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PubMed2003

Diagnosing night sweats.

Night sweats are a common outpatient complaint, yet literature on the subject is scarce. Tuberculosis and lymphoma are diseases in which night sweats are a dominant symptom, but these are infrequently found to be the cause of night sweats in modern practice. While these diseases remain important diagnostic considerations in patients with night sweats, other diagnoses to consider include human immunodeficiency virus, gastroesophageal reflux disease, obstructive sleep apnea, hyperthyroidism, hypoglycemia, and several less common diseases. Antihypertensives, antipyretics, other medications, and drugs of abuse such as alcohol and heroin may cause night sweats. Serious causes of night sweats can be excluded with a thorough history, physical examination, and directed laboratory and radiographic studies. If a history and physical do not reveal a possible diagnosis, physicians should consider a purified protein derivative, complete blood count, human immunodeficiency virus test, thyroid-stimulating hormone test, erythrocyte sedimentation rate evaluation, chest radiograph, and possibly chest and abdominal computed tomographic scans and bone marrow biopsy.

Circadian Rhythm↗

PubMed1992

Use of a semi-quantitative sweat test in thoroughbred horses.

A practical test for evaluating the sweating response to various concentrations of the specific beta 2 agonist, salbutamol sulphate, is described. The results of performing this test on horses (n = 54) considered to be "free sweaters", horses (n = 6) that showed signs of heat stress following exercise, and horses with complete anhidrosis (n = 2) are presented. The results indicate that intradermal injections of 0.1 ml of salbutamol sulphate at dilutions of 10(-7) or less are suitable stimuli to elicit a visually detectable local sweating in horses with a normal sweating response. Horses that only sweated at the sites where salbutamol solutions with dilutions of between 10(-4) and 10(-6) were injected, probably had a reduced sweating response and could be considered to be suffering from partial anhidrosis. Horses with severe anhidrosis of long duration did not sweat, even in response to salbutamol solutions with dilutions of 2 x 10(-3).

Albuterol↗

PubMed1985

Influence of digoxin and diuretic therapy on sweat fluid composition.

The effect of digitalis and diuretic therapy on sweat fluid composition was investigated. Patients treated for congestive heart failure with a combination of digoxin and diuretics demonstrated a higher concentration of sodium and chloride in their sweat fluid when compared to age-matched controls. The administration of diuretics alone did not affect sweat fluid composition. The digoxin-induced increase in sodium concentration was significantly higher than that observed for chloride. These data suggest that digoxin markedly inhibits sodium reabsorption along the sweat gland tubule, whereas chloride transport is affected to a lesser degree. A significant correlation between sweat fluid sodium and serum digoxin concentrations was observed. We conclude that the increased digoxin-induced sweat sodium and chloride losses may affect sodium homeostasis in patients with congestive heart failure.

Aged↗

PubMed1988

A population study on the density of palmar sweat pores.

A study of density of sweat pores in 594 individuals indicated that the average number of pores per cm2 in the hypothenar area was 490.4 for white newborns, 513.6 for black newborns, 652.4 for white children, 629.2 for black children, 519.6 for white adult males, 533.6 for white adult females, 379.2 for black adult males, and 519.2 for black adult females. The present study failed to demonstrate that newborns have the greatest density of pores when compared with children and adults. However, it should be kept in mind that many of the palmar impressions were taken during the first or second day of life. Those impressions did not reproduce the sweat pores clearly. It appears from this study that an optimal time to take palmar impressions on newborns is after the sweat glands are mature and functioning. Figure 1 shows that this occurs 2 weeks after birth. No differences in the density of sweat pores was found between blacks and whites. No differences in the density of sweat pores between the sexes was found in any group except for adult blacks: males had fewer pores than females. A review of the density of sweat pores in subjects with hypohidrotic ectodermal dysplasia is also given.

Adult↗

PubMed1977

Reflex sweating in patients with spinal cord injury: a review.

