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PubMed1978

Scintigraphy of hyperfunctioning adrenal tissue after total adrenalectomy.

The significance of scintigraphic examination in four patients with hyperfunction of adrenal tissue after total adrenalectomy is described. The scintigraphic examination was done 7--8 days after the injection of 1 mCi of 131I-19-iodocholesterol using the Jumbo Thoshiba 202 scintillation camera and Informatek SIMIS 3 data processing system. Noticeable concentration of 131I-19-iodocholesterol occurred in all four patients of, in three cases in the region of the right adrenal gland and in one case in the region of the left one. Scintigraphic examination confirmed the clinical hypothesis that of cushing's syndrome recurred in these patients because of hyperfunctioning adrenal tissue left in the body after the operation. This diagnosis was given confirmed in two cases undergoing repeated operations. The scintigraphic examination allowed accurate localization of the adrenal tissue and facilitated finding it during the next operation. The authors believe that adrenal scintigraphy is at the present time one of the best methods of locating the hyperfunctioning adrenal tissue left in the body during total adrenalectomy.

Adrenal Glands↗
PubMedDate not supplied

[The ectopic ACTH syndrome].

INTRODUCTION: Endogenous Cushing's syndrome is a clinical state resulting from prolonged, inappropriate exposure to excessive endogenous secretion of cortisol and hence excess circulating free cortisol, characterized by loss of the normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis and the normal circadian rhythm of cortisol secretion [2]. The etiology of Cushing's syndrome may be excessive ACTH secretion from the pituitary gland, ectopic ACTH secretion by nonpituitary tumor, or excessive autonomous secretion of cortisol from a hyperfunctioning adrenal adenoma or carcinoma. Other than this broad ACTH-dependent and ACTH-independent categories, the syndrome may be caused by ectopic CRH secretion, PPNAD, MAH, ectopic action of GIP or catecholamines, and other adrenel-dependent processes associated with adrenocortical hyperfunction. CASE REPORT: A 31 year-old men with 6-month history of hyperpigmentation, weight gain and proximal myopathy was refereed to Institute of Endocrinology for evaluation of hypercortisolism. At admission, patient had classic cushingold habit with plethoric face, dermal and muscle atrophy, abdominal strie rubrae and centripetal obesity. The standard laboratory data showed hyperglycaemia and hypokaliemia with high potassium excretion level. The circadian rhythm of cortisol secretion was blunted, with moderately elevated ACTH level, and without cortisol suppression after low-dose and high-dose dexamethason suppression test. Urinary SHIAA was elevated. Abdominal and sellar region magnetic resonance imaging was negative. CRH stimulation resulted in ACTH increase of 87% of basal, but without significant increase of cortisol level, only 7%. Thoracal CT scan revealed 14 mm mass in right apical pulmonary segment. A wedge resection of anterior segment of right upper lobe was performed. Microscopic evaluation showed tumor tissue consisting of solid areas of uniform, oval cells with eosinophilic cytoplasm and centrally located nuclei. Stromal tissue was scanty, and mitotic figures were infrequent. Tumor cells were immunoreactive for synaptophysin, neuron-specific enolase, and ACTH. The postoperative course was uneventful and the patient was discharged on glucocorticoid supplementation. Signs of Cushing's syndrome were in regression, and patient remained normotensive and normoglycaemic without therapy. DISCUSSION: A multitude of normal nonpituitary cells from different organs and tissues have been shown to express the POMC gene from which ACTH is derived. The tumors most commonly associated the ectopic ACTH syndrome arise from neuroendocrine tissues, APUD cells. POMC gene expression in non-pituitary cells differs from that in pituitary cells both qualitatively and quantitatively [8]. Aggressive tumors, like small cell cancer of the lung (SCCL) preferentially release intact POMC, whereas carcinoids rather overprocess the precursor, releasing ACTH and smaller peptides like CLIP. Some tumors associated with ectopic ACTH syndrome express other markers of neuroendocrine differentiation like two specific prohormone convertases (PCs). Assessment of vasopressin (V3) receptor gene expression in ACTH-producing nonpitultary tumors revealed bronchial carcinoid as a particular subset of tumors where both V3 receptor and POMC gene may be expressed in pattern indistinguishable from that in corticotroph adenoma [9]. In most, but not all, patients with ectopic ACTH syndrome, cortisol is unresponsive to high-dose dexamethason suppression test, what is used as diagnostic tool. It is not clear if the primary resistance resulted from structural abnormality of the native glucocorticoid receptor (GR), a low level of expression, or some intrinsic property of the cell line [9]. It appears that ectopic ACTH syndrome is made of two different entities. When it is because of highly differentiated tumors, with highest level of pituitary-like POMC mRNA, expressing PCs, high level of V3 receptors and GR, like bronchial carcinoids, it might be called ectopic corticotroph syndrome. In contrast, when it is caused by aggressive, poorly differentiated tumors, with much lower expression of V3 receptor, like SCCL, it might be called aberrant ACTH secretion syndrome. Carcinoid tumors have been reported in a wide range of organs but most commonly involve the lungs, bronchi, and gastrointestinal tract. They arise from neuroendocrine cells and are characterized by positive reactions to markers of neuroendocrine tissue, including neuron specific enolase, synaptophysin, and chromogranina [11]. Carcinoid tumors are typically found to contain numerous membrane-bound neurosecretory granules composed of variety of hormones and biogenic amines. One of the best characterized is serotonin, subsequently metabolized to 5-hydrohy-indolacetic acid (5-HIAA), which is excreted in the urine. In addition to serotonin, carcinoid tumors have been found to secrete ACTH, histamine, dopamine, substance P, neurotensin, prostaglandins and kallikrein. The release of serotonin and other vasoactive substances is thought to cause carcinoid syndrome, which manifestations are episodic flushing, weezing, diarrhea, and eventual right-sided valvular heart disease. These tumors have been classified as either well-differentiated or poorly differentiated neuroendocrine carcinomas. The term "pulmonary tumorlets" describes multiple microscopic nests of neuroendocrine cells in the lungs [12]. Pulmonary carcinoids make up approximately 2 percents of primary lung tumors. The majority of these tumors are perihilar in location, and patients often presents with recurrent pneumonia, cough, hemoptisis, or chest pain. The carcinoid syndrome occurs in less than 5 percent of cases. Ectopic secretion of ACTH from pulmonary carcinoid accounts for 1 percent of all cases of Cushing's syndrome. They are distinct clinical and pathologic entity, generally peripheral in location. Although they are usually typical by standard histologic criteria, they have mush greater metastatic potential than hormonally quiescent typical carcinoids [13]. Surgical treatment therefore should be one proposed for more aggressive malignant tumors. In all cases of ACTH-dependent Cushing's syndrome with regular pituitary MRI and bilateral inferior petrosal sinus sampling, thin-section and spiral CT scanning of the chest should be routine diagnostic procedure [14]. We present thirty-one year old patient with typical pulmonary carcinod with ACTH ectopic secretion consequently confirmed by histology.

