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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of thyroid carcinoma is multifactoral. The examples of etiologic factors are: deficit of iodine, genetic predisposition's, female sex, older age, irradiate in childhood, thyroid growth stimulating factors, and epidermal growth factor. Epidemiological data suggested that differentiated thyroid carcinoma depends on sex hormones, especially estrogen. The author have immunohistochemically studied estrogen receptors (ER) in many benign and malignant thyroid tumours. The cases included 8 papillary, 4 follicular, 4 anaplastic, and 1 Hurthle cell carcinomas, 15 follicular adenomas, 4 Hurthle cell adenomas, 8 adenomatous goiter, and 12 parenchymal goiter. Incidences of ER-positive cases were 4/8 in papillary carcinoma, 2/4 follicular carcinoma, 1/1 Hurthle cell carcinoma, 0/4 anaplastic carcinoma, 2/4 Hurthle cell adenoma, and 0/15 follicular adenoma, 0/8 adenomatous goiter, 0/12 parenchymal goiter. Estrogen receptors are commonly detectable in thyroid carcinomas (papillary carcinoma). Estrogens may play an important role as as a promoting factor in thyroid carcinoma. The results of future investigation will explain the possible role of hormones in thyroid pathology and the importance of the sex hormones receptors expression analysis for therapeutic detection.
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PMID:[Estrogen receptors in the malignant and benign neoplasms of the thyroid]. 1010 61

In hepatic adenomatosis, multiple liver cell adenomas (usually > or = 10) generally affects patients with no prior history of oral contraceptive use, androgenic steroid use, or glycogen storage disease. We report a rare case of a 44 year-old female who underwent emergency surgery for hemoperitoneum due to spontaneous rupture of a liver cell adenoma in hepatic adenomatosis, after prolonged use of two different contraceptives (Gestodene and Ethinylestradiol).
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PMID:Ruptured hepatic adenoma in liver adenomatosis: a case report of emergency surgical management. 1043 Mar 73

Colorectal cancer is the third leading cause of cancer death in women. Studies on the potential protective effect of postmenopausal hormone replacement on the incidence of colon cancer have been contradictory. To attempt to clarify the potential protective effect of hormone replacement therapy (HRT), an English-language key word (KW) search of MEDLINE, up to August 1999, was performed for KW colon cancer or colorectal adenoma or colon adenoma or adenomatous polyp and KW estrogen replacement or hormone replacement. Additional references were obtained from reading of the reference lists. Thirty-five studies, including 3 meta-analyses, were found. Of these, 23 suggested any degree of protective effect of HRT, 11 reported neutral results, and 1 reported negative impact of hormone replacement. The single prospective randomized controlled trial included small numbers of inpatients taking high-dose estrogen. However, studies did not uniformly specify hormone type, dose, duration, and potential differential effects on right and left colon. Estrogen and progesterone effects were not often considered separately. Many studies had inadequate control of confounders, for example, family history of colon cancer or indication for endoscopy. Therefore, although the majority of studies, especially more rigorously designed recent studies, support the conclusion that postmenopausal estrogen replacement therapy (ERT) has a protective effect against colon adenomas and colon cancer, methodological limitations preclude practical application of study results at present. Prospective studies are needed to confirm the existence and degree of protective effect, as well as to specify the mechanism of protection.
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PMID:Estrogen replacement therapy and colon cancer: a clinical review. 1059 28

Carcinoma of the colon is common and its incidence varies according to the geographical location and dietary habits. The aims of this paper are, first, to review the current epidemiological data on the incidence and mortality of colon cancer in postmenopausal women using hormone replacement therapy (HRT); second, to review the published data on the prevalence of estrogen receptors in healthy and malignant colonic tissue; and third, to examine the available evidence of gene silencing as applicable to this and other neoplastic conditions. Estrogen use confers overall protection, with a reduction in the incidence of colon adenoma and carcinoma of about 30%. Estrogen use reduces the colon cancer-related mortality. The risk of colon cancer is decreased among current and recent users of postmenopausal HRT but the molecular mechanisms involved remain unclear. Estrogen acts either on a single major transformation step in the oncogenetic process, or is involved in multiple events that avert the course of this transformation. Aberrant methylation of the CpG islands in the promoter regions of the estrogen receptor gene, as well as of other genes, is equivalent to the silencing of that gene, with the consequence of inactivation, or reduced expression, of a number of genes downstream, including tumor suppressor genes. This epigenetic mechanism, when reversed, suppresses the growth of cancer cells in vitro and in vivo. The ubiquitous distribution of the estrogen receptor genes and their isoforms, in a tissue-specific manner, opens new avenues for the understanding of cellular behavior in health and disease.
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PMID:Estrogen and colon cancer: current issues. 1197 57