Sweat glands derive their innervation from the sympathetic nervous system. The spinal sympathetic structures that are located in the intermediolateral areas extend from T1-L2 segments and are under the control of hypothalamic centers. Cord transection abolishes the supraspinal control of sudorimotor function. Since sympathetic innervation does not follow a clear segmental distribution, normal sweating may be preserved at a higher or lower level than skin sensation. Nonthermoregulatory reflex sweating is an indication of unchecked spinal cord facilitation and is precipitated by afferent stimuli from bladder, rectum, and various other sources. It is usually a manifestation of mass reflex or autonomic crisis and occurs particularly in cervical or high thoracic lesions. Transection below T8-T10 is not accompanied by reflex sweating. The phenomenon of thermal relfex sweating is controversial. Although some aspects of nonthermoregulatory reflex sweating are still unclear, proper immediate and continuing preventive management will reduce the incidence of this and other autonomic manifestations. Chemical sympathectomy should be a last resort in case of emergency or when the source of facilitation cannot be ascertained.

Autonomic Nervous System↗

PubMed1987

[Sweat collection and osmometry in the diagnosis of cystic fibrosis: a new method].

Two methods of sweat testing (Gibson and Cooke's vs. sweat osmolality) for the diagnosis of cystic fibrosis were compared in 33 subjects (26 healthy subjects and 7 patients aged 23 days to 28 years). Sweat was collected with a "macroduct"-sweat collection-system, osmolality was measured with the Wescorvapor-pressure osmometry. In a further 18 subjects (13 healthy, 5 patients) electrolytes were determined from filter-paper and the Vescor-macroduct-system. The osmolality in sweat of healthy subjects and patients with CF differed significantly (p less than 0.001). In healthy subjects maximum osmolality was 198 mmol/kg (means 158 +/- 21.3 mmol/kg), in patients with CF 283.9 +/- 10.2 mmol/kg. Assessment of sweat osmolality is a highly reliable procedure for confirming the diagnosis of CF provided borderline-values between 180 and 220 mmol/kg are reevaluated with the conventional filter-paper assay.

Cystic Fibrosis↗

PubMed1986

Sweat gland response to local heating during sleep in man.

In order to assess whether the fluctuations in the sweating response occurring during sleep are related to changes in central drive or in peripheral sweat gland reactivity, 4 healthy male subjects spent 6 non-consecutive nights in a climatic chamber. Air temperature was 25 degrees C, dew-point temperature was 10 degrees C and air velocity was 0.3 m X s-1, while wall temperature was either 38 degrees C, 46 degrees C or 48.7 degrees C giving 3 levels of operative temperature (To = 30, 33 or 34 degrees C). During the whole night, 2 local sweating rates on the right and the left sides of the upper chest were continuously recorded from 12 cm2 area capsules using a dew-point hygrometer technique, while applying local thermal clamps, a constant 2 degrees C difference in local skin temperatures being imposed between the two symmetrical skin areas. Continuous measurements were made of rectal temperature, 10 local skin temperatures, 2 EEGs, 2 EOGs, 1 EMG and 1 ECG. Results show that the multiplicative relationship between the peripheral influence of local skin temperature and the central drive for sweating described in waking subjects, is still valid in sleeping subjects. No peripheral change appears in sweat gland reactivity between the different sleep stages. Changes in the sensitivity of the thermoregulatory system occurring during sleep cannot be explained by a local factor acting at the sweat gland level.

Body Temperature Regulation↗

PubMed1984

Neonatal 6-hydroxydopamine treatment eliminates cholinergic sympathetic innervation and induces sensory sprouting in rat sweat glands.

