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A method is described for the determination of urinary 17-hydroxycorticosteroids using fluorescence high-performance liquid chromatography. After enzymatic hydrolysis, 17-hydroxycorticosteroids were extracted using an Extrelut column and then labeled with Dns-hydrazine in hydrochloric acid-ethanol solution. The labeled steroids were chromatographed on a microparticulate silica gel column, the mobile phase was dichloromethane-ethanol-water (900:60:40). The eluate was monitored on a fluorophotometer at 365 nm (excitation) and 505 nm (emission). Linearity of the fluorescence intensities (peak heights) of various 17-hydroxycorticosteroids were obtained between 60 pg and 20 ng. The assay was sensitive, precise and accurate. Comparison with the results obtained by radioimmunoassay gave correlation coefficients of 0.932 for tetrahydrocortisol and 0.930 for tetrahydrocortisone. The proposed method is clinically useful for the routine analysis of urinary 17-hydroxycorticosteroids.
The effects of levodopa on the plasma concentration of 11-hydroxycorticosteroids and glucose were examined in mice. In fasted, nialamide treated mice, but not in fed mice, levodopa produced a significant decrease in the plasma concentration of 11-hydroxycorticosteroids. This was accompanied by a significant and marked decrease in the plasma glucose concentration. These effects of levodopa could be mimicked by relatively small doses of dopamine injected intracerebroventricularly but not intravenously. The integrity of the hypothalamic-pituitary adrenal axis in nialamide-treated mice was suggested by the elevation in plasma 11-hydroxycorticosteroids produced by fasting or by insulin induced hypoglycaemia. These results indicate that in the mouse, as in other species, levodopa can inhibit stress provoked increases in the secretion of 11-hydroxycorticosteroids.
Previous papers dealt with the discovery that hydrolysis of 17-hydroxycorticosteroid glucuronides in urine with beta-glucuronidase preparations from bovine liver is increased by adding sodium sulfate to the incubation medium. Here, we conclude that sodium sulfate not only increases the activity of bovine liver beta-glucuronidase on 17-hydroxycorticosteroid glucuronides and p-nitrophenyl glucuronides, but also removes the inhibitory activity of substances of high molecular weight in urine and, moreover, inhibits urine putrefaction during the hydrolysis. The net effect is an increased yield of urinary 17-hydroxycorticosteroids. In the incubation with sodium sulfate (Na2SO4, final concentration 80 g/liter, 500 Fishman units of beta-glucuronidase per milliliter of urine, pH 5.0, 48 degrees C, 18 h) the analytical recovery of 17-hydroxycorticosteroid glucuronides added to 12 urine samples proved to be 98 +/- 1.8% (95-100).
We evaluated the usefulness of the basal urinary 24-h excretion rates of free cortisol versus 17-hydroxycorticosteroids in the diagnosis of Cushing's syndrome. On an outpatient basis, both urinary free cortisol and 17-hydroxycorticosteroids levels were determined in 48 patients with Cushing's syndrome, as well as in 95 obese and 94 healthy control persons of normal weight. Determination of the urinary free cortisol content allowed a clear-cut distinction between the patients with hypercortisolism and the controls, resulting in a sensitivity of 100% and specificity of 98% for the diagnosis of Cushing's syndrome. The diagnostic accuracy of urinary free cortisol was distinctly superior to that of 17-hydroxycorticosteroids, which showed a wide overlap of values between the groups, with a sensitivity of 73% and a specificity of 94%. In conclusion, the measurement of basal urinary free cortisol provided an excellent diagnostic sensitivity and specificity in the assessment of adrenocortical function. This simple and accurate test thus seems to be particularly useful in the outpatient evaluation of patients with suspected Cushing's syndrome.
Urinary levels of free adrenaline, noradrenaline and 11-hydroxycorticosteroid were measured in 30 surgeons while they operated, to test the hypothesis that sympathetic and adrenocortical systems are overactivated by occupational environment of surgery procedures. They were divided in two groups according to a crossover design in which the surgeons had taken alternatively an oral dose of 40 mg oxprenolol and placebo. During operations with placebo urinary free adrenaline, noradrenaline and 11-hydroxycorticosteroid rose significantly compared with the control values obtained during ward-round performed by the same surgeons. The increase of adrenaline, noradrenaline and 11-hydroxycorticosteroid was abolished by 40 mg of oxprenolol which contained their urinary concentration to the control values. These data support the concept that operating stress of surgeons influences the adrenosympathetic and adrenocortical systems and they indicate a possible role of beta-blocking drugs in minimizing the adverse reactions of a such hormonal overactivity.
A study was undertaken to develop a method that could be used an an indication of the absorption of steroids. It was demonstrated that 17-hydroxycorticosteroids in urine could be quantitatively determined via absorptivity values obtained through the use of standard hydrocortisone-alcohol solutions or standard solutions of hydrocortisone in urine utilizing the blue tetrazolium assay method. This method is dependent upon the hydrolysis of conjugated urinary steroids by beef liver glucuronidase. The resultant concentration of 17-hydroxycorticosteroids is determined colorimetrically using blue tetrazolium.
