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At least 127 records · Page 7Linked to original sources
PubMed1996

A case of silent 21-hydroxylase deficiency with persistent adrenal insufficiency after removal of an adrenal incidentaloma.

A case of an adrenal incidentaloma in a 57-year-old man with silent 21-hydroxylase deficiency is reported. Abdominal computed tomography revealed a right adrenal tumour of 6cm in diameter. There was no evidence of adrenal hormone excess. However, after surgical removal of the adrenal tumour, the patient developed acute adrenal insufficiency. Adrenocortical function has remained low ever since surgery. Pathological examination of the tumour revealed a cortical adenoma. On the basis of increased plasma renin activity and serum 17 alpha-hydroxyprogesterone concentration and decreased 21-hydroxylase activity of the adenoma tissue, the patient was diagnosed as having systemic 21-hydroxylase deficiency. There are two possible mechanisms for the persistent adrenal insufficiency; first the residual left adrenal gland may have been originally hypo-functioning for some reason and, second, the left gland may have lost the ability to regenerate following prolonged suppression by the adenoma. In cases of adrenal incidentalomas with 21-hydroxylase deficiency, the indications for surgical removal should be carefully considered.

Adenoma↗
PubMed2004

High expression of neuropeptide y receptors in tumors of the human adrenal gland and extra-adrenal paraganglia.

PURPOSE: Recently, a role of neuropeptide Y (NPY) in tumor biology was suggested based on the high density of NPY receptors in breast and ovarian cancers. The high frequency of NPY receptors in steroid hormone-producing ovarian sex cord-stromal tumors, together with the known influence of NPY on steroid hormone and catecholamine secretion in the rodent adrenal gland, led to the investigation of NPY receptor expression in the human adrenal gland and related tumors. EXPERIMENTAL DESIGN: Fifteen adrenal cortical tumors, 20 paragangliomas, 23 pheochromocytomas, 20 neuroblastomas, and 8 normal adrenal glands were investigated by in vitro NPY receptor autoradiography using 125I-labeled peptide YY in competition experiments with receptor subtype selective analogs. RESULTS: Ninety three percent of cortical tumors express Y1, 35% of pheochromocytomas and 61% of paragangliomas express Y1 and Y2, and 90% of neuroblastomas express Y2 receptors. The NPY receptors in pheochromocytomas, paragangliomas, and neuroblastomas are often expressed concomitantly with the NPY hormone detected immunohistochemically. The adrenal cortex strongly expresses Y1, whereas no NPY receptors are found in the adrenal medulla. CONCLUSIONS: These receptor data suggest a role of NPY in adrenal cortical tumors and, together with the strong NPY innervation of the cortex, a physiologic role in the adrenal gland, mediated by Y1 receptors. These NPY receptors are a potential new molecular target for the therapy of malignant tumors.

Adrenal Cortex Neoplasms↗
PubMed1976

Sex differences in adrenocortical structure and function. III. The effects of postpubertal gonadectomy and gonadal hormone replacement on adrenal cholesterol sidechain cleavage activity and on steroids biosynthesis by rat adrenal homogenates.

In rats postpubertal orchiectomy results in an increase in the adrenal weight, testosterone replacement restores the adrenal weight to the normal level. Neither ovariectomy (8 weeks of duration) nor estradiol replacement has an effect on adrenal weight in female rats. Pregnenolone synthesis as well as corticosterone and blue tetrazolium-positive steroids secretion is significantly higher in homogenates of adrenals from female rats than from males. Orchiectomy results in a marked increase in pregnenolone biosynthesis, testosterone replacement restores the value to the normal levels. Neither ovariectomy nor estradiol replacement has an effect on pregnenolone synthesis in v i t r o. In both sexes gonadectomy causes a marked decrease in corticosterone output by adrenal homogenates, concomitantly the increase in the adrenal 5alpha-reductase activity is observed. The ratio of secreted corticosterone to pregnenolone is significantly lower in gonadectomized rats of both sexes than in control animals. Estradiol or testosterone replacement inhibits the adrenal 5alpha-reductase activity and restores the corticosterone output as well as corticosterone/pregnenolone ratio to the normal values. The above described findings show that the sex differences in steroids secretion by the rat adrenal are partially conditioned by a cholesterol sidechain cleavage activity. Testosterone inhibits this activity while estradiol under applied experimental conditions has no effect on the cholesterol sidechain cleavage activity.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1989

Adrenal insufficiency after operative removal of apparently nonfunctioning adrenal adenomas.

