AN ALTERATION IN CORTISOL METABOLISM IN PATIENTS WITH CUSHING'S SYNDROME AND BILATERAL ADRENAL HYPERPLASIA.
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Addison Disease↗
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Results for “ADRENAL CORTEX HYPERFUNCTION”
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[The hypophyseal-adrenal axis in chronic alcoholism].
In order to reveal the morphologic basis of clinically recognized pseudo Cushing syndrome in chronic alcoholism, we performed an analysis of histologic characteristics of hypothalamo-hypophyseal adrenal axis components. The experiment included Wistar rats which were given 15% ethanol solution in water for three months. By methods of classical histology, histochemistry and immunofluorescence adrenal and hypophyseal sections of experimental animals exposed to continual effects of alcohol and those from the control group were examined. ACTH (adrenocorticotropin) cells of the experimental group show expressed immunofluorescence as a proof of their high secretory granules present in numerous cytoplasmic endings which contribute to significantly increased number of these cells comparing to the control group. In the adrenal cortex of animals exposed to alcohol, in the zona fasciculata and zona reticularis, under the influence of hypophyseal corticotropin (ACTH) secretion, there is a statistically significant increase of the compact cells region, as synthetic active elements, in regard to vacuolized cells, as inactive elements, which has been established stereologically. Simultaneous hyperfunction of hypophyseal ACTH cells and ACTH dependent zones of the adrenal cortex in chronic alcoholism, proves that alcohol primarily acts at the level of hypothalamus and hypophysis, while adrenals react to hypersecretion of ACTH cells. The way alcohol affects neurotransmitters is the topic of the discussion, whereas stimulated synthesis of acetylcholine is pointed out.
Adrenal Cortex↗
[Morphofunctional reaction of the cortical lamina of the adrenal gland to reparative osteogenesis and administration of thyrocalcitonin].
A complex of morphofunctional changes of the adrenal cortex was studied on 150 albino male rats in case of thyrocalcitonin (TCT) administration and experimental fracture. There proved to be an increase of functional activity of the gland under conditions of reparative osteogenesis. The state of hyperfunction developed the first five days of TCT administration in a dose of 5 Units daily. The following saturation of the organism with TCT caused depression of the adrenal gland, particularly of its glucocorticoid function. It is supposed that the inhibitory effect of TCT on the adrenal cortex served as one of the mechanisms accelerating the repair processes in the bone tissue.
Adrenal Cortex↗
Influence of L-triodothyronine on steroid hormone metabolism: studies in a patient with adrenal hyperplasia (Cushing's syndrome).
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Adrenal Cortex Hormones↗
Endocrine adjustments in a wild lemming population during the 1969 summer season.
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Adrenal Cortex Hormones↗
Effect of ACTH-induced hypercortisolemia on the EEG in patients with stress-related epilepsy.
PURPOSE: We assess the effect of acute hypercortisolemia induced by ACTH stimulation on seizures and EEG interictal spike activity in patients with localization-related epilepsy (LRE) and stress-related seizures. METHODS: Seven patients (3 males, 4 females) with LRE and stress-related seizures were studied. All patients underwent ACTH stimulation with 0.25-0.75 mg Cosyntropin intravenously at 8 am. Serum cortisol and ACTH levels were monitored half- to one-hourly for 4 to 6 hours. Video/EEG monitoring was also performed. RESULTS: ACTH injection induced hypercortisolemia in all patients. Hypercortisolemia was not associated with seizures or interictal spike facilitation in any patient. Two patients experienced seizures on the day of ACTH injection, one 8 hours after and another 15 and 12 hours after the injection, during a period when their cortisol levels had returned to normal. CONCLUSION: No reproducible interictal EEG changes occurred in any of the patients following ACTH injection.
Adolescent↗
Secretion of the adrenal androgen, dehydroepiandrosterone sulfate, during normal infancy, childhood, and adolescence, in sick infants, and in children with endocrinologic abnormalities.