3 conditions may be responsible for absence of menstruation in women taking the minipill: pregnancy, extrauterine pregnancy, or endometrial atrophy which is the most frequent cause but should be treated only after the other 2 possibilities are excluded. The most frequent cause of pregnancy while taking minipills is error in pill consumption due to forgetting, but malabsorption due to vomiting less than 2 hours after taking the pill or an interaction with some other medication may be responsible. The possibility of extrauterine pregnancy should be systematically considered, and the possibility that a micropill and not a minipill is involved should be ruled out. With a sequential minipill contraceptive efficacy does not reach 100% but iatrogenic amenorrhea is infrequent because of the strong dose of ethinyl estradiol. In the case of a preexisting amenorrhea that does not respond to the estrogen or progestin dose, a prolactin adenoma may be suspected. After 2 consecutive beta tests of pregnancy 8 days apart have been negative, it may be concluded that endometrial atrophy is the cause of the amenorrhea. Unprotected sexual relations should be avoided and the patient should be given a fast-acting combined oral contraceptive such as Lutestral to induce bleeding, after which the minipill can be resumed. If unprotected intercourse occurs there is a risk of pregnancy since amenorrhea and anovulation are not synonymous. A morning after pill can be used if the unprotected sexual relations occurred within the last 72 hours. If a pill was forgotten or probably forgotten before the emenorrhea, the most prudent attitude would be to consider the pill to have been ineffective during the preceding 21 days and to test for pregnancy. Unprotected intercourse should be avoided, a fast-acting combination pill should be prescribed to induce bleeding, and the minipill should then be resumed. Amenorrhea in the 1st month of use after an abortion is not significant. This secondary effect of the minipill should be explained to the patient to avoid unnecessary worry.
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PMID:[Do's and don'ts in treating amenorrhea in women taking the minipill]. 1226 2

The effects of dose and duration of estrogen treatment on cholestasis, hepatic regeneration, and the genesis of liver tumors are evaluated in this work. Estrogens, especially at high doses during pregnancy or after long use of oral contraceptives (OCs), cause a constant diminution of bile secretion which remains subclinical in the great majority of cases. Ethinyl estradiol causes a constant but reversible cholestasis in the rat. 2 categories of cholestasis related to estrogens are distinguished in clinical practice; cholestasis induced by estrogens in pregnancy or in OCs, and cholestasis aggravated or revealed by estrogens, such as primitive biliary cirrhosis. Cholestasis induced by estrogens is dose-dependent, but few clinical data are available on this point. Experience has shown that a woman predisposed to cholestasis due to condition even with low-dose combined OCs. OCs are contraindicated for women genetically predisposed to cholestasis. Evidence has been found of an interaction between estrogen and DNA in the initiation of regenerative processes after experimental hepatectomy. 2 benign liver tumors, hepatic adenomas and focal nodular hyperplasias, have become more common with widespread diffusion of OCs. The role of estrogens in the genesis of hepatic adenomas is well established, but is more controversial with focul nodular hyperplasia. The appearance of low- dose OCs does not seem to have decreased the incidence of benign liver tumors. On the other hand, 2 series totalling 113 cases have demonstrated that the risk of adenoma increases significantly with the duration of treatment, and another study of 32 cases of focal nodular hyperplasia and 12 adenomas showed that most of the women had used OCs for more than 5 years. Both types of tumor carry risks of hemorrhagic accidents, and adenomas at least also carry carcinoma appears more significant in a country like Great Britain with a very low prevalence of such cancers. Benign liver tumors are very rare and should not affect prescription of OCs. A hepatobiliary sonogram should be obtained for women seeking OCs. A sonographic image of a tumor less than 5 cm in diameter with the characteristics of a benign tumor should prompt termination of OCs and reexamination in 4 weeks. If the tumor is over 5 cm in diameter the diagnosis should be confirmed by another technique. The nodular hyperplasias that are large, painful, and easily accessible. Recent epidemiologic studies suggest that the prevalence of asymptomatic lithiases is not very different in OC users and nonusers, but the frequency of complications leading to cholecystectomy is greater in women receiving longterm estrogen treatment. An asymptomatic lithiasis in a young OC user does not necessarily require termination of OCs.
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PMID:[Hepatic and biliary repercussions of estrogens: dose or duration of treatment effect]. 1231 61

