhidrosis. OBJECTIVES: To compare the variation of sweating in patients with primary palmar hyperhidrosis with healthy individuals during daily activities. METHODS: Twenty patients with primary palmar hyperhidrosis and 20 healthy age- and sex-matched subjects were studied. Each participant self-assessed rates of sweating for 7 days on an hourly basis using a subjective evaluation scale (SES) ranging from 0 to 10. RESULTS: The 3763 assessments showed clear differences between patients and healthy controls (median SES score 5 and 0, respectively; P < 0.0001). Stress and exercise significantly increased SES by scores of 2-5 in both groups, with stress influencing patients more than controls. SES scores in patients varied significantly, from 0 to 2 during mornings and evenings, and between 5 and 6 at mid-day, while scores in control subjects remained consistently close to 0. The pattern of change depended weakly on sex and weekday/weekend distinction. Dynamic responses to stress and exercise in patients had the tendency to return to baseline more slowly than in controls. CONCLUSIONS: Hourly changes in sweating rates can be assessed successfully through self-assessment. Patients with primary palmar focal hyperhidrosis reported significantly increased palmar sweating and daily patterns of sweating showing considerable variation dependent on factors such as time of day and emotional stimuli.

Adolescent↗

Assessment of cellular proliferation of eccrine acrospiromas and eccrine sweat gland carcinomas by AgNOR counting and immunohistochemical demonstration of proliferating cell nuclear antigen (PCNA) and Ki-67.

Argyrophil nucleolar organizer regions (AgNORs) were counted and immunostaining using antibodies raised against proliferating cell nuclear antigen (PCNA) and Ki-67 was carried out on eccrine acrospiroma and eccrine sweat gland carcinoma, to determine the malignant potential and prognosis of these tumours. Formalin-fixed and paraffin-embedded tissue specimens surgically excised from 25 patients with eccrine sweat gland carcinoma (20 cases of eccrine porocarcinoma, four cases of ductal sweat gland carcinoma and one case of malignant clear cell hidradenoma) and 25 patients with eccrine acrospiroma (16 cases of eccrine poroma, four cases of poroid hidradenoma and five cases of clear cell hidradenoma) were used. PCNA and Ki-67 labelling indices were categorized semiquantitatively into four grades. Significant differences were noted between eccrine sweat gland carcinoma and eccrine acrospiroma with these three methods (P < 0.01). When a cut-off of 5 was chosen, the AgNOR value distinguished eccrine sweat gland carcinoma from eccrine acrospiroma with high specificity and sensitivity. Moreover, we compared the results of these three methods between stages 1 or 2 (17 cases) and stage 3 (eight cases) eccrine sweat gland carcinomas, and no significant differences were observed. From these findings, these three methods are useful in discriminating malignant from benign lesions of eccrine tumours, but have no value in estimating the aggressiveness of eccrine sweat gland carcinomas.

Acrospiroma↗

A sweat-patch test for alcohol consumption: evaluation in continuous and episodic drinkers.

We evaluated the sweat-patch test for its ability to detect alcohol consumption. During an 8-day study, volunteers drank whisky while wearing sweat-patches that collected sweat continuously at a steady rate. We offered 1.0, 2.0, or 5.0 g ethanol/kg/day to 6 continuous drinkers, and 5.0 g ethanol/kg/day for 2 days to 8 episodic drinkers, and removed sweat patches after 2, 4, 6, and 8 days. The concentration of ethanol in the collected sweat (Cs) rose: (1) progressively with the amount of alcohol consumed: and (2) linearly with the mean concentration of ethanol in the blood (Cb) during the sweat collection period (In Cs = 0.80 In Cb - 1.40; r = 0.93, p < 0.001). The test clearly distinguished drinkers from nondrinkers (Cs < 0.0022 G/L when no ethanol consumed; Cs > 0.0067 G/L when 0.5 G ethanol/kg/day consumed and when Cb > 0.013 G/L). The sweat patch test provides an objective index of drinking behavior with potential applications in clinical practice and research.

Alcohol Drinking↗

Coexpression of cytokeratin and vimentin intermediate filaments in benign and malignant sweat gland tumors.

