Diss. (sammanfattning) Linköping : Univ., 2001. / Härtill 4 uppsatser.

I found that 2.6ml of 0.5% levobupivacaine had similar clinical characteristics as the same volume of 0.5% bupivacaine in spinal anaesthesia. Both were effective for spinal anaesthesia in urological surgery, when a sensory block up to at least T10 dermatome was required. In comparing the use of levobupivacaine alone and levobupivacaine with fentanyl, there were no significant differences in haemodynamic changes and quality of sensory and motor block, when 2.6ml of levobupivacaine alone or 2.3ml of levobupivacaine with fentanyl 15mcg (0.3ml) were used in spinal anaesthesia. Both were effective for spinal anaesthesia in urological surgery. In comparing the use of ropivacaine 10mg and bupivacaine 10mg, both with fentanyl 15mcg in spinal anaesthesia for urological surgery, all the patients achieved adequate level of sensory block up to T10 dermatome or higher. The two drugs were similar in the onset time of motor block, the characteristics of sensory block and haemodynamic changes; however, the duration of motor block was shorter with ropivacaine. I concluded that both studied solutions, ropivacaine-fentanyl and bupivacaine-fentanyl, were effective for spinal anaesthesia in urological surgery and the duration of motor block was shorter with the ropivacaine-fentanyl solution. The dose-response relationship of ropivacaine in spinal anaesthesia for lower limb surgery requiring a sensory block up to at least the T12 dermatome was defined. Anaesthesia was successful in 0, 0, 42, 83 and 100% when ropivacaine at doses of 2, 4, 7, 10 and 14mg respectively were given. The derived values for ED50 and ED95 were 7.6mg and 11.4mg respectively. The cephalic level of sensory block and the degree of motor block increased with larger doses of ropivacaine. Finally, the median effective dose (ED50) of bupivacaine, levobupivacaine and ropivacaine in spinal anaesthesia for lower limb surgery were defined as 5.50mg (95% CI: 4.90--6.10mg), 5.68mg (95% CI: 4.92--6.44mg), and 8.41mg (95% CI: 7.15--9.67mg) respectively. The relative potency ratios were 0.97 (95% CI: 0.81--1.17) for levobupivacaine/bupivacaine, 0.65 (95% CI: 0.54--0.80) for ropivacaine/bupivacaine and 0.68 (95% CI: 0.55--0.84) for ropivacainellevobupivacaine. / In this series of studies, I have shown that levobupivacaine and ropivacaine are effective local anaesthetic agents for spinal anaesthesia in lower limb and urological surgery. This proved my hypothesis. Both are suitable alternatives to bupivacaine for spinal anaesthesia. Furthermore, these studies showed that ropivacaine is less potent than levobupivacaine and bupivacaine and the potency is similar between levobupivacaine and bupivacaine at median effective dose. / Levobupivacaine and ropivacaine are two relatively new local anaesthetics which were developed in view of their potential for less cardiotoxicity in comparison with bupivacaine, the most common local anaesthetic used in spinal anaesthesia for many years. Both are produced in pure S(-) enantiomer form in contrast to bupivacaine which is a racemic mixture. They have been shown to be effective in peripheral nerve blocks, and epidural analgesia and anaesthesia; nevertheless, experience of their use in spinal anaesthesia is limited. The objective of this thesis was to evaluate their use in spinal anaesthesia for surgery in non-obstetric patients. My hypothesis was that levobupivacaine and ropivacaine are effective local anaesthetic agents for spinal anaesthesia in lower limb and urological surgery. In order to test this hypothesis, I conducted five clinical studies on 269 patients who had urological surgery or lower limb surgery under spinal or combined spinal-epidural anaesthesia. First, I investigated the efficacy and clinical characteristics of levobupivacaine and the mixture of levobupivacaine with fentanyl in spinal anaesthesia. Next, I compared the use of ropivacaine-fentanyl with bupivacaine-fentanyl in spinal anaesthesia. Finally, I defined the dose-response relationship of ropivacaine in spinal anaesthesia using traditional dose-response methodology and defined the relative potency among levobupivacaine, ropivacaine and bupivacaine by comparing the defined ED50 in spinal anaesthesia using up-down sequential allocation method. / Lee, Ying Yin. / Source: Dissertation Abstracts International, Volume: 73-06, Section: B, page: . / Thesis (M.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 133-150). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.

