Urinary 17-KS Research Articles

Elevated levels of urinary 17-ketosteroids in central Indian children residing near sewage treatment plant and solid waste disposal plant: A preliminary study

ABSTRACTUrinary excretion of 17-ketosteroid (17-KS) was assessed in male pre-pubertal subjects aged (8–11 years; n = 90). Children living near sewage treatment plant and solid waste disposal plant (Group P) showed significantly higher levels of urinary 17-KS (Group P: 3.27 ± 1.63 µg/mL/CRE; p < 0.01) than children living in cleaner area (0.50 ± 0.53 µg/mL/CRE; Group C). Occurrence of urinary dibutyl phthalate in representative subjects of Group P (odds ratio: 9; p < 0.05; 95% of Confidence interval (CI) 1.93–72.99) was higher compared to Group C. Urinary concentrations of Cd (0.85 µg/g CRE ± 0.11), Mn (24.25 µg/g CRE ± 6.11) and Pb (12.39 µg/g CRE ± 2.86) in Group P were significantly (p < 0.01) higher than those found in Group C (Cd (0.28 µg/g CRE ± 0.03), Mn (13.33 µg/g CRE ± 3.20) and Pb (5.67 µg/g CRE ± 0.53)). Analyses of ambient air samples (PM10) in polluted area revealed major occurrence of phthalates, whereas derivatives of trifluoromethyl, dione, etc. were identified in PM2.5 fraction. Metal (Cd, Co, Mn and Pb) concentrations in ambient air (24 h, PM10) were higher in polluted area compared to cleaner area. We conclude that elevated levels of urinary 17-KS in Group P could be attributed to higher exposure of these subjects to Endocrine disrupting chemicals (EDCs) compared to Group C.

Changes of Urinary 17-OHCS & 17-KS in Patients with “Jin Yo Kyo & Jin Yin Kyo”

Changes of Urinary 17-OHCS & 17-KS in Patients with “Jin Yo Kyo & Jin Yin Kyo”

尿中17-KS, 17-OHCS, VMA排泄量の季節並びに日々の変動と気象条件

尿中17-KS, 17-OHCS, VMA排泄量の季節並びに日々の変動と気象条件

室内冷房と尿中17-KS, 17-OHCS, VMA

室内冷房と尿中17-KS, 17-OHCS, VMA

Transposition of pedicled adrenal gland for the treatment of adrenocortical and medullary hyperplasia

Objective To investigate the clinical efficacy of pedicled adrenal transposition for the treatment of adrenocortical and medullary hyperplasia, Methods Twenty cases of adrenal hyperpla-sia (6 men and 14 women; mean age,36 years ) had history of hypertension from 0.5 to 5 years. Of all cases, 15 had centripetal obesity and purple striae, 2 had weakness and polyuria, 3 had durative hypertension. Serum potassium and aldosterone were increased in 4 and 3 cases, respectively. Urinary 17-OH and 17-KS were increased in 15 cases. Epinepgrine, norepinephrine and dopamine increased in 3 cases, VMA increased in 4 cases. CT scan and MRI revealed adrenal diffuse enlargement with in-creased thickness or nodules in 18 and 3 cases, respectively, 131I-MIBG scan showed positive in 3 ca-ses. Preoperative diagnoses were Cushing's syndrome in 11 cases, hyperaldosteronism in 2 cases, pheochromocytoma in 1 case, adrenomedullary hyperplasia in 2 cases, Cushing's syndrome-cate-cholamine syndrome in 4 cases. All cases were treated with transposition of pedicled adrenal gland into the subcutaneous tissues. Results All operations were successful. The average operation time was 120 min, the average blood loss was 40 ml and the average hospital stay was 10 d. No obvious surgical complications occurred. Pathological studies of all the cases revealed the coexistence of adrenocortical and medullary hyperplasia. Seventeen cases were followed up for 0.5-8 years. Thirteen cases had no symptom and normal biochemical results. Four cases still had hypertension and abnormal biochemical results. They were recovered after adrenal operation of the ther side. Conclusion Transposition of pedicled adrenal gland could be an available option to treat patients with adrenocortical and medullary hyperplasia. Key words: Adrenocortical and medullary hyperplasia; Transposition, operation

Urinary 17-KS and 17-OHCS as markers of endocrine disruption by air pollution in primary school children.

