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PubMedDate not supplied

[Evaluation of the secretory activity of the adrenal cortex and gonads in women with epilepsy. I. Urinary excretion of metabolites of adrenal cortex hormones in women with epilepsy during the 2 days preceding menstrual bleeding].

In 32 women with seizures occurring mainly in the premenstrual phase and during bleeding, (group A) and in 31 women with epilepsy without this relationship of the seizures to the menstrual cycle (group B) the metabolites of adrenocortical hormones (17-ketosteroids and 17-hydroxycorticosteroids) were determined in 24-hour urine. The investigations were done during 2 days preceding menstrual bleeding, in most cases during three menstrual cycles. A significant reduction of the excretion of 17-ketosteroids and total 17-hydroxycorticosteroids was found in both groups as compared to the accepted normal value (p less than 0.01). However, no significant difference was observed in the excretion of these hormones between these groups of patients, although in group A he values of 17-ketosteroids were lower than in group B. On the basis of these results it is suggested that deficiency of androgenic hormones may contribute to the occurrence of seizures on the days before the onset of menstrual bleeding, and the effect of anticonvulsant treatment on the decreased excretion of these hormones is discussed.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

[The fetal adrenal gland in risk pregnancy].

INTRODUCTION: The role of the adrenal gland in the metabolism of foetus and its role in maturation of foetal organs are the principal motives for paying more attention to this vital organ, which is still a great enigma for gynaecologists. The control of the gland is important in normal as well as in risk pregnancies. Of the entities that most often imperil the growth of foetus and adrenal glands are diabetes and hypertension in pregnancy. A consequence of the maternal diabetes may be macrosomy of foetus manifested by increase in foetal body mass and enlargement of organs sensitive to increased concentration of insulin in the foetal blood [6], i.e., the liver, fat tissue, lungs, adrenal glands, heart. Brown and Singer (1988) [2] established that adrenal glands of foetus are imperiled in pregnancies complicated by mother's hypertension. Their conclusion was derived from pathologic findings in foetuses from unsuccessful pregnancies of patients with hypertension. The glands were of reduced sizes. The way to perform precise measuring of glands, which are of dilapidated composition during post mortem examination, is not quite acceptable, since during the manipulation the size may, to some degree, be altered. By introduction of the ultrasound method in medical practice the problem of biometry has been overcome. Besides measuring, of great importance for the study of physiology of the gland is also the analysis of the foetal fluid and foetal blood. The first successful measuring of the adrenal gland of foetus by ultrasound was performed in mid 80s of the last century by Jeanty and Romero [3] via transabdominal path. The aim of our study is the comparison of foetal adrenal glands in normal and high-risk pregnancies. MATERIAL AND METHODS: During a prospective follow-up carried out at the Institute of Gynaecology and Obstetrics, Clinical Centre of Serbia, 213 patients, aged from 19 to 44 years were examined. Gestation periods were from the 11th to the 40th week. We divided the patients in 3 groups. The first group consisted of 131 patients with no pathologic changes and whose children were born alive. The second group was formed of 75 pregnant women in whom the course of pregnancy was impaired and disorders in the foetal. From these pregnancies the children were born alive. The third group was composed of 7 patients in whom abortion was indicated. The measured values of foetal adrenal glands diameter in the first group (131 patients), were used for making a nomogram of the glands growth. The measuring was performed with ultrasound apparatus "Toshiba 100 SSA". Transabdominal examination with a probe of 3.75 MHz and transvaginal examination with probes of 5 and 7 MHz were performed. Since the picture of the adrenal gland resembled an ellipse, on the basis of measured diameters and using the formula for circumference of this geometric figure [O = (d1 + d2) x pi/2], we obtained the desired value, which increased with advancement of pregnancy. Patients included in the study were with one-foetus pregnancy, whose last menstruation was precisely dated. Data are presented in a chart. For analysis of the obtained data, in addition to parameter methods, we also used the linear correlation and regression and one-factor analysis of variance. Data base analysis was made in the SPSS for DOS package. RESULTS: In making a nomogram of adrenal glands growth of a foetus old between 11 and 40 weeks, 131 of 213 patients were included, while the other foetuses were excluded as they belonged to high-risk pregnancies. Correlation of the growth of adrenal glands circumference and gestation period of pregnancy are also highly statistically important. The correlation coefficient of the straight line which represents this dependancy, is R = 0.8916, for the significance level of p < 0.01 (GRAPH 1). We observed how the course of pregnancy influenced the growth of foetal adrenal gland in normal pregnancies and in foetuses impaired by a pathological pregnancy course. By the method of one-way variance analysis, we obtained the value of the test, which was F = 2.79; p = 0.07. The graphical presentation of adrenal glands of a foetus in the appropriate week of gestation revealed that dimensions of glands in pregnancies impaired by diabetes were larger than those in normal gestations, and that they were at the top of border value of +2 SD or even over this limit. The statistically obtained value was F = 1.81; p > 0.05 (p = 0.06 and it was close to the border value for the significance level of p < 0.05); however, for glands of pregnancies complicated with hypertension the value was F = 1.61; p = 0.063 and the border value near -2 SD. Data are presented in a chart, regarding nomograms and adrenal glands of risk pregnancies. DISCUSSION: In 1993 Bronstein and colleagues [1] proved that the route of visualization of an adrenal gland was not only transabdominal. They succeeded in detecting the glands by transvaginal ultrasound examination in the 12th week. Jeanty and Romero [3] performed a successful transabdominal visualization in the 23rd week of gestation. By ultrasound prenatal examination we can determine the existence of hyperplasia of adrenal glands (Kelnar 1993) [5]. With ultrasound examination we can also diagnose tumours of the medulla, such as neuroblastoma (Jennings and colleagues 1993) [4]. In our study we reported on the visualization and growth of foetal adrenal glands in the period from the 11th to the 40th week of gestation. We presented the growth of foetal adrenal glands in normal gestations with the growth nomogram. The coefficient of correlation of adrenal glands circumference was R = 0.8916. The level of significance was p < 0.01. In conclusion, we can say that risk factors in pregnancy could impair the growth of adrenal glands. We have found that foetal adrenal glands in pregnancies impaired with maternal diabetes were hypertrophic, while those in pregnancies impaired with hypertension were almost at hypotrophic border. The nomograms of adrenal glands growth were of clinical importance, since they help us to control the state of a foetus in high-risk pregnancies. CONCLUSION: Improvement of the methods used in prenatal diagnosis will contribute to a timely detection of a diseased foetus, and will be the first step in its recovery. Regulating the pathological condition of the mother will surely contribute to decrease the risk of delivering children with an increased risk of morbidity.

