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PubMed1979

Evaluation of steroid laboratory tests and adrenal gland imaging with radiocholesterol in the aetiological diagnosis of Cushing's syndrome.

Basal values of the urinary excretion of 17-oxogenic steroids and serum levels of cortisol were not satisfactory in the differentiation of 'suspected' subjects from patients with true Cushing's syndrome. With an RIA method for serum cortisol determination, the overnight dexamethasone suppression test provided the most reliable single test in establishing adrenocortical hyperfunction. Thirty-five normal subjects, fifty-nine obese patients, thirteen 'suspected' patients, and thirteen patients with disease states other than Cushing's syndrome had suppressed values below 4.0 microgram/100 ml. None of the ten patients with Cushing's syndrome had a cortisol concentration less than 16.3 microgram/100 ml. Adrenal gland scintigraphy after radiocholesterol injection is a more valuable tool than the metyrapone test and the high-dose dexamethasone suppression test in the localization and differential diagnosis of adrenocortical lesions causing Cushing's syndrome. It obviates the need for angiographic procedure in the localization of adenomas. It is a reliable technique for identifying functioning adrenal remnants. We therefore propose a schedule for studying patients with suspected adrenocortical hyperfunction.

17-Ketosteroids↗

PubMed1985

The use of the corticotropin-releasing hormone test to monitor the recovery of patients with Cushing's disease or Cushing's syndrome due to an adrenal adenoma after adenomectomy.

Six patients with Cushing's disease and three with Cushing's syndrome due to an adrenal adenoma were monitored after their adenomectomy with the corticotropin-releasing hormone test to evaluate the progress of recovery of their pituitary adrenal function. Before surgery the patients with Cushing's disease showed either high, normal or low responses of plasma ACTH and cortisol to 100 micrograms synthetic ovine corticotropin-releasing hormone (CRH) administered intravenously, whereas all three patients with Cushing's syndrome due to an adrenal adenoma showed no response of plasma ACTH or cortisol to CRH. One or two months after surgery, the patients who had Cushing's disease had low levels of basal plasma ACTH and cortisol and their responses to CRH were extremely low. However, the same patients were tested later, it was found that their responses to CRH gradually increased and reached normal ranges approximately within one year after tumor removal, which coincided with the overall improvement in their clinical signs and symptoms due to adrenal insufficiency. In contrast, the recovery of the pituitary adrenal function in patients who had Cushing's syndrome due to an adrenal adenoma was not complete even one year after surgery. Thus the corticotropin-releasing factor test is a useful criteria to evaluate the recovery of the pituitary adrenal function in these patients after surgery, since the responses of plasma ACTH and cortisol to the administered CRH are parallel with the improvements in clinical signs and symptoms due to adrenal insufficiency in patients with Cushing's disease.

Adenoma↗

PubMed2003

Adrenal insufficiency during septic shock.

