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PubMed1982

Incidental asymptomatic adrenal masses detected by computed tomographic scanning. Is operation required?

Until recently, adrenal masses came to clinical attention either from local symptoms due to massive enlargement or from manifestations of excess hormones production. During the last year, an adrenal mass was identified as an incidental finding in nine patients undergoing abdominal computed tomographic (CT) scanning for unrelated problems. These five men and four women ranged in age from 41 to 73 years. Eight were hypertensive. After the CT scan, each was evaluated for catecholamine or steroid hypersecretion. Only one had clearly elevated urinary vanillylmandelic acid, metanephrine, and catecholamine levels. Equivocal evidence of catecholamine excess was seen in five patients who had slight elevation of one urinary metabolite or of plasma epinephrine or norepinephrine levels. Three patients had no evidence of medullary or cortical hyperfunction on repeated testing. Eight patients were good operative risks and underwent unilateral adrenalectomy without complication. Masses ranging in size from 1 to 4 cm were found in each. These included four cortical adenomas, two adrenal cysts, one adrenal lipoma, and one pheochromocytoma. The pheochromocytoma occurred in the patient with strong biochemical evidence of disease. With wider application of CT imaging, increasing numbers of asymptomatic adrenal masses will be detected. Care in interpreting the clinical significance of these masses and caution in recommending treatment are required.

Adenoma↗
PubMed1993

[Pheochromocytoma with ectopic secretion of ACTH].

Pheochromocytoma is a tumor displaying a considerable degree of clinical polymorphism both with respect to its location and the secretion of different types of catecholamines and its capacity to synthesize several ectopic hormones. The present work reports on a case of pheochromocytoma with secretion of ACTH that exhibited several clinical and biological peculiarities. Firstly, the clinical picture of the patient was characterized by a predominance of manifestations of adrenal hyperfunction as compared with those of the original tumor. Secondly a striking finding was an important degree of neutrophilia without band forms and a marked hypokalemia produced by the joint secretion of catecholamines and steroid hormones, as demonstrated later. Finally, the images obtained with computerized tomography were very characteristic, such that together with the above data it was possible to establish a preoperative diagnosis.

Adrenal Gland Neoplasms↗
PubMed2003

Trilostane treatment of a dog with functional adrenocortical neoplasia.

A 13-year-old, crossbreed dog presented with a history of recent onset polydipsia, progressive lethargy, weakness and reduced appetite. Blood tests showed raised concentrations of alkaline phosphatase and alanine aminotransferase with marginally low serum potassium. There was a leucocytosis with a mature neutrophilia and no eosinophils. Endocrine tests showed a normal aldosterone concentration and an exaggerated adrenocorticotropic hormone (ACTH) stimulation test, consistent with a diagnosis of hyperadrenocorticism (HAC). A diagnosis of adrenal-dependent HAC was made, based on the presence of a calcified mass involving the left adrenal gland, and hepatomegaly, on radiography and ultrasonography. The owners declined surgical adrenalectomy. Medical management with trilostane rapidly improved the clinical signs and normalised the serum chemistry. ACTH stimulation tests showed an improvement in post-ACTH cortisol concentrations and were used to make dose adjustments where necessary. At the time of writing, no adverse side effects had been seen and the dog remained well after 80 weeks of treatment.

3-Hydroxysteroid Dehydrogenases↗
PubMed1992

Dominant familial syndromes with endocrine hyperfunction: an additional syndrome?

At least 8 separate dominant syndromes have been described which have hyperfunctioning endocrine tumors as an important component. Scattered reports in the literature suggest that there may be an additional syndrome, in which extra-adrenal paragangliomas (often multiple), pituitary adenomas, and parathyroid hyperplasia coexist. Of 3 such cases described to date, 2 have included information about the family history, which in each case suggested dominant inheritance. This would presumably be a less common syndrome than the others recognized previously, so that full evaluation of endocrine findings and family history in future cases will be important for developing our understanding of the syndrome.

Acromegaly↗
PubMedDate not supplied

Adrenal tissue characterization with 0.5-T MR imaging: value of T2*-weighted images.