Adrenal Glands↗
PubMed2002

Adrenal insufficiency in critically ill patients with human immunodeficiency virus.

OBJECTIVE: The adrenal gland is the endocrine organ most commonly involved in patients infected with human immunodeficiency virus (HIV). It is important to recognize patients with adrenal insufficiency, because this disorder may be fatal if untreated. The incidence of adrenal insufficiency in critically ill HIV-infected patients is unclear, partly because different criteria are used to diagnose adrenal insufficiency. To help clarify the incidence of adrenal insufficiency in HIV-infected critically ill patients, we compared the incidence based on the stress cortisol concentration, low-dose corticotropin stimulation test, and high-dose corticotropin stimulation test. SETTING: Medical intensive care unit. PATIENTS: Twenty-eight critically ill patients with HIV, mean age 43 +/- 9 years; 20 were male; 54% died. INTERVENTIONS: We performed a 1-microg (low-dose adrenocorticotropic hormone; LD-ACTH) and 249 microg (high-dose; HD-ACTH) corticotropin stimulation test in HIV-infected critically ill patients not receiving corticosteroids. According to results of the stress serum cortisol concentration and LD-ACTH and HD-ACTH tests, patients were classified as having adrenal insufficiency or as normal. The results of newly revised diagnostic criteria for adrenal insufficiency (i.e., stress cortisol concentration and cortisol response to LD-ACTH <25 microg/dL) were compared with the traditional criteria (i.e., stress cortisol level and response to HD-ACTH <18 microg/dL). In addition, the associations between adrenal insufficiency and the CD4 count, human cytomegalovirus antigenemia, and other risk factors for adrenal insufficiency were determined. MEASUREMENTS AND MAIN RESULTS: When we used a stress cortisol concentration <18 microg/dL as the sole diagnostic threshold for diagnosis of adrenal insufficiency, 50% (14 of 28) of patients had adrenal insufficiency. The incidence was 75% (21 of 28) when we used a diagnostic threshold of <25 microg/dL for the stress cortisol concentration. When we used both the stress cortisol concentration and LD-ACTH test with a diagnostic cortisol threshold concentration <18 microg/dL, 21% (six of 28) had adrenal insufficiency. The incidence was 46% (13 of 28) when we used a cortisol diagnostic threshold concentration of <25 microg/dL. When we used both the stress cortisol concentration and the HD-ACTH stimulation test with a diagnostic cortisol threshold of <18 microg/dL, 7% (two of 28) had adrenal insufficiency. The incidence of adrenal insufficiency was 21% (six of 28) with a cortisol diagnostic threshold value of <25 microg/dL. Human cytomegalovirus antigenemia was the only variable assessed that was associated with adrenal insufficiency. CONCLUSION: There is a high incidence of adrenal insufficiency in critically ill HIV-infected patients that varies with the criteria used to diagnose adrenal insufficiency. The LD-ACTH stimulation test is more sensitive than the high-dose test for diagnosing adrenal insufficiency in this population. Because of the high incidence of inadequate adrenal function, all critically ill HIV-infected patients should undergo an evaluation for adrenal insufficiency with the stress cortisol concentration and LD-ACTH stimulation tests.

