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PubMed1983

Nodular adrenal hyperplasia with elevated adrenocorticotropic hormone levels.

Micronodular adrenal hyperplasia is an uncommon adrenal disorder characterized by failure of urinary corticosteroid excretion to be suppressed by high-dose dexamethasone therapy. Thus, micronodular adrenal hyperplasia demonstrates dexamethasone suppressibility that resembles primary adrenal neoplasia. However, since some cases have been reported to have measurable plasma adrenocorticotropic hormone (ACTH) levels, it is unclear whether this disorder arises primarily in the pituitary-hypothalamic region or in the adrenal gland. Our patient had clinical features of Cushing's syndrome and elevated urinary corticosteroid excretion that did not suppress with even high doses of dexamethasone; however, ACTH levels were elevated and were suppressible with high-dose dexamethasone therapy. At operation, enlarged adrenal glands with multiple micronodules were found. This case is compatible with the hypothesis that hypothalamic-pituitary hyperfunction precedes the development of micronodular adrenal disease in some cases.

Adrenal Glands↗
PubMed1982

Progression of endocrinological and neurological dysfunction in adrenoleukodystrophy. Endocrinological evidence of an affection of the adrenal cortex independent of the cerebral disorder.

In a boy suffering from adrenoleukodystrophy (ALD) the function of the adrenal cortex and pituitary gland was followed prospectively. At the onset of the disease an autonomic hyperfunction of the adrenal cortex was shown. Subsequently the secretion of cortisol dropped to low levels despite high plasma levels of ACTH. The results suggest a primary disorder of the adrenal cortex in ALD, which up till now could only be postulated on anatomical evidence. With the use of computerized tomography and electroencephalography abnormalities characteristic for ALD were shown. The progression of the disease was followed using these noninvasive methods of examination.

Adrenal Cortex↗
PubMed1974

A functioning black adenoma of the adrenal cortex: a clinico-pathological entity.

A 25-year-old woman is described who had suspected hyperfunction of the adrenal cortex. She complained of fatiguability, excessive hair growth, and attacks of swelling of the face, hands, and ankles. Moreover she had a ;moon face', hypertension, a ;buffalo hump', and livid striae of the loins and hypogastrium. Adrenal function tests yielded values which could not be clearly interpreted. Operation showed a ;black adenoma' of the adrenal cortex on the right side. As far as it is known this is the first published case of this extremely rare lesion which was operated upon and caused nearly complete remission of the endocrine disturbance.

Adenoma↗
PubMed2002

Adrenal cortical and medullar hyperplasia--a retrospective analysis of 6 cases.

The features of the symptoms, laboratory tests and pathological characteristics of adrenal cortical and medullary hyperplasia were studied. In 6 cases of hypercatecholaminenia, plasma norepinephrine (NE), epinephrine (E), catecholamine (CA) and 24-h urinary vanillylmandelic acid (VMA), 17-hydroxycorticosteroid (OHCS) and 17-ketosteroid (KS) were determined. Adrenal glands were examined by CT scan and 131I-MIBG imaging. Pathological examination was performed after operation. The results showed that in 6 cases of hypercatecholaminenia (3 men and 3 women) aged from 34-50 years, the clinical features were just like "pheochromocytoma", for example, episodic headache, perspiration, palpitation, pallor, apprehension, nausea, tremor, anxiety and so on. Plasma levels of CA, NE and E were elevated in all 6 cases. 24-h urinary samples obtained at the onset revealed elevated VMA in 1 case. 24-h urinary cortisol was obviously elevated in all 6 cases. 24-h urinary 17-OHCS, 17-KS was normal. B-type ultrasound, CT, MRI and 131I-MIBG revealed 9 lateral adrenal gland diffuse or nodular enlargement in 6 cases. Pathologic examination showed adrenal cortical and medullary hyperplasia. Clinically, adrenal cortical and medullary hyperplasia resembled "pheochromocytoma". The most significant feature of this disease was both elevated plasma CA and 24-h urinary cortisol obviously. Pathologic examination showed adrenal cortex nodular hyperplasia and medullar diffuse or limit hyperplasia. Whether it is an independent disease or symptoms of the other disease has not final conclusion up till now.

Adrenal Cortex↗
PubMed1975

Primary aldosteronism. A study in contrasts.