The present study was undertaken to determine the effects of air pollution on urinary excretion of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids (17-OHCS), which are markers of adrenal cortex functions, in primary school children from five schools with different levels of air pollution. One hundred and twentynine fourth-grade children were included in the study. Urinary excretion of 17-KS and 17-OHCS were significantly lower in male children living in polluted areas than in children living in clean areas. We conclude that adrenal cortex functions before puberty can serve as practical markers of endocrine disruption by environmental factors in epidemiological studies.

Serum 3α-androstanediol glucuronide measurements in children with congenital adrenal hyperplasia

To determine the value of 3 alpha-androstanediol glucuronide (3-AG) measurements in children with congenital adrenal hyperplasia, we compared serum 3AG, 17-hydroxyprogesterone (17-OHP), androstenedione (A), testosterone (T) and dihydrotestosterone (DHT) levels and 24-h urinary 17-ketosteroid (17-KS) excretion in 42 female children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency, including 27 with the simple virilizing and 15 with the salt-losing form. Their mean age was 74.5 +/- 48.5 months (range, 6-194 months). Twenty-four-hour urinary 17-KS excretion and serum 3-AG, A, T, DHT and 17-OHP levels were measured in the patients. The values were less than the mean + 2 SD of the control group in 63%, 74%, 67%, 69%, 60% and 31% of the patients, respectively. Serum 3-AG levels correlated with 24-h urinary 17-KS excretion (r = 0.66) and plasma A (r = 0.80), 17-OHP (r = 0.56), T (r = 0.79) and DHT (r = 0.62) levels. We conclude that serum 3-AG is a useful metabolic index in the management of children with congenital adrenal hyperplasia.

A Case of Stunted Growth Caused by Glucocorticoid Ointment Treatment for Psoriasis Universalis

Stunted growth has been rarely reported as a side effect of treatment with glucocorticoid ointment. We report a 14-year-old boy who visited our clinic complaining of short stature. Since 9 years of age, he had been treated for psoriasis universalis with bethamethasone ointment by a dermatologist. The dosage of the ointment was approximately 30g/week, i. e. 4-5g/day. At the first visit, cushingoid features were noted as well as short stature (-2.9 SD). Serum cortisol concentrations were very low (1.0-1.7μg/dL) and their diurnal variation had disappeared. Administration of ACTH demonstrated a failure of the cortisol response. Urinary 17-OHCS and 17-KS were 0.8 and 2.2mg/day, respectively. From these data suppression of the pituitaryadrenocortical axis was obviously present in this patient. A diabetic pattern was also observed by an oral glucose tolerance test. After reducing the dosage, the response of cortisol to exogenous ACTH recovered to some extent. However, plasma ACTH remained low in a CRF test.

Clinical study on 26 cases of incidental adrenal tumors: a consideration on surgical indication

At our medical center we have seen 151 patients who have undergone adrenalectomy from 1971 up until June 1992. There has been a recent increase in the number of cases since 99 patients have been seen in the last eight years from 1985. This increase is related to the increase in the number of incidental tumors. Of those 99, 26 have been incidental tumors. Twenty-four of those have been endocrine inactive tumors, and the remaining 2, both active endocrinologically, were pheochromocytoma. We propose that our tentative indications for surgical treatment of incidental tumors are 1) tumors of diameter 3.5 cm or greater, 2) tumors undeniably malignant by imaging diagnosis, 3) tumors that tend to increase in size with every six-month re-examination, even though the original size is less than 3.5 cm in diameter, and 4) tumors endocrinologically active. The main purpose of this study was to make a differential diagnosis of malignant tumors among incidental tumors. Diagnostic modalities included 1) imaging diagnosis such as echography, CT, MRI, and angiography, 2) analysis of DNA ploidy and BrdU uptake utilizing flow cytometry of excised adrenal tumor tissues, and 3) analysis of urinary steroid fraction. It is generally thought that there are currently no methods by which malignant tumors can be differentiated with certainty, even with modern diagnostic technology, and review of the literature, finds approval or disapproval with regard to the methods we selected to evaluate tumors. What has aroused interest in our results is urinary 17KS fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

