Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Adrenal Cortex Function Tests”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 955 records · Page 53Linked to original sources
PubMed1999

Serum cortisol levels in very low birth weight infants of substance-abusing mothers.

OBJECTIVE: Recently, hypoadrenalism was described in extremely low birth weight infants. We have been measuring serum cortisol levels in very low birth weight (VLBW) infants to assess their adrenal function. It was noticed that infants of substance-abusing mothers (ISAM) had unusually high serum cortisol levels. To our knowledge, there are no data regarding serum cortisol levels in VLBW ISAM. The objective of our study was to determine if serum cortisol levels of VLBW ISAM are different from serum cortisol levels in VLBW infants without a history of maternal substance abuse. METHODS: We reviewed medical records of infants with birth weight between 400 and 1300 gm who were born between July 1994 and June 1995. Seven ISAM who had serum cortisol levels drawn before 48 hours of life were identified. Seven infants matched for gestational age, antenatal steroid exposure, and birth weight served as control infants. Clinical characteristics, serum cortisol levels, and clinical outcome were compared between the two groups. Serum cortisol levels of all infants were measured by radioimmunoassay. RESULTS: The mean birth weight of the ISAM group was 834 gm (range 480 to 1175 gm), and the mean gestational age was 27.4 weeks. The mean birth weight of the control group was 921 gm (range 525 to 1230 gm) with a mean gestational age of 27.8 weeks. The mean serum cortisol level of the ISAM group was 65.3 micrograms/dl (range 11.9 to 144 micrograms/dl); it was significantly higher than that of the control group (mean cortisol level of 20.5 micrograms/dl; range 4.9 to 62.7 micrograms/dl) (p = 0.01, two-tailed). CONCLUSION: Our data suggest that maternal substance abuse significantly increases serum cortisol levels in VLBW infants. Studies in larger scale are needed to confirm our findings and to correlate cortisol levels in this group of patients with clinical outcome.

Adrenal Cortex Function Tests↗
PubMed2000

Adrenal responsiveness to high, low and very low ACTH 1-24 doses in obesity.

OBJECTIVE: To investigate adrenal activity in visceral obesity in which adrenal hyperactivity has been hypothesized. This could reflect hypothalamus-pituitary alterations leading to slight hyperfunction of the adrenal. Primary adrenal hypersensitivity to ACTH drive in obesity has also been suggested. However, it has also been reported that dehydroepiondrosterone (DHEA) levels in obesity are reduced and it has been hypothesized that this could play a role in the increased cardiovascular risk in obese patients. SUBJECTS: We have studied seven obese women with visceral adiposity (OB, age: 33.6+/-3.3 years, BMI: 33.8+/-1.3 kg/m2, WHR: 0.88+/-0.01). The results in OB were compared with those recorded in a group of age-matched normal women (NS, age: 30+/-1.3 years, BMI: 19.9+/-0.4 kg/m2, WHR: 0.76+/-0.02). METHODS: We have studied the cortisol (F), aldosterone (A) and DHEA responses to ACTH 1-24 administered at low (LD, 0.5 microg/m2) or very low (VLD, 0.125 microg/m2) dose followed by a second challenge with supramaximal dose (HD, 250 microg). RESULTS: Basal F, A and DHEA levels in OB were similar to those in NS. The peak F responses to ACTH were dose-related in both groups. At each dose the F peaks in OB (VLD: 495.6+/-43.9 nmol/l, HD: 722.3+/-67.7 nmol/l; LD: 519.2+/-46.0 nmol/l, HD: 729.6+/-44.7 nmol/l) were similar to those in NS (VLD: 556.7+/-45.9 nmol/l, HD: 704.8+/-20.7 nmol/l; LD: 511.8+/-22.8 nmol/l, HD: 726.7+/-26.5 nmol/l). The peak A responses to ACTH were dose-related in both groups. At each dose, the A peaks in OB (VLD: 0.55+/-0.03 pmol/l, HD: 0.79+/-0.09 pmol/l; LD: 0.63+/-0.04 pmol/l, HD: 0.78+/-0.09 pmol/l) were similar to those in NS (VLD: 0.8+/-0.10 pmol/l, HD: 0.86+/-0.09 pmol/l; LD: 0.8+/-0.10 pmol/l, HD: 0.95+/-0.12 pmol/l). The peak DHEA responses to ACTH were dose-related in both groups. At each dose the DHEA peaks in OB (VLD: 58.6+/-13.3 nmol/l, HD: 61.9+/-13.1 nmol/l; LD: 55.18+/-6.4 nmol/l, HD: 72.3+/-9.8 nmol/l) were similar to those in NS (VLD: 54.3+/-8.2 nmol/l, HD: 57.8+/-8.2 nmol/l; LD: 42.2+/-3.7 nmol/l, HD: 56.9+/-4.3 nmol/l). CONCLUSIONS: This study shows that the cortisol, aldosterone and dehydroepiondrosterone responses to high, low and very low ACTH doses in obese women overlap with those in age-matched lean controls; these findings suggest normal sensitivity of the different zones of the adrenal cortex to ACTH in obesity.