Serum concentrations of the adrenal androgen, dehydroepiandrosterone sulfate, were measured by radioimmunoassay in normal infants and children, in sick premature and full-term newborn infants, and in patients undergoing evaluation of the hypothalamic-pituitary-gonadal and -adrenal systems. Premature infants had significantly greater (p less than 0.001) levels of DHAS (263 +/- 40)[SE]migrong/dl) than did full-term infants (58.9 +/- 5.2) during the first ten days of life; further increments occurred in stressed "sick" infants. A gradual age- and maturity-related rise in serum concentrations of DHAS was observed during childhood with the earliest increase occurring prior to the onset of pubertal production of gonadal steroids. Serum levels of DHAS rose following administration of ACTH and were increased in patients with congenital adrenal hyperplasia, in whom rapid decrements followed treatment with dexamethasone. hCG or LH-RH treatment did not alter DHAS concentrations. These data suggest that direct secretion of DHAS by the adrenal gland and/or peripheral sulfation of DHA, rather than gonadal secretion, accounts for the majority of DHAS production. The involvement of adrenal androgens in the pubertal maturation of the reproductive endocrine system thus may be evaluated by quantitation of serum DHAS.
Adolescent↗
Endocrine disorders of the pancreas and adrenal cortex in pediatric patients.
Hyperinsulinemia, a common cause of persistent hypoglycemia in infants and children, can result in permanent damage to the central nervous system. Thus, early diagnosis and treatment are important. The typical clinical manifestation of hyperinsulinemic hypoglycemia is symptomatic hypoglycemia that responds poorly to medical therapy. Affected infants may have tremors, jitteriness, apnea, cyanosis, or seizures. If initial medical therapy (frequent feedings, large amounts of intravenously administered glucose, diazoxide, and glucocorticoids) fails to stabilize plasma glucose levels, subtotal pancreatectomy is indicated. This surgical intervention does not completely correct the hypoglycemia in all patients, but it effectively reduces the severity of the condition. Surgical treatment of pediatric patients with Cushing's syndrome or aldosteronoma has also been effective. In our experience, survival of patients with adrenocortical adenomas has been 100%, whereas only five of nine children with adrenocortical carcinomas survived, and four of the five were younger than 10 years of age.
Adrenal Cortex Neoplasms↗
Diagnosis and treatment of functioning and nonfunctioning adrenocortical neoplasms including incidentalomas.
The most important functional tumors of the adrenal cortex are those that secrete cortisol or aldosterone in excess. Biochemical testing when appropriately utilized can diagnose and differentiate the cause of Cushing's syndrome, and when an adrenal adenoma is found, surgical excision is curative. The diagnosis and surgical treatment of primary aldosteronism are straightforward today, and localization of the usual small cortical tumor producing the syndrome can be achieved by CT and NP-59 scanning or selective venous assays. Adrenocortical carcinomas are relatively rare, are usually incurable when diagnosed, and are an important consideration in the incidentally discovered adrenal mass found by CT scanning.
Adenoma↗
Alcohol-induced pseudo-Cushing's syndrome.
In 4 patients corticosteroid hypersecretion associated with excessive intake of alcohol led initially to an erroneous diagnosis of Cushing's syndrome. If diagnostic errors are to be avoided, a history of alcohol intake should always be sought in a patient in whom the diagnosis of Cushing's syndrome is entertained. The abnormalities of pseudo-Cushing's syndrome revert to normal on ethanol withdrawal.
Adrenal Cortex Function Tests↗
Adrenal suppression after long-term exposure to occupational corticosteroids followed by rapid recovery.
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Adrenal Cortex Hormones↗
Diagnosis of canine hyperadrenocorticism.
Canine hyperadrenocorticism is one of the most common endocrinopathies in dogs. Diagnosis remains difficult in some cases due to factors such as the presence of non-adrenal illness and limitations in the tests. Differentiation between the pituitary and adrenal forms is important for providing accurate prognostic information and delineating treatment options and protocols. This article reviews the tests available for diagnosis (screening) and differentiation and evaluates their advantages and disadvantages. Recommendations for testing are made.
Abdomen↗
Diagnosis of canine hyperadrenocorticism.