OBJECTIVE: To determine whether a baseline (random) cortisol concentration <25 microg/dL in patients with septic shock was a better discriminator of adrenal insufficiency than the standard (250 microg) and the low-dose (1 microg) corticotropin stimulation tests as assessed by the hemodynamic response to steroid replacement. SETTING: Intensive care unit. PATIENTS: Fifty-nine patients with septic shock. Their mean age was 57 +/- 16.7 yrs; 29 were male. INTERVENTIONS: A baseline cortisol concentration was obtained. Patients then received an intravenous injection of 1 microg of corticotropin (low-dose test) followed 60 mins later by an injection of 249 microg of corticotropin (high-dose test). Cortisol concentrations were obtained 30 and 60 mins after low- and high-dose corticotropin. All patients were administered hydrocortisone (100 mg every 8 hrs) for the first 24 hrs while awaiting results of cortisol assessment. Patients were considered steroid responsive if the pressor agent could be discontinued within 24 hrs of the first dose of hydrocortisone. MEASUREMENTS AND MAIN RESULTS: Forty-seven percent of patients died. Twenty-two percent of patients met the diagnostic criteria of adrenal insufficiency by the low-dose test and 8% by the high-dose test. However, 61% of patients met the criteria of adrenal insufficiency when we used a baseline cortisol concentration of <25 microg/dL. Twenty-two patients (37%) were steroid responsive; the baseline serum cortisol was 14.1 +/- 5.2 microg/dL in the steroid-responsive patients compared with 33.3 +/- 18 microg/dL in the steroid-nonresponsive patients (p <.0001). Ninety-five percent of steroid-responsive patients had a baseline cortisol concentration <25 microg/dL. Fifty-four percent of steroid responders had a diagnostic low-dose test and 22% a diagnostic high-dose test. Receiver operating characteristic curve analysis revealed that a stress cortisol concentration of 23.7 microg/dL was the most accurate diagnostic threshold for determination of the hemodynamic response to glucocorticoid therapy. CONCLUSIONS: Adrenal insufficiency is common in patients with septic shock, the incidence depending largely on the diagnostic test and criteria used to make the diagnosis. There is clearly no absolute serum cortisol concentration that distinguishes an adequate from an insufficient adrenal response. However, we believe that a random cortisol concentration of <25 microg/dL in a highly stressed patient is a useful diagnostic threshold for the diagnosis of adrenal insufficiency.

Adrenal Cortex Function Tests↗

PubMed1980

Functional significance of idiopathic adrenal calcification in the adult.

Two young adults with idiopathic adrenal calcification are described. In one patient the calcification was probably secondary to adrenal haemorrhage in the neonatal period. Neither patient exhibited clinical features suggestive of adrenal cortical insufficiency, and baseline serum cortisol levels were normal. The corticosteroid responses to ACTH administration and to other provocative tests indicated that both glucocorticoid and mineralocorticoid reserve was normal. One patient showed an appropriate epinephrine response to insulin-induced hypoglycaemia. We conclude that even extensive adrenal calcification may be compatible with completely normal adrenal function. Since, however, little is known of the natural history of this condition, lifelong follow-up of such patients is advised.

Adrenal Cortex Function Tests↗

PubMed1987

Effect of nonadrenal illness on adrenal function in the cat.

Adrenal function was assessed by a combined dexamethasone suppression-ACTH stimulation test in 18 healthy cats, 17 diabetic cats, and 19 sick nondiabetic cats. In all groups, plasma cortisol concentrations decreased after dexamethasone was administered and increased after ACTH was administered. There were no significant (P greater than 0.05) differences among groups in time trend changes in cortisol concentration. There was considerable variation in adrenal response between cats in each group. Diabetic cats had more variation in base-line and postdexamethasone plasma cortisol concentrations (P less than 0.05) than did other groups. In sick, nondiabetic cats, cortisol concentrations tended to be higher in cats with hyperthyroidism (P = 0.06) than in cats with other diseases.

Adrenal Cortex Function Tests↗

PubMed1998

Long-term effects of allogeneic bone marrow transplantation (BMT) on pituitary, gonad, thyroid and adrenal function in adults.

To evaluate the late-effects of allogeneic bone marrow transplantation (BMT) on endocrine function 20 adults (10 females, 10 males) with hematological malignancies were studied after a mean of 3.2 years (range 1.0-10.0) following BMT. The mean age of patients at the time of BMT was 39 years. Dynamic tests of the hypothalamic-pituitary axis included growth hormone releasing hormone (GHRH), gonadotropin releasing hormone (GnRH) and thyrotropin releasing hormone (TRH) stimulations with measurements of serum growth hormone (GH), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyrotropin (TSH) and prolactin (PRL) responses. Adrenal function was assessed with the adrenocorticotropin (ACTH) test. Five patients (25%) had a subnormal GH response to GHRH stimulation, but all had a normal serum insulin-like growth factor I (IGF-I) value. There was an inverse nonlinear relationship between the body mass index (BMI; kg/m2) and GH response but no relation between the GH response and total body irradiation (TBI), intrathecal treatment or occurrence of graft-versus-host disease. In females, serum FSH and LH basal levels and responses to GnRH, in spite of oestrogen substitution therapy in 9/10 patients, indicated ovarian failure and early menopause. Most responses to GnRH were delayed. All males had elevated serum basal FSH levels indicating damage in seminiferous tubulus and infertility. Serum basal LH was elevated only in four males but testosterone values were all within normal limits. However, the mean free androgen index (FAI) was in the low normal range, and two subjects had abnormally low FAI. Serum free thyroxine (fT4) levels were normal in all but one, but an exaggerated TSH response to TRH occurred in seven patients (35%). Four of them had received TBI and one total nodal irradiation suggesting radiation-induced damage to the thyroid gland. In 19 of the 20 patients, adrenal function judged with ACTH test was normal. We conclude that functional impairments of the hypothalamus-pituitary-gonad/thyroid axis are common while disturbances in GH, adrenal and prolactin occur less often in patients after intensive treatment and BMT. Typically, the target organ is more commonly affected than the hypothalamus-pituitary axis. In spite of normal serum testosterone and LH values, serum FAI may reveal androgen deficiency.