Adolescent↗
PubMed1986

[Vegetative hyperthermia: a thermoregulation disorder or a variant from the norm?].

A diagnosis of low-grade idiopathic fever was made in 85 women and 15 men, examined for subfebrile temperature of unknown origin, after organic disease had been excluded. Compared with 100 healthy control subjects these patients had inadequate movement-dependent temperature elevations with a usually pronounced discrepancy between the rectal temperature, predominantly more than 38 degrees C, and a normal or only slightly raised axillary temperature recorded after bodily movement. Other characteristics were that the elevated temperature was uninfluenced by antipyretic drugs. Almost all patients initially complained about general lassitude as well as frequently about atypical functional complaints and psychological symptoms. These observations indicate that low-grade fever is a functional syndrome due to a harmless faulty regulation of body temperature. In addition to a special constitutional reactivity, psychological factors and possibly previous febrile infections are likely to be involved as precipitating causes.

Adolescent↗
PubMedDate not supplied

Endocrine and reproductive dysfunction in men associated with occupational inorganic lead intoxication.

In an attempt to define a postulated effect of lead on male endocrine function, seven men with symptomatic occupational lead intoxication (maximum whole blood lead levels 66-139 micrograms/dl) underwent in-patient endocrine evaluation at the time of diagnosis. Defects in thyroid function, probably of central origin, were present in three patients. Six patients had subnormal glucocorticoid production measured by 24-hr urinary 17-hydroxycorticosteroids and plasma cortisol responses to vasopressin- and/or insulin-induced hypoglycemia. Although serum testosterone concentration was normal in six patients, five had defects in spermatogenesis, including two with oligospermia and two with azoospermia. Repeat examinations after chelation therapy showed only partial improvement. It is concluded that heavy occupational exposure to lead, sufficient to cause clinical poisoning, may be associated with diffuse disturbances of endocrine and reproductive functions in men which are not rapidly reversible with standard treatment. Since men without overt poisoning have not been studied, these results cannot yet be included as sequelae of low-dose exposures.

Adrenal Cortex Function Tests↗
PubMed1981

Cushing's syndrome: problems in diagnosis.

Cushing's syndrome, an unusual group of disorders characterized by hypercortisolism, must be considered in the differential diagnosis of such common clinical problems as hirsutism, menstrual irregularity, hypertension, diabetes mellitus, and obesity. Its distinct forms--pituitary-dependent Cushing's syndrome (Cushing's disease), adrenal tumor and ectopic ACTH syndrome--must be identified correctly so that specific therapy can be administered. In the majority of cases, use of a relatively simple diagnostic sequence will provide accurate and rapid diagnosis. However, in our experience with more than 60 patients, diagnostic difficulties may arise from a variety of conditions (e.g., drug interference, alcohol ingestion, and depression). In addition, unusual circumstances, such as unexpected responses to dexamethasone, may complicate the diagnosis. Our approach to these problems is illustrated through a report of seven cases, and we emphasize that the proper management of Cushing's syndrome mandates a thorough marshalling of all the available data.