Adrenal Gland Diseases↗
PubMed2006

Adrenal-exhaustion syndrome in patients with liver disease.

OBJECTIVE: Adrenal failure is emerging as an important cause of excess morbidity and mortality in critically ill patients. We have recently reported the high incidence of adrenal failure in patients with liver disease, the so called "hepato-adrenal syndrome." It has been noted that patients who on initial testing may have "normal" adrenal function subsequently progress to overt adrenal failure, the adrenal-exhaustion syndrome. The goal of this study was to further characterize this syndrome. DESIGN: Retrospective review of the "Hepatic Cortisol Research and Adrenal Pathophysiology Study" database. SETTING: Liver transplant ICU of a tertiary care university hospital. PATIENTS AND METHODS: Patients who on initial testing had "normal" adrenal function were followed, and adrenal function testing was repeated in those who failed to improve. The patients were grouped as follows: (1) patients who developed adrenal failure on follow-up testing; and (2) patients who had normal adrenal function during their ICU stay. The incidence and risk factors for the development of adrenal-exhaustion syndrome were determined. MEASUREMENTS AND RESULTS: The study cohort consisted of 221 patients, of whom 120 (54%) were diagnosed with adrenal insufficiency on initial diagnostic testing and were excluded from further analysis. The remaining 101 patients comprised those who made up the group of interest. On follow-up, 16 (16%) of these developed adrenal failure a mean of 3 days after initial testing. The only factor that predicted the development of adrenal-exhaustion syndrome was a low HDL level (p<0.001). CONCLUSION: This study demonstrates that adrenal failure is a dynamic process and that repeat adrenal function testing is indicated in patients who remain hemodynamically unstable or fail to improve with aggressive supportive treatment. Low HDL levels may be pathogenetically linked to the development of adrenal failure.

Adrenal Cortex Function Tests↗
PubMed1998

Immunohistochemical staining of normal, hyperplastic, and neoplastic adrenal cortex with a monoclonal antibody against alpha inhibin.

AIMS: To investigate the immunohisto-chemical staining of normal, hyperplastic, and neoplastic adrenal cortex with a monoclonal antibody against alpha inhibin. Also, to determine whether immunostaining with this antibody is useful in differentiating between adrenal cortical neoplasms and other tumours involving the adrenal gland that might mimic them. METHODS: Normal adrenal tissue (n = 20) and specimens from cases of adrenal hyperplasia (n = 13), adrenal cortical adenoma (n = 15), adrenal cortical carcinoma (n = 4), phaeochromocytoma (n = 8), and adrenal metastatic tumour (n = 7) were stained with a monoclonal antibody against the alpha subunit of human inhibin. RESULTS: Positive staining with the anti-alpha inhibin monoclonal antibody was seen in all normal adrenal glands. Immunoreactivity was largely confined to the inner cell layers of the adrenal cortex, with no staining of the adrenal medulla. All hyperplastic adrenal glands and adrenal cortical adenomas and carcinomas were also immunoreactive. The other tumours studied were negative. CONCLUSIONS: There is consistent immunoreactivity with the anti-alpha inhibin monoclonal antibody in normal adrenal cortex and in hyperplastic and neoplastic adrenal cortical lesions. In the normal adrenal cortex, positive staining is mainly confined to the zona reticularis. Other neoplasms involving the adrenal gland are negative. Immunohistochemical staining with anti-alpha inhibin monoclonal antibody, performed as part of a panel, may prove to be of value in the distinction between adrenal cortical carcinoma and phaeochromocytoma or metastatic tumour.