We describe a woman who developed adrenal insufficiency after removal of an apparently nonfunctional adrenal adenoma. She displayed no stigmata of Cushing's syndrome and had normal plasma and urinary cortisol levels. A second patient without clinical findings of Cushing's syndrome also had normal basal steroid levels. This patient displayed partial suppressibility with dexamethasone, had low-normal levels of serum corticotropin, and excreted a low concentration of urinary 17-ketosteroids. She also developed mild adrenal insufficiency after the operation. We believe the adrenal adenomas in these patients secreted enough cortisol to suppress the contralateral adrenal gland but not enough hormone to elevate basal steroid levels. Therefore, we suggest that all patients with adrenal masses be studied with the overnight dexamethasone suppression test rather than basal steroid hormone measurements to detect low levels of autonomous cortisol secretion. In addition, patients with adrenal masses that are not removed surgically should have serial adrenal function tests performed.

Adenoma↗
PubMed1997

Prevalence of adrenal carcinoma among incidentally discovered adrenal masses. A retrospective study from 1989 to 1994. Gruppo Piemontese Incidentalomi Surrenalici.

BACKGROUND: The incidental discovery of an adrenal mass poses the problem of distinguishing between the frequent benign masses and the infrequent malignant ones that require surgery. Univocal guidelines to approach this problem are unavailable. OBJECTIVE: To perform a survey of the clinical management of incidentally discovered adrenal masses (ie, adrenal incidentalomas). DESIGN: A multicentric retrospective analysis of hospital medical records of adrenal incidentalomas diagnosed during a 5-year period; the medical records were scrutinized for demographic data and clinical details by means of a specifically tailored questionnaire. SETTING: The major surgical and medical centers of Piedmont, a northern Italian region with approximately 4 million inhabitants. The recruitment pattern of these centers was unselected. PATIENTS: The definition of adrenal incidentaloma was limited to patients with a physical examination and a clinical history unindicative of adrenal disease. Exclusion criteria also included hypertension of suspected endocrine origin and a history of neoplasms known to metastasize frequently in the adrenal glands. Two hundred twenty-four medical records were collected, and 210 were analyzed (14 excluded a posteriori). RESULTS: Most patients were in their 50s and 60s, and women were predominantly affected. The frequency of adrenocortical cancer was 13% among patients operated on. The tumor diameter was highly correlated with the risk of cancer; a cutoff at 5 cm had a sensitivity of 93% with a specificity of 64% in discriminating between benign and malignant cortical lesions. CONCLUSIONS: The occurrence of adrenocortical carcinoma among adrenal incidentalomas is not rare. The evaluation of the mass size is a simple and effective method for selecting patients at risk for cancer. The indication for surgery of masses larger than 5 cm, or of masses of any diameter that have suspicious imaging characteristics, limits unnecessary operations and costs.

Adrenal Gland Diseases↗
PubMed1993

Comparison of the adrenalytic activity of mitotane and a methylated homolog on normal adrenal cortex and adrenal cortical carcinoma.

Mitotane is an important adrenalytic drug for the treatment of adrenal cancer whose use is limited by toxicity. Reports from another laboratory indicated that a methylated homolog of Mitotane (Mitometh) tested in guinea pigs possessed comparable adrenalytic activity but was less toxic than Mitotane. This observation prompted us to undertake a comparative study of these two drugs on the basis that Mitometh may be a superior agent for the treatment of adrenal cancer. Preliminary studies in guinea pigs failed to show a significant adrenalytic effect for either Mitotane or Mitometh. Thus, we extended the study to 13 mongrel dogs weighing 12-15 kg that were treated daily with Mitometh or Mitotane (50-100 mg/kg) for 6 or 12 days. Cortisol decreased to undetectable levels and adrenocorticotropic hormone (ACTH) rose to 10 times the baseline levels within 72 h in Mitotane-treated animals. Despite the achievement of similar drug levels, Mitometh treatment in dogs failed to suppress cortisol or increase ACTH. To determine whether these differences were due to differences in bioavailability, we measured the relative concentration of Mitotane and Mitometh in homogenates of adrenal cortex obtained from Mitotane- and Mitometh-treated dogs. The adrenal concentration of Mitometh determined in Mitometh-treated dogs was 5 times higher than the concentration of Mitotane measured in Mitotane-treated animals. Whereas the adrenal glands of Mitotane-treated dogs showed hemorrhage and necrosis, the Mitometh-treated animals showed no adrenal damage. Despite the lack of adrenalytic activity, Mitometh maintained its toxicity as demonstrated by microscopic evidence of hepatic necrosis and an increase in hepatic enzymes. The adrenalytic effects of both agents was also studied in vitro using a human functioning adrenal cortical carcinoma cell line, NCI-H295. Whereas Mitotane strongly suppressed cell growth, Mitometh had a weaker effect. We conclude that Mitometh is not likely to be effective in the therapy of adrenal cancer. Moreover, the results of this study are supportive of the view that metabolic transformation of Mitotane is in some way linked to its adrenalytic action.