ACTH Syndrome, Ectopic↗
PubMed1990

Long-term follow-up of hypopituitary patients treated with human growth hormone.

Thirty-six former human growth hormone (hGH) recipients underwent comprehensive physical, endocrine and lipoprotein evaluations as adults. Treatment was associated with a decrease in height standard deviation score (SDS) in males from 4.0 pretreatment to 2.1 as adults, and in females from 4.2 to 2.5. Males showed a better growth response to treatment than did females. Plasma somatomedin-C levels were subnormal in 30 patients, but were higher in isolated growth-hormone-deficient patients than in others. Three men and 1 woman showed evidence suggesting a disturbance in pulsatile gonadotropin release despite the previous documentation of normal serum gonadotropin levels. Hypertriglyceridemia was not observed, and the women's plasma cholesterol levels were unremarkable. Men, however, showed higher-than-expected total cholesterol, LDL-cholesterol, and HDL-cholesterol concentrations. The last finding may explain the lack of increased cardiovascular morbidity in this group.

Adolescent↗
PubMed2003

High prevalence of decreased cortisol reserve in brain-dead potential organ donors.

OBJECTIVE: To investigate the adrenocortical function in brain-dead patients, potential organ donors. DESIGN: Prospective study. SETTING: Intensive care units in two teaching hospitals. PATIENTS: A total of 37 patients (28 men, nine women) with severe brain injury, having a mean age of 42 +/- 18 yrs, were included in the study. Group A consisted of 20 brain-injured patients who did not deteriorate to brain death. Group B included 17 brain-injured patients who were brain dead; of these, ten patients developed brain death during ICU stay and seven patients were admitted to the ICU after clinical brain death. INTERVENTIONS: In all patients (group A and group B), a morning blood sample was obtained at admission to the ICU to determine baseline plasma cortisol. Subsequently, 1 microg of corticotropin (adrenocorticotropic hormone, Synacthen) was administered intravenously, and a blood sample was taken 30 mins after the injection. In group B patients who became brain dead while being treated in the ICU (n = 10), the same procedure was repeated the morning after the confirmation of brain death. Patients having a cortisol level of at least 18 microg/dL after the administration of adrenocorticotropic hormone were defined as responders. MEASUREMENTS AND MAIN RESULTS: After the occurrence of brain death, group B patients had significantly lower values for baseline (8.5 +/- 6.2 vs. 17.0 +/- 6.6 microg/dL, p <.001) and stimulated (16.9 +/- 6.3 vs. 23.9 +/- 5.7 microg/dL, p =.001) plasma cortisol compared with group A patients. Thirteen group B patients (76%) and two group A patients (10%) were nonresponders to adrenocorticotropic hormone (p <.001). In group B patients, baseline and stimulated cortisol concentrations were significantly related (r =.71, p =.001), whereas there was no correlation between baseline cortisol and the increment in cortisol (r = -.37, p =.15). Mean hormonal data of the ten brain-dead patients studied at admission in the ICU and after the occurrence of brain death were the following: baseline plasma cortisol (23.5 +/- 11.4 vs. 6.8 +/- 4.2 microg/dL, p =.003) and stimulated serum cortisol (28.8 +/- 9.9 vs. 16.3 +/- 4.3 microg/dL, p =.008). CONCLUSIONS: Adrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors.

Adolescent↗
PubMed1985

Effects of single and multiple doses of ketoconazole on adrenal function in normal subjects.

The plasma cortisol response to 0.25 mg tetracosactrin given by intramuscular injection was suppressed by nine oral doses of 200 mg ketoconazole given 12 hourly to nine normal female subjects. No effect was noted following a single 200 mg oral dose of ketoconazole. This suppressive effect was reversible within at least 5 days of discontinuation of ketoconazole.

Adrenal Cortex↗
PubMed1984

Glomerulosa failure in congenital adrenocortical unresponsiveness to ACTH.