The authors investigated the value of magnetic resonance (MR) imaging at 0.5 T for distinguishing adrenal adenomas from adrenal metastases. The series included 23 adrenal adenomas (18 nonhyperfunctioning, five hyperfunctioning) and 23 adrenal metastases from various organs. Adrenal tumor-liver signal intensity ratios on T1-, T2-, and T2*-weighted images were calculated for adrenal tissue characterization. Adrenal adenomas were more precisely distinguished from adrenal metastases on T2*-weighted images (21 of 23, 91%) than on T2-weighted images (15 of 23, 65%). T1-weighted images were not useful for this distinction. In conclusion, T2*-weighted images were better than routine T2-weighted images for distinguishing adrenal adenomas from adrenal metastases. It can be postulated that the total signal intensity of adrenal adenomas, which contain some fat components, decreased on T2*-weighted images because of an out-of-phase effect.

Adenoma↗
PubMed2005

[Diagnosis of autoimmune thyroid disease].

Autoimmune thyroid disease (AITD) is the most common organ specific autoimmune disorder usually resulting in dysfunction (hyperfunction, hypofunction or both) of the thyroid gland. The syndromes comprising autoimmune thyroid disease are many intimately related illnesses: Graves' disease with goitre, hyperthyroidism and, in many patients, associated ophthalmopathy, Hashimoto's thyroiditis with goitre and euthyroidism or hypothyroidism but also thyroid dysfunction occurring independently of pregnancy and in 5-6% of postpartum women and thyroiditides induced by different drugs and other environmental influences. The immunological mechanisms involved in these diseases are closely related, while the phenotypes probably differ because of the specific type of immunological response that occurs. The syndromes are connected together by their similar thyroid pathology, similar immune mechanisms, co-occurrence in family groups, and transition from one clinical picture to another within the same individual over time. In some patients, other organ specific and nonorgan specific autoimmune syndromes are associated with autoimmune thyroid disease, including pernicious anemia, vitiligo, myasthenia gravis, primary adrenal autoimmune disease, celiac disease, rheumatoid arthritis or lupus. Thyroid peroxydase, TPO, the primary enzyme involved in thyroid hormonogenesis, was initially identified in 1959 as the 'thyroid microsomal antigenn. It is uncertain whether TPO autoantibodies or TPO-specific T cells are the primary cause of thyroid inflammation, which can lead, in some individuals, to thyroid failure and hypothyroidism. TPOAbs are the hallmark of AITB and are present in almost all patients with Hashimoto's thyroiditis, in two-thirds of patients with postpartum thyroiditis and also in 75% of patients with Graves' hyperthyroidism. The antibodies are mainly produced by lymphocytic infiltrate in the thyroid gland and only to a small extent by regional lymph nodes or the bone marrow. Unlike antibodies against thyroglobulin (Tg), TPO antibodies are capable of inducing antibody-dependent cell-mediated cytotoxicity. Antibodies to TSH-R mimic the function of TSH, and cause disease by binding to the TSH-R and stimulating (or inhibiting) thyroid cells. The TSHR, a member of the G protein-coupled receptor family with seven membrane-spanning segments. Patients with autoimmune thyroid disease may have both stimulating and blocking antibodies in their sera, the clinical picture being the result of the relative potency of each species; blocking antibodies seem more common in Graves' patients with ophthalmopathy compared to those without this complication. The major T cell epitopes are heterogeneous and T cell reactivity against certain TSH-R epitopes has been present in high proportion in normal subjects. More diversified response to TSH-R, with heterogeneity of epitope recognition by TSAb, is predictive of likely remission after antithyroid drug treatment for Graves' disease.

Autoimmune Diseases↗
PubMed1983

Surgery of the endocrine glands in pregnancy.