Diagnosis of canine hyperadrenocorticism can only be made when a suspicion of the disorder persists after completion of a thorough history and physical examination. The first diagnostic testing steps include a complete blood count, serum biochemical tests, and urinalysis with urine culture. Radiography or ultrasonography may also be necessary, depending on physical findings. Screening tests are next applied to support or exclude the clinical diagnosis of hyperadrenocorticism. After the diagnosis has been made, discrimination tests are applied to determine whether the cause is pituitary or adrenal. The limitations of screening tests, particularly in the presence of nonadrenal diseases, cannot be overemphasized. We recommend that neither screening tests nor discrimination tests for hyperadrenocorticism be used in dogs with concurrent nonadrenal disease.
Abdomen↗
Transsphenoidal hypophysectomy for treatment of pituitary-dependent hyperadrenocorticism in 7 cats.
OBJECTIVE: Evaluation of microsurgical transsphenoidal hypophysectomy for the treatment of pituitary-dependent hyperadrenocorticism (PDH) in cats. STUDY DESIGN: Prospective clinical study. ANIMALS OR SAMPLE POPULATION: Seven cats with PDH. METHODS: Urinary cortisol/creatinine ratios, pituitary-adrenocortical function tests, and computed tomography (CT) were performed on 7 cats that presented with a provisional diagnosis of hyperadrenocorticism. All cats underwent microsurgical transsphenoidal hypophysectomy with histologic examination of the excised specimen. Follow-up consisted of clinical evaluation, repeat adrenocortical function testing, and CT. RESULTS: Four cats had concurrent diabetes mellitus. In all cats, the urinary cortisol/creatinine (C/C) ratios were elevated. The dexamethasone screening test showed that 2 cats did not meet the criterion for hyperadrenocorticism. The response of the cats' plasma concentrations of cortisol and adrenocorticotrophic hormone to a high dose of dexamethasone varied from very sensitive to completely dexamethasone resistant. Basal plasma alpha-melanocyte-stimulating hormone concentrations were elevated in 2 cats with a pars intermedia adenoma and in 3 cats with an adenoma that originated from the anterior lobe. Preoperative CT enabled accurate assessment of pituitary size (5 nonenlarged pituitaries with a height <4 mm and 2 enlarged pituitaries with a height >5 mm) and localization relative to intraoperative anatomic landmarks. Two cats died within 4 weeks after surgery of a nonrelated disease. In the remaining 5 cats, the hyperadrenocorticism went into both clinical and biochemical remission. Hyperadrenocorticism recurred in 1 cat after 19 months, but no other therapy was given and the cat died at home 28 months after surgery. CT evaluation of this cat had identified pituitary remnants 6 weeks after surgery. The main postoperative complications were oronasal fistula (1 cat), complete dehiscence of the soft palate (1 cat), and transient reduction of tear production (1 cat). One cat died at 6 months (undefined anemia), and another cat at 8 months (recurrent nose and middle ear infection secondary to soft palate dehiscence) after surgery. In the surviving 2 cats, the remission periods at the time of writing were 46 and 15 months. In the 2 cats with sufficient follow-up time, the concurrent diabetes mellitus disappeared, ie, insulin treatment could be discontinued at 4 weeks and 5 months after hypophysectomy. In all 7 cats, the histologic diagnosis was pituitary adenoma. CONCLUSIONS: Microsurgical transsphenoidal hypophysectomy is an effective method of treatment for feline PDH in specialized veterinary institutions having access to advanced pituitary imaging techniques. Concurrent diabetes mellitus is usually reversible after hypophysectomy. Thorough presurgical screening for coexisting diseases is imperative. CLINICAL RELEVANCE: PDH in cats can be effectively treated by hypophysectomy. The neurosurgeon performing hypophysectomy must master a learning curve and must be familiar with the most frequent complications of the operation to treat them immediately and effectively. Urinary C/C ratios are sensitive indicators for the assessment of remission and recurrence of hyperadrenocorticism.
Adenocarcinoma↗
Results of adrenalectomy in 36 dogs with hyperadrenocorticism caused by adreno-cortical tumour.
