A perimenopausa é caracterizada como o período de transição da vida reprodutiva para a não reprodutiva em mulheres, e inicia-se com o aparecimento dos sintomas clínicos, prolongandose até um ano após a última menstruação. Esta fase é caracterizada pela ocorrência de ciclos menstruais irregulares, alterações na produção hormonal, bem como por mudanças comportamentais, neuroendócrinas e metabólicas, sendo o período de maior vulnerabilidade a desordens afetivas quando comparado às outras fases da vida. Apesar dos diversos estudos desenvolvidos acerca das manifestações destes sintomas durante a perimenopausa, ainda pouco se sabe a respeito das modificações na atividade do eixo hipotálamo-hipófise-adrenal (HPA) e da resposta ao estresse. O reagente químico diepóxido de 4-vinilciclohexeno (VCD) acelera o processo natural de atresia folicular, possibilitando estudos desta fase da vida reprodutiva. Assim sendo, sua aplicação em roedores constitui um excelente modelo experimental capaz de simular em animais o que ocorre durante a perimenopausa. Assim, os objetivos deste trabalho foram avaliar, neste modelo animal de perimenopausa: 1) as respostas endócrinas (corticosterona e progesterona) e neuroniais (atividade das subdivisões parvocelulares medial e posterior - PaMP e PaPo do núcleo paraventricular do hipotálamo (PVN) e do locus coeruleus - LC) ao estresse de contenção e 2) a influência da terapia hormonal sobre estas respostas. Para tanto, ratas Wistar receberam injeções subcutâneas de Óleo ou VCD por 15 dias consecutivos, a partir do 28° dia de vida. Ao redor do 56º ao 66º dia do início da administração de Óleo ou VCD, as ratas dos grupos a serem estressados receberam implantes subcutâneos de um pellet contendo placebo (PL), estradiol (E2), progesterona (P4) ou estradiol+progesterona (E2P4). O estresse de contenção foi aplicado por 30 minutos entre 09:00h e 10:00h na fase do diestro, ou 20 dias após o início da terapia hormonal (grupos VCD+E2, VCD+P4 e VCD+E2P4), de 75 a 85 dias após o início da administração de VCD/Óleo. O sangue foi coletado imediatamente (0min) e 60min após o final do estresse, quando os animais foram anestesiados e perfundidos para obtenção do tecido cerebral e posterior estudo imunohistoquímico das áreas de interesse. As concentrações basais de corticosterona foram semelhantes entre os grupos Óleo e VCD não estressadas. Contudo, asecreção de corticosterona em resposta ao estresse das ratas em periestropausa foi 72% menor que a do grupo controle. As concentrações basais de progesterona das ratas em periestropausa foram menores do que aquelas das ratas controles, mas o aumento da secreção deste hormônio induzido pelo estresse agudo por contenção não foi diferente entre os grupos. Centralmente, nas subdivisões PaMP e PaPo do PVN, assim como no LC, o número de neurônios c-Fos positivos expressos não foi diferente entre ratas VCD e óleo e o estresse aumentou de maneira semelhante o número de neurônios ativados em ambos os grupos. A secreção de corticosterona de animais em periestropausa tratados com estradiol, associado ou não à progesterona, foi ainda mais atenuada. Por outro lado, nas ratas tratadas com progesterona, as concentrações de corticosterona após o estresse mostraram-se mais elevadas que as do grupo VCD estressado sem tratamento hormonal. Todos os grupos tratados com hormônios aumentaram a secreção de progesterona em resposta ao estresse, no entanto esta resposta foi amplificada pelo estradiol. Nenhum dos tratamentos hormonais modificou a atividade neuronial após o estresse na PaMP, embora todos tenham atenuado esta resposta na PaPo. No LC, todos os tratamentos bloquearam o aumento de atividade neuronial induzida pelo estresse. Uma hora após o final do estresse, as concentrações de corticosterona e progesterona retornaram aos níveis basais observados nas ratas não estressadas. No entanto, nos grupos tratados com estradiol, os níveis de progesterona não retornaram aos basais, sendo estes níveis significantemente maiores após o fim do estímulo. Em conjunto, nossos resultados demonstram que na periestropausa, embora a secreção de progesterona em resposta ao estresse esteja preservada, a capacidade da adrenal em secretar corticosterona está reduzida. Esta redução parece não estar associada à deficiência central no funcionamento do eixo HPA (PVN) ou do sistema simpático central (LC), mas sim, a disfunções na esteroidogênese adrenal, que foram parcialmente corrigidas pela progesterona exógena. A diminuição da atividade neuronial do LC pelos esteróides ovarianos sugere uma possível atenuação do tônus simpático por estes