"Polywater" and sweat:similarities between the infrared spectra.

The infrared spectrum of "polywater" is remarkably similar to that of sodium lactate, the primary constituent of sweat. It is proposed, therefore, that this property of "polywater," and possibly others, results from accidental biological contamination. Such contamination is consistent with chemical analyses of "polywater" samples prepared both here and abroad.

Sweat in schizophrenic patients: identification of the odorous substance.

The substance causing the peculiar odor in sweat of schizophrenic patients has been isolated and identified as trans-3-methyl-2-hexenoic acid by gas chromatography, mass spectrometry, and nuclear magnetic resonance spectroscopy. The natural and the synthetic compounds were cleaves across the double bond to give 2-pentanone and oxalic acid, thereby confirming the structure.

L-Lactic acid: a mosquito attractant isolated from humans.

L-Lactic acid was the major component in material isolated from humans that was active as an attractant for female yellow fever mosquitoes, Aedes aegypti (L.). The L(+)-isomer was several times as attractive as the D-isomer. Good correlation was found between the attractiveness of an individual to mosquitoes and the quantity of lactic acid present in an acetone washing of his hand.

Micropuncture studies of the sweat formation in cystic fibrosis patients.

In order to determine whether the precursor solution of sweat is abnormal in cystic fibrosis, osmolality and concentrations of sodium and chloride were measured in fluid obtained by micropuncture from the sweat gland coil of the nail fold of patients with this disease. Osmolality was 323+/-4.8 SE (mOsm/kg of water), sodium concentration was 151+/-1.1 SE (mEq/liter), and chloride concentration was 124+/-6.0 SE (mEq/liter). The sweat:plasma ratio for osmolality averaged 1.1+/-0.015 SE. These values are not significantly different from the corresponding ones obtained previously in normal individuals. It is concluded therefore that the disturbance of sweat gland function as far as electrolytes are concerned is restricted to the excretory ducts. In a second series of experiments the stop-flow pressure which is generated by sweat glands during secretion was measured. Values up to 500 mm Hg were found in both patients and normals. According to van't Hoff's law (DeltaP = RTDeltaC) hydrostatic pressure differences of this magnitude can be generated by the osmotic difference of 27 mOsm/kg of water observed between precursor sweat and plasma in the present experiments. With respect to the mechanism of sweat secretion this finding supports the hypothesis that active solute transport creates an osmotic gradient which causes osmotic water flux.

The effect of supplemental oral phosphate on the bone mineral changes during prolonged bed rest.

Five healthy young men were studied during 24-30 wk of continuous bed rest. During the first 12 wk of bed rest, untreated subjects increased calcium excretion in the urine by 109 mg/day and in the feces by 147 mg/day. The rate of total body calcium loss was 0.5-0.7% per month. Losses of central calcaneus mineral, assessed by gamma ray transmission scanning, occurred at a tenfold higher rate, whereas the mineral content of the radius did not change. Changes in phosphorus balance resembled the calcium pattern, and increased excretion of nitrogen and hydroxyproline also occurred during bed rest. Upon reambulation, the subjects' calcium balance became positive in 1 month and recovery of their calcaneus mineral was complete within 10-20 wk. Treatment with potassium phosphate supplements (1327 mg P/day) entirely prevented the hypercalciuria of bed rest, but fecal calcium tended to increase. During the first 12 wk, calcium balance was slightly less negative (mean - 193 mg/day) than during bed rest without added phosphate (mean - 267 mg/day). This effect was not seen during the second 12 wk of bed rest. The patterns of magnesium excretion were similar to those of calcium. Fecal and urinary phosphorus excretions were doubled, and phosphorus balance became positive (+ 113 mg/day). Mineral loss from the central calcaneus was similar to that of untreated subjects. It is concluded that this form of phosphate supplementation reduces urinary calcium excretion but does not prevent bone loss during bed rest.

Recurrent respiratory disease, azoospermia, and nasal polyposis. A syndrome that mimics cystic fibrosis and immotile cilia syndrome.

Three adult men with chronic sinopulmonary disease, nasal polyposis, and azoospermia were studied. All had normal sweat chloride values and pancreatic function. The azoospermia was due to a block in the epididymis that was distinguishable from the defect in the vas deferens seen in cystic fibrosis. Cilia structure was normal in sperm tails from testicular biopsy specimens and in cilia from tracheal biopsy specimens. These cases represent a clinical entity distinct from cystic fibrosis and known immotile cilia disorders.

Electrophoretic patterns of proteins in cystic fibrosis sweat.

The abnormal gene product in cystic fibrosis has not been identified. We report that two-dimensional polyacrylamide gel electrophoresis of 125I-labeled sweat proteins coupled with fluorography and rare earth screen radioautography reveals an absence of an acidic protein of molecular weight 60,000 in sweat collected from 9 patients with cystic fibrosis. The protein spot was present in sweat from heterozygotes and from controls.