FUNCTIONING ADRENOCORTICAL TUMOR -REPORT OF A CASE-

A 61-year-old female was admitted to the hospital because of general fatigue and hoaresness. An elastic soft, smooth surfaced and nontender mass was palpable in the left lobe of the thyroid gland. Radiographic examinations revealed a benign thyroid adenoma. Abdominal ultrasonography, however, a 9×7cm solid tumor presenting as well-defined heterogenous internal echoic picture between the spleen and left kidney. CT and MRI indicated a well-defined homogenous adrenal mass. In endocrinologic examination elevated serum DHEA-sulfate, progesteron, and urinary 17-KS were noted. Functioning adrenocortical tumor was suspected and adrenalectomy was performed. The removed adrenal tumor was 10×8×7cm in sizeand 295g in weight and covered with thin fibrus capsule. Its cut surface was brown. It was a elastic hard and solid tumor, scatering with hemorrhagic and necrotic lesions. Histologically the tumor was adrenocortical carcinoma. The patient is well as of half year after the operation.

3α-Androstanediol Glucuronide in Virilizing Congenital Adrenal Hyperplasia: A Useful Serum Metabolic Marker of Integrated Adrenal Androgen Secretion*

To determine whether serum 3 alpha-androstanediol glucuronide (3AG) reflects the overall effect of integrated adrenal androgen secretion in the virilizing form of congenital adrenal hyperplasia (CVAH), circadian levels (0800, 1200, 1600, and 2000 h) of serum 3AG and 17-hydroxyprogesterone (17OHP) or 11-deoxycortisol (S), androstenedione (A), testosterone (T), and 24-h urinary 17-ketosteroids (17KS) were examined in seven patients (pts) with classical 21-hydroxylase deficiency (21OHD) and one pt with classical 11 beta-hydroxylase deficiency (11 beta OHD). Hormonal studies were conducted during the second day of dexamethasone (Dex) administration (2 mg/day). In five poorly controlled CVAH pts, including the 11 beta OHD pt, highly elevated baseline morning (AM) serum 17OHP or S as well as A levels, and elevated AM T levels in three pts decreased markedly in the evening (PM), while elevated serum 3AG showed no significant circadian changes; 17KS levels were markedly elevated for age. During Dex, moderately or slightly elevated AM 17OHP, A, or T in two to four pts with 21OHD decreased to the normal range in the PM. In the pt with 11 beta OHD, S, A, and T levels were suppressed. 3AG levels were modestly elevated or normal, without circadian changes, in these pts; 17KS levels were elevated or normal. In two other 21OHD pts, modestly elevated AM baseline 17OHP and A levels decreased in the PM; elevated AM T decreased in one pt in the PM; modestly elevated 3AG levels showed no circadian changes; 17KS levels were modestly elevated. During Dex, normal or slightly elevated serum steroids and 17KS levels were associated with normal or high normal 3AG levels without circadian changes. In one postpubertal female with 21OHD, modestly elevated AM baseline 17OHP levels decreased at 2000 h; normal A and T levels throughout the day and low normal 17KS were associated with slightly low 3AG levels, without circadian variation. During Dex treatment, normal 17OHP, A, T, and low 17KS levels were associated with low 3AG levels without circadian variation. In all pts as a group, an excellent correlation (r = 0.9) was found between either 0800 h or mean, or 2000 h serum 3AG levels and 17KS. In addition, AM and PM serum 3AG levels in five normal women were similar. We conclude that the high correlation between serum 3AG and urinary 17KS and the absence of a significant circadian variation in 3AG indicate that serum 3AG, regardless of sample time, is a useful metabolic index of integrated adrenal androgen secretion in CVAH.

Successful Treatment of a Metastatic Hormone-Producing Adrenal Cancer by a Combination of Mitotane, Tegafur and Surgical Resection.

A 34-year-old man had a huge hormone-producing adrenal cancer with multiple lung metastases, direct liver invasion and a tumor thrombus in the inferior vena cava. Initial treatment was mitotane alone. The dose of mitotane was 2 g/day initially and gradually increased to 15 g/day in combination with 600 mg of tegafur per day. During the initial phase of chemotherapy, the serum mitotane level was relatively low (2.9-4.6 micrograms/ml) and the pulmonary metastases tended to grow in size in spite of a gradual decline in urinary 17-KS and 17-OHCS and a regression of the primary tumor. A seemingly marked increase in serum mitotane (20.5-34.5 micrograms/ml) was coincident with the addition of tegafur. Rapid and consistent regression of the primary tumor occurred. This excellent response to the chemotherapy made the primary tumor with liver invasion and the metastases resectable. The adverse effect of mitotane, central nervous toxicity, appeared to be serum mitotane level dependent. The present results, together with previous reports in the literature, seem to recommend the following therapeutic approaches to advanced adrenal cancer: monitoring of the serum level may be useful in predicting the efficacy as well as the occurrence of side effects of mitotane, surgical treatment of the lesions should be performed whenever possible, even though it may be only palliative, and the combination of mitotane and tegafur is a choice of chemotherapy which should be evaluated in future studies.