hormônios. Ainda, a capacidade de recuperação pós-estresse da secreção de corticosterona e de progesterona se mostrou preservada neste modelo experimental. / Perimenopause is characterized as the period of transition from reproductive to nonreproductive life in women, and begins with the onset of clinical symptoms, lasting up to one year after the last menstrual period. This phase is characterized by irregular menstrual cycles, alterations in hormonal production, as well as by behavioral, neuroendocrine and metabolic changes, and increased vulnerability to affective disorders when compared to other phases of life. Despite the various studies on the manifestations of these symptoms during perimenopause, little is known about the changes in hypothalamic-pituitary-adrenal (HPA) axis activity and the response to stress. The chemical reagent diepoxide 4-vinylcyclohexene (VCD) accelerates the natural process of follicular atresia, enabling studies of this phase of reproductive life. Therefore, its application in rodents constitutes an excellent experimental model capable of simulating in animals what occurs during perimenopause. Thus, the objective of this study was to evaluate, in an animal model of perimenopause: 1) the endocrine responses (corticosterone and progesterone) as well as the neuronal response (parvocellular subdivisions of PVN, medial- PaMP) and posterior-PaPO and locus coeruleus - LC) to restraint stress and 2) the influence of hormonal therapy on these responses. Female Wistar rats received subcutaneous injections of Oil or VCD for 15 consecutive days, from the 28th day of life. Around the 56th to 66th day of the onset of Oil or VCD administration, the rats of the groups to be stressed received subcutaneous implants of a pellet containing placebo (PL), estradiol (E2), progesterone (P4) or estradiol + progesterone (E2P4 ). Restraint stress was applied for 30 minutes between 09:00 and 10:00 in the diestrus phase, or 20 days after the onset of hormonal therapy (VCD + E2, VCD + P4 and VCD + E2P4 groups), from 75 to 85 days after starting VCD / Oil administration. The blood was collected immediately (0min) and 60min after the end of stress, when the animals were anesthetized and perfused to take the brain for immunohistochemistry of PVN and LC. Basal corticosterone concentrations were similar between the non-stressed Oil and VCD groups. However, corticosterone secretion in response to stress was 72% lower than that of the control group. The basal progesterone concentrations of periestropausal rats were lower than those of the control rats, but the increase in the secretion of this hormone induced by stress was not different between thegroups. Centrally, in the PaMP and PaPO subdivisions of PVN as well as LC, the number of c-Fos positive neurons expressed was not different between VCD and Oil rats and the stress increased similarly the number of activated neurons in both groups. Corticosterone secretion from estradiol-treated periestropause rats, associated or not with progesterone, was further attenuated. On the other hand, in rats treated with progesterone, post-stress corticosterone concentrations were higher than those in the stressed VCD group without hormonal treatment. All groups treated with hormones increased progesterone secretion in response to stress, however this response was amplified by estradiol. None of the hormone treatments modified neuronal activity after stress in PaMP, although all hormone treatment attenuated this response in PaPo. In the LC, all treatments blocked the increase of neuronal activity induced by stress. One hour after the end of stress, corticosterone and progesterone concentrations returned to the baseline levels observed in the non-stressed rats. However, in the estradioltreated groups, progesterone levels did not return to the basal levels, these levels being significantly higher after the end of the stimulus. Taken together, our results demonstrate that in periestropause, although progesterone secretion in response to stress is preserved, the ability of the adrenal to secrete corticosterone is reduced. This reduction appears not to be associated with a central deficiency in HPA axis (PVN) or central sympathetic (LC) function, but rather to dysfunctions in adrenal steroidogenesis, which have been partially corrected by exogenous progesterone. The reduction of neuronal LC activity by ovarian steroids suggests a possible attenuation of sympathetic tone by these hormones. Furthermore, the post-stress recovery capacity of corticosterone and progesterone secretion seems to be preserved in this experimental model.

