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Results for “Adrenocortical Hyperfunction”

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At least 253 records · Page 14Linked to original sources
PubMed1987

Familial hypersecretion of adrenal androgens transmitted as a dominant, non-HLA linked trait.

Clinical evidence of adrenal androgen hyperfunction (premature pubarche, hirsutism, amenorrhea) occurred in the studied proband, her mother, maternal aunt (twin sisters), and maternal great-grandmother. The basal levels of androgen in the first three were variably elevated. In all the members of this family who were tested, the response of 17-hydroxyprogesterone and progesterone to adrenocorticotropic hormone stimulation was either normal or of the type seen in heterozygotes for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Of particular importance is the fact that neither the proband nor her mother or maternal aunt had the type of response seen in homozygotes presenting the attenuated form of congenital adrenal hyperplasia. The disorder appears to be a familial condition resulting in excessive levels of adrenal androgens beginning during childhood years, causing hirsutism and amenorrhea and interfering with normal pubertal and adult ovarian function. Glucocorticoid therapy suppresses adrenal androgen levels; in two individuals, conception occurred twice in each during such treatment in otherwise amenorrheic individuals. The pattern of transmission of the disorder appears to be either autosomal or X-linked dominant, and not linked to the homologous leucocytic antibodies (HLA) region of the sixth chromosome.

Adolescent↗
PubMed2004

Growth in disorders of adrenal hyperfunction.

This article reviews how growth is affected in disorders of adrenal hyperfunction. Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Adrenal androgens, when in excess, lead to advanced linear growth and skeletal maturation, and prolonged hypercortisolemia leads to the suppression of growth hormone (GH) secretion and inhibition of somatomedin C and other growth factor effects on their target tissues. In virilizing adrenal tumors height is increased at diagnosis, but after surgical cure the final height is usually in the normal range. In congenital adrenal hyperplasia height is usually compromised by advanced skeletal maturation or by suppressed growth, particularly in the first years of life, due to excess glucocorticoid treatment. The final height is reduced in both clinical forms (salt wasting and simple virilizing) and sexes in patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Growth impairment is also the hallmark of Cushing syndrome of whatever etiology when it occurs in children and growing adolescents, and the final height of these patients, even after surgical cure, remains compromised. This is apparently due to direct or indirect growth impairment by the hypercortisolism during the disease, followed by inadequate catch-up growth. Although it seems that GH treatment might be beneficial for improving final height both in patients with congenital adrenal hyperplasia who have poor height predictions and in patients with Cushing disease and GH deficiency, a larger number of studies is needed to confirm this suggestion.

Adrenal Cortex Hormones↗
PubMed2002

Growth in disorders of adrenal hyperfunction.

Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 +/- 0.42 and 1.3 +/- 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m(2)/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4-17.8 years, with Cushing's disease (CD). At diagnosis, mean height SDS was -1.81 (1.2 to -4.17), 53% < -1.8 SDS, height velocity in 6 was 0.9-3.8 cm/year and mean BMI SDS 2.29 (0.7-5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1-108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10-29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 +/- 3.4 years, growth after cure was studied for 9.1 +/- 5.0 years. Nine had no catch-up growth in the interval of 0.3-1.1 years after cure (mean HV 5.3 +/- 2.4 cm/year). All these had GH deficiency peak GH 0.5-20.9 mU/l, and received hGH 2.7 mg/m(2)/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS-target Ht SDS) -1.72 +/- 1.26 improving to -0.83 +/- 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (-2.9 to 3.0), -0.8 (6.0 to 2.2), 0.7 (-7.9 to 9.5) respectively, whereas SHBG was reduced at -2.1 (-5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height.

Adolescent↗
PubMed2002

Adrenal function in the human immunodeficiency virus-infected patient.

Although clinical manifestations of adrenal dysfunction are uncommon in patients infected with human immunodeficiency virus (HIV), subclinical functional abnormalities of the hypothalamic-pituitary-adrenal axis are frequent. Patients infected with HIV usually have higher basal serum cortisol and lower serum dehydroepiandrosterone concentrations than HIV-seronegative individuals. This imbalance has been related to progression of the infection by inducing a shift from T(H)1 to T(H)2 immunologic responses. Although, adrenal reserve may be marginal in HIV-infected patients, clinically evident adrenal insufficiency is uncommon and, when present, it is observed in advanced stages of the infection. Hypocortisolemia should be treated regardless of the existence of associated symptoms. On the contrary, hypercortisolemia in the absence of features of Cushing syndrome is common and should not promote treatment nor specific studies. The possible influence that alterations of the adrenal function could have on the patients' immune status and the eventual effect of antiretrovirals on these alterations merit further investigation.

Adrenal Insufficiency↗
PubMed1978

The diagnosis of Leydig cell tumors in childhood.

We report the clinical and hormonal findings in two boys with isosexual precocity secondary to Levdig cell tumor of the testis. The hormonal profile at the initial evaluation was quite different in the two cases suggesting differences in steroid biosynthesis by the tumors. These differences indicate that a dexamethasone suppression test may be required to differentiate between Leydig cell tumors and congenital virilizing adrenal hyperplasia with adrenal rest tissue located within the testes.

Adrenocortical Hyperfunction↗
PubMed1978

Preadolescent and adolescent endocrinology: physiology and physiopathology. II. Hormonal changes during abnormal pubertal development.

Based on the knowledge of the physiology of regulation of gonadotropins and gonadal steroids, basal levels of these hormones might be indicative of the etiologic factors of abnormal pubertal development. In addition, stimulatory tests may help in the diagnosis of such conditions. It is interesting that the pubertal maturation of the adrenal cortex is independent of the hypothalamic-pituitary-gonadal axis. The role of the adrenal cortex for the pubertal development remains questionable: adrenal androgens are low in isosexual precocious puberty, low in delayed adolescence, and normal in hyper- or hypogonadotropic hypogonadism. The importance of this role is doubled in congenital virilizing adrenal hyperplasia. When the disease is untreated, although adrenal androgens in excess advance bone age and hypothalamic maturation, girls remain prepubertal. When the therapeutic control is good, normal puberty occurs. The action of the adrenal androgens on growth and puberty remains to be determined.

Adolescent↗
PubMed1989

Hypercortisolism among socially subordinate wild baboons originates at the CNS level.

Recent studies suggest that the hypercortisolism and dexamathasone resistance of depression arise, at least in part, at the level of the brain, ie, cortisol-releasing factor (CRF) and/or other corticotropin-secretagogues are hypersecreted. This article suggests a similar cause of the hypercortisolism of social subordinance. Two troops of wild olive baboons, living freely in the Serengeti Ecosystem of East Africa, have been under long-term study. Consistently, in stable dominance hierachies, subordinate males are hypercortisolemic relative to dominant animals. Furthermore, hypercortisolemic males are dexamethasone resistant. There are no rank-related difference in cortisol clearance or adrenal sensitivity to corticotropin, suggesting a pituitary and/or neural locus of the hypercortisolism. Subordinate males were shown to secrete less corticotropin in response to a CRF-challenge than did dominant males. Following the logic used in similar studies with depressives, if subordinate males were hypercortisolemic despite decreased pituitary sensitivity to CRF, then this implies that the hyperactivity of the adrenocortical axis is driven at the level of the brain. Furthermore, subordinate males were hyporesponsive to CRF after administration of metyrapone, which blocks cortisol secretion and disinhibits the pituitary from feedback inhibition. Thus, the pituitary appears to have lost sensitivity to CRF itself in these low-ranking males. These observations are interpreted in light of behavioral data suggesting that these subordinate males are under sustained social stress.

Adrenocortical Hyperfunction↗