IgE in human eccrine sweat.

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

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.

Urine pH and phencyclidine excretion.

Subeffective doses (0.5 mg) of 3H-phencyclidine (PCP) were given intravenously to three healthy men under two regimens designed to alkalinize or acidify their urine (oral sodium bicarbonate or ammonium chloride). The concentrations of PCP and its metabolites in saliva, plasma, and urine for 7 hr after injection were determined by high-performance liquid radiochromatography. A sample of perspiration from one subject was analyzed. The effects of physical exercise on the plasma concentration and urinary excretion of PCP were also studied. Multiple linear regression analysis showed the logarithm of renal clearance the renal clearance of PCP. PCP and its metabolites are also excreted in perspiration. Our results support clinical reports of the importance of vigorous acidification of urine and diuresis in treatment of PCP intoxication.

Effect of strenuous exercise on serum lithium level in man.

The authors examined the effect of strenuous exercise on the serum lithium levels of four healthy, conditioned athletes who were stabilized on lithium carbonate for 7 days and who ran a 20-km race under hot, humid conditions. The subjects became substantially dehydrated during the race, and their serum lithium levels decreased, suggesting that sweat lithium loss may be substantial. (The sweat-to-serum ratio for lithium exceeded that for sodium by a factor of 4.) The authors conclude that contrary to widely held belief, heavy sweating may not increase the risk of lithium intoxication.

Iron losses in sweat.

The losses of iron in whole body cell-free sweat were determined in eleven healthy men. A new experimental design was used with a very careful cleaning procedure of the skin and repeated consecutive sampling periods of sweat in a sauna. The purpose was to achieve a steady state of sweat iron losses with minimal influence from iron originating from desquamated cells and iron contaminating the skin. A steady state was reached in the third sauna period (second sweat sampling period). Iron loss was directly related to the volume of sweat lost and amounted to 22.5 micrograms iron/l sweat. The findings indicate that iron is a physiological constituent of sweat and derived not only from contamination. Present results imply that variations in the amount of sweat lost will have only a marginal effect on the variation in total body iron losses.

Copper status and urinary and salivary copper in young men at three levels of dietary copper.

Eleven young men were confined to a metabolic research unit for 90 d to determine the effect of the amount of dietary copper on copper nutriture. The study was divided into three metabolic periods (MP): 1) with an adequate-copper diet (1.68 mg/d) for 24 d, 2) with a low-copper diet (0.79 mg/d) for 42 d, and 3) with a high-copper diet (7.53 mg/d) for 24 d. Three indices of copper status, urinary copper, and salivary copper were determined at intervals throughout the study. Neither copper status, urinary copper, nor salivary copper differed among MPs. Sweat collections from three subjects suggested that losses of copper through sweat were very low and would not contribute significantly to copper balance. These results suggest that an amount of dietary copper slightly less than 0.8 mg/d is adequate to maintain copper status for greater than or equal to 42 d in normal, healthy men and that neither urinary nor salivary copper is affected by the amount of Cu in the diet.

Dietary potassium and heavy exercise: effects on muscle water and electrolytes.

Eight men were studied during two 4-day exercise-dietary regimens, once under a control diet (80 mEq K+/day) and again with a diet low in K+ (25 mEq/day). Muscle K+ increased 5 to 6% as a result of the two exercise-dietary regimens, while no change was observed for muscle Na+ or Mg++. Plasma volume increased throughout the 4 days of each exercise-diet sequence, with the low K+ regimen resulting in the largest plasma volume gain (+15%) and a marked reduction in urinary K+ excretion. Despite the losses of K+ in sweat and the low K+ intake, there was a relatively small decrease in total body K+ content (less than 2% of body content). Based on these measurements of extracellular (plasma) and tissue (muscle) water and electrolytes, we have concluded that in combination with 4 days of heavy exercise and sweating, a low K+ diet will not significantly diminish the total body K+ content.

Low sweat electrolytes in a patient with cystic fibrosis.

A patient with the clinical syndrome of cystic fibrosis characterized by chronic pulmonary disease, infection with mucoid Pseudomonas aeruginosa, sinusitis, nasal polyposis, abnormal pancreatic bicarbonate response to secretin stimulation, but normal levels of trypsin and chymotrypsin in the duodenal drainage, and a sibling with autopsy-documented cystic fibrosis, is described. Sweat chloride ranged from 20 to 44 meq/liter and sweat sodium from 36 to 55 meq/liter. Immunoglobulin deficiency, alpha 1-antitrypsin deficiency, tuberculosis and abnormalities of ciliary ultrastructure were excluded. Review of sweat electrolytes in 213 patients with cystic fibrosis revealed that patients with normal pancreatic enzyme release have significantly lower sweat sodium and chloride concentrations (p < 0.0005) than do patients with pancreatic insufficiency. Chronic pulmonary disease, pancreatic insufficiency and elevated levels of sweat electrolytes comprise the classic diagnostic triad for cystic fibrosis. The expression of these features may be variable, but the sweat test remains the cardinal laboratory confirmation of the diagnosis. Over 98 percent of patients with cystic fibrosis have sweat chloride values greater than 60 meq/liter, 1 to 2 percent between 50 and 60 meq/liter, and only about one in 1,000, like our patient, less than 50 meq/liter. Patients with cystic fibrosis with borderline sweat chloride values frequently have chronic pulmonary disease but intact pancreatic enzyme release. In such patients, family history, ancillary clinical features and systemic exclusion of other syndromes assume special diagnostic importance.