Tsang Yuen-Man. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 200-218). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABBREVIATIONS --- p.iii / ABSTRACT --- p.vii / CHINESE ABSTRACT --- p.xi / TABLE OF CONTENTS --- p.xiii / Chapter CHAPTER 1: --- GENERAL INTRODUCTION / Chapter 1.1 --- Hematopoiesis --- p.1 / Chapter 1.1.1 --- An Overview on Hematopoiesis --- p.1 / Chapter 1.1.2 --- Role of Cytokines in the Control of Hematopoiesis --- p.4 / Chapter 1.2 --- Leukemia --- p.5 / Chapter 1.2.1 --- Abnormalities in Hematopoietic Cell Development --- p.5 / Chapter 1.2.2 --- Classification of Leukemia --- p.7 / Chapter 1.2.3 --- Etiology and Symptoms of Leukemia --- p.9 / Chapter 1.2.4 --- Therapeutic Strategies for Leukemia --- p.10 / Chapter 1.2.4.1 --- Conventional Therapies --- p.10 / Chapter 1.2.4.2 --- Differentiation Therapy and Induction of Apoptosis in Leukemia --- p.11 / Chapter 1.2.5 --- Regulation of Apoptosis and Cell Cycle Progression --- p.12 / Chapter 1.2.5.1 --- Apoptosis --- p.12 / Chapter 1.2.5.2 --- Cell Cycle --- p.13 / Chapter 1.2.5.3 --- Disregulation of Apoptosis and Cell Cycle Contribute to the Development of Leukemia --- p.14 / Chapter 1.3 --- Licorice --- p.16 / Chapter 1.3.1 --- Chemistry of Licorice --- p.16 / Chapter 1.3.2 --- Pharmacological Activities of Glycyrrhizin and 18-β Glycyrrhetinic Acid --- p.22 / Chapter 1.3.2.1 --- Mineralocorticoid Activity --- p.22 / Chapter 1.3.2.2 --- Anti-inflammatory Effect --- p.23 / Chapter 1.3.2.3 --- Anti-allergic Effect --- p.24 / Chapter 1.3.2.4 --- Enhancement of Immune Response --- p.24 / Chapter 1.3.2.5 --- Anti-hepatotoxic Effects --- p.26 / Chapter 1.3.2.6 --- Anti-viral Activity --- p.27 / Chapter 1.3.2.7 --- Anti-carcinogenic and Anti-tumor Effects --- p.28 / Chapter 1.3.3 --- Other Biological Activities of Licorice --- p.30 / Chapter 1.3.4 --- A 96-kDa Glycyrrhizin-Binding Protein (gb96) --- p.31 / Chapter 1.3.5 --- Evaluation of Health Hazard --- p.32 / Chapter 1.4 --- Aims and Scopes of This Research --- p.34 / Chapter CHAPTER 2: --- MATERIALS AND METHODS / Chapter 2.1 --- Materials --- p.37 / Chapter 2.1.1 --- Animals --- p.37 / Chapter 2.1.2 --- Cell Lines --- p.37 / Chapter 2.1.3 --- "Cell Culture Medium, Buffers and Reagents" --- p.39 / Chapter 2.1.4 --- Recombinant Cytokines --- p.42 / Chapter 2.1.5 --- [methyl-3H] Thymidine (3H-TdR) --- p.43 / Chapter 2.1.6 --- Liquid Scintillation Cocktail --- p.44 / Chapter 2.1.7 --- Reagents and Buffers for Flow Cytometry --- p.44 / Chapter 2.1.8 --- Monoclonal Antibodies --- p.45 / Chapter 2.1.9 --- Reagents for DNA Extraction --- p.47 / Chapter 2.1.10 --- Reagents for Total RNA Isolation --- p.48 / Chapter 2.1.11 --- Reagents and Buffers for RT-PCR Study --- p.49 / Chapter 2.1.12 --- Reagents and Buffers for Gel Electrophoresis --- p.55 / Chapter 2.1.13 --- Reagents and Buffers for Western Blot Analysis --- p.56 / Chapter 2.2 --- Methods --- p.63 / Chapter 2.2.1 --- Culture of the Tumor Cell Lines --- p.63 / Chapter 2.2.2 --- "Isolation, Preparation and Culture of Primary Mouse Cells" --- p.63 / Chapter 2.2.3 --- Determination of Cell Proliferation by [3H]-TdR