1/38. recurrence of adrenal aldosterone-producing adenoma.Conn's syndrome (adrenal aldosterone-producing adenoma) and bilateral adrenal hyperplasia are the most common causes of primary aldosteronism. The treatment of choice for patients with aldosterone-producing adenoma is unilateral total adrenalectomy. recurrence after adequate surgery is exceptional. We present a patient with recurrence of an aldosterone-producing adenoma in the right adrenal gland 9 years after adenomectomy of a aldosterone-producing adenoma in the same adrenal gland. We conclude that adenomectomy is not an adequate therapy for patients with adrenal aldosterone-producing adenoma.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
2/38. adenocarcinoma of the prostate with ectopic antidiuretic hormone production: a case report.An 88-year-old patient with a poorly differentiated adenocarcinoma of the prostate gland was found to have all cardinal findings of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Elevated levels of antidiuretic hormone were found in the patient's serum and in the prostatic tumor and the cytoplasms of the tumor was positive for prostate specific antigen and was faintly positive for antidiuretic hormone (ADH). He responded well to combination therapy of androgen blockade with leuprorelin acetate and flutamide, and laboratory findings of SIADH and serum ADH level returned to normal. However, he died of sudden profuse bleeding caused by gastric ulcers 6 months after the therapy. Ten cases of SIADH caused by prostatic cancer have been reported including the present case.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
3/38. Prostatic carcinoma producing syndrome of inappropriate secretion of antidiuretic hormone.The syndrome of inappropriate secretion of antidiuretic hormone was recognized in a sixty-year-old man with a poorly differentiated metastatic adenocarcinoma of the prostate gland. Elevated levels of antidiuretic hormone were found in the patient's serum and in the prostatic tumor but not in the cerebrospinal fluid. The patient's clinical course is detailed, and the pathophysiology of this syndrome is discussed.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
4/38. acromegaly and somatotroph hyperplasia with adenomatous transformation due to pituitary metastasis of a growth hormone-releasing hormone-secreting pulmonary endocrine carcinoma.CONTEXT: GHRH excess from extracranial endocrine tumors is known to cause somatotroph hyperplasia and acromegaly. Hypothalamic gangliocytomas producing GHRH are also known to be associated with pituitary adenomas causing acromegaly. OBJECTIVES: The objective of this study was to describe a case of acromegaly due to a pulmonary GHRH-secreting endocrine carcinoma with metastasis to the pituitary gland and to look at the peculiar histological features of this case. SUBJECT: The patient was a 44-yr-old woman who was diagnosed with a biopsy-proven metastatic pulmonary endocrine tumor during pregnancy. After delivery, she underwent radiation and chemotherapy for pulmonary and skeletal metastases. Her disease was clinically stable for 7 yr until she developed bitemporal hemianopia. She had symptoms and signs of acromegaly. methods: Imaging, biochemical, and histological studies were performed. RESULTS: magnetic resonance imaging (MRI) of the brain confirmed the presence of a 2.6-cm lesion within the sella turcica extending above the sella and compressing the optic chiasm. Endocrine studies showed elevated serum levels of GH, prolactin, alpha-subunit of glycoprotein hormones, IGF-I, chromogranin a, and GHRH. The patient underwent uneventful transsphenoidal resection of the sellar tumor. Postoperatively, she noted an improvement in symptoms of acromegaly. Histological examination confirmed metastatic endocrine carcinoma to the pituitary, and immunohistochemistry localized GHRH to the tumor cells. The adjacent pituitary exhibited somatotroph hyperplasia with abundant reactivity for GH and alpha-subunit. In addition, there was focal neoplastic transformation to a sparsely granulated somatotroph phenotype with fibrous bodies. CONCLUSION: This is the first report of a GHRH-producing endocrine tumor metastasizing to the pituitary and causing local hyperstimulation with somatotroph hyperplasia and adenomatous transformation.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
5/38. Primary aldosteronism due to a malignant ovarian tumor.A case of a young woman with the syndrome of primary aldosteronism and malignant ovarian tumor is reported. Hormone studies revealed extremely high urinary aldosterone, undetectable plasma renin activity, elevated plasma 17beta estradiol and testosterone, and low plasma FSH and LH. plasma cortisol and urinary 17-hydroxycorticoids were at the upper normal limits. autopsy disclosed an ovarian tumor, histologically an arrhenoblastoma, with polymorphic aspects. The adrenal glands grossly were normal. aldosterone was found by the double radioisotopic technique in the neoplastic tissue.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
6/38. Ectopic ACTH syndrome due to salivary gland adenoid cystic carcinoma.A 68-year-old woman developed cushing syndrome associated with a submaxillary salivary gland adenoid cystic carcinoma. High levels of immunoreactive adrenocorticotrophic hormone (ACTH) were found in the tumor and peripheral blood. Urinary 17-hydroxycorticosteroid levels decreased following administration of dexamethasone, suggesting possible suppression of ectopic ACTH production. however, there was no specific in vitro binding of dexamethasone by tumor cytosol. A trial of metyrapone therapy resulted in control of hypokalemia and hyperglycemia. Both plasma cortisol and 11-deoxycortisol levels decreased with metyrapone administration, suggesting that this agent may inhibit not only 11-beta-hydroxylation, but also possibly earlier steps in glucocorticoid synthesis.- - - - - - - - - - ranking = 2.5keywords = gland (Clic here for more details about this article) |