Adrenal Cortex↗
PubMed2001

Adrenal incidentalomas: surgical treatment in 28 patients and update of the literature.

INTRODUCTION: Adrenal masses discovered by imaging techniques for reasons unrelated to adrenal diseases are called adrenal incidentalomas (Al). The aim of this study was to find out the clinical outcome of 28 patients operated for incidentally discovered adrenal mass and to update the literature concerning this topic. PATIENTS AND METHODS: From September 1976 to December 1999 we operated on 28 patients for adrenal incidentaloma. Adrenal masses were unilateral in 25 cases and bilateral in 5. Average age was 57 years (range 10-73). Hormonal study was performed in all patients. All patients underwent adrenalectomy by the transabdominal subcostal approach. RESULTS: Histopathology assessed the adrenal masses as primary in 19 patients and secondary in 9. 24-hour urinary vanillylmandelic acid (VMA) excretion was elevated in 2 patients. Adrenal insufficiency was detected in 1 case. Average tumor diameter resulted 5.8 cm (range 2-17). Histopathologic features of primary adrenal masses included pheochromocytoma in 5 cases, cysts in 4, myelolipomas in 3. nodular hyperplasia in 2, tuberculous mass in 1, cortical adenoma in 1, extra-bone marrow hemopoiesis in 1, cortical carcinoma in 1 and neuroendocrine tumor of the adrenal medulla in 1. The 9 adrenal metastasis resulted by renal cell carcinoma in 7 patients, urothelial carcinoma of the upper urinary tract in I and primary renal lymphoma in 1. Average follow-up was 68 months (range 6-246). Patients alive were 18 (64%), deal 10 (36%). Of the 19 patients with primary adrenal tumors 16 (84%) were alive and disease free and 3 (16%) died (I for disease and 2 for reasons unrelated to the primary tumor). Of the 9 patients with adrenal metastasis 2 (22%) were alive (I disease free and I with progression of the disease) and 7 (78%) died for disease. Replacement therapy for adrenocortical hormones was given 5 patients. CONCLUSIONS: Management of Al need CT or MRI and hormonal investigation in order to detect malignancy and subclinical hypersecretory syndromes. Subclinical functional adrenal masses, single adrenal metastasis and primary nonhypersecretory adrenal tumors sized 4 cm are treated by surgery. A close morpho-functional follow-up is indicated for primary adrenal incidentalomas when nonhypersecretory and smaller than 4 cm.

Adolescent↗
PubMed1987

Neural control of adrenal medullary and cortical blood flow during hemorrhage.

Hemorrhagic hypotension produces an increase in adrenal medullary blood flow and a decrease in adrenal cortical blood flow. To determine whether changes in adrenal blood flow during hemorrhage are neurally mediated, we compared blood flow responses following adrenal denervation (splanchnic nerve section) with changes in the contralateral, neurally intact adrenal. Blood pressure was reduced and maintained at 60 mmHg for 25 min by hemorrhage into a pressurized bottle system. Adrenal cortical blood flow decreased to 50% of control with hemorrhage in both the intact and denervated adrenal. Adrenal medullary blood flow increased to four times control levels at 15 and 25 min posthemorrhage in the intact adrenal, but was reduced to 50% of control at 3, 5, and 10 min posthemorrhage in the denervated adrenal. In a separate group of dogs, the greater splanchnic nerve on one side was electrically stimulated at 2, 5, or 15 Hz (n = 4 each group) for 40 min. Adrenal medullary blood flow increased 5- to 10-fold in the stimulated adrenal but was unchanged in the contralateral, nonstimulated adrenal. Adrenal cortical blood flow was not affected by nerve stimulation. We conclude that activity of the splanchnic nerve profoundly affects adrenal medullary vessels but not adrenal cortical vessels and mediates the observed increase in adrenal medullary blood flow during hemorrhagic hypotension.

Adrenal Cortex↗
PubMed1992

Inherited congenital adrenal hyperplasia in the rabbit: absent cholesterol side-chain cleavage cytochrome P450 gene expression.