The coexpression of cytokeratin and vimentin intermediate filaments has been immunohistochemically evaluated in 124 benign and malignant sweat gland tumors of various types in comparison to normal sweat glands. In addition, all neoplasms have been stained by an antibody to alpha-smooth muscle actin. Epithelial cells reacted with the pan-cytokeratin antibody lu-5. In normal sweat glands, vimentin immunoreactivity was restricted to myoepithelial cells and to some cells of the coiled duct. In benign sweat gland tumors (n = 88), coexpression of vimentin and alpha-smooth muscle actin was frequently found in basal cells of neoplasms considered to differentiate towards the secretory coil of the eccrine or apocrine gland. These included eccrine spiradenoma, apocrine cystadenoma, hidradenoma papilliferum, syringocystadenoma papilliferum, and cylindroma. Thus, in these tumors, vimentin-reactive cells corresponded to myoepithelial cells. Vimentin-positive cells were also found in 14 of 36 sweat gland carcinomas, including 1 case of sclerosing sweat duct carcinoma, 1 case of porocarcinoma, 4 cases of eccrine adenocarcinoma, 1 case of mucinous eccrine carcinoma, and 5 cases of apocrine adenocarcinoma. Co-expression of vimentin and alpha-smooth muscle actin was observed in some cells of eccrine and apocrine adenocarcinomas. Therefore, in these neoplasms, some vimentin-positive cells appear to represent myoepithelial cells. In contrast, vimentin-positive cells in all other malignant tumors did not express alpha-smooth muscle actin. Our results indicate that coexpression of cytokeratin and vimentin may be frequently found in a variety of benign and malignant sweat gland tumors. In the majority of these neoplasms, vimentin-positive cells correspond to myoepithelial cells. Because vimentin is not specific for myoepithelial cells, additional stains for alpha-smooth muscle actin should be performed to prove the myoepithelial nature of vimentin-positive cells.

Humans↗

Ectopic breast tissue and breast-like sweat gland metaplasias: an overlapping spectrum of lesions.

There are many similarities in the morphology of benign and malignant lesions of the sweat glands and the breasts. The recently described cutaneous mammary-like sweat glands, also known as mixed sweat glands or apoeccrine glands, are also a likely source of selected proliferations that closely mimic those of the breast. We present three cases of breast-like lesions arising in the skin that demonstrate the ways in which the morphologic and pathologic continuum of the mammary glands, cutaneous mammary-like glands, and sweat glands can produce difficulties in precise diagnosis. The examples demonstrate that an anatomic location outside the milk line does not preclude the diagnosis of ectopic mammary tissue, and that lesions closely resembling those of the breast may also arise outside the milk line from conventional sweat glands or mixed sweat glands. The concept of homologous lesions of the breast, breast-like glands and sweat glands, in which morphology is partially mirrored by biochemical similarities, provides a perspective for classification of problematic cases of breast-like cutaneous lesions.

Adult↗

Improved sweat test method for the diagnosis of cystic fibrosis.

We describe a new technique of collecting sweat for measurement of osmolality and sodium concentrations. Eighty two subjects were studied--39 controls and 43 patients with cystic fibrosis. Adequate amounts of sweat were obtained in 81 subjects and sweat was analysed for both osmolality and sodium concentrations in 73 subjects. The 34 controls gave sweat osmolality and sodium values ranging from 62 to 196 mmol/kg and 9 to 72 mmol/l respectively. The 39 cystic fibrosis patients gave osmolality values ranging from 220 to 416 mmol/kg and sodium concentrations ranging from 60 to 150 mmol/l. Sweat osmolality alone was determined in eight infants under 50 days of age--four later developed the clinical features of cystic fibrosis and four, in whom cystic fibrosis was suspected, were later excluded. Sweat osmolality values in these two groups ranged from 255 to 345 mmol/kg and 87 to 123 mmol/kg respectively. The simplicity of collecting sweat and the measurement of osmolality offer distinct advantages over techniques previously described.

Adolescent↗

Quantitative sweat test in diabetics with neuropathic foot lesions.