Incorporation Assay --- p.64 / Chapter 2.2.4 --- Determination of Cell Viability --- p.65 / Chapter 2.2.5 --- Cell Morphology Study --- p.66 / Chapter 2.2.6 --- Apoptosis Study by DNA Fragmentation --- p.66 / Chapter 2.2.7 --- Flow Cytometric Analysis --- p.67 / Chapter 2.2.8 --- Cell Cycle/DNA Content Evaluation --- p.68 / Chapter 2.2.9 --- Gene Expression Study --- p.69 / Chapter 2.2.10 --- Protein Expression Study --- p.72 / Chapter 2.2.11 --- Statistical Analysis --- p.75 / Chapter CHAPTER 3: --- THE ANTI-TUMOR EFFECTS OF GLYCYRRHIZIN AND 18-β GLYCYRRHETINIC ACID ON VARIOUS LEUKEMIC CELL LINES / Chapter 3.1 --- Introduction --- p.76 / Chapter 3.2 --- Results --- p.78 / Chapter 3.2.1 --- The Growth Inhibitory Effects of Glycyrrhizin on Various Leukemic Cell Lines --- p.78 / Chapter 3.2.1.1 --- Differential Anti-proliferative Effects of Glycyrrhizin on Various Leukemic Cell Lines In Vitro --- p.78 / Chapter 3.2.1.2 --- Effects of Glycyrrhizin on the Viability of Various Leukemic Cell Lines and Normal Hematopoietic Cells In Vitro --- p.89 / Chapter 3.2.1.3 --- Induction of DNA Fragmentation in Leukemia Cells by Glycyrrhizin --- p.94 / Chapter 3.2.1.4 --- Effect of Glycyrrhizin on the Cell Cycle Kinetics of HL-60 Cells In Vitro --- p.97 / Chapter 3.2.1.5 --- Effect of Glycyrrhizin on the Cell Cycle Kinetics of JCS Cells In Vitro --- p.100 / Chapter 3.2.1.6 --- Effect of Glycyrrhizin on the In Vivo Tumorigenicity of the Murine Myeloid Leukemia JCS Cells --- p.103 / Chapter 3.2.2 --- The Growth Inhibitory Effects of 18-β Glycyrrhetinic Acid on Various Leukemic Cells Lines --- p.105 / Chapter 3.2.2.1 --- Differential Anti-proliferative Effect of 18-β Glycyrrhetinic Acid on Various Leukemic Cell Lines In Vitro --- p.105 / Chapter 3.2.2.2 --- Effects of 18-β Glycyrrhetinic Acid on the Viability of Various Leukemic Cell Lines and Normal Hematopoietic Cells In Vitro --- p.115 / Chapter 3.2.2.3 --- Induction of DNA Fragmentation in Leukemia Cells by 18-β Glycyrrhetinic Acid --- p.120 / Chapter 3.2.2.4 --- Effect of 18-β Glycyrrhetinic Acid on the Cell Cycle Kinetics of HL-60 Cells In Vitro --- p.123 / Chapter 3.2.2.5 --- Effect of 18-β Glycyrrhetinic Acid on the Cell Cycle Kinetics of JCS Cells In Vitro --- p.126 / Chapter 3.2.2.6 --- Effect of 18-β Glycyrrhetinic acid on the In Vivo Tumorigenicity of the Murine Myeloid Leukemia JCS Cells --- p.129 / Chapter 3.3 --- Discussion --- p.131 / Chapter CHAPTER 4: --- THE DIFFERENTIATION-INDUCING EFFECTS OF GLYCYRRHIZIN AND 18-β GLYCYRRHETINIC ACID ON MURINE MYELOID LEUKEMIA CELLS / Chapter 4.1 --- Introduction --- p.135 / Chapter 4.2 --- Results --- p.138 / Chapter 4.2.1 --- Morphological Changes in Glycyrrhizin or 18-β Glycyrrhetinic Acid-treated JCS Cells --- p.138 / Chapter 4.2.2 --- Surface Antigen Immunophenotyping of Glycyrrhizin or 18-β Glycyrrhetinic Acid-treated JCS Cells --- p.141 / Chapter 4.2.3 --- Endocytic Activity of Glycyrrhizin or 18-β Glycyrrhetinic Acid-treated JCS Cells --- p.155 / Chapter 4.3 --- Discussion --- p.158 / Chapter CHAPTER 5: --- MECHANISTIC STUDIES ON THE ANTI LEUKEMIC ACTIVITIES OF GLYCYRRHIZIN AND 18-P GLYCYRRHETINIC