Virilizing granulosa cell tumor responsive to human chorionic gonadotropin and oral contraceptive with 8-year followup

Urinary and serum steroid measurements were obtained in a 48-year-old female before and after the removal of a virilizing granulosa cell tumor (GCT). Preoperatively, serum testosterone was markedly elevated while 17-ketosteroid (17-KS) and estrogen excretion were normal. Chorionic gonadotropin administration effected a marked rise in urinary 17-KS excretion and serum testosterone while oral contraceptive therapy for 21 days decreased serum testosterone to normal. With tumor resection, serum testosterone fell to normal and subsequent administration of HCG had no stimulatory effect on serum testosterone or urinary 17-KS excretion. The patient's clinical response and 8-year followup attest to the tumor's unusual virilizing role.

THE EFFECT OF TREATMENT ON FINAL HEIGHT IN CLASSICAL CONGENITAL ADRENAL HYPERPLASIA (CAH)

One of the goals of glucocorticoid therapy in classical CAH is to suppress excess androgen production to prevent premature epiphyseal closure and resultant short stature. This retrospective study was conducted to determine if the final height (FH) of 45 adult patients (pts) with CAH was influenced by the clinical variant (salt-wasting (SW) vs simple virilizing (SV)), age diagnosis was made and treatment initiated, and the degree of hormonal control. Good or poor hormonal control were determined from levels of 24 hr urinary 17-KS, serum Δ4-androstenedione (Δ4-A) and 17-OHP. The patient was assigned to the category of good control if more than 50% of daily urinary 17-KS or serum Δ4-A were normal for age (mean±2SD) or if 50% of the serum 17-OHP levels were < 1000 ng/dl. All others were assigned to the poor control category; 3 pts had insufficient data for assignment. Final height was compared to the mid-parental height (MPH), to the normal population, and to 5 never treated pts with SVCAH. The mean final Ht for all male patients was 163.2 cm and for all female patients was 153.3 cm. Conclusion: The adult height of 3 never treated females was not different from any treated females, whether in good or poor control, SW or SV, or treated early or late. Among the treated males, height was not different whether they were in good or poor control, SW or SV, or treated early or late. Although the 2 never treated males are shorter than treated males, the small number of pts precludes statistical analysis. The mean final heights of all pts were significantly less than the mean heights of males and females in the normal population.

FAMILIAL ADRENAL FEMINIZATION PROBABLY DUE TO INCREASED STEROID AROMATIZATION

5 of 10 members of a non-related North African family(father, 2 male, 2 female siblings) were observed or reported to have had gynecomastia, early growth spurt for chronologic age(CA), and short final stature. The extensively studied 8 year old propositus had advanced bone age (BA, 13 yrs) and height 135.6cm (normal for CA (+1.1SD), short for BA(-2.5SD)). He presented with facial acne, gynecomastia (B3), pubic hair (Tanner 2), and testicular volume 2ml. Blood pressure was normal (90/70 mmHg). Urinary total 17-KS (2.1mg/d),17-OHC(2.4mg/d), and individual steroids (gas chromatography) were normal .Cortisol, S, and 17OHP in plasma responded normally to ACTH. Basal estrone (E1, 181 pg/ml) was elevated, and increased with ACTH (223 pg/ml). After hCG, testosterone(T) responded normally(55 to 164ng/dl), but neither E1(135 to 139pg/ml), nor estradiol(E2,86 to 85 pg/ml) did increase. The assumption of ACTH-dependent adrenal feminization was confirmed by a reduction of breast tissue with dexamethasone or cyproterone acetate treatment. However, this effect was only transient. Subsequent testolactone treatment (450 mg/d) resulted in an increase of the T/E2 (5.6 to 20.3),and A/E1(3.4 to 31.4) ratios, and in reduction of breast tissue. It is concluded that this is a familial type of non-tumorous adrenal feminization with increased adrenal androgen aromatization for unknown reasons.