The volume of sweat produced by axon reflex stimulation using acetylcholine was measured in one foot each of 35 control subjects and 52 feet of 37 diabetic patients (28 with neuropathic ulceration, 11 with Charcot arthropathy, nine with somatic neuropathy but no foot lesion and four with no evidence of somatic neuropathy). In controls, the volume of sweat was greater in males than females. A flare response was seen in 94% of control feet. In diabetics, the volume of sweat was within the control range in 17 feet, increased in one, reduced in seven, and absent in 27. Sweating was absent in 75% of feet with a neuropathic ulcer; a flare response was absent in 86% of them. Sweating was only absent in 36% of feet with Charcot arthropathy and was increased in one, whereas the flare response was absent in all. Autonomic cardiovascular reflexes were more frequently abnormal than the sweat test; sweating was absent in only one patient with normal cardiovascular reflexes.

Acetylcholine↗

Relationship between quin2-determined cytosolic [Ca2+] and sweat secretion.

Although both methacholine (MCh)- and A23187-induced sweat secretion are known to be strictly dependent on extracellular Ca2+, the role of intracellular calcium concentration ([Ca2+]i) in eccrine sweating has not been clarified. Partially purified eccrine secretory cells were prepared from 400 to 600 isolated secretory coils of monkey sweat glands by serial collagenase digestion and Percoll gradient centrifugation. The quin2 method was used for semiquantitative determination of [Ca2+]i, MCh increased [Ca2+]i in a dose-dependent, reversible, and pharmacologically specific manner (from the resting [Ca2+]i of 80-320 nM) but failed to increase [Ca2+]i in a Ca2+-free medium. A23187 (10(-7) M) increased [Ca2+]i to approximately 900 nM. Theophylline (TH), isoproterenol (ISO), and forskolin (FK) had no effect on the resting [Ca2+]i but, in combination, attenuated the effect of subsequently added MCh and A23187. A23187 at 10(-7) M failed to stimulate sweat secretion or CO2 production in vitro from the quin2-loaded intact isolated sweat glands and dispersed sweat secretory cells, respectively. The observed dissociation between the increase in [Ca2+] may suggest either that MCh stimulation induces some unknown excitatory signal in addition to a rise in [Ca2+] or that A23187-induced Ca2+ influx into the secretory cells is much lower in undissociated sweat glands.

Aminoquinolines↗

Control of thermoregulatory sweating during exercise in the heat.

The purposes of this study were the following: 1) to determine whether erythrocyte infusion alters the control of thermoregulatory sweating and 2) to demonstrate how increases and decreases of both plasma tonicity and blood volume influence the thermoregulatory control parameters of threshold temperature and sweating sensitivity. Six non-heat-acclimated and five heat-acclimated males attempted heat stress tests (HSTs) both before and shortly after (48-96 h) autologous erythrocyte infusion. The non-heat-acclimated subjects were euhydrated for both HSTs, whereas the heat-acclimated subjects were studied in a euhydrated and a hypohydrated (-5% body wt) condition both pre- and postinfusion (500 ml of solution containing approximately 60% hematocrit of autologous erythrocytes). The HSTs consisted of treadmill exercise (335 W.m-2) in a hot (35 degrees C, 45% relative humidity) environment, and esophageal temperature and local sweating rate were continuously measured during 25 min of exercise. These experiments resulted in a matrix of conditions where both plasma tonicity and blood volume were increased or decreased relative to control conditions (euhydration, preinfusion). The findings concerning thermoregulatory sweating during exercise in the heat were summarized as follows: 1) acute polycythemia decreases the threshold temperature and increases the sweating sensitivity, 2) both threshold temperature and sweating sensitivity are increased or decreased from control levels dependent on the combined influence of plasma tonicity and blood volume, and 3) equations are presented that describe how plasma tonicity and blood volume alter threshold temperature and sweating sensitivity values.

Acclimatization↗

Sweating responses to central and peripheral heating in spinal man.