7/38. Ectopic ACTH, prostatic oat cell carcinoma, and marked hypernatremia.Locally recurrent, poorly differentiated carcinoma of the prostate was associated with hypokalemic alkalosis, marked hypernatremia, diabetes mellitus of recent onset, and hyperosmolar syndrome. These findings, with mild hypertension, in the absence of clinical features of Cushing's syndrome, suggested an ectopic ACTH syndrome. plasma ACTH and cortisol levels were markedly elevated, and failed to suppress in response to either low or high-dose dexamethazone administration. The patient's condition deteriorated rapidly. autopsy findings included carcinoma extensively infiltrating the prostate with extension to the urinary bladder, and metastases confined to the pelvic nodes and soft tissues. The adrenal glands weighed 23 g and showed diffuse hyperplasia. Extract of the prostatic tumor was analyzed for ACTH and showed approximately 40 times normal plasma levels (or about 4,010 pg/g of tissue); ultrastructural features showed secretory granules consistent with ACTH content of the tumor cells. Such cells were positive when stained for ACTH by peroxidase-tagged immunochemical methods. The case fulfills all established criteria for relating excess corticosteroid production and nonpituitary tumors.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
8/38. female pseudohermaphroditism due to a maternal adrenocortical tumor.A 15-yr-old, apparently male, patient presented with a 2-yr history of gynecomastia and poor genital development. A normally formed, but small, penis with a phallic urethra was present, and testes were impalpable. The karyotype was 46,XX, and at laparotomy a uterus, fallopian tubes, and ovaries were found, but there was no testicular tissue. The mother had had regular periods ever since menarche at 14 yr. She had complained of hirsutism since the birth of the child, and on examination 15 yr later had marked clitoromegaly. serum androgens were elevated: testosterone, 4.5 nmol/L (normal, 0.5-3); dehydroepiandrosterone sulfate, 18 mumol/L (normal, 3-12); and androstenedione, 35 nmol/L (normal, 3-8). All failed to suppress with dexamethasone. Abdominal computed tomographic scan revealed a 9 X 6-cm mass in the position of the left adrenal gland. This was removed at laparotomy and found to be an adrenocortical tumor. Postoperatively, the androgens returned to normal. Virilization of a female fetus due to androgens secreted by a maternal adrenal tumor has only been described three times previously, and the presentation has never been delayed so long.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
9/38. Steroidogenesis in an estrogen-producing adrenal tumor in a young woman: comparison with steroid profiles associated with cortisol- and androgen-producing tumors.There is only one previous report of an estrogen-secreting adrenal tumor occurring in a woman during reproductive years. Our patient presented with mild hirsutism associated with menstrual bleeding every 3-6 weeks. The occurrence of apparently intermenstrual bleeding prompted an evaluation of estrogen levels. Markedly elevated plasma estrone levels were found (860-2305 pmol/L; normal, 50-340). Lesser relative elevations in 11-deoxycortisol and androstenedione were noted. Computed tomographic scanning of the adrenal glands identified a large tumor, which was subsequently resected. estrone levels fell to 120 pmol/L, and all other abnormalities were corrected. Eighteen months after adrenalectomy, ovulation occurred regularly, and steroid levels were entirely normal. Steroid production in a cell suspension made from tissue obtained from the 190-g tumor was compared with that occurring in normal human adrenal cells. The production of estrone by the tumor cells was 40-fold greater than that by normal adrenal cells. There was also a mild excess of 11-deoxycortisol produced by tumor cells, but the tumor cells were less than 50% as efficient as normal cells in producing cortisol, dehydroepiandrosterone, androstenedione, testosterone, and dehydroepiandrosterone sulfate. Examination of the steroid profile in plasma occurring in three other patients with adrenal tumors reveals that while elevations in estrone occur frequently, this is usually due to the peripheral conversion of very high levels of androstenedione. estrone, androstenedione, and 11-deoxycortisol plasma levels were elevated in all four patients; dehydroepiandrosterone sulfate was elevated in only two of four patients. After resection of one of these tumors, all steroid levels remained normal despite the occurrence of extensive metastases. These observations confirm the difficulty of making a diagnosis of estrogen excess in a woman during reproductive years because of the paucity of physical signs. The acquisition of aromatase activity was clearly demonstrated by tumor cells from our patient in vitro. Elevated plasma concentrations of estrone, androstenedione, and 11-deoxycortisol provide useful markers for adrenal tumors, but no one steroid can be relied upon in all tumors, and metastases may lack the steroidogenic capabilities of the primary tumor.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
10/38. Ectopic production of parathyroid hormone by small cell lung cancer in a patient with hypercalcemia.Severe hypercalcemia (serum calcium, 4.37-4.84 nmol/L) was found in a 70-yr-old man who had a small cell carcinoma of the lung with multiple metastases. The plasma immunoreactive PTH concentration was markedly elevated, as measured in three different PTH assays [N-terminal PTH, 4,650 ng/L (normal, 230-630); midregion PTH, 13,850 ng/L (normal, 180-560); C-terminal PTH, 9,900 ng/L (normal, less than 1,300)], but at autopsy the parathyroid glands were histologically normal. The PTH concentration of a liver metastasis was 503.5 ng/g wet wt (normal liver, less than 4.2-5.9), and the PTH in the tumor extract eluted at nearly the same position as synthetic human PTH-(1-84) on gel filtration chromatography. Northern blot analysis revealed PTH mRNA in the tumor as a single band of 0.9 kilobase. These results indicate that the ectopic PTH production by the lung cancer was the cause of hypercalcemia in this patient.- - - - - - - - - - ranking = 0.5keywords = gland (Clic here for more details about this article) |
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