Atropine, administered to cats just prior to the time of the expected circadian rise in levels of 17-hydroxycorticosteroid in plasma, blocks this rise. Atropine does not alter this circadian pattern when administered at other times in the circadian cycle. Results similar to those obtained with atropine have been observed with short-acting barbiturates. Dibenzyline administered just prior to the time of the expected circadian rise is ineffective in blocking this rise. These findings support the hypothesis that the circadian pattern of plasma 17-hydroxycorticosteroid levels reflects activation, by the central nervous system, of the hypothalamicpituitary-adrenal axis during a "critical time period" in the circadian cycle.
The discriminatory power of three clinical tests for adrenal activity are compared by measuring the variability of the results obtained in 40 normal control subjects, 35 patients with mild essential hypertension, and 13 patients with Cushing syndrome. The variance of the 24-h integrated plasma concentration of cortisol was significantly (P < 0.0001) smaller than the variance of the 24-h urinary excretion of 17-hydroxycorticosteroids and free cortisol. While the 24-h urinary excretion of 17-hydroxycorticosteroids and free cortisol of the patients with Cushing syndrome overlapped with the corresponding values of the normal and hypertensive subjects, their integrated cortisol concentration did not exhibit any overlap.
Eleven patients presenting with acute necrotizing ulcerative gingivitis (ANUG) collected 24-hour urine samples during and after the course of their ANUG. The Porter-Silber technique was used to determine the 17-hydroxycorticosteroid concent of the urine, a physiological measure of stress. All of the patients had significantly higher levels of 17-hydroxycorticosteroid during the course of their ANUG than after it had resolved.
Falsely high fluorimetric readings were obtained in plasma and urine 11-hydroxycorticosteroids (mostly cortisol) assays during the administration of bencyclan to hypertensive patients. No valid conclusion can be drawn from 11-hydroxycorticosteroids assays in bencyclan treated patients.
Sodium sulfate increases the hydrolysis of urinary 17-hydroxycorticosteroid glucuronides with beta-glucuronidase preparations derived from Helix pomatia because it removes the inhibitory activity of urinary high-molecular-weight substances. For maximum hydrolysis of urinary 17-hydroxycorticosteroid glucuronides, the hydrolysis [5 ml of urine, 0.5 ml of 2 mol/liter acetate buffer (pH 5.0)] should be conducted in the presence of sodium sulfate (final concentration: 80 g/liter) with (a) 600 Fishman units of the enzyme per milliliter of urine (18 h at 52 degrees C) or (b) with 1500 units of the enzyme per milliliter of urine (3 h at 57 degrees C). Under conditions a, analytical recovery of steroid glucuronides added to 12 urine samples was 99 +/- 2.1% (96-102%). Values obtained for 20 urine samples with this method were 99 +/- 2.7% (93-104%) as great as those yielded by a method in which 600 units of the enzyme from bovine liver are used together with sodium sulfate (18 h at 48 degrees C).
The authors investigated the effect of thymectomy and TP2 thymic polypeptide extract administration on total, esterified and free cholesterol in the plasma and the adrenals, as well as on plasma Na and K and plasma free total 11-hydroxycorticosteroids. The results showed that total, esterified and free cholesterol decrease in the adrenals by 23.20%, 28.57% and 17.70% maximum respectively, in the thymectomized rat and that under the influence of the TP2 extract the values increase by 14.81%, 15.38% and 12.67%, respectively. Plasma cholesterol did not change. Thymectomy caused an increase in the plasma 11-hydroxycorticosteroids value by 13.4% and administration of the TP2 extract lowered their value by 58.11%. The plasma Na and K values did not change.
Cefoxitin interferes with determination of urinary 17-hydroxycorticosteroids. The apparent concentration of hormone is increased from three- to 10-fold in samples from patients receiving cefoxitin when the Amberlite XAD-2 "Clini-Skreen" column is used. To determine the mechanism of interference, we reacted aqueous solutions of cefoxitin, cortisol, cortisone, and 11-deoxycortisol with phenylhydrazine; recorded the adsorption spectra; and determined the molar absorptivities and the equilibrium and rate constants. Also, we recorded the absorption spectra of phenylhydrazine with eight other cepha antibiotics and benzylpenicillin. Cortisol, cortisone, 11-deoxycortisol, and cefoxitin react with phenylhydrazine and absorb light with superimposable spectra and absorption maxima of 410 nm. The other antibiotics react with phenylhydrazine but absorbance maxima of the products vary, none being at 410 nm. Cortisol, cortisone, and 11-deoxycortisol react with phenylhydrazine 35-fold faster, have equilibrium constants ninefold greater, and have molar absorptivities 1.6 times that of cefoxitin. Thus, cefoxitin interferes with determination of urinary 17-hydroxycorticosteroids by forming a chromophore with the same absorbance maximum and with a molar absorptivity similar to cortisol, but much more slowly.