ACID / Chapter 5.1 --- Introduction --- p.161 / Chapter 5.2 --- Results --- p.164 / Chapter 5.2.1 --- Combining Effect of Glycyrrhizin or 18-β Glycyrrhetinic Acid with Hematopoietic Cytokines in Modulating the Proliferation of the Murine Myeloid Leukemia JCS Cells --- p.164 / Chapter 5.2.1.1 --- Combining Effect of Glycyrrhizin and IL-lα on the Proliferation of JCS Cells --- p.164 / Chapter 5.2.1.2 --- Combining Effects of Glycyrrhizin with IFN-γ or TNF-α on the Proliferation of JCS Cells --- p.166 / Chapter 5.2.1.3 --- Combining Effect of 18-β Glycyrrhetinic Acid and IL-lα on the Proliferation of JCS Cells --- p.169 / Chapter 5.2.1.4 --- Combining Effects of 18-β Glycyrrhetinic Acid with IFN-γ or TNF-α on the Proliferation of JCS Cells --- p.169 / Chapter 5.2.2 --- Elucidation of the Molecular Mechanisms of Glycyrrhizin or 18-β Glycyrrhetinic Acid on Leukemic Cell Differentiation and Growth Arrest --- p.173 / Chapter 5.2.2.1 --- Modulatory Effects of Glycyrrhizin and 18-β Glycyrrhetinic Acid on the Expression of Cytokine Genes in the Leukemia JCS Cells --- p.173 / Chapter 5.2.2.2 --- Modulatory Effects of Glycyrrhizin and 18-β Glycyrrhetinic Acid on the Expression of PKC Isoforms in the Leukemia JCS Cells --- p.176 / Chapter 5.2.2.3 --- Modulatory Effects of Glycyrrhizin and 18-β Glycyrrhetinic Acid on the Expression of Growth- regulatory Genes in the Leukemia JCS Cells --- p.180 / Chapter 5.2.2.4 --- Modulatory Effects of 18-β Glycyrrhetinic Acid on the Expression of Apoptosis-related Genes in the Leukemia JCS Cells --- p.183 / Chapter 5.2.2.5 --- Modulatory Effects of 18-β Glycyrrhetinic Acid on the Expression of Growth-regulatory and Apoptosis-related Proteins in JCS Cells --- p.185 / Chapter 5.3 --- Discussion --- p.187 / Chapter CHAPTER 6: --- CONCLUSIONS AND FUTURE PERSPECTIVES --- p.194 / REFERENCES --- p.200

Zhao Zheng. / "December 2000." / On t.p. "2" is subscript. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 187-241). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Clopidogrel is an antiplatelet drug prescribed to prevent stent thrombosis after a percutaneous coronary intervention (PCI). Previous evidence suggests that some widely prescribed statins may inhibit the antiplatelet effects of clopidogrel via competitive metabolism of its activating enzyme cytochrome P450 3A4 (CYP3A4). / The objective was to investigate the possibility of an interaction post-PCI between statins and clopidogrel. / We carried out a population-based cohort study identifying 10,491 patients using clopidogrel post-PCI (2001-2004). The outcome was a composite of death of any cause, myocardial infarction, unstable angina, repeat revascularization, and cerebrovascular events. We found that co-prescription of CYP3A4-metabolized statins (hazard ratio (HR) 0.95, 95% confidence interval (CI) 0.79-1.15), or non-CYP3A4-metabolized statins (HR 0.82, 95% CI 0.63-1.07) with clopidogrel was not associated with increase in adverse outcomes. / We observed no evidence of interaction between clopidogrel and statins in a large population cohort of PCI patients, suggesting unlikelihood of an important interaction.