A total of 38 adrenocortical tumours were removed from 36 dogs with hyperadrenocorticism. The surgical approach was by way of a unilateral flank laparotomy (32 dogs; 14 left and 18 right), a bilateral flank laparotomy (3 dogs) or a midline celiotomy (1 dog). Two dogs were euthanized during surgery because their tumours could not be resected. Eight dogs died from post-operative complications. Pancreatic necrosis with peritonitis was the most common cause of death. Eight of the 26 dogs that survived had signs of recurrence of hyperadrenocorticism. Unsuppressible hyperadrenocorticism was found in four dogs; one dog had probably pre-existent pituitary-dependent hyperadrenocorticism, and adrenocortical function could not be re-examined in the remaining three dogs. Among the 37 tumours examined microscopically expansion of neoplastic tissue into blood vessels was found in 22 of them. Four adrenal glands with adrenocortical tumours also contained phaeochromocytomas. Necropsy was performed in eight dogs. Metastases were found in the lungs of two dogs and in the lungs and liver in one dog. In combination with the data of previous reports, it is suggested that histological findings in surgery specimens are not good predictors for the clinical outcome.
Adrenal Cortex Neoplasms↗
Multiple endocrine neoplasias in a dog: corticotrophic tumour, bilateral adrenocortical tumours, and pheochromocytoma.
In a 10-year-old ovariohysterectomized standard Schnauzer, the finding of dexamethasone-resistant hypersecretion of cortisol, the results of computed tomography, and elevated plasma concentrations of ACTH suggested the presence of both adrenocortical tumour and pituitary-dependent hyperadrenocorticism. The dog made an uneventful recovery after bilateral adrenalectomy and remained in good health for 31/2 years with substitution for the induced hypoadrenocorticism. Then the enlarged pituitary caused neurological signs and eventually euthanasia was performed. The surgically excised right adrenal contained a well-circumscribed tumour of differentiated adrenocortical tissue and in the left adrenal there were two adrenocortical tumours and a pheochromocytoma. The unaffected parts of the adrenal cortices were well developed and without regressive transformation. At necropsy there were no metastatic lesions. The cells of the pituitary tumour were immunopositive for ACTH and had characteristics of malignancy. The present combination of corticotrophic tumour, adrenocortical tumours, and pheochromocytoma may be called 'multiple endocrine neoplasia' (MEN), but does not correspond to the inherited combinations of diseases known in humans as the MEN-1 and the MEN-2 syndromes. It is suggested that the co-existence of hyperadrenocorticism and pheochromocytoma may be related to the vascular supply of the adrenals. Some chromaffin cells of the adrenal medulla are directly exposed to cortical venous blood, and intra-adrenal cortisol is known to stimulate catecholamine synthesis and may promote adrenal medullary hyperplasia or neoplasia.
Adrenal Cortex Neoplasms↗
Effects of hyperadrenal states on luteinizing hormone in cattle.
The effect of an induced hyperadrenal state on luteinizing hormone (LH) secretion and subsequent ovarian function was examined in both intact and adrenalectomized (ADRX) heifers. Treatments were begun on Day 2 or Day 16 of an estrous cycle in order to examine their effect on corpus luteum development or ovulation, respectively. In Experiment I, continuous intravenous infusion of ACTH (1.0 mg/24 h) to intact heifers decreased LH concentrations during the early phase of the cycle (Days 3-5). Treatment of ADRX heifers with hydrocortisone succinate (HS) (100 mg/24 h) did not appear to change mean LH concentrations, although da Rosa and Wagner (1981) have reported reduced plasma concentrations of progesterone at mid-cycle in these ACTH-treated intact heifers and HS-treated ADRX heifers. ACTH treatment of ADRX heifers had no effect on LH or progesterone. In the second study, there were similar frequencies of LH surges at the anticipated time of ovulation in all treatment groups. HS (100 mg/24 h) in ADRX heifers and ACTH (0.5 mg/24 h) in intact heifers was given continuously beginning on Day 16 of an estrous cycle. Although some animals in all groups exhibited LH surges, the ACTH-treated intact and HS-treated ADRX heifers failed to show a consistent subsequent increase in progesterone concentrations in plasma, suggesting a failure of luteal development. Although no difference was seen in baseline concentrations of LH, there was a greater difference between basal and overall mean LH concentrations in control groups than was observed in ACTH- or HS-treated animals. These induced hyperadrenal states resulted in depression of ovarian function as shown by decreased plasma progesterone during the luteal phase of the cycle. It is not known if other noncorticoid steroids from the adrenal cortex are necessary for a full expression of this effect.
Adrenal Cortex Hormones↗
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↗