Contexte : Il est établi que les traitements hormonaux de la ménopause à base d’estroprogestatifs augmentent le risque de cancer du sein, mais ce risque pourrait varier selon les types de progestatifs utilisés. Par ailleurs, le rôle des traitements à base de progestatifs seuls dans le cancer du sein a été peu étudié. Du fait des particularités françaises dans la prescription de ces traitements, nous avons analysé le risque de cancer du sein en fonction des types de traitement hormonaux prescrits chez les femmes en France.Le surpoids et l’obésité sont associés à une diminution du risque de cancer du sein en préménopause, mais augmentent le risque en période post-ménopausique. Les mécanismes sous-jacents ne sont pas complètement élucidés et des questions restent en suspens quant au rôle du gain de poids à différentes périodes de la vie. Méthodes : Ce travail porte sur les données d’une étude cas-témoins réalisée en population générale en France, incluant 1232 cas et 1317 témoins recrutés chez les femmes des deux départements d’Ille-et-Vilaine et de Côte d’Or, entre 2005 et 2007. Des informations détaillées sur l'utilisation des traitements hormonaux, sur le poids à différentes périodes de la vie et sur diverses caractéristiques reproductives et médicales ont été obtenues au cours d'entretiens en face-à-face. Les odds ratios et intervalles de confiance à 95% après ajustement sur les facteurs de risque du cancer du sein ont été calculés à l’aide de modèles de régression logistique. Des analyses de trajectoires d’indice de masse corporelle entre l’âge de 20 ans et l’âge au moment du diagnostic ont été pratiquées.Résultats : Le risque de cancer du sein était augmenté chez les utilisatrices de progestatifs de synthèse combinés ou non avec un estrogène. Ce risque était restreint à la prise récente du traitement hormonal et augmentait avec la durée d’utilisation. A l’inverse, les traitements à base de progestérone naturelle n’étaient pas associés à une augmentation du risque de cancer du sein. Chez les femmes non ménopausées, un IMC élevé et un gain de poids antérieur étaient associés à une diminution du risque de cancer du sein. Chez les femmes ménopausées, seul un gain de poids dans la période précédant la ménopause (entre 40 et 50 ans) était associé à une augmentation du risque de cancer du sein. Cette association était plus marquée chez les femmes maigres à 20 ans (IMC≤ 18,5 kg/m²), ou chez les femmes plus âgées. Conclusion : Ce travail confirme d’une part les effets cancérogènes des traitements hormonaux à base de progestatifs de synthèse, et d’autre part l’absence d’effet délétère de la progestérone naturelle sur le risque de cancer du sein. L’utilisation de progestérone naturelle doit toutefois être évaluée au regard des bénéfices et des risques qu’elle peut entraîner. Nous avons également pu préciser les relations existant entre le gain de poids et le risque de cancer du sein, et suggéré qu’un gain de poids pendant la période précédant la ménopause pouvait être plus favorable à la survenue de cancer du sein en post-ménopause. / Background: There is evidence that menopausal combined estrogen-progestagen therapy increases the risk of breast cancer, but the risk may vary depending on the types of progestagen used. Moreover, the role of progestagen-only therapy in breast cancer has been little studied. Because of French specificities in prescribing these treatments, we analyzed the risk of breast cancer based on these different types of hormone treatment prescribed among women in France.Overweight and obesity are associated with a reduced risk of premenopausal breast cancer, but increase the risk in postmenopausal period. The underlying mechanisms are not fully understood, and questions remain about the role of weight gain in different periods of life.Methods: This work relates on data from a case-control study in the general population in France, including 1232 cases and 1317 controls recruited among women in two departments of Ille-et-Vilaine and Côte d'Or, between 2005 and 2007. Detailed information on hormonal treatments use, on weight at different periods of life and various reproductive and medical characteristics were obtained during a face-to-face interview. Odds ratios and 95% confidence intervals after adjustment for breast cancer risk factors were calculated using logistic regression models. Analyzes of BMI trajectories between the age of 20 and the age at diagnosis were performed.Results: The risk of breast cancer was increased in users of synthetic progestagen combined or not combined with an estrogen. This risk was restricted to the recent use of the hormone treatment and increased with the duration of use. Conversely, the natural progesterone based treatment was not associated with an increased risk of breast cancer.In premenopausal women, higher BMI and a previous weight gain were associated with a decreased risk of breast cancer. In postmenopausal women, only weight gain in the period preceding the menopause (40 to 50 years) was associated with an increased risk of breast cancer. This association was stronger among women who were lean women at the age of 20 (IMC≤ 18.5 kg / m²), or in older women.Conclusion: This study confirms the carcinogenic effects of hormonal treatments with synthetic progestagen, and the absence of deleterious effects of natural progesterone on breast cancer risk. However, the use of natural progesterone must be evaluated according to the benefits and risks that may result. We could also clarify the relationship between weight gain and the risk of breast cancer, and suggested that weight gain during the period before menopause could be more favorable to the occurrence of breast cancer in post-menopausal .

ABSTRACT/SUMMARY Background: The clinical efficacy of tamoxifen therapy may be modified by the drug-metabolizing enzymes and transporting molecules involved into the pharmacokinetics of tamoxifen. The aim of this study was to evaluate the association of CYP2D6, ABCB1 polymorhisms and comedication with efficacy and safety of tamoxifen treatment. Methods: Totally 258 women with hormonal positive breast carcinoma were retrospectively evaluated in relation to CYP2D6, ABCB1 polymorphisms and comedication. Results: CYP2D6 polymorphisms or co-medication affecting CYP2D6 activity demonstrated no statistically significant effect on the efficacy of tamoxifen therapy or adverse event incidence; there was only a trend towards shortening the time to event (TTE) in CYP2D6 poor metabolizers. ABCB1 polymorphism rs2032582 was not associated with clinical outcomes, while a trend towards an increase of TTE in variant allele carriers was noted. The ABCB1 polymorphism rs1045642 demonstrated statistical significance in premenopausal patients (p = 0.0012, HR 0.69 (95% CI 0.21 to 2.31), and its significant association was noted with gynaecological /vasomotor adverse events (p = 0.0221, HR = 1.0588), with no evidence of the influence on the incidence and onset of venous complications. Conclusions: Although this work did not show...