Two adult familial cases of selective hypoaldosteronism due to insufficiency of conversion of corticosterone to aldosterone.

A 57-year-old woman (case 1) and her daughter aged 29 (case 2) with hyperkalemia exhibited subnormal plasma aldosterone (ALD) in the face of elevated plasma renin activity. Their physical findings were normal. Their arterial blood gas analysis showed that metabolic acidosis and renal function of these cases were slightly impaired. Urinary 17-OHCS and 17-KS excretions in these cases were normal. Baseline levels of corticosterone (B) and 18-hydroxycorticosterone (18-OH-B) were clearly elevated. Plasma deoxycorticosterone (DOC), B and 18-OH-B as well as cortisol remarkable increased after ACTH injection, but the increase in plasma ALD was very small. Angiotensin II infusion in case 1 resulted in a clear rise in plasma 18-OH-B but in slight depletion of B, and no increase in ALD. 9-alpha-fludrocortisone acetate treatment was performed in case 1. Serum potassium was normalized and blood pressure elevated from 82/52 to 120/78 mmHg. Arterial blood gas analysis was corrected. We concluded that these two cases with subnormal plasma ALD and hyperreninemia may exist as a congenital and familial abnormality of the final step of aldosterone boisynthesis due to the impairment of the conversion of B to ALD.

Insulin resistance and secretion in polycystic ovarian disease.

In order to verify the relationship between insulin resistance and hyperandrogenism in Polycystic ovary disease (PCOD), circulating levels of insulin in response to oral glucose tolerance test (OGTT) were assessed in 23 PCOD patients and 10 matched control subjects without obesity, acanthosis nigricans and impaired glucose tolerance. In PCOD patients serum total testosterone (T), dehydroepiandrosterone sulfate (DHEA-S), LH and LH/FSH ratio were significantly higher than in control subjects; whereas urinary 17-ketosteroids (17-KS) and glycemic response to OGTT were not different. PCOD patients were clearly hyperinsulinemic before and during OGTT compared to the control group: mean +/- SD basal insulin (Io) (23.4 +/- 10.3 vs 11.3 +/- 4.6 microU/ml, p less than 0.001) and the sums of insulin levels (sigma I) during OGTT (341.4 +/- 148.9 vs 162.2 +/- 56 microU/ml, p less than 0.001). In the two groups serum T, but not DHEA-S, LH, urinary 17-KS and the degree of obesity, was strongly associated with Io (r = 0.458, p less than 0.01) and sigma I (r = 0.419, p less than 0.02), as well as with insulin resistance as assessed by basal (r = 0.425, p less than 0.02) and postglucose challenge (r = 0.384, p less than 0.05) insulin to glucose ratio. These results confirm that the hyperinsulinism and insulin resistance in PCOD is not related to obesity and suggest that the hyperandrogenism may be partially responsible of the observed imbalance in glucose-insulin homeostasis.

Black (or Brown) Adrenal Cortical Adenoma: Its Characteristic Features on Computed Tomography and Endocrine Data

Seventeen patients with adrenal adenoma causing Cushing's syndrome, eight patients with Cushing's disease due to hypersecretion of ACTH, and five patients with primary aldosteronism due to an aldosteronoma were studied for their computed tomographic (CT) patterns, hormonal profiles, and macroscopic and microscopic findings of the adrenal gland. Black (or brown) adrenal adenomas were found in 71% of the patients with Cushing's syndrome, but not in patients with aldosteronoma. The adrenal tissue of patients with Cushing's disease was predominantly yellow. The number of compact cells was larger in black or brown adenomas than in yellow tumors or hyperplastic adrenal tissue. In patients with Cushing's syndrome, urinary excretion of 17-ketosteroids (17-KS) and serum aldosterone concentrations were lower in those with black or brown adenomas than in those with yellow adenomas (P less than 0.05). Patients with Cushing's disease had even higher 17-KS and serum aldosterone levels. No difference was found in serum cortisol concentrations and dexamethasone suppressibility in two types of adenomas causing Cushing's syndrome. Visual estimation of radiological density of the adrenal tissue relative to the kidney on CT scan and quantitative measurement of it by CT number revealed a difference between the two types of adrenal tumors causing Cushing's syndrome. Adrenal tumors with decreased density on CT scan were yellow adenomas with predominantly clear cells, and those with equal or increased density were black or brown adenomas with predominantly compact cells. All aldosteronomas had decreased density and consisted of clear cells. It is suggested that black or brown adenomas of the adrenal gland have higher radiological density and accompanying lower serum aldosterone and urinary 17-KS levels than ordinary yellow tumors. The abundance of compact cells may have some significance for the development of this particular type of adrenal tumor.