Previous studies of the development of cholinergic sympathetic innervation of sweat glands in rat footpads suggested that these terminals initially exhibit noradrenergic properties which are lost as the glands and their innervation mature. We have treated neonatal and adult rats with 6-hydroxydopamine (6-OHDA), a toxic congener of norepinephrine, and compared its effects on the cholinergic sympathetic innervation of sweat glands and the noradrenergic sympathetic innervation of the iris, salivary gland, and blood vessels. As reported by others, 6-OHDA treatment of neonates caused the destruction of noradrenergic fibers in the iris and salivary gland but did not affect other fibers projecting to these targets that stain for acetylcholinesterase (AChE). We found that 6-OHDA treatment of neonatal animals also caused the destruction of the sympathetic axons in immature sweat glands that possess catecholamine histofluorescence and tyrosine-hydroxylase-like immunoreactivity. Furthermore, when such animals were examined as adults, we found no AChE staining, vasoactive intestinal peptide (VIP)-like immunoreactivity, or characteristic sympathetic axonal varicosities. However, the denervated glands were invested by a plexus of sensory axons, some of which exhibited substance P-like immunoreactivity (SP-IR). An increase in the number of SP-IR fibers also occurred in the sympathetically denervated irides of these animals. Chronic treatment of neonates with guanethidine, another adrenergic sympathetic neurotoxin, resulted in similar loss of cholinergic sweat gland innervation. Treatment of adults rats with doses of 6-OHDA identical to those used to treat neonates caused the loss of noradrenergic fibers from the iris, salivary gland, and many blood vessels but did not noticeably affect AChE and VIP staining or axonal ultrastructure in the sweat glands. However, treatment with higher doses of 6-OHDA did cause significant axonal degeneration. The response of the sympathetic innervation of developing but not mature sweat glands to 6-OHDA provides evidence for a transition from noradrenergic to cholinergic phenotype during the development of sympathetic neurons in vivo similar to the transition observed in cell culture. The sprouting of sensory axons may be caused by NGF-like trophic influences present in some sympathetically denervated tissues.

Animals↗

PubMed1984

The use of sweat osmolality in the diagnosis of cystic fibrosis.

Sweat osmolality determination with 7-10 microliter of sweat for the establishment of the diagnosis of cystic fibrosis (CF) was evaluated in 297 probands. In 12 out of 26 infants below 2 months of age and in 3 out of 271 older probands not enough sweat could be collected at the first attempt. A final diagnosis was established before the age of 2 months in 21 out of 26 infants. In 27 CF patients sweat osmolality was 285.86 +/- 41.25 mmol/kg (mean +/- SD), the mean value - 2 SD being 203.36 mmol/kg. In 266 control subjects sweat osmolality was 107.38 +/- 29.49 mmol/kg (mean +/- SD), the mean value + 2 SD being 166.36 mmol/kg. There was no overlap between CF patients and controls in each age group. The method is simple, rapid and reliable, and improves diagnostic possibilities especially in young infants. Sweat osmolality values above 180 mmol/kg should be repeated and checked for final confirmation or exclusion of the diagnosis of cystic fibrosis.

Adolescent↗

PubMed1994

Prognostic value of immunohistochemical staining for proliferating cell nuclear antigen, p53, and c-erbB-2 in sebaceous gland carcinoma and sweat gland carcinoma: comparison with histopathological parameter.

Thirteen cases of sebaceous gland carcinoma and 10 cases of sweat gland carcinoma were studied using immunohistochemical staining for proliferating cell nuclear antigen (PCNA), c-erbB-2, and p53 to examine correlations among them, and to determine the best predictor of patient prognosis. Many sebaceous gland carcinomas and sweat gland carcinomas showed nuclear accumulation of p53, and patients with tumors showing a PCNA index (percentage of nuclei stained for PCNA) higher than 20%, and a p53 index (percentage of nuclei stained for p53) higher than 10% had short survival. Sebaceous gland carcinomas and sweat gland carcinomas showing c-erbB-2 expression had high PCNA (> 20%) and p53 (> 10%) indices, and were associated with poor prognosis. Histologically, sebaceous gland carcinomas showing a high degree of differentiation and severe nucleolar atypia had high PCNA and p53 indices. A growth pattern of small solid nests and strands, a low degree of differentiation, and the presence of lymphatic permeation in sweat gland carcinoma were often associated with high PCNA and p53 indices. These results suggest that nuclear accumulation of p53 plays an important role in the development of sebaceous gland carcinoma and sweat gland carcinoma. Assessment of PCNA and p53 indices together was very useful for prognostication of patient outcome, using cut-off values of 20% and 10%, respectively, to separate good prognosis from poor. Differentiation of sebaceous gland carcinoma, and c-erbB-2 expression by sweat gland carcinoma were significant independent prognostic indicators.

Adult↗

PubMed1994

The role of sweat in maintaining the stimulation of effort homeostasis in horses.

