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PubMed1997

[Usefulness of measurement of hormones in urine samples collected during the night period for the diagnosis of endocrine disorders].

It has been known that the measurement of adreno-cortical and medullary hormones in urine for 24 hours is the best way for diagnosis of the disease state. This is not only because hormone release shows circadian rhythm but also because the urinary excretion of hormones reflects the total amount of hormones produced for 24 hours. However, the civilized people, particularly the workers, are too busy to correct urine for 24 hours. Therefore, we aimed to evaluate whether the urine sample corrected for only 12 hours during night is useful for the diagnosis of adrenal diseases. Circadian rhythm of hormones in urine was evaluated by correcting urine every 4 hours in 18 normal adults. Diurnal variations of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids (17-OHCS) were evident; they showed the peak value during 8 AM and 12 AM, and the trough during 0 AM and 4 AM. Similarly, urinary noradrenaline and adrenaline showed the peak value at day time and the trough at night time. However, the rhythm was not observed in urinary dopamine and vanilyl mandelic acid (VMA). Under consideration of outpatient's convenience, urine sampled during night (between 8 PM and 8 AM) was evaluated. The amount of hormones during night was 35.9-46.9% of the total amount of the day, and the deviation was relatively small. The reference intervals (mean +/- 2SD) were as follows; 17-KS (n = 56, 2.8 +/- 2.4 mg/12 hours), 17-OHCS (n = 56, 2.0 +/- 2.0 mg/12 hours), 17-KGS (n = 52, 3.6 +/- 3.6 mg/12 hours), free cortisol (n = 43, 14.3 +/- 14.2 micrograms/12 hours), noradrenaline (n = 50, 12.9 +/- 9.8 micrograms/12 hours), adrenaline (n = 50, 2.1 +/- 4.0 micrograms/12 hours), dopamine (n = 50, 134 +/- 194 micrograms/12 hours), VMA (2.3 +/- 2.4 mg/12 hours). When the night periods urine in patients with adrenal disorders such as virilizing adrenocortical carcinoma, pituitary adenoma, adrenocortical hydroxylase deficiency, Addison's disease, hypopituitarism, Cushing's syndrome, pheochromocytoma was analyzed, the respective urinary hormone level corresponding to each disease was significantly changed from the reference interval. These results indicate that analysis of urine sample during night has advantage over the daily urine because the difference between normal and disease state is augmented when measured urinary during night.

Adenoma↗
PubMed1988

[2 surgically treated cases of adrenocortical carcinoma producing steroid hormones without endocrinological symptoms--case report and a review of cases in the Japanese literature].

We have experienced two male cases of an adrenocortical carcinoma that have produced steroid hormones without endocrinological symptoms. Both men were admitted to hospital because of an abdominal pain and left hypochondral tumors. In each case, an abdominal CT, an ultrasonogram and an angiogram demonstrated a left adrenal tumor, and levels of blood dehydroepiandrosterone sulfate, etiocholanolone, pregnenolone sulfate and urine 17 KS were elevated. The tumors were resected and the histology revealed that they were adrenocortical carcinomas. Postoperatively, the levels of their urine hormones returned to normal values, though in one man recurrence occurred a year later. Only 8 cases of an adrenocortical carcinoma that has produced steroids without specific endocrinological symptoms have been reported in Japan, and we also report on two cases herein.

17-Ketosteroids↗
PubMed1990

Clinical features of adrenocortical carcinoma, prognostic factors, and the effect of mitotane therapy.

Adrenocortical carcinoma is a rare tumor, and only limited information is available about its natural history and the effects of therapy. We studied 105 patients (75 female and 30 male; mean age, 46 years) with adrenocortical carcinoma who were referred to us between 1963 and 1987. The average duration of symptoms before diagnosis was 8.7 months. At the time of diagnosis, 68 percent of the patients had endocrine symptoms, and 30 percent had distant metastases. Hormonal studies showed that 79 percent of the tumors were functional. Eighty patients underwent surgery, and 59 also received the adrenal cytotoxic agent mitotane. The median disease-free interval after surgery was 12.1 months (range, 1 to 175). Tumor dissemination occurred in 82 percent of the patients, most commonly to the lung, liver, and adjacent organs. The median survival time was 14.5 months (range, less than 1 to 175), and the five-year survival was 22 percent. Age over 40 years and the presence of metastases at the time of diagnosis were the only factors recognized as indicating a poor prognosis. Mitotane controlled hormonal secretion in 75 percent of the patients. Eight mitotane-treated patients had partial tumor regression, but the drug did not have a significant effect on survival. We conclude that adrenocortical carcinoma carries a poor prognosis. Mitotane therapy may offer transient benefits, particularly in controlling endocrine symptoms.