Adolescent↗

PubMed2004

The effect of a single course of antenatal corticosteroids on maternal adrenal function at term.

OBJECTIVE: To determine if one course of antenatal corticosteroids at 32 weeks produces maternal adrenal suppression at term. METHODS: The adrenocorticotropic hormone (ACTH) stimulation test was administered at 38 weeks to 11 pregnant women who had received a single course of antenatal betamethasone prior to 33 weeks and to six control subjects. RESULTS: There was no difference in basal cortisol levels (mean+/-standard deviation) between the two groups: 41.6+/-6.9 microg/dl for controls versus 36.0+/-7.8 microg/dl for the steroid group, p=0.16. Peak cortisol levels at 45 min following ACTH stimulation were not different: 61.6+/-3.5 microg/dl for controls versus 55.0+/-2.6 microg/dl for the steroid group, p=0.16. The power of the study to detect a statistical difference in the observed peak cortisol levels was greater than 95%. None of the study subjects had laboratory criteria or clinical signs of adrenal suppression. CONCLUSIONS: A single course of betamethasone for women at risk for preterm delivery does not produce adrenal insufficiency at term and stress dose steroids are not recommended.

Adrenal Cortex Function Tests↗

PubMed1998

Mitotane (o,p'-DDD) resistance in a dog with pituitary-dependent hyperadrenocorticism and phaeochromocytoma.

A dog was presented with a 2 year history of polyuria and polydipsia due to pituitary-dependent hyperadrenocorticism. A low-dose dexamethasone suppression test and measurement of plasma ACTH concentration confirmed the diagnosis. Treatment was instituted with mitotane at 44 mg/kg/day and then 88 mg/kg/d without complete resolution of signs. The dog collapsed with signs consistent with liver disease and was euthanased. Necropsy revealed a phaeochromocytoma of the left adrenal medulla with extensive metastases to the liver. A chromophobe adenoma of the pars intermedia of the pituitary was found.

Adrenal Cortex Function Tests↗

PubMed1978

Adrenocortical suppression in workers manufacturing synthetic glucocorticoids.

A man who had worked for 16 years in the manufacture of a potent corticosteroid was found to be suffering from chronic adrenocortical insufficiency attributed to chronic absorption of the glucocorticoid. Eleven other symptom-free workers were therefore screened. Two of these workers, like the first patient, gave grossly abnormal responses to the Synacthen (tetracosactrin) test; one had been employed for only seven months. All 12 men had facial plethora, suggesting absorption of the drug in spite of their having adhered to the safety precautions. All workers manufacturing potent steroids should therfore be screened regularly by measurement of their plasma cortisol concentrations and should be moved regularly to processing other drugs.

Absorption↗

PubMed1981

Adrenocortical suppression in the dog after a single dose of methylprednisolone acetate.