The surgical endocrinology of the pregnant patient is special with respect to the additional hazards of maternal and fetal loss under the stress of pregnancy, labor, and delivery. The added threat of drug, radiation, radioisotope, anesthetic, and surgical management requires extra precaution in diagnostic and therapeutic manipulation, and limitations are imposed by appropriate reluctance to employ radioisotopes or external radiation in localizing or treating focal endocrine tumors. The state of pregnancy itself causes some endocrine hyperfunction that is normal, and the normal types must be distinguished from those that are pathologic, with consideration of the hormone values that would be pathologic in the nonpregnant state. The physician must be concerned with hyperfunctioning and hypofunctioning endocrine systems in their effect on the mother and their frequently reciprocal effects on the fetus in the maternal/fetal unit. The most directly life-threatening concerns of endocrine surgery in the pregnant patient are those of thyrotoxicosis, hyperparathyroidism, insulinoma, and, most particularly, pheochromocytoma. The severe consequences of unsuspected pheochromocytoma in the pregnant patient are evident in maternal and fetal mortality that approximates nearly 50%. The only reduction in the lethal consequences in the combination of pheochromocytoma and pregnancy can be made through continual suspicion and early diagnostic efforts with patients who manifest cardiovascular, neurologic, blood sugar, or blood pressure abnormalities in pregnancy. Some of the endocrine syndromes may not only affect and be affected by pregnancy but may be passed on through it to kindred in familial syndromes. The multiple endocrine adenopathies that are known are genetically expressed as autosomal dominant traits. Careful screening methods for case-finding among affected families is important follow-up to genetic counseling.

Adrenal Gland Neoplasms↗
PubMed1984

Ovarian and adrenal vein steroids in seven patients with androgen-secreting ovarian neoplasms: selective catheterization findings.

Standardized bilateral ovarian-adrenal vein catheterization was utilized to preoperatively assess glandular steroid release in seven consecutive cases of occult virilizing gonadal neoplasms. Peripheral testosterone (T) exceeded 1.5 ng/ml in all instances (range, 1.51 to 8.67 ng/ml). Endoscopy and radiography failed to locate the functional lesions. Catheterization showed a unilateral elevation of the ovarian-peripheral vein gradient for T greater than 2.7 ng/ml in six women. In the remaining patient, gradient analysis ruled out an adrenal tumor but did not facilitate lateralization of the gonadal lesion due to subselective ovarian effluent sampling. In addition to the consistent hypersecretion of T, variable excess gonadal output of dihydrotestosterone, androstenedione, dehydroepiandrosterone, and 17 alpha-hydroxyprogesterone was evident. Associated adrenal androgenic hyperfunction was documented in three subjects. Histologic evaluation of the implicated ovaries revealed three lipid cell, two Leydig cell, and two Sertoli-Leydig cell tumors, respectively, measuring between 0.6 and 2.2 cm in diameter. No correlation was found between any of the following parameters: peripheral or glandular vein steroid levels, androgen gradients, severity of symptoms, tumor morphology, and tumor size. In conclusion, appropriate application of selective catheterization may considerably reduce the frequency and extent of operative intervention.

Adrenal Glands↗
PubMed2005

[The use of suprarenal scintigraphy in the differential diagnosis of suprarenal incidentaloma].

OBJECTIVES: To assess the usefulness of adrenal scintigraphy for clinical evaluation of adrenal incidentalomas, and its relation with pathological diagnosis and follow-up. PATIENTS AND METHODS: We have studied 46 patients with unilateral adrenal incidentaloma of size between 10 and 100 mm (average 30.5 +/- 19 mm). The lesions were discovered with abdominal computerized tomography in the study of a primary tumor (22%) or in the evaluation of benign pathology (78%). Adrenal scintigraphy assessed uptake in adrenal incidentaloma. Hormonal study included urinary catecholamines, plasma cortisol after dexamethasone, adrenal androgens, and renin and aldosterone in hypertensive patients. Five patients were operated, FNAB was carried out in three patients, and in the rest average follow-up was 29 +/- 21 months. Adrenal incidentaloma was considered nonfunctional if the lesion did not modified its size nor showed analytical alterations along a follow-up higher than 8 months. RESULTS: Of 46 adrenal lesions, seven didn't show uptake (three metastases, one cyst, one adrenal carcinoma, one pheochromocytoma, and one angiomyolipoma), 34 showed excessive uptake (29 nonfunctional adrenal nodules and 5 hyperfunctional adrenal nodules), and five had normal uptake (nonfunctional adrenal nodules). Adrenal scintigraphy was compatible in all cases with cytological study or the response to chemotherapy. Along the follow-up, growth of the lesion was demonstrated in 23%, and reduction or disappearance of the lesion in 11%, with no hormonal significant changes. CONCLUSIONS: Detection of a lesion with no uptake in adrenal scintigraphy forces to carry out complementary explorations in order to rule out malignant pathology. A lesion with excessive uptake is indicative of a benign process and should be assessed with hormonal determinations.

