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At least 361 records · Page 20Linked to original sources
PubMed1976

Microcysts of the permanent adrenal cortex in perinates and infants,.

Microscopic cysts in the permanent cortices of adrenal glands were studied in a series of 274 infants, some of whom had been stillborn and none of whom were more than 12 months old. After correction for length of gestation, there were no significant relationships between the occurence and number of microcysts and various maternal, placental, and perinatal diseases. A significant direct correlation was demonstrated statistically with shorter gestational period and shorter survival time after birth. We concluded that the adrenal microcysts are either a developmental feature or the result of a greater susceptibility to stress in the fetus and newborn than in older infants.

Adrenal Cortex↗
PubMed1977

Adrenoleukodystrophy (Siemerling-creutzfeldt disease): Heterozygote with two clonal fibroblast populations.

On the fifth day after subcultivation,, fibroblasts of two unrelated patients with adrenoleukodystrophy (Siemerling-Creutzfeldt disease (SCD)) developed typical morphologic anomalies which could be seen by light microscopy. From skin biopsy material of an obligatorily heterozygous womam, both normal and morphologically defective colonies could be isolated. These findings suggest that the morphologic alterations are an expression of the defect in Siemerling-Creutzfeldt disease. Futhermore, they suggest that the SCD locus is subject to lyonization.

Adrenal Cortex Diseases↗
PubMed1983

Computed tomographic evaluation of the retroperitoneum in infants and children.

With many retroperitoneal diseases in infancy and childhood, computed tomography will give information unavailable by any other single imaging technique. This maxim applies particularly to the adrenal, where the percolating nature of neuroblastoma with its propensity toward spinal involvement is exquisitely shown with computed tomography. Renal neoplasms and trauma can be illustrated effectively with computed tomography, as can pancreatic disease and spinal and paraspinal inflammatory and neoplastic disease. In addition to diagnostic studies, computed tomography may be used as guidance for invasive procedures.

Administration, Oral↗
PubMed1989

[ACTH secretion in adrenocortical disorders].

Secretion of cortisol is under stimulatory regulation by ACTH, and cortisol secreted, in turn, inhibits ACTH secretion by the pituitary. Therefore, measurement of plasma ACTH is indispensable in the diagnosis of the adrenocortical diseases. The adrenal cortex is included in the hypothalamo-adenohypophysial-adrenocortical system, and the pathogenesis of these disorders must be evaluated. An interaction between the hypothalamo-adenohypophysial-adrenal system and the immune system have been suggested. We studied the effect of interleukin-1 (IL-1) on ACTH secretion by cultured rat pituitary cells in vitro. Our results suggest that IL-1 stimulates the ACTH secretion by enhancing its synthesis by the pituitary, rather than ACTH release.

Adrenal Cortex Diseases↗
PubMed1980

[Ultrastructure of the adrenal cortex in burn disease].

Submicroscopic changes in adrenocorticocytes and sinusoid capillaries on days, 1, 2, 7, 14, 21 and 28 of burn disease were studied in experiments on pubertal male guinea pigs. During the first week the hormogenic gland cells showed predominant hyperplastic processes which proceeded in the presence of functionally excited sinusoids. On the 14th day the destruction of organella significantly increased along with hyperplasia and hypertrophy in parenchymatous and endothelial cells. Increased disorganization and destruction of the cell membrane components led to dramatic abnormalities in vascular-parenchymatous correlations and to the development of deep dystrophic processes and necrobiotic injuries to the adrenal cortex in later periods of the disease.

Adrenal Cortex↗
PubMed1986

Familial Cushing's syndrome due to nodular adrenocortical dysplasia. A putative receptor-antibody disease?

Two sisters aged 13 and 19 years suffering from familial Cushing's syndrome due to nodular adrenocortical dysplasia are described. Pituitary adrenocortical function tests indicated the presence of adrenal autonomy. Adrenal scintigraphy showed bilateral symmetrical uptake indicating the bilateral character of the autonomous process. Complete adrenalectomy was performed in both girls. The adrenals were of about normal weight showing numerous dark brown pigmented nodules and small perivascular lymphocytic infiltrates. Serum immunoglobulin preparations obtained from both girls stimulated adrenocortical cell growth in a cytochemical bioassay system. It is proposed that circulating growth factors may be involved in the pathogenesis of the disease.

Adolescent↗
PubMedDate not supplied

[Renin-angiotensin and hypophyseo-adrenal systems in children suffering from congenital adrenocortical hyperplasia resulting from 21-hydroxylase deficiency].

A study was made of the activity of plasma renin (APR), and the blood levels of ACTH, 17-hydroxyprogesterone (17-OHP) and aldosterone (A) in 50 children suffering from congenital adrenocortical hyperplasia as a result of 21-hydroxylase deficiency; 38 girls and 12 boys aged 1.5 mos. to 14 years were divided into 2 groups: (1) 35 with a salt losing type of disease; (2) 15 with a common virile type of disease. ARP in the 1st group did not exceed the control values and was unaccompanied by adequate secretion of A. Moderate ARP in parallel with a high level of A was noted in the 2nd group. Mineral corticoid therapy resulted in reduced ARP and A concentration, and a tendency to a decrease in the levels of ACTH and 17-OHP was noted. Variations in ARP and in the level of A did not manifest themselves clinically and were unaccompanied by electrolytic disorders. In the authors' opinion, a choice of adequate therapy for both types of disease must be based on the results of investigation of the above hormonal parameters.

17-alpha-Hydroxyprogesterone↗
PubMed1997

Growth hormone receptor messenger ribonucleic acid in normal and pathologic human adrenocortical tissues--an analysis by quantitative polymerase chain reaction technique.

GH receptor (GHR) has been reported to express in both normal rat and human adrenals. However, no study examined GHR expression in diseased human adrenal cortex. We quantitated, with RT-PCR, GHR messenger RNA (mRNA) in both normal and diseased human adrenal cortex with the following results: GHR mRNA levels in four histologically normal, not steroid-stimulated, control adrenal cortices was 1.5-11 x 10(4) molecules/microgram total RNA; in three diffusely hyperplastic adrenals (DH): 6.7-17.7 x 10(4); in two nonfunctioning tumors (NF): 0.84-1.9 x 10(4); in five androgen-producing neoplasms (AP): 4.6-34 x 10(4); and in five glucocorticoid-producing neoplasms (GP): 6.7-87 x 10(4). GHR transcript levels among adrenal cortices, DH, NF, AP, and GP reached statistically significant difference (P < 0.03). The GP group exhibited higher GHR mRNA levels than controls (P < 0.006). NF, as well as GP and AP, tumors had less GHR mRNA than their histologically normal adjacent cortex (P < 0.05). A positive correlation between urinary cortisol and GHR messenger RNA (mRNA) levels from GP and DH was observed (r = 0.93, P < 0.003). Our data suggest that GHR is expressed in both normal and diseased adrenal cortex and that GHR mRNA accumulation is less efficient in adrenocortical neoplasm than their adjacent nonneoplastic cortex. GHR expression in adrenal cortex provides an evidence of direct GH action in this tissue.

Adrenal Cortex↗