Sweat secretion was analyzed quantitatively and qualitatively in 20 horses after a 5 min. gallop at 450 m/min. The analysis revealed concentration of proteins 63.3 +/- 6.47 g/l, mainly albumins, a high level of sodium 254.43 +/- 62.84 mM/,l chloride 268.68 +/- 98.46 mM/l, potassium 98.95 +/- 49.62 mM/l and calcium 4.14 +/- 0.8 mM/l. A dependence was found between the protein concentration in serum and its quantity in sweat and between the level of potassium in sweat and its loss from the cells within a range 8.6 to 25.8 mM/l. The hypertonic horse sweat protects organism for excessive water loss, the loss taking place by imperceptible evaporation. The loss of body weight amounted to 5.64 +/- 2.36 kg and the loss with the sweat was only 1.56 kg. Besides its thermoregulation function, the sweat ensures a proper effort homeostasis-isoosmic and isoionic status.

Animals↗

PubMed1976

Detection of HBsAg and HBsAb in sweat.

HBsAg was detected in the sweat of 9/18 seropositive, but 0/20 seronegative probands. Frequency of detection correlated to serum titer of HBsAg, blood contamination and efficiency of sweat concentrating. On base of quantitative evaluations it is assumed, that blood and/or plasma contaminations are responsible for the presence of HBsAg in sweat. Since HBsAg and hepatitis virus B are of similar diameter, this mechanisms should work on the infectious agent too. Thus HBsAg could prove a marker, to calculate the infectivity of sweat in comparison to the corresponding serum specimen (10(-6) to 10(-7). HBsAb was detected in sweat too and was confined to HBsAb-seropositive probands (4/5). It is discussed, that the presence of HBsAb in sweat could provide protection against reinfections by contact and thus contribute to homologous immunity in hepatitis B.

Antibodies↗

PubMed1960

Electrical impedance changes of the cat's foot pad in relation to sweat secretion and reabsorption.

Impedance across the cat's foot pad, the glands being at rest, has a high quite constant value in a given preparation. Stimulation of the sudomotor nerves causes a decrease to a low constant value. After cessation of stimulation impedance returns slowly over a course that is linear with respect to the logarithm of time. The resistive and capacitative components vary with each other. Sweat reabsorption during recovery progresses linearly with respect to time. Hence impedance varies as the logarithm of reabsorption, and therefore as the mean level of sweat columns in the ducts. This relation can be accommodated by supposing that the sweat duct epithelium resembles a core conductor. An electrical model constructed on this principle is shown to behave as does the foot pad. During stimulation at a fixed frequency impedance change varies as the logarithm of duration showing that the amount of sweat produced per impulse at a given frequency is a constant. With frequency of a fixed number of stimuli varied the impedance change varies with it in a manner consistent with the view that the amount of sweat produced per impulse is a constant regardless of frequency.

Animals↗

PubMed2001

Olfactory receptors on the antennae of the malaria mosquito Anopheles gambiae are sensitive to ammonia and other sweat-borne components.

Electrophysiological studies on female An. gambiae s.s. mosquitoes revealed a receptor neuron within a subpopulation of the antennal grooved-peg sensilla sensitive to the odour of incubated sweat, but not responding to fresh sweat. This receptor neuron was sensitive to ammonia as well, a sweat-borne component which attracts female An. gambiae in a windtunnel bioassay. Neurons innervating a different subpopulation of grooved-peg sensilla did not show a response to incubated sweat. In the latter sensilla, however, one type of neuron responded to water or water containing solutions, while another receptor neuron was inhibited when stimulated with dry air, ether or ethanol. Neurons innervating sensilla trichodea, a more abundant antennal type of olfactory sensillum, did not respond to fresh or incubated sweat at the doses offered. However, receptor neurons within the sensilla trichodea responded with excitation to several sweat-borne components. A subpopulation of the sensilla trichodea was innervated by neurons sensitive to geranyl acetone. A second subpopulation housed receptor neurons sensitive to indole. 3-Methyl-1-butanol and 6-methyl-5-hepten-2-one evoked excitation of receptor neurons within both subpopulations of sensilla trichodea. Neurons were most sensitive to indole and geranyl acetone with a threshold of 0.01%. These findings are discussed in the context of host-seeking behaviour.