Adrenal Gland Neoplasms↗
PubMed2006

Androgen excess in women--a health hazard?

A significant body of evidence suggests that androgens in women may play a role in the genesis of central adiposity and type 2 diabetes. There are two principal sources of circulating androgens in females: the ovary and the adrenal gland. In hyperandrogenic women, there are elevated serum concentrations of androstenedione and testosterone and, in up to 50% of the women, dehydroepiandrosterone sulfate (DHEAS). The androgen precursor DHEAS is of exclusive adrenal origin, suggesting that hyperandrogenic women have an elevated proportion of adrenal androgen production and secretion. Another cause of androgen excess in reproductive-age women is a decreased conversion of testosterone to estradiol by the aromatase enzyme complex. In this review, we will discuss the hypothesized clinical sequel of elevated androgens in women - an aspect of women's health highly neglected. Furthermore, an attempt is made to appreciate what causes the androgens to initially rise from normal levels, allowing the onset of pathophysiological processes towards diseases.

Adiposity↗
PubMed2005

[Management of adrenal incidentaloma combined with high blood pressure].

Hypertension (HTA) is a very common disease but its origin is well known only in 1 to 5% of the cases. HTA is present in half of the patients who have an adrenal incidentaloma. Clinical data, hormonal sampling, computed tomography and adrenal scintigraphies are necessary to identify hyperfunctioning adrenal tumors. Adrenalectomy is indicated in case of potential malignant tumors and hyperfunctioning tumors. If HTA seems to be not in relation with the adrenal mass, it is recommended to recognize a congenital enzymatic block in order to ovoid an unnecessary adrenalectomy and to search for a preclinical Cushing's syndrome. The last one is associated with HTA in 91% of the cases, and with a morbid obesity, mellitus diabetes or dyslipidemia in 50% of the cases. The removal of the adrenal mass improves the HTA for half of the patients. If the adrenocortical tumor is nonfunctioning, patients have to be followed during a long time. HTA will be considered as "essential" after a new comprehensive analysis performed 3 years later.

Adrenal Gland Neoplasms↗
PubMed1991

Activating mutations of the stimulatory G protein in the McCune-Albright syndrome.

BACKGROUND: The McCune-Albright syndrome is a sporadic disease characterized by polyostotic fibrous dysplasia, café au lait spots, sexual precocity, and hyperfunction of multiple endocrine glands. These manifestations may be explained by a somatic mutation in affected tissues that results in activation of the signal-transduction pathway generating cyclic AMP (cAMP). We analyzed DNA from tissues of patients with the McCune-Albright syndrome for the presence of activating mutations of the gene for the alpha subunit of the G protein (Gs alpha) that stimulates cAMP formation. METHODS: Genomic DNA fragments encompassing regions (exons 8 and 9) previously found to contain activating missense mutations of the Gs alpha gene (gsp mutations) in sporadically occurring pituitary tumors were amplified in tissues from four patients with the McCune-Albright syndrome by the polymerase chain reaction. The amplified DNA was analyzed for mutations by denaturing gradient gel electrophoresis and allele-specific oligonucleotide hybridization. RESULTS: We detected one of two activating mutations within exon 8 of the Gs alpha gene in tissues from all four patients, including affected endocrine organs (gonads, adrenal glands, thyroid, and pituitary) and tissues not classically involved in the McCune-Albright syndrome. In two of the patients, histidine was substituted for arginine at position 201 of Gs alpha, and in the other two patients cysteine was substituted for the same arginine residue. In each patient the proportion of cells affected varied from tissue to tissue. In two endocrine organs, the highest proportion of mutant alleles was found in regions of abnormal cell proliferation. CONCLUSIONS: Mutations within exon 8 of the Gs alpha gene that result in increased activity of the Gs protein and increased cAMP formation are present in various tissues of patients with the McCune-Albright syndrome. Somatic mutation of this gene early in embryogenesis could result in the mosaic population of normal and mutant-bearing tissues that may underlie the clinical manifestations of this disease.

