白细胞介素6与雌激素受体基因对绝经后妇女骨密度的联合效应

目的：探讨白细胞介素（IL）6基因和雄激素受体（ER）基因多态性对绝经后妇女骨密度的联合效应。方法：应用双能X吸收测量法检测205例绝经后妇女的腰椎和股骨颈骨密度;以聚合酶链反应（PCR）扩增IL-6基因多态性区域、产物行7％聚丙酰胺凝胶电泳,根据条带位置,以A-F等位基因命名;ER基因的PCR扩增产物经PvuII和XbaI内切酶酶切后,行1.5％琼脂糖凝胶电泳,其多态性分别用P和p(PvuII)及X和x(XbaI)表示。结果：12位绝经后妇女的IL-6基因型为C/D、C/C和E/E型。193例妇女的IL-6基因为D/D和D/E型,腰椎、股骨颈骨密度和骨生化指标等没有差异,ER基因为pp型妇女股骨颈骨密度显著高于Pp型（P=0.036）;XX型妇女的腰椎骨密度显著高于Xx型（P=0.005）和xx型妇女（P=0.031）,无Pz单倍型（PPXX、ppxx）妇女的腰椎骨密度明显高于有Px单倍型者（PPxx、PPXx、Ppxx、PpXx（P=0.029）。合并IL-6基因D/D、D/E型和ER基因Px单倍型妇女,DD*无Px单倍型者腰椎骨密度显著高于DE*有Px单倍型者（P=0.036）。结论：同时检测ER基因Px单倍型和IL-6基因型,有助于准确发现绝经后妇女骨密度低者。     

北京地区汉族绝经后妇女雌激素受体基因多态性与尺桡骨骨密度相关性研究

目的　研究雌激素受体（ER）基因多态性在北京地区汉族绝经后妇女中的分布及其与骨密度的相关性。方法　对绝经1～4年、年龄49～55岁未行激素替代治疗且无对骨密度有影响疾病的健康绝经后北京市区汉族妇女99例,采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）方法测定ER基因的XbaⅠ和PvuⅡ酶切多态性,用双能X线吸收测量法检测桡骨骨密度（以骨密度T-score值表示）,方差法分析ER基因多态性与骨密度的关系。结果　ER基因PvuⅡ酶切多态性与尺桡骨松质骨（尺桡骨远端）、密质骨（尺桡骨近端）的骨密度无相关性(P>0.05),而ER基因XbaⅠ酶切多态性与尺、桡骨松质骨、密质骨的骨密度有相关性(P<0.05);XX基因型骨密度值最低密质骨为-1.55±0.37、松质骨为-2.54±0.38,xx基因型骨密度值最高密质骨为-0.95±0.24、松质骨为-1.74±0.16。结论　ER基因XbaⅠ酶切多态性与尺、桡骨松质骨、密质骨的骨密度间显著相关,不同个体的基因差异可能影响骨质疏松症的发生、发展。     

影响绝经后妇女骨密度变化的候选基因研究

目的探讨有关候选基因对绝经后妇女骨密度变化的影响。方法对205例绝经后妇女,应用双能X线骨密度仪测定腰椎和股骨颈骨密度。采用PCR测序法,检测护骨素基因多态性;采用PCR-限制性片段长度多态性方法,检测甲状旁腺激素、降钙素受体、骨钙素及瘦素受体基因多态性;采用PCR-琼脂糖凝胶电泳法,检测瘦素基因多态性。结果在护骨素基因第1外显子中,发现1个G-1181C单核苷酸多态性。在校正年龄及体重指数对骨密度的影响后,携带护骨素基因CC型及甲状旁腺激素基因bb型妇女的腰椎骨密度较高,分别为(1.042±0.142)g/cm2及(1.196±0.133)g/cm2。降钙素受体、骨钙素、瘦素及瘦素受体基因与骨密度之间无相关关系。经多元逐步回归分析,护骨素、甲状旁腺激素及骨钙素基因与腰椎骨密度变异有关,甲状旁腺激素基因与股骨颈骨密度的变异有关。结论护骨素及甲状旁腺激素基因与绝经后妇女骨量变异有一定关系,降钙素受体、骨钙素、瘦素及瘦素受体基因与绝经后妇女骨密度变异无关。护骨素基因可能是绝经后妇女发生骨量减少的遗传性标记。     