Journal Article↗

PubMed1995

Impaired sweating as an exocrine manifestation in Sjögren's syndrome.

To examine the prevalence of hypohidrosis and to quantitate sweating as an exocrinopathy in Sjögren's syndrome (SS), 49 patients with SS (primary form, 38; secondary form, 11) were studied. Sweating was induced by mental stimulation such as deep breathing or hand grasping. Statistically significant reductions of sweat volume were seen in SS (P < 0.005). Patients under 50 years old showed impaired sweat function compared with normal controls (P < 0.0005). In a control study, only haemodialysis patients showed impairment of sweating and this was greater than in patients with SS aged under 50 years. These results suggest that patients with SS develop impaired sweating as an exocrine manifestation in addition to the known symptoms of xerostomia and xerophthalmus.

Adolescent↗

PubMed2005

Are patients better than the laboratory in assessing sweating? Validation study.

BACKGROUND: Primary focal hyperhidrosis is a hereditary condition characterized by excessive sweating affecting a variety of areas, including the palms. In most cases, the decision to treat a patient is based only on the patient's own description of the symptoms because laboratory tests have not been established in clinical practice. OBJECTIVE: To validate a subjective self-assessment scale for sweating in comparison with an objective method of quantifying evaporation from the skin surface. METHODS: We studied palmar sweating in 20 patients with primary focal hyperhidrosis and 20 age- and gender-matched controls. Four times in each subject, we obtained measurements of the evaporation in palms and the self-evaluation scale (SES) scores on a proportional scale from 0 (no sweating) to 10 (worst imaginable sweating). RESULTS: Good correlation was found between the SES score and evaporation assessment (R = .65). The SES score was easier to obtain and provided better diagnostic sensitivity and specificity. They leveled out at over 80% when a score of 3 was used as the threshold level; for evaporimetry, sensitivity equalled specificity at 70% at the threshold 90 mg -2h(-1). CONCLUSION: We confirm the usefulness of the SES in assessing palmar sweating and discuss the current restrictions in its use in clinical diagnosis. We propose that the scale can be added effortlessly to research or clinical protocols to provide the necessary validation in wider spectra of patients.

Adolescent↗

PubMed2005

The relevance of sweat testing for the diagnosis of cystic fibrosis in the genomic era.

Cystic fibrosis (CF) is the most common inherited disorder of childhood. The diagnosis of CF has traditionally been based on clinical features with confirmatory evidence by sweat electrolyte analysis. Since 1989 it has been possible to also use gene mutation analysis to aid the diagnosis. Cloning of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has advanced our understanding of CF, in particular the molecular basis of an expanded CF phenotype. However, because there are over 1000 mutations and 200 polymorphisms, many without recognised effects on CFTR, the molecular diagnosis can be troublesome. This has necessitated measurement of CFTR function with renewed interest in the sweat test. This review provides an overview of the clinical features of CF, the diagnosis and complex genetics. We provide a detailed discussion of the structure and function of CFTR and the classification of CFTR mutations. Sweat electrolyte analysis is discussed, from the physiology of sweating to the rigours of a properly performed sweat test and its interpretation. With this information it is possible to understand the relevance of the sweat test in the genomic era.

Journal Article↗

PubMed1991

Evaluation of severe reactions to sweat bee stings.

Thirteen patients with severe reactions to sweat bee stings were evaluated. Eleven patients had had systemic reactions and two, large local reactions. Skin testing and RAST with venom of other Hymenoptera and whole body extract of sweat bees disclosed negative reactions to both skin tests and RAST of all other insects tested in eight, while three showed sensitivity to honey bee. Only one patient had a positive RAST reaction to whole body extract of sweat bee. Whole body extract of sweat bee causes some irritant reaction when skin testing controls and is not a reliable diagnostic agent even though patients were more reactive than controls. Hypersensitivity reactions to sweat bee stings are distinct and not associated with reactions to other stinging insects. Currently, no reliable antigen is commercially available for diagnosing or treating this condition. Sweat bee venom or other venom antigens might be beneficial.

Adult↗