We report two children of a family with congenital adrenocortical unresponsiveness to ACTH. Repeated stimulation of the adrenal by Synthetic 1-24 ACTH (Synacthen) failed to increase cortisol secretion, but produced significant rises of serum aldosterone. This was, however, associated with increased plasma renin activity. Only when the renin-angiotensin effect was eliminated, by a converting enzyme blocker, did Synacthen fail to affect serum aldosterone. These data support the view that glucocorticoid deficiency in this disorder results from unresponsiveness to ACTH and that development of the zona glomerulosa and normal aldosterone secretion is achieved by action of the renin-angiotensin system.

Adrenal Cortex↗
PubMed1993

Isolated congenital ACTH deficiency: a cleavage enzyme defect?

The pro-opiomelanocortin (POMC) gene encodes adrenocorticotrophin (ACTH) which is derived from precursors by proteolytic cleavage. Congenital, isolated ACTH deficiency is rare but may be familial and fatal. The aetiology is unknown though defects at both hypothalamus and adenohypophysis have been postulated. We have studied a female presenting with hypoglycaemia in the neonatal period. When studied at 6 weeks of age, ACTH was unmeasurable even after injection of corticotrophin releasing hormone (CRH1-41). ACTH precursors, quantitated by two-site immunoradiometric assay, were clearly measurable prior to treatment and were stimulated by CRH1-41 and suppressed by glucocorticoid administration. Concentrations of POMC, N-terminal pro-opiocortin (N-POC) and beta-endorphin (beta-EP) were within the normal adult range during glucocorticoid replacement therapy; ACTH and beta-lipotrophin remained undetectable. The secretion of glucagon, measured by radioimmunoassay, in response to hypoglycaemia was normal. By sequencing polymerase chain reaction products from the patient's genomic DNA, the entire coding region of the POMC gene was established to be normal. The results are compatible with a cleavage enzyme defect.

Adrenal Cortex↗
PubMed1991

Adrenocortical insufficiency with normal serum cortisol levels and hyporeninaemia in a patient with acquired immunodeficiency syndrome (AIDS).

The acquired immunodeficiency syndrome (AIDS) has been associated with abnormalities of adrenocortical function, and hypoaldosteronism due to hyporeninaemic hypoaldosteronism (HHA). We here report the case of a woman with AIDS associated with orthostatic hypotension, persistent hyponatraemia and hyperkalaemia, in whom basal serum cortisol levels were normal and serum renin activity was low. Subsequent post-mortem examination revealed almost complete adrenocortical destruction. A possible explanation of this apparently contradictory combination of findings is discussed, together with the therapeutic implications for similar cases.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Diagnosis of X-adrenoleucodystrophy phenotypic variants.

We report the radiological and biochemical data of a familial X-adrenoleucodystrophy with an extreme phenotypic variability, in which the diagnosis of several affected members was delayed for several years. The propositus developed a progressive dementia, while two of his brothers were diagnosed of primary Addison's disease several years previously. MRI in two cases with different phenotypes revealed hyperintense diffuse white matter lesions, and the diagnosis was confirmed by increased serum levels of very long chain fatty acids. We conclude that X-adrenoleucodystrophy should be included in the differential diagnosis of adult Addison's disease even though no neurological involvement or family history is recorded, and that MRI is a useful tool for diagnosis and follow-up of neurological involvement in this disease.

Addison Disease↗
PubMed1995

Auxological, clinical and neuroradiological findings in infants with early onset growth hormone deficiency.

Sixteen infants less than 2 years of age with apparently idiopathic hypopituitarism were studied. At birth, 11 of 16 patients (69%) had subnormal length associated with relative adiposity and 10 of 16 (62%) showed significant deterioration in length deficiency from birth onwards. These findings suggest that: (a) growth hormone deficiency, in a number of patients, had started well before delivery; (b) growth hormones may play a role in intrauterine growth; and (c) growth hormone may also be involved in early postnatal growth. Magnetic resonance imaging in these patients was very similar to that described in hypopituitarism of later onset. This suggests that even in the latter case, hypopituitarism may have a prenatal onset. Finally, the severity of growth failure and the coexistence of other hypopituitary symptoms at the time of diagnosis in 31% of our patients indicate that early clinical screening of hypopituitarism is possible.

Adrenal Cortex Function Tests↗