ACTH Syndrome, Ectopic↗
PubMed1995

Compound adrenal medullary tumor.

Compound tumors of the adrenal medulla, characterized by a mixture of pheochromocytoma and ganglioneuroma, are rare, only 12 cases having been reported in the literature. We present the case of a 66-year-old woman with a left-sided incidentally discovered adrenal mass that was subsequently shown to contain elements of pheochromocytoma and ganglioneuroma. The patient had no history of hypertension but did have a history of "idiopathic" edema (dependent edema). A review of the literature shows hormonal hypersecretion in approximately three fourths of the reported cases. Because of the preoperative hypertensive crises from the pheochromocytoma component of the tumor, contemporary management of incidentally discovered adrenal masses must include preoperative hormonal evaluations to exclude endocrine hyperfunction.

Adrenal Gland Neoplasms↗
PubMed1989

[Long-term result in 22 cases of adrenal autotransplantation with arterio-venous anastomosis].

Since 1982 22 cases of Cushing's disease treated by bilateral adrenalectomy and left adrenal autotransplantation with A-V anastomosis have been followed up for 2-5 years. 3 cases with anastomosis of adrenal vein to the epigastric inferior artery failed completely. 19 cases with anastomosis of adrenal vein to the gastrodiploic artery stopped all steroid replacement therapy 7-40 days after operation and the short-term results within three months were good, but later 2 cases died, 5 cases developed adrenocortical hypofunction, 1 case recurred and 11 cases are satisfactory. The pathologic mechanism of occurrence of adrenocortical hypofunction and hyperfunction are discussed.

Adolescent↗
PubMed2001

[Diagnosis and surgical treatment of arterial hypertension of adrenal origin].

230 patients with arterial hypertension of adrenal origin were treated. 205 of them underwent adrenalectomy with surrounding paranephral fat. There were no lethal outcomes. Endogenic adrenocorticism was diagnosed in 134 patients. Cushing's syndrom was in 96 patients, Cushing's disease--in 34, ACTH-ectopic syndrome--in 2, adrenocortical cancer--in 2. Primary hyperaldosteronism was diagnosed in 42 cases: idiopathic hyperaldosteronism in 23 patients, aldosteronproducing adenoma (Conn's syndrome)--in 19. Tumors of chromaffine tissue were defected in 30 patients. All the patients underwent complex examination (hormonal profile, US, CT, MRT, angiography if it was necessary). Symptomatic arterial hypertension of adrenal origin was diagnosed during one year in 10% patients only because of absence of typical clinical picture. Use of complex examination has permitted to make a correct topical diagnosis and to choose optimum treatment policy in all the cases.

ACTH Syndrome, Ectopic↗