Adrenal Cortex↗
PubMed2004

Prevalence of ovarian adrenal rest tumours and polycystic ovaries in females with congenital adrenal hyperplasia: results of ultrasonography and MR imaging.

The aim of the investigation was to assess the prevalence of ovarian adrenal rest tumours and polycystic ovaries in female patients with congenital adrenal hyperplasia (CAH). Thirteen female CAH patients (median age 19.8 years, range 14.8-23.5 years) underwent transvaginal (n=6) or transabdominal (n=7) ultrasonography by a gynaecologist and MR imaging (n=13) of the ovaries (pre and post contrast-enhanced T1- and T2-weighted images). Ovarian adrenal rest tumours were defined as small hypoechoic and multifocal nodules on ultrasound and isointense lesions on T1- and hypointense on T2-weighted MR images (derived from characteristics of testicular adrenal rest tumours). Polycystic ovaries were defined as the presence of > or = 10 follicles arranged peripherally around or scattered throughout increased stroma. No ovarian adrenal rest tumours were found either on ultrasound, or by MR imaging. Polycystic ovaries were found in 2 of the 13 patients (15.4%), both with ultrasound and MR. No ovarian adrenal rest tumours were detected in these female CAH patients, which suggests that ovarian adrenal rest tumours in CAH females are rare. The prevalence of polycystic ovaries corresponded to that in the general population. From these results, we would suggest that routine ovarian imaging in CAH females is not indicated. However, when ovarian dysfunction is present, ovarian imaging is advised, first by ultrasonography, to detect ovarian adrenal rest tumours or polycystic ovaries.

Adolescent↗
PubMed1994

Effects of neuromedin U (NMU)-8 on the rat hypothalamo-pituitary-adrenal axis. Evidence of a direct effect of NMU-8 on the adrenal gland.

A 6-day subcutaneous (s.c.) treatment of adult rats with NMU-8 (1.5 or 6 micrograms/100 g/day) increased the average volume of zona fasciculata cells and decreased the number of zona reticularis cells in the adrenal cortex. The lower dose of NMU-8 did not change blood ACTH concentration and adrenal weight, but it notably enhanced serum corticosterone level and basal corticosterone output by adrenal slices. ACTH blood level increased after ether stress in both control and NMU-8-treated rats, but stress-evoked rise in serum corticosterone was observed only in control rats. The higher dose of NMU-8 increased the level of circulating ACTH; however, it decreased adrenal weight and had no effect on serum corticosterone concentration and basal corticosterone output by adrenal slices. NMU-8 (10(-10)/10(-6) M) did not affect basal and ACTH-stimulated corticosterone yield by isolated adrenocortical cells, nor did it change their cytosolic Ca2+ concentration. NMU-8 (10(-8) M) markedly raised basal corticosterone secretion by adrenal slices (including cortex and medulla); higher concentrations of NMU-8 (10(-7)/10(-6) M) were ineffective on basal corticosterone secretion, but strongly inhibited the response to ACTH stimulation. On the ground of these findings it seems reasonable to suggest that NMU-8 exerts a biphasic effect on the function of the peripheral branch of the hypothalamo-pituitary-adrenal axis in rats: NMU-8 at low doses directly stimulates the function and growth of the adrenal cortex, while at high doses exerts a direct inhibitory action.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed2006

[Acute adrenal insufficiency during unilateral adrenal hemorrhage secondary to the antiphospholipid syndrome].