Adrenal Cortex Hormones↗
PubMed1987

Studies on lipoprotein and adrenal steroidogenesis: II. Utilization of low density lipoprotein- and high density lipoprotein-cholesterol for steroid production in functioning human adrenocortical adenoma cells in culture.

We examined the utilization of human low density lipoprotein (LDL)- and high density lipoprotein (HDL)-cholesterol for steroid production in primary monolayer culture cells from adenomas of primary aldosteronism and Cushing's syndrome and an adrenal of nodular hyperplasia of Cushing's syndrome. We compared the data obtained with findings in the case of cultured normal human adrenocortical cells. In the presence of 10(-7) M adrenocorticotropin (ACTH), the addition of either LDL or HDL to the culture medium at a cholesterol concentration of 100 micrograms/ml led to a significant increase in the daily secretion rates of cortisol, dehydroepiandrosterone sulfate (DHEA-S) and aldosterone in the adenoma and nodular hyperplasia cells, as in the normal cells. Although LDL greatly increased the secretion of steroid hormones, no significant difference in steroid secretion following the treatments with LDL and HDL were observed in these cultured cells. The contribution of endogenous cholesterol to steroid production was also high, thereby indicating that the neoplastic transformation did not have untoward effects. Cells from adenomas of primary aldosteronism secreted not only aldosterone, but also cortisol and DHEA-S. The daily secretion rates of these steroids were markedly increased when ACTH was added to the medium. With prolonged exposure to ACTH, however, the rate of aldosterone secretion showed a gradual decrease with the incubation time. This decrease might be due to the impaired conversion of corticosterone to 18-hydroxycorticosterone. In case of adenomas in patients with Cushing's syndrome, the secretion of steroid hormones varied in quantity and quality, depending on the type of plasma cortisol response to the rapid ACTH test in vivo, thereby suggesting that the adrenocortical adenoma of Cushing's syndrome might be divided into two subtypes. These results indicate that human functioning adrenocortical adenoma cells utilize plasma lipoproteins as a source of cholesterol for steroidogenesis during the prolonged stimulation of steroid secretion.

Adenoma↗
PubMed1985

Nonfunctioning adrenocortical carcinoma in a young girl.

A 9 year old Japanese girl was admitted complaining of left hypochondrial pain and a large upper left abdominal tumor. There were no clinical or laboratory signs of hormonal abnormality. Intravenous pyelography showed marked compression and deformity of the kidney by a tumor. This tumor was excised together with the left kidney. The pathological diagnosis was adrenocortical carcinoma. Postoperatively, the child was given neither irradiation nor chemotherapy. Twenty-one months after the surgery, there was a hepatic metastasis, and she died 40 months after surgery from a combination of hepatic metastases and local tumor recurrence.

Adrenal Cortex Hormones↗
PubMed2004

Corticosteroids--from an idea to clinical use.

Corticosteroids form the basis of treatment in many inflammatory rheumatic diseases, both as systemic treatment and as treatment with local injections to reduce inflammation. In 1948 the first systemic treatment of a patient with a rheumatic disease was given to a woman with severe rheumatoid arthritis (RA); the impressive effect in this patient, and in another 15 patients, was reported by Dr Hench and co-workers in 1949. Systemic corticosteroid treatment was rapidly adopted and used not only for patients with RA but also for those with other rheumatic diseases such as systemic lupus erythematosus-as well as other disorders such as asthma-with a similar positive effect. In the following year, 1950, the Nobel Prize was awarded for the discovery of the structure and biological effects of the adrenal cortex hormones. This open trial was followed by several controlled trials conducted in the UK in which the effects of cortisone were compared with the effects of aspirin in patients with RA-interestingly, without any significant clinical benefit for the cortisone-treated patients. It was not until 1959, in yet another multi-centre trial in Britain, that a significant effect on functional capacity and general well-being was reported after 2 years of treatment with prednisolone, compared to aspirin, in patients with early RA. Despite the dramatic effects that were observed in the severely ill RA patients reported by Hench and co-workers it took 10 years to demonstrate that this effect was superior to the effect of aspirin when the two compounds were compared in controlled trials. Why was this so? One explanation could be in the study designs and the different outcome measures used in the various studies. Perhaps the results in the first comparative studies would have been different if individual response criteria had been used. This is discussed in this chapter.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Reassessment of the role of theophylline in the current therapy for nocturnal asthma.