A recent case-control study by a team of University of Southern California investigators follows published observations on a total of 107 liver tumors among young women. Most of them were, or had been, oral contraceptive users. The importance of duration of use in the etiology of these tumors was shown by data on 58 women reported at the 1976 annual meeting of the American College of Obstetricians and Gynecologists. Of the 58 women who developed these tumors, 85% had used the pill continuously for more than 4 years. An increasing number of such reports has induced the National Cancer Institute to undertake an investigation regarding these tumors. Almost all of the reported tumors have been benign and described as adenomas, hamartomas, or focal nodular hyperplasia. Some have been without symptoms. Others have been associated with severe abdominal pain or sudden bleeding. A case-control study of 34 young women diagnosed as having benign liver tumors in 1955-1976 was made with appropriate controls. Of the 34 tumor cases, 29 had used oral contraceptives but 26 of the controls had done so also. The tumor patients had taken the pills for significantly longer periods than the controls. The risk of developing liver tumors increased with duration of use and was 2.5 times greater than after 3-5 years than for 1 year or less of use. After 5 years of use, the risk increased sharply to 25 times greater after 9 or more years of pill use. A palpable mass was present in 34% of the cases and severe abdominal pain in 29% of 1 series. Pills containing mestranol seemed more likely to cause liver tumors than those containing ethinyl estradiol. Another report was of 44 case histories published within the past 5 years and 27 new cases reported to the Registry for Liver Tumors Associated with Oral Contraceptives. This Registry was established in 1975. Duration and type of pill use was recorded for 58 of them. Of these, 85% had taken the pill for over 4 years. Mestranol-containing pills had been mostly used. Norethindrone was often used. Of these tumors, 18 ruptured resulting in the death of 8 of the 71 women. In Louisville, 9 cases of benign liver tumors were diagnosed between 1968 and 1974 in women who had used oral contraceptives. No similar tumors had been observed in a comparable age group of women in the previous 13 years. In 1 case, a patient had the tumor removed and resumed the pills. After 6 years a 2nd similar tumor developed. It was not removed but regressed somewhat in 5 months when the oral contraceptive was omitted. In Britain and the U.S., 3 prospective studies of pill users are being conducted. The different types of liver tumors involved seem to have different etiologies. Focal nodular hyperplasia is sometimes found in men but liver-cell adenoma is almost exlusively found in women, many of whom have used oral contraceptives. The Central Registry may resolve some questions.
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PMID:Case control study finds long-term pill use is associated with higher risk of benign liver tumors. 1233 49