We investigated adrenal steroidogenic enzymes, their activity and mRNA expression, and in vitro biosynthesis of an enzyme in rabbits with congenital adrenal hyperplasia (CAH; weight: CAH, 19 +/- 5 mg/adrenal; normal, 2.7 +/- 1.0 mg/adrenal). Serum pregnenolone (delta 5-P) levels in CAH newborn rabbits (12-36 h) were normal (mean/range, 438/51-2191 ng/dl), but corticosterone levels were low [0.05 +/- 0.05 microgram/dl; P less than 0.001 vs. normal (0.66 +/- 0.57)]. Serum Na+ levels in CAH newborn rabbits were in the normal range (143 +/- 30 meq/liter), but K+ levels were elevated [7 +/- 1.1 meq/liter; P less than 0.05 vs. normal (5.9 +/- 0.6 meq/liter)]. Minced normal adrenal tissue incubated with [3H] cholesterol (30-100 pmol/flask) and ACTH (100 mU/flask) produced [3H]delta 5-P (newborn, 21 and 45 fmol/100 mg; adult, 3 and 5 fmol/100 mg) and [3H]corticosterone (newborn, 23 fmol/100 mg; adult, 11.3 fmol/100 mg), but CAH adrenals produced no product (less than 1.3 fmol/100 mg). Adrenal mitochondria from normal newborn rabbits produced delta 5-P (4.4-7 nmol/mg protein), but CAH adrenals did not, while CAH adrenal mitochondria demonstrated over 4 times greater 11 beta-hydroxylase activity. A Western blot of adrenal homogenate from normal newborn rabbits revealed a cholesterol side-chain cleavage cytochrome P450 (P450scc)-immunoreactive species (mol wt, 53 x 10(3), but this species was absent in CAH adrenals; CAH adrenals had a normal adrenodoxin and intensified 17 alpha-hydroxylase cytochrome P450 (P450(17)alpha) band compared to normal adrenals. In vitro translation of RNA in a cell-free rabbit reticulocyte lysate system containing [35S] methionine yielded a precursor P450scc protein (mol wt, 58.5 x 10(3)) with normal adrenal RNA, but not with CAH adrenal RNA. P450scc mRNA was detected in all normal adrenals, but was not detected in all CAH adrenals. 21-Hydroxylase cytochrome P450 mRNA expression was detected at a similar level in both normal and CAH adrenals. We conclude that CAH in the rabbit is caused by inherited absent P450scc gene expression. The clinical, pathological, and biochemical manifestations of P450scc deficiency in the rabbit are nearly identical to the human disorder. Increased 11 beta-hydroxylase activity and increased P450(17)alpha on Western blot of CAH adrenals indicate altered gene expression of other steroidogenic enzymes due to CAH. Further molecular analysis of the P450scc gene in this animal CAH model will facilitate understanding of P450scc deficiency CAH.

Adrenal Glands↗
PubMed2002

Role of ultrasonography in the detection of small adrenal masses.

AIM: Computed tomography (CT) scanning is commonly used for evaluation of adrenal masses in adults. In this prospective study we evaluated whether adrenal gland masses of less or equal than 20 mm in diameter could be detected by modern abdominal ultrasonography (US). METHOD: Between July 1999 and June 2000, 44 consecutive patients with 50 adrenal masses documented by contrast-enhanced CT (left adrenal gland, n = 31; right adrenal gland, n = 19; bilateral, n = 6; median size, 15 [5 +/- 80] mm) and, additionally, 50 patients without CT findings of an adrenal mass were prospectively evaluated by high-resolution US performed by physicians. Based upon CT measurement, 34 adrenal masses were </= 20 mm and 16 were > 20 mm in diameter. RESULTS: The overall sensitivity of US for the detection of adrenal masses was 96 % (48/50) (94 % [29/31] for left and 100 % [19/19] for right adrenal masses, respectively). The overall specificity of US for the detection of adrenal masses was 92 % (92/100) (90 % [45/50] for left and 94 % [47/50] for right adrenal masses, respectively). Thus, the diagnostic accuracy of US for the detection of adrenal masses is 93 % (140/150). Sensitivity and specificity of US for the detection of adrenal masses </= 20 mm (n = 34) did not differ significantly from those > 20 mm (n = 16). CONCLUSION: US is effective for detecting small adrenal masses. In rare cases small masses of the left adrenal gland might be missed and nodular adrenal hyperplasia or retroperitoneal lymph nodes might be misinterpreted as adrenal masses.

Adrenal Gland Neoplasms↗