BACKGROUND: Symptoms of asthma commonly increase at night for a variety of reasons. While different options are available for the management of nocturnal asthma, theophylline has maintained a prominent role in treating this problem, and it is widely promoted as a first-line agent. Very recent reports stress the use of anti-inflammatory agents as the drugs of choice for the long-term treatment of asthma. METHODS: Using the key words "asthma," "theophylline," "bronchodilators," "adrenal cortex hormones," "beclomethasone," "triamcinolone acetonide," and "disodium cromoglycate," the MEDLINE files were searched from 1982 to the present. Articles dating before 1982 were accessed from cross-reference of the more recent articles. RESULTS: Sustained-release theophylline preparations are effective in decreasing the rate of exacerbations of nocturnal asthma symptoms, but theophylline has risks of major toxicity and serum concentrations must be monitored. Inhaled corticosteroids are also useful in controlling nocturnal asthma, and they reduce inflammation, which is the basic problem in asthmatics. Inhaled anticholinergics and oral controlled-release albuterol are also helpful in reducing symptoms of nocturnal asthma. CONCLUSIONS: A suggested approach to managing nocturnal asthma includes corticosteroids inhaled through a spacer device at optimum doses, adding inhaled albuterol or oral sustained-release albuterol and then ipratropium with a spacer. If control is not maintained with this regimen, sustained-release theophylline may add benefit to inhaled steroid therapy in reducing nighttime asthma symptoms. Long-acting inhaled beta 2 agonists show promise and could be the adjunctive treatment of choice when they become available in the United States.

Adrenal Cortex Hormones↗
PubMed2005

Complications associated with the use of corticosteroids in the treatment of athletic injuries.

BACKGROUND: The potent anti-inflammatory pharmacologic effects of the corticosteroids (cortisone and synthetic derivatives) has led to their extensive usage in the management of rheumatologic diseases and athletic musculoskeletal injuries. The efficacy and risks of locally injected or systemically administered corticosteroids in the treatment of athletic injuries are unclear. OBJECTIVE: To review critically the medical literature and determine complications and risks associated with corticosteroid treatment of athletic injuries. DATA SOURCES: A search of 3 databases-MEDLINE, CINAHL, and Cochrane Clinical Trial Register-was performed using the OVID interface for all years between 1966 and 2003. The search first combined all references under the medical subject headings adrenal cortex hormones, glucocorticoids, and glucocorticoids, synthetic. A second search combined all references under the medical subject headings athletic injuries, sprains and strains, tendon injuries, shoulder injuries, rotator cuff disease, tennis elbow, and lateral epicondylitis. The references identified by these 2 searches were intersected and limited to human only to produce 130 articles. Relevant review articles were scanned, references reviewed, and additional articles retrieved for consideration of inclusion. STUDY SELECTION: For inclusion in this critical review, articles must meet the following criteria: (1) subjects were human, (2) subjects had athletic-related injuries, and (3) subjects received corticosteroid treatment. Ultimately, 43 studies met inclusion criteria. DATA EXTRACTION AND SYNTHESIS: Selected articles were then categorized as to whether the primary focus was usage/efficacy of corticosteroid injection therapy, occurrence of complications of corticosteroid injection therapy, or usage or complications of systemic corticosteroid therapy. MAIN RESULTS: Twenty-five selected studies primarily examined the usage/efficacy of corticosteroid injections in the treatment of various athletic injuries. Of the 983 total subjects who received corticosteroid injections among these studies, only minor complications of treatment were reported. Eighteen selected studies primarily described complications of corticosteroid injections in the treatment of athletic injuries. Of these, tendon and fascial ruptures were the predominant complications reported. The search identified no articles that addressed the usage of or complications of systemic corticosteroids in the treatment of athletic injuries, although tibial stress fracture and multifocal osteonecrosis occurred in individuals being treated for nonathletic injury conditions. CONCLUSIONS: This critical review reveals that the existing medical literature does not provide precise estimates for complication rates following the therapeutic use of injected or systemic corticosteroids in the treatment of athletic injuries. Tendon and fascial ruptures are often reported complications of injected corticosteroids, whereas tibial stress fractures and multifocal osteonecrosis were described with systemic corticosteroids.