Adrenal function was assessed in dogs after intramuscular administration of a single dose of methylprednisolone acetate (MPA). Twelve dogs were test challenged with adrenocorticotropic hormone (ACTH) and then assigned randomly to 1 of 3 groups and given MPA. Individual groups were test challenged with ACTH 2, 3, or 4 weeks later. All dogs were rechallenged 5 weeks after MPA administration. Plasma cortisol concentration was determined by radioimmunoassay. Basal plasma cortisol (time 0) was depressed on weeks 2 and 3, but not on weeks 4 and 5. Adrenal response to ACTH (increment of cortisol change) was suppressed on weeks 2, 4, and 5, but not on week 3. It was concluded that a single dose of MPA is capable of altering adrenal cortical function in dogs for at least 5 weeks.

Adrenal Cortex↗

PubMed1980

HLA typing and ACTH stimulation in the detection of carriers for 21-hydroxylase deficiency.

Two methods of carrier detection were applied to the siblings of two children with congenital adrenal hyperplasia due to 21-hydroxylase (21-OH) deficiency. HLA geno-typing showed that the affected children were HLA identical. One of the siblings possessed only one of the relevant haplotypes, and was shown to be heterozygous for 21-OH deficiency by the 17 alpha hydroxyprogesterone response to ACTH stimulation. The other sibling had a maternal recombination between the DR and glyoxylase-1 (GLO) loci. The ACTH stimulation test was normal and therefore confirms recent reports suggesting that the 21-OH gene is between the HLA-A and the GLO loci. Although HLA typing of family members will identify heterozygous 21-OH deficiency in most instances, biochemical definition is still required for some cases with recombinations in the short arm of chromosome 6.

Adrenal Cortex Function Tests↗

PubMed1992

[A case of Cushing's disease associated with a non-functioning adrenal tumor].

A 52-year-old woman was admitted to our hospital for further examination of central obesity, hypertension and hirsutism suggesting Cushing's syndrome. Hirsutism had been remarkable for two years, and muscle weakness of the lower extremities gradually developed during the past year. CT scan revealed a tumor in the left adrenal gland which was 1 cm in diameter, round, well-circumscribed, homogeneous and not enhanced. Endocrine data disclosed increased urinary 17-OHCS (11.5-16.4 mg/day) and elevated plasma ACTH (125 pg/ml) and cortisol (19 micrograms/dl) with a lack of diurnal rhythm. Administration of the single-dose dexamethasone (1mg) did not suppress plasma cortisol. However, consecutive administration of either 2mg or 8mg of dexamethasone for 2 days suppressed both plasma cortisol and urinary 17-OHCS. Administration of metyrapone raised both urinary 17-OHCS and plasma ACTH levels. Rapid ACTH test resulted in a hyperresponse of plasma cortisol. CRF injection raised plasma ACTH and cortisol. Bilateral adrenal glands were well demonstrated by 19-iodocholesterol (I-131) scintigraphy during the administration of dexamethasone. MRI with Gd-contrast revealed a microadenoma in the sella turcica. With the diagnosis of Cushing's disease, the microadenoma was removed by the transsphenoidal approach and adrenal function was normalized. However, the left adrenal tumor remained on CT scan but was not demonstrated by scintigraphy. These findings indicate that this is a very rare case of Cushing's disease which was associated with an unilateral non-functioning adrenal tumor.

Adenoma↗

PubMed1995

Use of ACTH stimulation tests to monitor the treatment of canine hyperadrenocorticism.

The case histories of 60 dogs with hyperadrenocorticism were reviewed. Fifty-four of the dogs were treated with mitotane at a mean daily dose rate of 48.8 mg/kg (range 25.6 to 84 mg/kg) for between four and 21 days. The mean weekly maintenance dose of mitotane was 48.8 mg/kg. An adrenocorticotrophic hormone (ACTH) stimulation test was performed before the treatment began, and in 30 cases at the end of the induction course, and the response to ACTH was measured at regular intervals thereafter. Nine of the treated dogs developed complete hypoadrenocorticism during treatment and required permanent mineralocorticoid replacement therapy. Twelve of the dogs had normal responses to an ACTH stimulation test before treatment, and the diagnosis of hyperadrenocorticism was based on the result of a low-dose dexamethasone suppression test. These 12 dogs had consistently lower cortisol levels before and after stimulation with ACTH and four of them developed complete hypoadrenocorticism. In general the clinical signs were well controlled when the cortisol levels were less than 105 nmol/litre before and after the stimulation test. Dogs in which the clinical signs recurred had cortisol levels between 210 and 580 nmol/litre after the test, a level which is within the normal pretreatment range. Twenty-seven of the treated dogs died and six of these deaths were attributable directly to the disease or therapy. The median survival time of the 54 treated dogs was 30 months; eight dogs died during the first 16 weeks of treatment, and the dogs which survived this period had a median survival time of 39 months (mean 50 months).