The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25D), is a key calcium (Ca++) regulatory hormone. It is also associated with functions unrelated to Ca++ homeostasis. Here, special attention is paid towards the anticancer properties of 1,25D. 1,25D strongly inhibits the growth of well-differentiated head and neck squamous cell carcinoma (HNSCC) derived cell lines. However, advanced, less differentiated, HNSCC cell lines (e.g. SCC4) are partially resistant to 1,25D. Resistance to nuclear receptor (NR) agonists is a common event that occurs in other NR-related treatments. For example, some leukemias develop resistance to the usually effective retinoic acid (RA) treatment. However, treating RA-resistant cells with HDAC inhibitors (HDACi) sensitizes them to RA. Thus, this study aims to investigate how treatment with TSA, an HDACi, would affect the response of SCC4 cell lines to 1,25D. We found that TSA had a variety of effects on 1,25D-regulated gene expression. Combined treatment with 1,25D and TSA increased the expression of cell-cycle regulating proteins, but also enhanced the downregulation of key target genes. Given the potential of the 1,25D/HDACi combination in combating cancers, two chimeric compounds, each containing parts of 1,25D and an HDACi, were synthesized in collaboration with Dr. James Gleason (Dept. of Chemistry, McGill). These 1,25D analogs have the HDACi-like structure replacing the 1,25D side chain. Both compounds proved to be agonists of the vitamin D receptor. Moreover, the TSA-substituted compound, called triciferol, effectively induced a-tubulin as well as histones acetylation. This study underlines the potential of combining 1,25D and TSA in cancer treatment, and reveals that bi-functional 1,25D analogs can be produced with potentially enhanced therapeutic activity.

5-Bromo-2'-deoxyuridine (BrdU), a thymidine analogue, is genotoxic and teratogenic. The exposure of mouse embryos to BrdU at doses that cause malformations induces oxidative stress and an embryonic stress response characterized by an increase in c-Fos dependent AP-1 DNA binding. The goal of this thesis was to test the hypothesis that development is disturbed at sites where BrdU is incorporated into DNA, triggering oxidative stress and c-Fos induction. Gestation day 9 CD-1 mice were treated with BrdU and embryos were obtained for immunolocalization of BrdU, 8-oxoguanine, a biomarker for oxidative stress, and c-Fos. BrdU incorporation into DNA was dispersed throughout the embryo. In contrast, the staining for 8-oxoguanine and c-Fos were highest in the neuroepithelium. BrdU incorporation was not affected by the pre-administration of N-acetyl-cysteine (NAC), an anti-oxidant, although both 8-oxoguanine and c-Fos staining were decreased. Thus, the response of the embryo to insult is tissue specific.

Dissertation (Ph.D.)--University of South Florida, 2008. / Title from PDF of title page. Document formatted into pages; contains 187 pages. Includes vita. Includes bibliographical references.

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / Este trabalho tem por objetivo avaliar mulheres portadoras de endometriose em uso de anÃlogos de GnRH investigando o metabolismo Ãsseo e massa Ãssea atravÃs da dosagem de marcadores sÃricos e realizaÃÃo de ultra-sonometria do calcÃneo, respectivamente. Trata-se de estudo observacional transversal tipo caso â controle prospectivo. Foi desenvolvido na Maternidade-Escola Assis Chateaubriand (MEAC) â UFC. Foram avaliadas 99 mulheres, divididas em 3 grupos, sendo 32 portadoras de endometriose diagnosticada cirurgicamente e tratadas com goserelina 3,6mg SC a cada 28 dias (4 doses) â grupo endometriÃtico. O segundo grupo foi composto de 25 mulheres nÃo endometriÃticas e no menacme (controle negativo). O terceiro grupo foi composto de 42 mulheres nÃo endometriÃticas e menopausadas por no mÃnimo dois anos, os dois Ãltimos grupos sem uso de medicaÃÃes. Foi realizada avaliaÃÃo Ãssea atravÃs da ultra-sonometria do calcÃneo com o aparelho Achilles, da LunarÂ, sendo determinado o âstiffnessâ de cada grupo (uma combinaÃÃo de velocidade do som e grau de atenuaÃÃo ultra-sonogrÃfica), juntamente com as dosagens sÃricas de magnÃsio, fosfato, urÃia, creatinina, cÃlcio, fosfatase alcalina (FA), PTH, cortisol e hidroxiprolina, alÃm das dosagens de cÃlcio urinÃrio, cÃlcio urinÃrio/creatinina, e hidroxiprolina/creatinina. O grupo endometriÃtico somente foi submetido a esta avaliaÃÃo apÃs o uso da medicaÃÃo. A