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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A histopathologic review of 1985 cases of endometrial carcinoma yielded 31 undifferentiated carcinomas (1.6%). Forty-eight percent were large cell type and 52%, intermediate/small cell type. Twenty-one tumors were examined immunohistochemically. All stained for keratin. Eleven tumors reacted with vimentin antibodies, two with carcinoembryonic antigen antibodies, and ten with neuron-specific enolase (NSE) antibodies (four of which stained for bombesin, two for beta-endorphin, one for prealbumin, five for Leu7, and four for synaptophysin). The mean age at diagnosis was 63.9 years (range, 45 to 86). The crude 5-year and 10-year survival was 58% and 48%, respectively. Seventy-nine percent of the patients in surgicopathologic Stage I and 33% in Stage II survived 5 years. The intermediate/small cell types had a somewhat better prognosis than the large cell type, but the difference was not statistically significant. The presence or absence of NSE and vimentin immunoreactivity had no influence on survival. All patients with tumors infiltrating less than one half of the myometrium survived 5 years in contrast with 46% of the patients with deep infiltrating tumors. Fifty-four percent of the patients with demonstrable vessel invasion survived 5 years in contrast with 89% not so affected.
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PMID:Undifferentiated carcinoma of the endometrium. A histopathologic and clinical study of 31 cases. 204 61

As is obvious from the previous discussions, obesity is associated with a wide variety of changes in endocrine parameters (Table 1). Some of these changes, such as the reduction in SHBG without change in serum free testosterone levels, reflect merely laboratory abnormalities that may influence interpretation of diagnostic tests but have no important physiologic relevance. Other abnormalities have major clinical impact, such as hyperestrogenemia-endometrial carcinoma and hyperlipidemia-coronary artery disease. In some cases, endocrine changes in obesity are beneficial--that is, hyperestrogenemia leading to lower incidence of osteoporosis. In other cases, such as the profound suppression of growth hormone output in obesity, the physiologic relevance is unknown. Several endocrine changes in obesity, such as the impaired response of many hormones (growth hormone, prolactin, vasopressin, corticotropin) to insulin-induced hypoglycemia and elevated endorphin levels, suggest hypothalamic dysfunction. Furthermore, the failure of all of these abnormalities to be normalized after weight reduction raises the possibility of an underlying disorder leading to both endocrine dysfunction and obesity, rather than the endocrine dysfunction being simply a consequence of the obesity. Successful elucidation of the pathogenesis of obesity, which might then lead to much needed specific treatment modalities, may be advanced if we can solve some of these puzzles.
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PMID:Endocrine aspects of obesity. 264 1

Fourteen of fifty-three cases of endometrial carcinoma (26 per cent) contained varying, usually small numbers of argyrophil cells, as demonstrated by Grimelius silver nitrate staining of formalin-fixed paraffin-embedded sections. In eight cases the argyrophilia was present in the apical region of glandular cells (type 1 cells) or throughout the cytoplasm of glandular or squamous cells (type 2 cells). The distribution of argyrophilia in these cells closely paralleled that of mucin or glycogen, and pretreatment of the sections with disease resulted in a loss of argyrophilia in the glycogen-rich tumors. In six cases individual round, ovoid, and flask-shaped argyrophilic cells were present also within the glandular epithelium (type 3 cells). In all six cases, similarly distributed cells were positive immunohistochemically for serotonin. Immunohistochemical staining for a battery of polypeptide hormones (calcitonin, gastrin, somatostatin, adrenocorticotropin [ACTH], and neurotensin) revealed positive staining for ACTH in one of the six tumors that contained type 3 cells and positive staining for somatostatin in another. Ultrastructural examination of the ACTH- and serotonin-positive tumor disclosed cells with granules 80 nm in diameter. Types 1 and 2 argyrophil cells were found in small numbers in several specimens of normal proliferative and secretory endometrium, but type 3 argyrophil cells were not identified in these specimens. Although focal argyrophilia is a frequent feature of endometrial carcinomas (26 per cent), the presence of type 3 argyrophil cells containing hormones, as evidenced by the immunohistochemical demonstration of serotonin and occasionally polypeptide hormones, is much less common (11 per cent).
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PMID:Endometrial carcinoma with argyrophil cells: a histochemical and immunohistochemical analysis. 614 92

Studies in our laboratory and elsewhere have demonstrated numerous abnormalities of steroid and polypeptide hormone secretion in obesity: hyperestrogenemia and hypogonadotropic hypogonadism in obese men; diminished SHBG levels in both sexes; elevated free testosterone and free estradiol in obese women; PCOS-like gonadotropin and sex-hormone abnormalities in obese women; elevated serum insulin in both sexes; blunted stimulability of prolactin, growth hormone, and vasopressin in both sexes; and elevated basal levels and blunted stimulability and suppressibility of beta-endorphin in both sexes. All of these abnormalities have been clearly shown to be partly or completely reversible with weight loss, with the exception of the endorphin abnormalities. In that area, four out of the five studies reported show no reversibility with weight loss. Reversibility of nearly all the hormonal abnormalities of obesity (i.e., all but the hyperendorphinemia) by weight loss suggests that none of them is causative of obesity. Nevertheless, some of the reversible abnormalities may secondarily amplify the morbidity associated with obesity: the hyperinsulinemia may be related to the increased risk of hypertension, hyperlipidemia, coronary disease, and Type II diabetes; the elevated levels of free estradiol in obese women may be related to their increased risk of breast and endometrial cancer. The role of hyperendorphinemia in obesity clearly requires further investigation, since it is the only observed hormonal abnormality that appears to be non-reversible by weight loss, and also since there seems to be increased sensitivity to beta-endorphin in obesity. The possibility that endorphin abnormalities may be causal in obesity cannot be ruled out.
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PMID:A perspective on the hormonal abnormalities of obesity: are they cause or effect? 1635 9

Small-cell carcinoma (SCC) of neuroendocrine type is an uncommon tumor of the endometrium. No previous report has documented Cushing's syndrome due to ectopic ACTH production by SCC of the endometrium. We describe a 56-year-old Japanese woman with SCC of the endometrium and multiple lung metastases presenting as Cushing's syndrome. The patient was referred to our hospital because of general fatigue with facial and leg edema, and multiple nodular lesions in the bilateral lungs on chest X-ray examination. A physical examination revealed that the patient had moon face, buffalo hump, and truncal obesity. Endocrinological examinations confirmed ACTH-dependent Cushing's syndrome. Thoracic computed tomography imaging showed multiple nodular lesions in the bilateral lungs. Abdominal magnetic resonance imaging suggested a malignant tumor of the uterus. The patient received a lung tumor biopsy and surgical hysterectomy. The endometrial carcinoma was histologically a SCC admixed with endometrioid adenocarcinoma. The SCC of the endometrium showed immunoreactivity for pro-opiomelanocortin, ACTH, and vimentin, but not for thyroid transcription factor-1. The lung biopsy specimen had the same features. These findings indicated that the SCC originated from the endometrium, and the ectopic ACTH-producing tumor caused Cushing's syndrome. This study provides the evidence that SCC of endometrial origin was an ectopic ACTH-producing tumor causing Cushing's syndrome.
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PMID:Small-cell carcinoma of the endometrium presenting as Cushing's syndrome. 1983 52