Adrenal Cortex Function Tests↗

PubMed1986

Adrenal imaging with technetium-99m-labelled low density lipoproteins.

Evaluation of adrenal cortical function by external imaging is currently accomplished by injection of radiolabelled analogs of cholesterol. Although the adrenals do utilized exogenous cholesterol for steroid hormone synthesis, the cholesterol is delivered to the glands not as free cholesterol but through the uptake of low density lipoproteins (LDL), which are subsequently degraded within the adrenal cortical cells to provide cholesterol. Thus, we sought to assess the use of 99mTc-labelled LDL injected into rabbits to obtain external images of the adrenal glands. Adrenal images of all nine rabbits tested were obtained within 18 to 21 hours after injection of 99mTc-LDL. Seven of the rabbits were subjected to adrenal cortical suppression with dexamethasone and then all nine rabbits were imaged a second time. In the untreated animals, visualization of the adrenal glands was accompanied by normal serum cortisol concentrations and accumulation of radiolabel in the adrenals, whereas in the dexamethasone-treated animals, lack of visualization of the adrenal glands was correlated with low serum cortisols, and greatly decreased accumulation of the radionuclide in the adrenals. These findings demonstrate for the first time that LDL, when labelled with 99mTc, can be used to evaluate adrenal cortical function by external imaging.

Adrenal Cortex Function Tests↗

PubMed2003

Critical size of residual adrenal tissue and recovery from impaired early postoperative adrenocortical function after subtotal bilateral adrenalectomy.

BACKGROUND: Subtotal bilateral adrenalectomy may preserve adrenocortical function. Little is known about the early postoperative function of the adrenal remnant. METHOD: In 10 patients with bilateral adrenal tumors (pheochromocytomas, adrenocortical nodular hyperplasia, and adrenal metastases), plasma adrenocorticotropic hormone (ACTH), serum cortisol, and maximal cortisol liberation were examined with an ACTH test after subtotal bilateral adrenalectomy, which left 15% to 30% of adrenal tissue in situ. RESULTS: In the early postoperative period, all patients had normal basal serum cortisol levels (mean, 415+/-208 nmol/L; normal morning range, 138-690 nmol/L) but pathologically increased plasma ACTH levels (mean, 55+/-42 pmol/mL; normal, <10.1 pmol/L). In 6 patients, a pathologic ACTH test result was observed. During follow-up (mean, 11.3+/-7.6 months), all patients were found to have a normal ACTH test result. None of the patients required steroid supplementation. However, in patients with both familial pheochromocytoma and impaired adrenocortical function during the early postoperative period, the maximal increase of serum cortisol after ACTH stimulation was significantly reduced (mean, 301+/-86.8 nmol/L) compared with control subjects (mean, 490+/-132.6 nmol/L; P=.019). CONCLUSION: After subtotal bilateral adrenalectomy left 15% to 30% of adrenal tissue in situ, functional recovery could be observed in all patients. However, subclinical impairment of the adrenocortical function with questionable clinical significance has to be considered in some of the patients. Especially during the early postoperative period, careful observation of the patients without exogenous steroid administration is required.

Adrenal Cortex Function Tests↗

PubMed1985

Effects of phenylbutazone and anabolic steroids on adrenal and thyroid gland function tests in healthy horses.