雌激素受体基因PvuⅡ和XbaⅠ酶切多态性及其上游TA重复序列多态性与子宫内膜癌关系的研究

目的　研究妇女的雌激素受体 (estrogenreceptor,ER)基因多态性与子宫内膜癌的关系 ,从而了解子宫内膜癌的发病因素及影响预后的因素 ,做到早预防、早诊断、早治疗 ,从而改善预后。方法　选取患者 5 2例 ,平均 5 7 5岁。患者的诊断均经手术病理证实。选取非子宫内膜癌患者 5 2例作为对照组 ,平均 5 9 3岁。所有入选者均未服用过激素类药物。用分子生物学的方法分析内切酶PvuⅡ、XbaⅠ限制性片段长度多态性 (re strictionfragmentlengthpolymorphism ,RFLP) ,观察ER基因多态性在实验组与对照组中的基因型分布。RFLP用Pp(PvuⅡ )和Xx (XbaⅠ )来表示。同时对人雌激素受体基因上游的高变区二核苷酸 (TA)重复序列进行纯化、克隆和序列分析 ,阐明该重复序列的重复多态性在实验组与对照组当中的分布情况及与子宫内膜癌的关系。结果实验组X基因型频率为 6 5 4 % ,对照组为 4 4 2 % ,OR值 :2 38(95 %CI 1 0 8～ 5 2 5 ) ,P =0 0 4 8;P基因型 ,OR值 :1 0 9(95 %CI 0 4 9～ 2 4 3) ,P =0 84。PvuⅡ、XbaⅠ限制性片段长度多态性在两组中均呈多态性分布。另外 ,TA重复序列在两组当中也存在着重复次数多态性。结论　实验人群中依XX >Xx >xx基因型子宫内膜癌发病危险呈递减趋势。TA重复序列分别在实验组及对照     

绝经前全子宫切除保留卵巢对妇女骨代谢及骨密度的影响

目的 :追踪观察绝经前妇女全子宫切除保留卵巢对远期骨代谢及骨密度的影响。方法 :对比观察绝经前行全子宫切除保留单侧卵巢 4 8例、全子宫切除保留双侧卵巢 15例和正常妇女 30例的血清钙 (Ca)、血清磷 (P)、血清碱性磷酸酶 (AKP)、血清骨钙素(BGP)、空腹尿Ca Cr及尿HYP Cr值、骨密度值的变化和差异。结果 :全子宫切除保留单侧卵巢组血AKP值、BGP值、空腹尿Ca Cr和尿HYP Cr均显著高于对照组 (P <0 0 5 ) ,而骨密度值则显著低于对照组 (P <0 0 5 )。保留双侧卵巢组尿HYP Cr显著高于对照组 (P <0 0 5 )。结论 :子宫全切除保留单侧卵巢者远期骨转换加快 ,导致骨丢失及骨密度下降 ,双侧卵巢保留者骨吸收亦加快 ,但骨密度无下降     

汉、维族子宫内膜异位症与雌激素受体基因多态性的关系

目的:观察雌激素受体(ER)基因多态性在新疆维吾尔族(维族)及汉族妇女中的分布及其与子宫内膜异位症(内异症)的关系。方法:应用PCR-RFLP技术,分别检测107名维吾尔族健康妇女(维族对照组)及65例内异症患者(维族内异症组),105名汉族健康妇女(汉族对照组)及85例内异症患者(汉族内异症组)的ER基因XbaⅠ和PvuⅡ酶切多态性。结果:ER基因型频率分布符合Harey-weinberg平衡定律。XbaI酶切多态性基因型频率,等位基因频率分别在维、汉族内异症组及对照组比较,差异无显著性(P>0.05)。但PvuⅡ酶切多态性基因型频率,等位基因频率在维族内异症组与对照组间比较,差异均有显著性(P<0.05),在汉族内异症组与对照组之间比较,差异无显著性(P>0.05)。维、汉族的内异症组和对照组比较,两内异症组的PvuII多态性和两对照组的XbaI多态性差异均有显著性(P<0.05)。结论:ER XbaⅠ酶切多态性与维、汉族内异症发病均无关,而PvuⅡ酶切多态性与维族内异症发病有关,与汉族无关。维、汉族内异症发病可能存在不同的遗传易感因素,PvuⅡ基因多态性可能是维族妇女子宫内膜异位症发病的危险因素之一。     