Administration, Oral↗
PubMed1993

Protein kinase C is a tonic negative regulator of steroidogenesis and steroid hydroxylase gene expression in Y1 adrenal cells and functions independently of protein kinase A.

The role of protein kinase C (PKC) in the regulation of basal steroidogenesis and steroid hydroxylase gene expression in Y1 adrenocortical cells was investigated. Treatment of Y1 cells with either staurosporine or calphostin C, inhibitors of PKC, increases steroid hormone production up to 7-fold. Induction of P450-cholesterol side chain cleavage enzyme (SCC) mRNA expression parallels induction of steroidogenesis by the PKC inhibitors. Staurosporine increases expression of a transiently transfected SCC promoter--human growth hormone construct in Y1 cells, indicating that PKC regulates expression of SCC mRNA at the level of transcription. Treatment with staurosporine increases expression of mRNA for two additional steroid synthetic enzymes, P450-11 beta-hydroxylase and 3 beta-hydroxysteroid dehydrogenase. These data indicate that PKC acts as a tonic negative regulator of basal steroidogenesis in Y1 cells by suppressing expression of mRNA encoding the steroid synthetic enzymes. Protein kinase A (PKA) and PKC have reciprocal effects on steroidogenesis and expression of the steroid synthetic enzymes in Y1 cells. However, the results of this study demonstrate that these signaling pathways are not interdependent. Steroid production by Y1 cells treated with (Bu)2cAMP and calphostin C together is equal to the sum of steroid production after treatment with either agent alone. Pretreatment of Y1 cells with Rp-8-Bromo-cAMP, a specific inhibitor of PKA, prevents induction of steroidogenesis by (Bu)2cAMP, but not by staurosporine, indicating that PKC is not dependent on PKA activity. In addition, induction of SCC mRNA expression by staurosporine, in Y1 cells which are defective in activation of PKA (Y1 kin-8), is equivalent to induction in Y1 cells. These data indicate that PKA and PKC regulate basal steroidogenesis through independent effects on expression of the steroid synthetic enzymes.

3-Hydroxysteroid Dehydrogenases↗
PubMed1983

Regulation by ACTH of steroid hormone biosynthesis in the adrenal cortex.

In this article, current knowledge about the mechanism of action of ACTH will be reviewed. Emphasis will be placed on events which occur subsequent to binding of ACTH to its receptor, stimulation of adenylate cyclase, and activation of protein kinase. In the first part of the review, the acute action of ACTH will be discussed with emphasis on present hypotheses as to the roles of calcium, phospholipids, sterol carrier proteins, and a "labile protein" activator of cholesterol side-chain cleavage. The presumptive role of these factors to increase the binding of cholesterol to the mitochondrial cholesterol side-chain cleavage enzyme will be discussed in the light of the concept that such binding is the step in steroidogenesis which is activated during the acute response of the adrenal cell to ACTH. In the second part of the article, the long-term action of ACTH to increase the levels of steroidogenic enzymes will be reviewed. Recent evidence is indicative that ACTH causes induction of the synthesis of key steroidogenic enzymes present in both the mitochondria and the microsomes. This appears to result from transcription of genes specific for these various species of cytochrome P-450 and ancillary proteins, resulting in increased synthesis of specific forms of mRNA. Whereas the mitochondrial steroidogenic enzymes are synthesized on cytoplasmic polysomes as precursor forms of higher molecular weight, the microsomal proteins are synthesized as forms of similar molecular weight to the mature forms.

Adrenal Cortex↗