The stimulatory role of estrogen on prolactin secretion and on proliferation of lactotropic cells is well established in terms of physiology but could this phenomenon be extended to include harmful effects of estrogens on prolactinoma? The aim of this review is to provide an up-to-date assessment of this subject with regard to pregnancy, use of contraceptive pills and postmenopausal hormone replacement therapy. Dopamine agonists allow women presenting prolactinoma to recover their ovulation cycles and become pregnant. There is no adverse data concerning the safety of dopamine agonists such as bromocriptine, if the woman is treated during the first trimester of pregnancy but there is little information regarding the most recent treatments such as cabergoline or quinagolide. In women with microadenomas, pregnancy generally has little impact on their adenoma, delivery is normal and breast-feeding is allowed. Concerning macroprolactinomas, tumor progression during pregnancy is possible and endocrine follow-up remains necessary. Contraceptive pills containing estrogen and progestins are currently the best-tolerated and the most effective contraception. This type of contraceptive has long been avoided in patients presenting prolactinoma. While the literature has little to say on this subject and provides no adverse information, professional experience suggests that this attitude should be amended and that women presenting microprolactinoma should be allowed to use current contraceptive pills (containing 30 microg or less of ethinyl estradiol). The most important problem to overcome with this type of prescription, which masks the clinical consequences of hyperprolactinemia, is the possibility of overlooking hypophyseal disease that could result from this approach. The problem of macroprolactinoma is different; the possibility of prescribing contraceptive pills must be evaluated on a case-by-case basis and the impact of the drug on the adenoma must be very closely monitored. Estrogen replacement therapy in patients presenting hypogonadism should be attempted in patients with a history of prolactinoma and standard-monitoring precautions should be taken. In menopausal women, when replacement therapy is desirable, the presence of a microprolactinoma should not by itself avoid this prescription.
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PMID:Prolactinoma and estrogens: pregnancy, contraception and hormonal replacement therapy. 1754 Mar 35

Aberrant crypt foci (ACF) are the earliest visible neoplastic lesions in the colorectum. The natural history of these lesions and their role in the adenoma-carcinoma sequence are unknown. We studied ACF in a subset of patients randomized to placebo (n = 17), celecoxib (200 mg twice daily; n = 15), or celecoxib (400 mg twice daily; n = 13) in the Adenoma Prevention with Celecoxib (APC) trial. Magnification chromoendoscopy was done to identify, count, and biopsy ACF within the rectum at baseline and after 8 to 12 months of treatment. A total of 655 ACF were identified in 45 patients. We examined 70 of these ACF histologically, and all 70 were nondysplastic. Cohort characteristics and APC trial treatment results for substudy patients were similar to those of the overall APC trial. There was no significant modulation of ACF by celecoxib (versus placebo; P = 0.77). Immunohistochemical comparison of ACF with adjacent normal mucosa showed that ACF had an increased proliferative index as determined by Ki-67 (P < 0.0001), but lacked other features of neoplasia such as increased cyclooxygenase-2 expression and microvessel density, nuclear localization of beta-catenin, or decreased expression of the tumor suppressors SMAD4, Estrogen Receptor alpha, or MGMT. Only baseline SMAD4 expression in ACF correlated with posttreatment adenoma recurrence (independent of treatment arm; P = 0.01). The presence or number of nondysplastic ACF did not correlate with a higher risk of synchronous advanced or recurrent adenomas. Our overall results indicated that nondysplastic ACF were not accurate surrogate endpoint biomarkers of recurrent colorectal adenomas in the APC trial.
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PMID:Aberrant crypt foci in the adenoma prevention with celecoxib trial. 1913 29

A rare case of an apocrine tumor in the male perineal region is reported. A dermal cystic lesion developed in the region between the anus and scrotum of a 74-year-old Japanese male. The cystic lesion, measuring 3.5 x 5.0 cm in size, was lined by columnar or flattened epithelium with occasional apocrine features and supported by a basal myoepithelium lining. A mural nodule, measuring 1 x 1.5 cm in size, protruded into the cystic space and consisted of a solid proliferation of tubular glands with prominent apocrine secretion and basal myoepithelial cells. Immunohistochemical examination showed that the luminal cells were partially positive for gross cystic disease fluid protein 15 and human milk fat globulin 1, and the basal myoepithelial cells were positive for alpha-smooth muscle actin and S-100 protein. Estrogen and progesterone hormone receptors were focally and weakly positive for luminal epithelium. Although no mammary-like glands were present in the dermis around the tumor, this unusual apocrine tumor has been suggested to be derived from male anogenital mammary-like glands and mimic a mammary-like gland adenoma in the male perineum.
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PMID:Unusual anogenital apocrine tumor resembling mammary-like gland adenoma in male perineum: a case report. 2057 61


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