446 TREATMENT OF ANDROGEN EXCESS IN ADOLESCENT PATIENTS

Fourteen hirsute girls, ages 12-22 yrs (M±SD 17.3±2.7 yrs), in whom 21OH deficiency was excluded by 1 h° IV bolus Cortrosyn test in 1981 were evaluated by a dexamethasone (dex) suppression test (0.5 mg QID) with measurement of serum androgens on d5 and then treated with a bedtime dose of dex (0.5 mg in 10, 0.25 mg in 4) for 7-41 mos (mean 15.7 mos) with visits q3 mos. Baseline free testosterone (FT) was ↑ in 14/14 (19-57 pg/ml); DHAS > 350 ug/dl in 10/14; DHA>790 ng/dl in 8/14; Δ4 > 300 ng/dl in 5/14; urinary 17KS > 15 mg/24 h in 8/14. With the dex test DHAS↓> 50% in all (mean 70%), FT<5 pg/ml in 8/14. With dex treatment DHAS ↓21-92% (mean 51%), FT was < 15 pg/ml in only 4 patients. Hirsutism did not change in 9, ↓ in 4, and ↑ in 1 with dex therapy. Of 9 patients with irregular menses, only 3 became regular on dex. Side effects (striae, weight gain and acne) occurred in 6 on 0.5 mg dex but not on 0.25 mg. The 2 patients with the most striking clinical response to dex did not recur 14 mos and 28 mos off dex. All others off treatment showed ↑ serum androgens. 7/14 (5 with ↑ DS) not responding well to adrenal suppression responded to oral contraceptive therapy with ↓ FT 0.4-6 pg/ml and improved control of hirsutism. The data suggest that single dose dex is satisfactory in patients who maintain FT <15 pg/ml without side effects. In others with adequate suppression by dex test, other schedules or glucocorticoids may be necessary. In hirsute adolescents without adequate suppression of FT, ovarian therapy is required.

432 LOW PLASMA DHEA AND DHEA SULFATE IN PROGERIA. DIMINISHED RESPONSE TO CORTROSYN

Progeria (Hutchinson-GiIford syndrome) manifests with apparent accelerated aging during youth. We studied a 21 mo. old female with marked growth retardation (Ht. 76cm, <2SD, Wt. 6.5 Kg <2SD), alopecia, small face, micrognathia, pinched nose and sclerodermic like changes of the skin. Osteoporotic changes were measured by the radiographic photodensitometry of Colbert et al, and compared to age and sex norms (25.7 vs 30-40 nl range). Pituitary and thyroid hormones were within normal limits (hGH 1.8 ng/ml; FSH 3.8 and LH 2.6 mIU/ml; Prolactin 8.0 ng/dl; TSH lμU/ml; T4 9.1 and T3 180 ng/dl). Insulin2.0μU/ml, Estrogens 1.7ng/dl. DHEA and DHEA sulfate have been reported to markedly decrease with normal aging. To study them in progeria we stimulated the patient's adrenals with 0.125 mg of cortrosyn I.M.(Organon Labs.) and 3 normal controls (Ages 5-9 yr.). Twenty-four hour urinary 17KS before were 0.4 and after 0.5 mg/24 hr. (controls 0.9 and 3.3); DHEA 0: 35 vs 190±72; 1 hr. 70 vs 256±70; 2 hr 35 vs 279±41 and 12 hr. 35 vs 226±186 ng/dl. DHEA-S O: undetectable = 0 vs 28+14; 1 hr 0 vs 29+21; 2 hr 0 vs 32±14; 12 hr 0 vs 26±20 mcg/dl. We concluded that there is a marked decrease in basal and post ACTH stimulation of DHEA and DHEA sulfate in our progeria patient. A deficienty of adrenal androgens might explain the growth retardation and osteoporosis seen in progeria. DHEA has been reported to have antiaging effects It's deficiency in progeria might not only be important as a biochemical marked for the disease but might also contribute to the premature aging.