Two patient with primary aldosteronism, one with a solitary adrenal adenoma and the other with bilateral nodular hyperplasia, are described. Both patients showed the classic features of primary aldosteronism in electrolyte and hormone patterns, but there were important differences in the biochemistry of their excised adrenal tissue. In addition, the injection of plasma from the patient with bilateral adrenal hyperplasia into the sheep's transplanted adrenal gland elicited a definite aldosterone secretory response, but there was no aldosterone response to the injection of plasma from the patient with a solitary adrenal adenoma. The findings support the hypothesis that an extra-adrenal stimulus may contribute to the pathogenesis of bilateral adrenal hyperplasia.

Adenoma↗
PubMed1977

Cholesterol side-chain cleavage enzyme activity and cytochrome P-450 content in adrenal mitochondria of a patient with congenital lipoid adrenal hyperplasia (Prader disease).

An autopsied case with congenital lipoid adrenal hyperplasia (Prader disease) was presented. The cholesterol side-chain cleavage (SCC) enzyme activity in adrenal mitochondria of this case was assayed with [3H]cholesterol as substrate, combined with purified bovine adrenodoxin and adrenodoxin reductase, by measuring the amount of [3H]pregnenolone formed. The cytochrome P-450 content was also measured by recording the difference absorption spectra of carbon monoxide-complexed P-450. The cholesterol SCC enzyme activity in adrenal mitochondria of Prader disease was 0.81 nmol pregnenolone/nmol P-450 per min, which was approximately 10% of that in normal tissue. The content of cytochrome P-450 was 0.074 nmol/mg protein, which was about half of that in controls. These results indicate that there is a cholesterol SCC enzyme deficiency in adrenal mitochondria in this disease.

Adrenal Glands↗
PubMed1979

A method for identification and follow-up of patients with a steroid-21-hydroxylase deficiency.

A method is described for the determination of 17 alpha-hydroxyprogesterone from blood samples obtained by heel prick and dried on filter paper. Discs (10 mm diameter) were cut from the filter paper and extracted in the assay tubes with 1 ml of a methanol/diethyl ether/ethyl acetate (50 :45 :5, v/v) solvent mixture. Antibody, tritium-labelled tracer and dextran-coated charcoal were added to assay tubes using a multichannel dispenser. The approach used permits one technician to analyze two series, each of 60 duplicate samples, within one working day. Thus the method is applicable for the centralized screening of suspected cases, while emergency samples may be analyzed at the same time within 4 h. Comparisons with a highly specific but more elaborate technique for the determination of blood 17 alpha-hydroxyprogesterone showed a correlation coefficient of 0.99, and the regression equation for the present method (y) against the established method (x) was y = 1.07x + 2.72. The calculated upper reference limit (mean +/- S.D.) for 17 alpha-hydroxyprogesterone in healthy infants from two days to eight years of age of 7.5 ng/ml of serum.

Adrenal Glands↗
PubMed2005

[What has changed in adrenalectomy? From open surgery to laparoscopy?].

INTRODUCTION: After the introduction of the laparoscopic approach in adrenal surgery, this technique has become the gold standard in surgical adrenal diseases. Nevertheless, comparative studies with open surgery are scarce and the impact of laparoscopic techniques on these diseases is unknown. OBJECTIVE: To evaluate our experience of adrenal surgery over a 14-year period, before and after the introduction of laparoscopic adrenalectomy, and to analyze the influence of this technique on the surgical management of adrenal diseases. PATIENTS AND METHOD: From January 1990 to June 2004, 78 patients underwent adrenalectomy. Between 1990 and 1998, open adrenalectomy was performed in 24 patients, while between 1999 and 2004, 54 patients underwent the laparoscopic approach and 1 underwent open surgery. Data for the open group were retrospectively reviewed while those for the laparoscopic group were prospectively registered in the advanced laparoscopic surgery database of Hospital Sant Pau (HSP). RESULTS: The mean age was 47 years (16-75) in the open group and was 49 years (17-77) (p = NS) in the laparoscopic group. Distribution by surgical indication was similar in both periods concerning primary hyperaldosteronism, hypercortisolism, and pheochromocytoma, with a significant increase in surgical cases indicated by malignancy (1 vs 4) or incidentaloma (2 vs 13) (p<.001). Operating time was reduced from 150 min (65-210) in the open group to 90 min (30-300) in the laparoscopic group (p<.01). Morbidity was also reduced (20% vs 6%, p<.01). The size of lesions resected by open or laparoscopic surgery (4 cm [0.4-16] vs 3.5 cm [1.2-14]) was similar. The mean length of hospital stay was reduced from 8 days (3-13) to 3 days (2-12) (p<.01). The number of adrenalectomies performed in HSP was 24 in the first period (1990-1997) vs 40 in the second (1998-2004). This represented an increase from 3/year to 6.6/year mainly due to the increase in the number of incidentalomas. CONCLUSIONS: The laparoscopic approach has improved immediate surgical results (operating time, morbidity, and length of hospital stay). There was a clear increase in the number of adrenalectomies, and especially of incidentalomas, due to improved diagnostic techniques and the availability of a less aggressive approach.