缓释左旋-18甲基炔诺酮皮埋避孕剂对骨密度和骨代谢的影响

对采用 Norplant R埋植剂和仿制 Norplant的国产埋植剂 型避孕的育龄妇女骨密度和骨代谢改变进行了 1年的随机前瞻性临床观察。 6 1例正常妇女被分为两组 :Norplant埋植剂组 30例 ,国产埋植剂组 31例。两组于埋植前和埋植后第 12个月时采用双能 X线骨密度测定仪 (DEXA)分别测定了腰椎 L2 ～ L4、股骨近端骨密度和骨矿含量。两组妇女埋植后第 12个月时腰椎 L2 ～ L4骨密度和骨矿含量均较埋植前明显增加 (P<0 .0 1) ,Norplant组骨密度平均增加2 .40 % ,骨矿含量平均增加 3.34 % ,国产埋植剂组分别增加 2 .75 %和 4.47% ;从年龄分析 ,以 2 5～ 2 9岁组腰椎 L2 ～ L4骨密度埋植后增加最为显著 ,Norplant组 P<0 .0 5 ,国产埋植剂组 P<0 .0 1。国产埋植剂组妇女埋植后第 12个月时股骨大粗隆骨密度和骨矿含量较埋植前明显增加 (P<0 .0 1) ;国产埋植剂组妇女空腹尿羟脯氨酸 /肌酐比值埋植后第 12个月时较埋植前明显下降 (P<0 .0 1) ;对使用妇女腰椎、股骨骨密度和骨代谢生化指标的影响 ,在两种埋植剂之间埋植前后比较均无显著差别 (P>0 .0 5 )。左旋 - 18甲基炔诺酮皮埋避孕剂对绝经妇女的骨骼是非有害的 ,对年轻妇女骨峰值的获得无明显影响。     

雌激素受体α基因多态性与妊娠肝内胆汁淤积症相关性研究

目的探讨雌激素受体α（ERα）基因多态性与妊娠肝内胆汁淤积症（ICP）发病的关系.方法应用PCR-限制性片段长度多态性（PCR-RFLP）技术,对100例ICP患者（ICP组）和100例正常孕妇（对照组）ERα基因1号内含子Xba Ⅰ和PvuⅡ酶切多态性进行分析.结果（1）对照组ERα基因的Xba Ⅰ基因型XX、Xx、xx频率分别为6%、33%、61%,ICP组分别为2%、33%、65%,两组比较,差异无统计学意义（P＞0.05）;对照组等位基因X、x频率分别为23%、78%,ICP组分别为19%、82%,两组比较,差异也无统计学意义（P＞0.05）.（2）对照组ERα基因的PvuⅡ基因型PP、Pp、pp频率分别为18%、42%、40%,ICP组分别为12%、53%、35%,两组比较,差异无统计学意义（P＞0.05）;对照组等位基因P、p频率分别为39%、61%,ICP组分别为39%、62%,两组比较,差异也无统计学意义（P＞0.05）.（3）ERα基因的Xba Ⅰ和PvuⅡ组合基因型在两组间分布比较,差异无统计学意义（P＞0.05）.结论ERα基因多态性与ICP发病无关.     

雷洛昔芬对绝经后妇女骨密度、骨代谢生化指标和血脂影响的随机对照研究

目的　确定盐酸雷洛昔芬 (RLX)对中国绝经后妇女骨密度、骨代谢生化指标及血脂的影响。方法　将来自 3所医院的 2 0 4例绝经后妇女 [平均年龄 (6 0± 5 )岁 ,平均体重 (6 3± 9)kg]随机分组 ,进行双盲安慰剂对照的临床研究 ,受试者每天接受RLX 6 0mg(n =10 2 ,RLX组 )或安慰剂 (n =10 2 ,安慰剂组 )治疗 12个月 ,并于服药前及服药 12个月后各进行一次骨密度、骨代谢生化指标及血脂的测定。结果　与安慰剂相比 ,RLX使腰椎和髋部骨密度显著升高 ,RLX组腰椎的骨密度增加2 30 % ,而安慰剂组降低 0 0 8% ,两组比较 ,差异有极显著性 (P <0 0 0 1) ;RLX组髋部骨密度增加2 4 6 % ,安慰剂组增加 1 0 7% ,两组比较 ,差异有显著性 (P <0 0 5 )。RLX组骨代谢生化指标血清骨钙素和血清C端交联肽分别降低 2 7 6 %和 2 4 0 % ,而安慰剂组则分别降低 10 6 %和升高 15 8% ,两组比较 ,差异有极显著性 (P <0 0 0 1)。RLX组总胆固醇和低密度脂蛋白胆固醇分别降低 6 4 %和34 6 % ,而安慰剂组则分别升高 1 4 %和降低 19 1% ,两组比较 ,差异有极显著性 (P <0 0 0 1)。两组间高密度脂蛋白胆固醇和甘油三酯水平未见差异。仅有 5例因不良事件而提前退出研究 (RLX组 3例 ,安慰剂组 2例 )。结论　RLX能增加绝经后中国妇女     