anÃlise estatÃstica foi realizada pelo programa SPSS for Windows 11.0.0. As dosagens de FA, cÃlcio urinÃrio e cÃlcio urinÃrio/creatinina foram semelhantes no grupo endometriÃtico (40,8Â7,7U/mL; 47,15Â10,8mmol/L; e 78,76Â23,0, respectivamente) e no grupo menopausado (38,65Â5,1U/mL; 36,8Â4,3mmol/L; e 55,21Â8,21, respectivamente) alÃm de significativamente superiores aos do grupo no menacme (28,5Â2,54U/mL; 26,4Â3,4mmol/L; e 39,52Â7,7, respectivamente). As dosagens de PTH do grupo endometriÃtico (23,99Â3,35nmol/L) foram semelhantes as das mulheres no menacme (29,15Â4,09nmol/L), ambas sendo significativamente menores que as mulheres menopausadas (41,14Â3,7nmol/L). As demais anÃlises foram semelhantes entre os grupos. Na avaliaÃÃo Ãssea o âstiffnessâ foi similar entre o grupo endometriÃtico (88,16Â2,86) e as mulheres menopausadas (83,70Â1,8), sendo ambos significativamente inferiores Ãs mulheres no menacme (97,02Â1,46). Conclui-se que as portadoras de endometriose apÃs tratamento com goserelina apresentaram intenso metabolismo Ãsseo e piora no padrÃo do tecido Ãsseo avaliada pela ultra-sonometria do calcÃneo aproximando-se do quadro encontrado em mulheres menopausadas hà pelo menos dois anos. NÃo se pode afirmar, no entanto, se tais alteraÃÃes sÃo devidas exclusivamente ao uso do anÃlogo do GnRH ou somam-se à prÃpria manifestaÃÃo da endometriose. Sugere-se que a endometriose e o uso de anÃlogos do GnRH sejam considerados como fatores de risco para o desenvolvimento de osteoporose, principalmente se associados a uma histÃria de uso crÃnico de corticÃides a qualquer Ãpoca da vida. / This research had as an objective of evaluate endometriotic women treated with GnRH analogues by investigating their bone turnover and bone structure using serum bone turnover markers and calcaneous ultrasonometry, respectively. This is a transversal, observational, prospective caseâcontrol study. It was developed at Maternidade-Escola Assis Chateaubriand (MEAC) â UFC. Ninety nine women, divided into three groups were analyzed. Thirty two endometriotic women were treated with goserelin 3,6mg SC 28/28d (4 doses) â Endometriotic group. Their disease had been confirmed by surgery. The second group had twenty five non endometriotic women and having menses (control group). The third group had 42 not endometriotic menopausal women, they were at menopause at least for 2 years. The latest two groups were not taking any treatment. The Achilles device from Lunar, had being used to analyse the bone structure through calcaneous ultrasonometry. We calculated the âstiffnessâ value for each group (a combination of sound velocity and ultrasonographic attenuation), and we also analysed the values of magnesium, phosphate, urea, creatinine, serum calcium, alkaline phosphatase (ALP), parathyroid hormone (PTH), cortisol, hydroxyproline, urinary calcium, urinary calcium/creatinine, and hydroxyproline/creatinine. The endometriotic group was evaluated only after the treatment. The statistical analysis had being done by SPSS program for Windows version 11.0.0. The values of ALP, urinary calcium and urinary calcium/creatinine were similar to endometriotic group (40.8Â7.7U/mL; 47.15Â10.8mmol/L; and 78.76Â23.0, respectively) and to menopausal group (38.65Â5.1U/mL; 36.8Â4.3mmol/L; and 55.21Â8.21, respectively) although significantly higher than control group (28.5Â2.54U/mL; 26.4Â3.4mmol/L; and 39.52Â7.7, respectively). The values of PTH from endometriotic group (23.99Â3.35nmol/L) were similar to control group (29.15Â4.09nmol/L), and both were significantly lower than menopausal one (41.14Â3.7nmol/L). The other values were equal between groups. At the evaluation of bone âstiffnessâ the values were similar between endometriotic (88.16Â2.86) and menopausal groups (83.70Â1.8), and both were significantly lower than control group (97.02Â1.46). Concluding the endometriotic women who received treatment with goserelin showed an intense bone metabolism and a bone deficit at calcaneous ultrasonometry almost like women at post-menopausal at least two years. Therefore, we can not affirm if these alterations were caused exclusively by the GnRH-analogue therapy or were influenciated by endometriosis itself. We suggest that endometriosis and treatment with GnRH analogues might be considered as risks factors for the development of osteoporosis, principally if they are associated with chronic corticoid treatment at any point in a lifetime.

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