Adrenal and/or thyroid gland function tests were evaluated in horses at various times during short-term therapy with phenylbutazone, stanozolol, and boldenone undecylenate. There were no significant treatment or time effects on mean basal plasma cortisol concentrations in horses during treatment with the following: phenylbutazone, given twice daily (4 to 5 mg/kg, IV) for 5 days; stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was no significant effect of phenylbutazone treatment on the changes in plasma cortisol concentration during the combined dexamethasone-suppression adrenocorticotropic hormone (ACTH)-stimulation test. Plasma cortisol concentration was significantly decreased from base line at 3 hours after dexamethasone administration and was significantly increased from base line at 2 hours after ACTH in all horses (P less than 0.05). Likewise, the stimulation of basal plasma cortisol concentrations at 2 hours after administration of ACTH (P less than 0.05) was not affected by treatment with stanozolol or boldenone undecylenate. There were no significant treatment effects on mean basal plasma concentrations of thyroxine (T4) or triiodothyronine (T3) among horses during the following treatments: stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was a significant time effect on overall mean basal plasma T4 and T3 concentrations (P less than 0.05): plasma T4 was lower on day 8 than on days 1, 10, and 12; plasma T3 was higher on day 8 than on days 4 and 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Function Tests↗

PubMed1992

Investigation of adrenal function in women with oligomenorrhoea and hirsutism (clinical PCOS) from the north-east of England using an adrenal stimulation test.

OBJECTIVE: To determine the prevalence of adrenal enzyme dysfunction in women presenting with oligomenorrhoea and hirsutism, two clinical features of polycystic ovary syndrome (PCOS). DESIGN: A prospective study of women attending outpatient clinics with these complaints. Androstenedione, dehydroepiandrosterone (DHEA), 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol and cortisol were measured before and after overnight dexamethasone suppression and at 60 minutes after adrenal stimulation by ACTH injection. SUBJECTS: Fifty women with clinical features of PCOS and 37 control women with regular cycles and normal hair distribution from the catchment area of the Royal Victoria Infirmary which includes Newcastle upon Tyne, Co. Durham, Cleveland, Cumbria and Northumberland. MEASUREMENTS: Number of women with steroid responses to ACTH beyond the normal range, as defined by the responses of the control group and in previous studies. RESULTS: Nineteen women (38%) were found to have some abnormality. One woman (2%) was identified with 21-hydroxylase (21-OHase) deficiency and a second (2%) had an increase in 17-OHP compatible with the heterozygote state for 21-OHase deficiency. Four women (8%) had isolated elevations in the DHEA response consistent with minimal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency. Thirteen women (26%) showed increases in both androstenedione and DHEA, or androstenedione alone, compatible with enhanced 17-20 lyase activity. CONCLUSIONS: Twelve per cent of the group showed evidence consistent with an adrenal enzyme deficiency; 26% had results in keeping with increased adrenal androgen production without an enzyme deficiency. These findings may be of relevance both in the pathogenesis of the features of PCOS and in determining appropriate treatment for individual patients.

3-Hydroxysteroid Dehydrogenases↗

PubMed1990

[Diagnosis of the heterozygote carrier state in 21-hydroxylase deficiency using steroids].

In an attempt to elaborate a method for screening heterozygous carriers of inborn adrenal hyperplasia caused by insufficiency of steroid 21-hydroxylase, the authors examined in 24 obligatory heterozygotes and in seven controls the concentrations of four steroids. Cortisol (F), 11 beta-hydroxyandrostendione (11-OH), 17 alpha-hydroxyprogesterone (17-OH) and androstendione (A) were estimated by the RIA method using non-commercial antisera. In the examined subjects an abbreviated ACTH test was made and the mentioned parameters were assessed at times 0, 30 and 60 minutes. The results (nmol/l) were expressed by the relationship R = F.11-OH/17-OH.A for all investigated time intervals. The coefficient R60 or difference of coefficients delta R = R60-R0 differed significantly and overlapped to a minimum extent in the group of heterozygotes and controls. The authors assume that the suggested method for the detection of carriership of 21-hydroxylase insufficiency could be used in genetic counselling.

17-alpha-Hydroxyprogesterone↗