缓释左旋-18甲基炔诺酮皮埋避孕剂

时采用NorplantR埋植剂和仿制Norplant的国产埋植剂I型避孕的育龄妇女骨密度和骨代谢改变进行了1年的随机前瞻性临床观察.61例正常妇女被分为两组Norplant埋植剂组30例,国产埋植剂组31例.两组于埋植前和埋植后第12个月时采用双能X线骨密度测定仪(DEXA)分别测定了腰椎L2～L4、股骨近端骨密度和骨矿含量.两组妇女埋植后第12个月时腰椎L2～L4骨密度和骨矿含量均较埋植前明显增加(P＜0.01),Norplant组骨密度平均增加2.40%,骨矿含量平均增加3.34%,国产埋植剂组分别增加2.75%和4.47%;从年龄分析,以25～29岁组腰椎L2～L4骨密度埋植后增加最为显著,Norplant组P＜0.05,国产埋植剂组P＜0.01.国产埋植剂组妇女埋植后第12个月时股骨大粗隆骨密度和骨矿含量较埋植前明显增加(P＜0.01);国产埋植剂组妇女空腹尿羟脯氨酸/肌酐比值埋植后第12个月时较埋植前明显下降(P＜0.01);对使用妇女腰椎、股骨骨密度和骨代谢生化指标的影响,在两种埋植剂之间埋植前后比较均无显著差别(P＞0.05).左旋-18甲基炔诺酮皮埋避孕剂对绝经妇女的骨骼是非有害的,对年轻妇女骨峰值的获得无明显影响.     

雌激素受体基因与女性骨密度的关系

目的观察雌激素受体基因型与妇女骨密度的关系。方法采用双能X线吸收骨密度仪测量78例绝经后妇女、23例围绝经期妇女和52例25～35岁妇女的骨密度,用聚合酶链反应限制性片段长度多态（PCR-RFLPs）方法分析雌激素受体基因型。结果在78例绝经后妇女中,各种基因型的骨密度差异无显著性（P>0.05）。在52例年轻妇女中,仅在Ward三角,pp型的骨密度（0.823±0.095）g/cm2,较PP型的（0.665±0.071）g/cm2高（P=0.037）,其他部位各基因型间的骨密度差异无显著性（P>0.05）;联合分析PvuⅡ和XbaⅠ位点,xxpp型的全身、腰椎、大转子、髋部和Ward三角的骨密度比其他几种组合基因型的骨密度高（P均<0.05）;在绝经后妇女中,各种组合基因型的骨密度差异无显著性（P均>0.05）。结论基因型xxpp型可能提示腰椎、大转子、髋部和Ward三角的峰值骨密度较高,但雌激素受体基因型与绝经后妇女的骨密度无相关性。     

Relationship between estrogen receptor-alpha polymorphism and serum levels of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, C-reactive protein and homocysteine in postmenopausal women.

BACKGROUND AND AIM: Genetic variation in the estrogen receptor-gene (ERalpha) may influence the risk of cardiovascular diseases in postmenopausal women. This effect, at least in part, may be dependent on the decrease in expression of injury and inflammatory markers in the vascular wall. The aim of the present study was to evaluate the relationship between ERalpha PvuII and XbaI polymorphisms and serum levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), C-reactive protein (CRP) and homocysteine in postmenopausal women. SUBJECTS AND METHODS: Subjects of the study were 64 postmenopausal women. PvuII and XbaI ERalpha gene polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Mean sVCAM-1 level was significantly higher in pp homozygotes in comparison with PP homozygotes and Pp heterozygotes, as well as higher in xx homozygotes in comparison with XX homozygotes and Xx heterozygotes. Levels of sVCAM-1 were also significantly higher in women with px haplotype compared with PX and Px haplotypes. There were no relationships between investigated genotypes or haplotypes and levels of sICAM-1, CRP and homocysteine. CONCLUSION: The results of our study suggest that genetic variation in ER gene may influence blood levels of VCAM-1 in women after the menopause.     