INTRODUCTION: Acute adrenal insufficiency during antiphospholipid syndrome is usually due to a bilateral adrenal hemorrhage. For a patient, an unilateral involvement has induced an acute adrenal insufficiency. CASE REPORT: A patient with an antiphospholipid syndrome has developed an acute adrenal insufficiency with an unilateral adrenal hemorrhage. This complication was caused by a concurrent steroid therapy, for an associated lupus, which resulted in a suppression of the contralateral adrenal gland. CONCLUSION: In patients with antiphospholipid syndrome and concurrent steroid therapy, usually for lupus, unilateral adrenal hemorrhage can cause acute adrenal insufficiency. Withdrawal of steroid might be difficult in case of undetected bilateral hemorrhage.

Adrenal Cortex Hormones↗
PubMed2003

Molecular pathogenesis of lipoid adrenal hyperplasia and adrenal hypoplasia congenita.

Congenital lipoid adrenal hyperplasia (lipoid CAH) is the most severe form of CAH in which the synthesis of all gonadal and adrenal cortical steroids is markedly impaired. Lipoid CAH may be caused by the defect in either the steroidogenic acute regulatory (StAR) protein or the P450scc. More than 34 different mutations in StAR gene have been identified. Clinically, most of the patients manifest adrenal insufficiency from 1 day to 2 months of age, but some patient show delayed onset of adrenal insufficiency. Affected 46, XY subjects do not show pubertal development, whereas affected 46, XX subjects undergo spontaneous feminization, breast development and cyclical vaginal bleeding at the usual age of puberty. X-linked adrenal hypoplasia congenital (AHC) is a rare congenital adrenal disorder characterized by severe adrenal insufficiency and hypogonadotropic hypogonadism. More than 80 different several intragenic mutations of DAX-1 have been identified. The failure of pubertal development may be caused by either abnormal hypothalamic or pituitary regulation of gonadotropin secretion. In addition, although the testicular steroidogenesis is largely intact, the functional maturity of Sertoli cells and also spermatogenesis are impaired. The type of mutation does not predict clinical phenotype. Thus, unified mechanism how DAX-1 gene defect gives rise to adrenal insufficiency, hypothalamic/pituitary hypogonadism and impaired spermatogenesis remains established.

Adrenal Gland Diseases↗
PubMed2000

Oral glucose tolerance testing but not intravenous glucose administration uncovers hyper-responsiveness of hypothalamo-pituitary-adrenal axis in patients with adrenal incidentalomas.

OBJECTIVE: Modern imaging techniques are detecting adrenal incidentalomas with increasing frequency. Recent data suggests food-dependent hypercortisolism in a subgroup of patients with bilateral macronodular hyperplasia due to aberrant adrenal responsiveness to gastric inhibitory polypeptide (GIP). We studied the putative influence of food intake on the hypothalamo-pituitary-adrenal (HPA) axis in patients with adrenal incidentalomas and possible mediation by GIP. PATIENTS AND MEASUREMENTS: We examined 15 mildly obese patients with adrenal incidentalomas, eight healthy, lean subjects, and seven obese patients with the metabolic syndrome, who were matched for body weight and age. Each individual underwent oral glucose tolerance testing (OGTT, 75 g glucose), i.v. glucose administration (IVGTT, 30 g glucose over 1 h) and i.v. glucose plus GIP infusion (body weight adapted leading to physiological postprandial GIP serum levels) on three occasions. Plasma glucose, ACTH and cortisol were measured from blood samples taken every 15 minutes from time - 30 minutes to + 75 minutes. RESULTS: OGTT, i.v. glucose administration and GIP infusion led to comparable glucose values within the groups. In contrast to normal subjects and patients with the metabolic syndrome, patients with adrenal incidentalomas had significantly higher mean cortisol values after oral glucose intake as compared to i.v. glucose administration or GIP infusion. The increase in cortisol levels was preceded by a corresponding ACTH increase. No significant effect of GIP administration on cortisol or on ACTH secretion could be detected. CONCLUSIONS: Patients with adrenal incidentalomas showed an abnormal responsiveness of the pituitary-adrenal axis to oral glucose administration. The cortisol peaks in these patients seemed to be ACTH-mediated and were not induced by GIP.

Adenoma↗
PubMed1980

Oestrogen dynamics in adrenal venous effluents in congenital virilizing adrenal hyperplasia.