Studies of central and peripheral heating of a resting spinal man (T6) were performed under various ambient temperatures (20-34 degrees C). It was found that at a constant core temperature, sweating could not be initiated by sentient skin heating alone, but skin cooling alone did produce a rapid decrease in sweating response. Central heating alone induced sweating responses and the central temperature thresholds of sweating were inversely related to the ambient (sentient skin) temperatures. The local and mean sweating rates were found to be linearly related to the core temperature. The slopes of local sweating rates versus the core temperature vary increasingly with the following locations: chest, forearm, and forehead; but the slopes of mean sweating rates versus core temperature were essentially constant.

Adult↗

Sweat ammonia excretion during submaximal cycling exercise.

This study was undertaken to investigate whether part of the ammonia formed during muscular exercise was excreted with the sweat. Male medical students volunteered for the experiment. They exercised 30 min on a bicycle ergometer at 80 and 40% of the predetermined maximal O2 uptake (VO2max). Exercise at 80% VO2max was performed twice, at room temperature (20 degrees C) and in a cold room (0 degrees C), whereas exercise at 40% was performed only at room temperature (20 degrees C). Blood was collected from the antecubital vein immediately before and after exercise. Sweat was collected from the hypogastric region by use of gauze pads. It was shown that the plasma ammonia level was elevated after exercise at 80% VO2max and remained stable after exercise at 40% VO2max. The volume of sweat produced during exercise at 80% VO2max at 20 degrees C was 428 +/- 138 ml and at 0 degrees C 245 +/- 86 ml and during exercise at 40% VO2max was 183 +/- 69 ml. The ammonia concentration in the sweat after exercise at 80% VO2max at 20 degrees C was 7,140 mumol/l and at 0 degrees C 11,816 mumol/l. After exercise at 40% VO2max, it was 2,076 mumol/l. The total ammonia lost through the sweat during exercise at 80% VO2max was similar at both temperatures, despite the difference in the sweat volume (at 20 degrees C, 3,360 +/- 2,080 mumol; at 0 degrees C, 3,310 +/- 1,250 mumol). During exercise at 40% VO2max, it was 350 +/- 230 mumol. These results show that part of ammonia formed during exercise is lost with sweat. The amount lost increases with increased work rate and the plasma ammonia concentration.

Adult↗

Attenuated thermoregulatory sweating and cutaneous vasodilation after 14-day bed rest in humans.

We investigated the effect of head-down bed rest (HDBR) for 14 days on thermoregulatory sweating and cutaneous vasodilation in humans. Fluid intake was ad libitum during HDBR. We induced whole body heating by increasing skin temperature for 1 h with a water-perfused blanket through which hot water (42 degrees C) was circulated. The experimental room was air-conditioned (27 degrees C, 30-40% relative humidity). We measured skin blood flow (chest and forearm), skin temperatures (chest, upper arm, forearm, thigh, and calf), and tympanic temperature. We also measured sweat rate by the ventilated capsule method in which the skin area for measurement was drained by dry air conditioned at 27 degrees C under similar skin temperatures in both trials. We calculated cutaneous vascular conductance (CVC) from the ratio of skin blood flow to mean blood pressure. From tympanic temperature-sweat rate and -CVC relationships, we assessed the threshold temperature and sensitivity as the slope response of variables to a given change in tympanic temperature. HDBR increased the threshold temperature for sweating by 0.31 degrees C at the chest and 0.32 degrees C at the forearm, whereas it reduced sensitivity by 40% at the chest and 31% at the forearm. HDBR increased the threshold temperature for cutaneous vasodilation, whereas it decreased sensitivity. HDBR reduced plasma volume by 11%, whereas it did not change plasma osmolarity. The increase in the threshold temperature for sweating correlated with that for cutaneous vasodilation. In conclusion, HDBR attenuated thermoregulatory sweating and cutaneous vasodilation by increasing the threshold temperature and decreasing sensitivity. HDBR increased the threshold temperature for sweating and cutaneous vasodilation by similar magnitudes, whereas it decreased their sensitivity by different magnitudes.

Adolescent↗

Prolonged head-down tilt exposure reduces maximal cutaneous vasodilator and sweating capacity in humans.