Adolescent↗
PubMedDate not supplied

Hyperadrenocorticism and hyperprogesteronemia in a cat with an adrenocortical adenocarcinoma.

A seven-year-old, neutered male domestic shorthair cat was evaluated for poorly regulated diabetes mellitus and increased skin fragility. Imaging studies revealed a right adrenal gland tumor, but cortisol testing did not support a diagnosis of hyperadrenocorticism. Serum concentrations of progesterone and testosterone were increased compared with a group of normal cats, and the clinical signs were attributed to hyperprogesteronemia. At necropsy, a diagnosis of adrenocortical adenocarcinoma was confirmed, and immunohistochemical staining confirmed the presence of progesterone within the tumor. Clinical signs of hyperadrenocorticism in cats may occur due to increased serum concentrations of hormones other than cortisol.

Adenocarcinoma↗
PubMed2006

A primary adrenal non-Hodgkin's lymphoma presenting as an incidental adrenal mass.

The primary adrenal localization of a non-Hodgkin's lymphoma (NHL) is a rare event. We report the case of a 70-yr-old woman, who was admitted at our Institute for a hormonal evaluation after the incidental discovery of a right adrenal mass during ultrasonography (US) performed for cardiovascular disease. At the physical examination, no sign of adrenal hyperfunction was present. She showed only an androgenetic alopecia and her blood pressure was 180/70 mm Hg, with an arrhythmic heart rate of 100 beats/min. No alterations in hormonal and biochemical data were observed. US studies showed a right adrenal mass (major diameter 16 mm), and an abdominal computed tomography (CT) scan confirmed this solid lesion (major diameter 15 mm) with a high density. [75Se] methylnorcholesterol adrenal scintigraphy exhibited a normal symmetrical radiotracer uptake. After 8 months of follow-up, an abdominal CT scan demonstrated a significant increase of the right adrenal mass (major diameter: 40 mm), with a solid tissue density and enhancement after i.v. contrast. [75Se] methylnorcholesterol adrenal scintigraphy showed an absent uptake on the right side versus the contralateral side. The hematological, hormonal and radiological evaluation did not reveal any sign of malignancy. Owing to the mass enlargement and the modification of scintigraphic pattern, the patient underwent unilateral adrenalectomy. Histological examination revealed a primary diffuse large B-cell NHL (REAL classification) of the adrenal gland. After surgery, she underwent a combined polychemotherapy (cyclophospamide, adriamycin, vincristine and prednisone) and subsequently one cycle of radiotherapy. At present, the patient is in good conditions and there are no signs or symptoms of recurrent disease.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

The possible role of apoptosis-suppressing genes, bcl-2 and mcl-1/EAT in human adrenal tumors.

The expression levels of bcl-2, mcl-1/EAT, and bax were examined by Northern blot analysis and semi-quantitative RT-PCR method in 25 adrenal tumors, including seven adrenal pheochromocytomas (PHE), seven aldosterone-producing adenomas (APA), four adrenal cortisol-producing adenomas (CS), one deoxycorticosterone-producing adenoma (DOC) and six non-hyperfunctioning adrenal cortical adenomas (NF). Northern blot analysis revealed both bcl-2 and mcl-1/EAT mRNAs in all of the adrenal tumors. The expression levels differed greatly among the tumor samples. Mcl-1/EAT mRNA levels were enhanced in APA and CS compared with those in NF. In contrast, bcl-2 levels in NF were higher than in other tumors. Our results suggest that deregulation of such apoptosis-suppressing genes may contribute to the multistep tumorigenesis of human adrenal tumors and that mcl-1/EAT, one of the bcl-2 family genes, has a different role from that of bcl-2 in such pathways.