Association of bone mineral density with vitamin D and estrogen receptor gene polymorphisms during GnRH agonist treatment

AIMS: This study examined whether or not a decrease in bone mineral density (BMD) induced by the use of gonadotropin-releasing hormone agonist (GnRHa) during sexual maturation is affected by vitamin D receptor and/or estrogen receptor gene polymorphisms, like the phenomenon observed during the postmenopausal period. METHODS: In 43 patients who received GnRHa therapy for 6 months to treat uterine myoma or endometriosis at our department and who were confirmed to have pituitary down-regulation, we measured bone density before and after GnRHa treatment using DXA and analyzed the bone metabolism turnover using bone metabolic markers. Polymorphisms were analyzed by RFLP using FokI and TaqI for the vitamin D receptor gene and PvuII and XbaI for the estrogen receptor gene. The then determined gene polymorphism was analyzed in relation to the percentage decreases in BMD following GnRHa treatment. RESULTS: The patients were divided by f, t into two groups: (f, t) < 2 (Group V-I) and (f, t) > or = 2 (Group V-II). They were also divided by P, x into two groups (P, x) < 3 (Group E-I) and (P, x) > or = 3 (Group E-II). The BMD change was significantly higher in Group V-II than in Group V-I. Group E-II tended to have a higher BMD change than Group E-I, although this difference was not statistically significant. CONCLUSION: Patients who often have f and t polymorphism are more likely to show BMD reduction following GnRHa therapy, like the phenomenon seen during the postmenopausal period, than patients with other gene polymorphisms. Measures to avoid BMD reduction are required when using GnRHa in such patients.     

PvuII genetic polymorphism of estrogen receptor alpha in the group of postmenopausal women with osteopenia and osteoporosis

DESIGN: It was suggested that genetic factors play an important role in the regulation of bone mineral density and in the pathogenesis of bone fracture in osteoporosis. PvuII restriction polymorphism in the intron 1 of the gene coding estrogen receptor alpha (ER-alpha) is indicated to play a significant role in osteopenia and osteoporosis development. The goal of our study was to determine the frequency and the significance of PvuII polymorphism of the ER-alpha gene in the group of postmenopausal women with osteopenia and osteoporosis. MATERIALS AND METHODS: 93 postmenopausal women with osteopenia and osteoporosis (t-score lower than (-1), and 141 healthy postmenopausal women have been investigated for PvuII polymorphism of the ER-a gene using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) assays. RESULTS: We have observed higher frequency of homozygous genotype PP (25.8 vs. 19.8%) and P allele (50.6 vs. 46.1%) in the group of women with low level of t-score. In the osteopenic women (-2.5 < T-score < -1.0) the significant difference in the distribution of t-score index and genotypes has been found. t-score index correlated with body mass index (BMI), mean body weight, BMD aged matched (AM) and BMD young adults (YA) index. The AM and YA index correlated with the number of pregnancies. CONCLUSIONS: The presence of PP genotype and P allele could be connected with higher bone loss and with the development of osteopenia and osteoporosis in postmenopausal women.     

The expression of the estrogen receptor in obese patients with high breast density (HBD)

Objective: Obesity has been associated with increased risk for breast cancer (BC) mortality. Verifying in women with high breast density (HBD) post-menopausal, the frequency of polymorphisms of estrogen receptor (ER)α-PvuII, ERα-XbaI and if they influence the body mass index (BMI).

Methods: Study with 308 women with HBD post-menopause divided into two groups according to BMI: 1st group?=?BMI?2, 2nd group?=?BMI?≥?25?kg/m². It was characterized in the clinical history: menarche, menopause, parity, family history of BC, smoking and alcohol intake.

Results: Allele and genotype frequencies for the ERα-397-Pvull and ERα-351-XbaI: P?=?43.99%, p?=?56.01%, pp?=?32.14%, Pp?=?47.73%, PP?=?X?=?20.13% and X?=?41.56%, x?=?58.44%; xx?=?33.44%; Xx?=?50.00%; XX?=?16.56%, respectively. Both PvuII and XbaI influenced BMI. When XbaI is mutated the tendency is toward higher BMI (0.039), and women with lower BMI were more frequent in PvuII genotype (p?=?0.002). More frequent risk factors for BC: menarche before the age of 12 years (35.38%), nulliparity or 1st child after 28 years old (41.66%), family history of BC (19.16%) and overweight/obesity (62.01%).