Adolescent↗
PubMed1980

Adrenal medullary hyperplasia: a clinicopathologic study of four cases.

This study presents the clinicopathologic findings in four new cases of adrenal medullary hyperplasia. The patients presented with episodic hypertension frequently associated with palpitations, headache, and diaphoresis. All four had elevated urinary catecholamine levels during attacks, and were thought clinically to have a pheochromocytoma. In each case laparotomy revealed a diffusely enlarged adrenal gland without a discrete tumor. Histologic examination of the adrenals demonstrated a diffuse and nodular expansion of the medulla confirmed by morphometric study. Of the four patients, three underwent unilateral and one bilateral adrenalectomy. Two patients who underwent unilateral adrenalectomy have been free of symptoms for three years. Thus, it would appear that adrenal medullary hyperplasia may occur unilaterally or asynchronously in the two glands. The bilaterally adrenalectomized patient has had persistent attacks, suggesting that the stimulus to adrenal medullary hyperplasia may possible affect other chromaffin tissues. On the basis of our cases and a review of the literature, we propose the following criteria for the diagnosis of adrenal medullary hyperplasia: a clinical history of episodic attacks suggesting pheochromocytoma (generally with associated increased urinary catecholamine levels), an adrenal gland showing diffuse expansion of the medulla into the alae or tail of the gland with or without nodule formation, a medulla composed of enlarged cells with or without pleomorphism, and, most important, an increased medulla/cortex ratio, together with an increased calculated medullary weight as determined by morphometric analysis.

Adrenal Cortex↗
PubMed1975

Early diagnosis of congenital adrenal hyperplasia by measurement of 17-hydroxyprogesterone.

Plasma 17-hydroxyprogesterone was measured by a simple radioimmunoassay technique in six infants, aged 3 days to 3 months, with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Hormonal levels in this group were compared to those of twenty normal newborns and to those found in sixty samples of umbilical vein blood from normal deliveries. Plasma 17-hydroxyprogesterone concentrations were markedly elevated in all congenital adrenal hyperplasia infants (range 544.7-1837 nmol/l, normal 3.03-19.06) at a time when urinary studies in some of these were either not diagnostic or inconclusive. In one infant whose cord blood was analysed, the level was also greatly raised. The data suggest that early definitive diagnosis of congenital adrenal hyperplasia can be established by measurement of plasma 17-hydroxyprogesterone.

Adrenal Glands↗
PubMed2002

Use of aminoglutethimide in the treatment of pituitary-dependent hyperadrenocorticism in the dog.

The aim of this study was to evaluate the efficacy and safety of aminoglutethimide in the treatment of dogs with pituitary-dependent hyperadrenocorticism (PDH). Ten dogs were diagnosed with PDH based on clinical and laboratory data, adrenal function tests (adrenocorticotropic hormone [ACTH] stimulation test and urinary cortisol/creatinine ratio [UCCR] combined with a high dose oral dexamethasone suppression test) and ultrasonographic evaluation of the adrenal glands. Aminoglutethimide was administered daily at a dose of 15 mg/kg bodyweight for one month. Median basal cortisol concentration and post-ACTH cortisol concentration one month after treatment were significantly lower than pretreatment values. Complete response was achieved in one dog, and partial response was obtained in three dogs. Severe side effects of anorexia, vomiting and weakness occurred in one dog and medication was withdrawn. Two further dogs developed decompensations of concurrent diseases and medication was stopped in these animals as well. Mild toxicity occurred in four dogs. Moderate to severe elevations in liver enzymes occurred in all dogs. The efficacy of this drug is lower than that observed using mitotane and ketoconazole, and adverse effects limit its use. Aminoglutethimide, using the protocol described, cannot be recommended for long-term management of PDH in the dog.

Adrenal Glands↗