Cutaneous vasodilation and sweat rate are reduced during a thermal challenge after simulated and actual microgravity exposure. The effects of microgravity exposure on cutaneous vasodilator capacity and on sweat gland function are unknown. The purpose of this study was to test the hypothesis that simulated microgravity exposure, using the 6 degrees head-down tilt (HDT) bed rest model, reduces maximal forearm cutaneous vascular conductance (FVC) and sweat gland function and that exercise during HDT preserves these responses. To test these hypotheses, 20 subjects were exposed to 14 days of strict HDT bed rest. Twelve of those subjects exercised (supine cycle ergometry) at 75% of pre-bed rest heart rate maximum for 90 min/day throughout HDT bed rest. Before and after HDT bed rest, maximal FVC was measured, via plethysmography, by heating the entire forearm to 42 degrees C for 45 min. Sweat gland function was assessed by administering 1 x 10(-6) to 2 M acetylcholine (9 doses) via intradermal microdialysis while simultaneously monitoring sweat rate over the microdialysis membranes. In the nonexercise group, maximal FVC and maximal stimulated sweat rate were significantly reduced after HDT bed rest. In contrast, these responses were unchanged in the exercise group. These data suggest that 14 days of simulated microgravity exposure, using the HDT bed rest model, reduces cutaneous vasodilator and sweating capacity, whereas aerobic exercise training during HDT bed rest preserves these responses.

Acetylcholine↗

Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans.

The purpose of the study was to examine the effect of 1) passive (assisted pedaling), 2) active (loadless pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), skin blood flow (SkBF), and sweating during recovery after 15 min of dynamic exercise. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, SkBF, and sweating during exercise recovery. Six male subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 15 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (T(sk)), esophageal temperature (T(es)), SkBF, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, and 15 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active and passive recovery modes, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining CO, SV, MAP, CVC, and sweat rate above inactive recovery. Sweat rate was different among all modes after 8 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the passive and inactive modes (P < 0.05). No differences in either T(es) or T(sk) were observed among conditions. Given that MAP was higher during passive and active recovery modes than during inactive recovery suggests differences in CVC may be due to differences in baroreceptor unloading and not factors attributed to central command. However, differences in sweat rate may be influenced by factors such as central command and mechanoreceptor stimulation.

Blood Pressure↗

Sweat chloride concentration in adults with pulmonary diseases.

In order to determine whether a high proportion of adults with pulmonary diseases have sweat chloride concentrations in the range usually considered diagnostic for cystic fibrosis (greater than 60 mEg/L), we performed the standard diagnostic "sweat test" of Gibson and Cooke prospectively on 187 subjects 18 to 85 yr of age who did not have cystic fibrosis (166 of them had some pulmonary or allergic disorder, and 21 were healthy). In this group, 99% had sweat chloride concentration less than 70 mEq/L, and 96%, less than 60 mEq/L. Those taking steroids had sweat chloride concentration slightly but significantly lower than those who did not take steroids, probably because of the mineralocorticoid effect. Six patients had pancreatitis, and 2 of those had sweat chloride concentration greater than 60 mEq/L, a distribution of values significantly different (p less than 0.005) from the rest of the population. Our results suggest that a very small proportion of adults with pulmonary diseases have sweat chloride concentrations in the range usually considered diagnostic for cystic fibrosis, and that the sweat test is a good discriminant for cystic fibrosis even in the adult age group.

Adolescent↗

Abnormal sweat electrolytes in a case of celiac disease and a case of psychosocial failure to thrive. Review of other reported causes.

Sweat electrolytes were initially elevated in a child who was diagnosed as having celiac disease and also in one with psychosocial failure to thrive. Subsequent sweat tests were normal after nutritional status of the patients had improved with therapy. The reports of elevated sweat electrolytes in conditions other than cystic fibrosis are discussed. It is emphasized that sweat test methods other than the quantitative pilocarpine iontophoresis method are not reliable. The occurrence of false-positive sweat tests demonstrates the need for care in the interpretation of elevated sweat electrolytes and the necessity of performing repeat quantitative pilocarpine iontophoresis for the establishment of the diagnosis of CF. Celiac disease and malnutrition from other causes may cause sweat electrolytes to be elevated.

Celiac Disease↗