Conclusion: Variations in the ERα gene affected the BMI in women with HBD, who already are at increased risk for BC.     

Estrogen receptor α gene (ESR1) polymorphisms associated with idiopathic premature ovarian failure in Chinese women

Objective: To evaluate the relationship between Estrogen receptor α gene (ESR1) polymorphisms and idiopathic premature ovarian failure (POF) in Chinese women. Methods: 155 idiopathic POF and 150 healthy controls were recruited in this study. All subjects were analyzed at the PvuII and XbaI loci of the ESR1 gene using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). Results: The frequency of the P allele of the PvuII polymorphisms was 38.1% in POF women, which was significantly higher than controls (28.0%) (p = 0.008). And for the XbaI polymorphisms, the X allele was 21.0% in POF patients, compared to 13.3% in control women (p = 0.013). Carriers of the PP genotype had higher increased risk of POF than those of the pp genotypes (p = 0.011), whereas in three genotypes of the XbaI polymorphisms, no difference was found in the prediction value of POF. In addiction, the P-X haplotype was associated with a significantly increased risk for idiopathic POF. Conclusion: These data suggest that the PvuII and XbaI polymorphisms of ESR1 gene are associated with POF, which may be a potential genetic risk factor of idiopathic POF. More researches are needed to determine whether the findings are generalizable to other populations.     

Association of CYP1A1 and CYP1B1 polymorphisms with bone mineral density variations in postmenopausal Mexican-Mestizo women

Herein, we investigated potential associations between polymorphisms of genes related to estrogen metabolism and bone mineral density (BMD) in postmenopausal women. This was a cross-sectional study, in which two hundred and ninety postmenopausal Mexican-Mestizo women were studied. The BMD of the lumbar spine (LS), total hip (TH), and femoral neck (FN) was measured. The distribution of the genetic polymorphisms, including rs1799814 and rs1048943 at CYP1A1 as well as rs1056836 at CYP1B1, were analyzed by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP), single-stranded conformational polymorphism (SSCP), and DNA sequencing. Deviations from Hardy–Weinberg equilibrium (HWE) were tested, and linkage disequilibrium (LD) was calculated by direct correlation (r²). Moreover, haplotype analysis was performed. All polymorphisms were in HWE. The genotype and allele distributions of the three single nucleotide polymorphisms (SNPs) studied showed no significant differences. However, statistical significance was reached when constructing haplotypes. The CG haplotype in CYP1A1 was associated with variations in LS and FN BMD after adjustment for covariates (p?=?0.021 and 0.045, respectively), but the association with TH BMD was not significant. These results suggested that the CG haplotype in CYP1A1 may play an important role in the mechanism of osteoporosis and may be useful as a genetic marker.     

Effects of aromatase inhibitors letrozole and anastrazole on bone metabolism and steroid hormone levels in intact female rats.

AIM: The present study was designed to investigate the effects of two aromatase inhibitors on steroid hormone levels, bone mineral density (BMD) and bone turnover markers in intact female rats. METHODS: Letrozole and anastrazole at two different dose levels were investigated for their effect on serum levels of estradiol, androstenedione, testosterone, dehydroepiandrosterone and dehydroepiandrosterone sulfate, BMD of femur and dorsal spine, and osteocalcin and pyridinoline levels as bone turnover markers. Fifty intact female rats were randomly divided in five groups (group 1 (n = 10): control, 2 ml saline; group 2 (n = 10): letrozole 1 mg/kg; group 3 (n = 10): letrozole 2 mg/kg; group 4 (n = 10): anastrazole 0.1 mg/kg; group 5 (n = 10): anastrazole 0.2 mg/kg, and oral gavages were applied for a period of 16 weeks. RESULTS: Both doses of letrozole and anastrazole did not change femoral and vertebral BMD. Serum estradiol levels were reduced significantly at all dose levels by both agents (p < 0.001); all androgen levels were significantly elevated by letrozole (p < 0.05), although anastrazole increased only androstenedione (p < 0.05). The higher dose of letrozole increased osteocalcin levels (p < 0.05), while pyridinoline levels were increased (p < 0.05) by the higher dose of anastrazole. CONCLUSION: Our results indicate that short-term use of letrozole and anastrazole had no clear effects on BMD in intact rats. Further investigations are needed to understand their effects on bone metabolism in intact females.