Cooperative study comparing three methods of performing sweat tests to diagnose cystic fibrosis.

Directors of cystic fibrosis centers in the United States have noted an increasing number of patients with histories of either false-positive or false-negative sweat tests. These inaccuracies were attributed to the use of rapid test methods which avoided actually weighing the sweat collected. These rapid tests have inherent difficulties which, theoretically at least, could lead to mistaken diagnoses. To evaluate methods of performing the sweat test, the National Cystic Fibrosis Foundation organized a combined study comparing the older Quantitative pilocarpine iontophoretic test (QPIT) method of performing the test with two newer and more rapid methods, the Orion skin electrode, and the Medtherm conductivity apparatus. Five cystic fibrosis centers participated in the study. Although two centers obtained considerably more accurate results with the Orion and the Medtherm than did the other three centers, the combined results of the study indicate that these procedures can be considered to be little more than screening tests.

Munchausen syndrome by proxy simulating cystic fibrosis.

The case of a child with apparent cystic fibrosis whose many signs, symptoms, and laboratory results were convincingly portrayed by his mother is presented. The mother falsified the history, and cunningly altered sweat tests and stool fat analyses, and stole sputum from patients with cystic fibrosis to make her child appear to have cystic fibrosis. This case of Munchausen syndrome by proxy highlights the extent to which the diagnosis of cystic fibrosis rests on reliable history and laboratory data and emphasizes the extremes to which perpetrators of this form of child abuse may go to make their case. Medical personnel must educate civil authorities about this syndrome and the dangers it represents to the child.

Dietary essential fatty acids in cystic fibrosis.

Analyses of serum lipids of children with cystic fibrosis (CF) have indicated a deficiency in essential fatty acids (EFA). In view of a report that intravenous administration of soybean oil emulsions normalized sweat sodium values in CF children, we studied the effects of orally administered essential fatty acids (as corn oil) for one year. Some improvement was noted in all patients, but no one consistent factor predominated. However, arachidonic acid, which was found only in trace amounts or was absent in sera of all children with CF before the clinical trial, was increased significantly in the sera after the oral administration of EFA for one year. Other findings included a significant decrease in sweat sodium and T3 in most patients.

Negative effects of oral fatty acid supplementation on sweat chloride in cystic fibrosis.

Essential fatty acid supplementation with oral safflower oil (1 gm/kg/day) to 11 cystic fibrosis patients (aged 6 months to 14 years) for one year produced no significant change in sweat chloride concentration (mEq/liter) or sweat rate (gm/min/m2), Addition of vitamin E (10 mg/kg/day) to the safflower oil had no effect on sweat chloride concentration or rate compared to placebo. No clinical improvement could be detected compared to a control group. These results do not support previous reports of the effects of fatty acid supplementation on sweat electrolyte concentrations in cystic fibrosis.

Studies of human lead metabolism by use of stable isotope tracers.

Dynamics of lead metabolism were studied by replacement of a portion of the dietary lead with stable isotope tracers, and maintaining subjects on controlled diets for about 6 months. Results for one subject have been previously reported. Preliminary data are now available for a second subject. Although the data on the two subjects are basically similar, there are also significant differences. The two subjects have different blood lead concentrations (0.25 and 0.18 mug/g). Both subjects received the same dietary and similar atmospheric lead exposure, and the lead concentration of their blood was shown to be nearly in a steady state. The difference in blood lead concentration appears primarily attributable to differences in the fraction of lead absorbed from the gut, although there are also differences in other physiological parameters, as well as probable small differences in their intake of atmospheric lead. The quantity of lead absorbed from a typical urban atmosphere (Pb concentration = 1-2 mug/m(3)) has been shown by our isotopic data and balance studies to be 15+/-3 mug/day. Measurement of the contribution of atmospheric lead to the lead intake of the second subject was also carried out by removal of lead from the atmosphere. Decline in the blood concentration of lead of normal isotopic composition was shown to be equivalent to the removal of 15 g/day. Measurements made during the course of a day show complexities in the absorption and distribution of lead, which are averaged out on a time scale of ca. 5 days.