Four patients with untreated congenital virilizing adrenal hyperplasia (partial 21-hydroxylase deficiency) were studied by bilateral adrenal vein catheterization. Simultaneous right and left adrenal and peripheral blood samples were collected for determination of oestrone (E1) and oestradiol (E2). The concentrations of both were higher in the adrenal effluents than in the peripheral blood samples, indicating their secretion by the adrenals. All patients were also studied during a sequential test of suppression (0.5 h after i.v. administration of 4 mg dexamethasone) and stimulation (5 min after i.v. administration of 250 microgram ACTH 1-24; Synacthen). Mean peripheral E2 concentrations did not change significantly whereas E1 increased above control levels after stimulation. In contrast, suppression of adrenal venous blood concentrations with dexamethasone, and stimulation with ACTH, was demonstrated for every patient. The results indicate that in congenital adrenal hyperplasia the adrenal glands secrete significant amounts of E1 and E2.

Adolescent↗
PubMed1989

Central regulation of adrenal tyrosine hydroxylase: effect of induction on catecholamine levels in the adrenal medulla and plasma.

The effect of induction of adrenal tyrosine hydroxylase (TH) by various centrally acting drugs on catecholamine levels in adrenal and plasma was investigated in rats. All the drugs tested, namely oxotremorine, Piribedil, B-HT 920, and HA-966, produced significant increases in adrenal dopamine content and plasma epinephrine level. Denervation of the adrenal abolished the increase in adrenal dopamine as it did the induction of tyrosine hydroxylase. The results suggest that the induced increase of adrenal TH activity, as mediated by certain drugs, results in an elevation of the plasma epinephrine level and that the adrenal dopamine content is a better indicator of the catecholamine-synthesizing capacity of the adrenal medulla than are the other catecholamines.

Adrenal Glands↗
PubMed1991

Different roles for the pituitary and adrenal cortex in the control of enkephalin peptide localization and cortico-medullary interaction in the sheep adrenal during development.

We have investigated the effect of adrenocorticotrophic hormone (ACTH) replacement after fetal hypophysectomy on the pattern of localization of enkephalin-containing peptides (enkephalins) and phenylethanolamine N-methyltransferase (PNMT) in the fetal sheep adrenal. We have also investigated the relative roles of the fetal pituitary and adrenal cortex in determining the extent of the interdigitation of the peripheral adrenaline (AD)-containing cells of the adrenal medulla with the inner zones of the adrenal cortex in the late gestation fetus. Fetal hypophysectomy (Hx; n = 12) or sham operations (n = 8) were performed at 109-118d. At 138 or 139d, ACTH (1-24) (10.5 micrograms/h) was infused intravenously for 72 h into 4 Hx fetuses (Hx + ACTH group). Saline was infused for 72 h into 4 Hx fetuses (Hx + Sal) and into 4 sham-operated fetal sheep (Intact + Sal). Fetal adrenal glands were collected at autopsy from 141/2d Intact + Sal, Hx + Sal and Hx + ACTH groups, from 4 intact fetal sheep at 145-147d gestation (145/7d Intact group) and 4 Hx fetal sheep at 147-164d gestation (147/64d Hx group). Adrenals were also collected from 4 newborn lambs at 10-12d after birth (10/12d Newborn group). Using the peroxidase-antiperoxidase immunocytochemical staining method, sections of adrenal glands (10-12 microns) from all groups were stained anti-PNMT. Sections of adrenal glands from the 141/2d groups were also stained separately with anti-dopamine-beta-hydroxylase (anti-D beta H) and anti-enkephalin (anti-ENK).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1980

Demonstration of glucocorticoid receptors in the adrenal cortex: evidence for a direct dexamethasone suppressive effect on the rat adrenal gland.

The adrenal cortex was evaluated for the presence of glucocorticoid receptors and functions. Substantial binding of [3H]dexamethasone was observed in aminoglutethimide-treated, hypophysectomized, and intact rats. Further studies demonstrated binding in cultured bovine adrenocortical cells and in Y-1 cells, a cloned murine cell line of adrenal cortical origin. Scatchard analysis of specific binding data in cytosol from hypophysectomized rats revealed an apparent Kd of approximately 15 nM and a receptor content (Nmax) of 123 fmol/mg cytosol protein. Analysis of Y-1 cell cytosol showed a Kd of approximately 17 nM and Nmax of 190 fmol/mg protein. The binding site in hypophysectomized rats had the following steroid specificities: high affinity for dexamethasone, corticosterone, and progesterone; moderate affinity for 11 beta-cortisol, and low affinity for testosterone, estradiol, pregnenolone, and 11 alpha-cortisol. Sedimentation in sucrose density gradients revealed 8S binding peaks in cytosols prepared from intact rat adrenal glands, Y-1 cells, and cultured bovine adrenocortical cells. Time- and temperature-dependent nuclear uptake of [3H]dexamethasone in Y-1 cells was demonstrated. In vivo treatment of hypophysectomized rats with dexamethasone significantly enhanced the rate of adrenal atrophy. ACTH stimulation tests in hypophysectomized rats showed a decreased corticosterone response in dexamethasone-treated rats compared to that in control animals. However, in vitro, there was no evidence for an effect of dexamethasone on ACTH-stimulated corticosterone production. The data indicate that the adrenal cortex possesses a high affinity binding site that fulfills the criteria for a glucocorticoid receptor. Glucocorticoid administration enhances adrenal atrophy and impairs adrenal function. We speculate that this action contributes to the suppressive effect of glucocorticoids on the pituitary-adrenal axis.