Adrenal Gland Neoplasms↗
PubMed1998

p53 protein and its messenger ribonucleic acid in human adrenal tumors.

The role of p53 tumor suppressor gene in the pathomechanism of adrenal tumors was investigated by measuring p53 protein and its messenger ribonucleic acid (mRNA) in 12 normal human adrenals as well as in 56 adrenal tumors (7 aldosterone-producing adenomas, 5 adrenocortical adenomas causing Cushing's syndrome, 19 non-hyperfunctioning adrenocortical adenomas, 5 adrenocortical carcinomas, 12 pheochromocytomas, 3 myelolipomas, 4 ganglioneuromas and 1 hemangioma). The p53 protein concentration was significantly increased in aldosterone-producing adenomas (394+/-36 pg/mg cytosolic protein, mean+/-SE, vs 266+/-18 in normal human adrenals), whereas the concentration of this protein in Cushing's adenomas, non-hyperfunctioning adrenocortical adenomas, pheochromocytomas, and in all but one adrenocortical carcinomas was similar to that measured in normal human adrenal tissues. One adrenocortical carcinoma tissue showed very high p53 protein content (3000 pg/mg cytosolic protein). By contrast, myelolipomas (23+/-20) ganglioneuromas (43+/-15) and a hemangioma (11 pg/mg cytosolic protein) had very low p53 protein content. Northern blot analysis revealed the presence of p53 mRNA in each adrenal tissue examined with highest levels in aldosterone-producing and Cushing's adenomas. It is possible that the differences in p53 protein and/or mRNA contents reflect corresponding differences in the pathogenetic importance of p53 alterations in these types of adrenal tumors.

Adenoma↗
PubMed1979

Uptake of 131I-19-cholesterol by normal and spontaneously hyperfunctioning canine adrenals.

In six normal dogs the adrenals could be visualized as separate areas of radioactivity at 7--10 days after injection of 20--40 muCi 131I-iodocholesterol per kg of body weight. Image analysis revealed uptake values of 0.15--0.3% of the injected dose. In five dogs with pituitary-dependent hyperadrenocorticism the adrenals became visible at 3--5 days after injection of the radiopharmaceutical, with uptake values of 0.38--2.2%. In six dogs with hyperadrenocorticism due to adrenocortical tumor the scintigraphy contributed to the diagnosis and the presurgical localization. The uptake values were within the normal range; the tumor could be observed at 3--10 days after injection. Additional findings on adrenal asymmetry and a case of fluctuating pituitary-dependent hyperadrenocorticism are discussed.

19-Iodocholesterol↗
PubMed1997

The natural history and treatment of adrenal myelolipoma.

PURPOSE: We determined the natural history and clarified the treatment of adrenal myelolipoma. MATERIALS AND METHODS: A retrospective review of medical records and radiographic imaging studies of 20 patients diagnosed with adrenal myelolipoma was performed. RESULTS: Of 20 patients 4 presented with abdominal pain and 1 had Cushing's syndrome. The remaining tumors were discovered incidentally. Four patients underwent surgery because of abdominal pain in 2, adrenal hyperfunction (Cushing's syndrome) in 1 and a tumor 10.5 cm. in largest dimension in 1. Of 15 patients (16 adrenal myelolipomas) followed without surgical intervention for an average of 3.2 years (range 0.3 to 10.8) 13 remained asymptomatic and 2 experienced persistent, vague abdominal discomfort. One patient was lost to followup. A total of 13 tumors from 12 patients was serially imaged, with tumor size increasing in 6, decreasing in 2 and remaining unchanged in 5. CONCLUSIONS: These data suggest that the majority of adrenal myelolipomas can be treated conservatively. While tumors can become enlarged, they also exhibit variable growth, and size and growth rate do not necessarily correlate with symptoms. Computerized tomography can be used for diagnosis.

Adrenal Gland Neoplasms↗