Adrenal Cortex↗
PubMed2000

Effects of aging on adrenal function in the human: responsiveness and sensitivity of adrenal androgens and cortisol to adrenocorticotropin in premenopausal and postmenopausal women.

We sought to determine the effects of aging on several aspects of adrenal steroidogenesis in the hopes of characterizing the possible causes of adrenal androgen deficiency in elderly women. To this end, we quantified basal morning concentrations of cortisol (F), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DS), and androstenedione (A4) and then evaluated the effects of overnight dexamethasone (DEX) suppression followed by adrenal responses to graded hourly infusions of ACTH, ranging from 20-1280 ng/1.5 m2 x h. Finally, we performed a standard 0.25-mg ACTH bolus stimulation test, with sampling at 1 h thereafter. Basal serum levels of DHEA, DS, and A4 were significantly reduced (approximately 50% each) in a group of 35 healthy postmenopausal women, 55-68 yr old, compared to those in 30 healthy, regularly menstruating women, 20-25 yr old. Post-DEX levels of these C19 steroids also were significantly lower in the older women than in the younger women; the percent decrease after DEX for A4 was greater in the older women, whereas those in DHEA and DS were not age related. Basal and post-DEX levels of F were similar in both groups. Secretory responses of DS to ACTH were not informative due to its large plasma pool and slow clearance rate. The maximally stimulated levels of DHEA after ACTH bolus were significantly lower in the older women than in younger women; those of A4 were similar in both age groups, and the maximally achieved levels of F were higher in the older women than in the younger women. The sensitivity of adrenal DHEA, A4, and F to ACTH (defined as the minimal dose of ACTH required to significantly increase the steroid levels above basal post-DEX values) was similar in older and younger women. The responsiveness of the steroids of interest to ACTH (defined as the slope of the dose-response curve over the linear portion of the dose-response curve) also was similar among younger and older women. These data demonstrate that the deficiency in adrenal androgen production in women is restricted to the delta5-pathway steroid products (DHEA and DS), whereas there is no reduction in the capacity of the adrenal to produce A4 or cortisol. As DHEA and DS are likely to be produced mainly in the zona reticularis of the adrenal cortex, we propose that these data point to an alteration in that cortical zone as the cause of adrenal androgen deficiency in aging. The reductions in A4 in aging are probably due to reduced ovarian secretion after menopause.

Adrenal Glands↗
PubMed1990

Transplantation of parathyroid, adrenal cortex and adrenal medulla using procedures which successfully prolonged islet allograft survival.

Life-long hormone replacement therapy is today the only form of therapy for several endocrine insufficiencies. Transplantation of endocrine tissues could represent a more physiological approach to the treatment of different syndromes such as adrenal insufficiency, diabetes or hypoparathyroidism. Successful experimental islet transplantation across major histocompatibility barriers using cultural pretreatment of the insulin producing tissue in conjunction with temporary immunosuppression of the recipients, encouraged us to attempt similar approaches with parathyroids, adrenal cortex and adrenal medulla. Either bilateral parathyroidectomy or bilateral adrenalectomy were performed on the recipient rats before transplantation, followed by the implantation of parathyroid, adrenal cortical or adrenal medullary tissue beneath the renal capsule. The tissue was transplanted either immediately after its dissection or after pretreatment with 1 week culture. Some of the recipients received a short term cyclosporine treatment. The results indicated that parathyroid and adrenal medulla transplants were often infiltrated by mononuclear cells 30 days after transplantation. In contrast, adrenal cortical tissue was well preserved 4 weeks after transplantation, without showing any sign of rejection when a combination of pre-transplant culture of the adrenal tissue and temporary cyclosporine treatment of the recipients was used.

Adrenal Cortex↗