A perimenopausa é caracterizada como o período de transição da vida reprodutiva para a não reprodutiva em mulheres, e inicia-se com o aparecimento dos sintomas clínicos, prolongandose até um ano após a última menstruação. Esta fase é caracterizada pela ocorrência de ciclos menstruais irregulares, alterações na produção hormonal, bem como por mudanças comportamentais, neuroendócrinas e metabólicas, sendo o período de maior vulnerabilidade a desordens afetivas quando comparado às outras fases da vida. Apesar dos diversos estudos desenvolvidos acerca das manifestações destes sintomas durante a perimenopausa, ainda pouco se sabe a respeito das modificações na atividade do eixo hipotálamo-hipófise-adrenal (HPA) e da resposta ao estresse. O reagente químico diepóxido de 4-vinilciclohexeno (VCD) acelera o processo natural de atresia folicular, possibilitando estudos desta fase da vida reprodutiva. Assim sendo, sua aplicação em roedores constitui um excelente modelo experimental capaz de simular em animais o que ocorre durante a perimenopausa. Assim, os objetivos deste trabalho foram avaliar, neste modelo animal de perimenopausa: 1) as respostas endócrinas (corticosterona e progesterona) e neuroniais (atividade das subdivisões parvocelulares medial e posterior - PaMP e PaPo do núcleo paraventricular do hipotálamo (PVN) e do locus coeruleus - LC) ao estresse de contenção e 2) a influência da terapia hormonal sobre estas respostas. Para tanto, ratas Wistar receberam injeções subcutâneas de Óleo ou VCD por 15 dias consecutivos, a partir do 28° dia de vida. Ao redor do 56º ao 66º dia do início da administração de Óleo ou VCD, as ratas dos grupos a serem estressados receberam implantes subcutâneos de um pellet contendo placebo (PL), estradiol (E2), progesterona (P4) ou estradiol+progesterona (E2P4). O estresse de contenção foi aplicado por 30 minutos entre 09:00h e 10:00h na fase do diestro, ou 20 dias após o início da terapia hormonal (grupos VCD+E2, VCD+P4 e VCD+E2P4), de 75 a 85 dias após o início da administração de VCD/Óleo. O sangue foi coletado imediatamente (0min) e 60min após o final do estresse, quando os animais foram anestesiados e perfundidos para obtenção do tecido cerebral e posterior estudo imunohistoquímico das áreas de interesse. As concentrações basais de corticosterona foram semelhantes entre os grupos Óleo e VCD não estressadas. Contudo, asecreção de corticosterona em resposta ao estresse das ratas em periestropausa foi 72% menor que a do grupo controle. As concentrações basais de progesterona das ratas em periestropausa foram menores do que aquelas das ratas controles, mas o aumento da secreção deste hormônio induzido pelo estresse agudo por contenção não foi diferente entre os grupos. Centralmente, nas subdivisões PaMP e PaPo do PVN, assim como no LC, o número de neurônios c-Fos positivos expressos não foi diferente entre ratas VCD e óleo e o estresse aumentou de maneira semelhante o número de neurônios ativados em ambos os grupos. A secreção de corticosterona de animais em periestropausa tratados com estradiol, associado ou não à progesterona, foi ainda mais atenuada. Por outro lado, nas ratas tratadas com progesterona, as concentrações de corticosterona após o estresse mostraram-se mais elevadas que as do grupo VCD estressado sem tratamento hormonal. Todos os grupos tratados com hormônios aumentaram a secreção de progesterona em resposta ao estresse, no entanto esta resposta foi amplificada pelo estradiol. Nenhum dos tratamentos hormonais modificou a atividade neuronial após o estresse na PaMP, embora todos tenham atenuado esta resposta na PaPo. No LC, todos os tratamentos bloquearam o aumento de atividade neuronial induzida pelo estresse. Uma hora após o final do estresse, as concentrações de corticosterona e progesterona retornaram aos níveis basais observados nas ratas não estressadas. No entanto, nos grupos tratados com estradiol, os níveis de progesterona não retornaram aos basais, sendo estes níveis significantemente maiores após o fim do estímulo. Em conjunto, nossos resultados demonstram que na periestropausa, embora a secreção de progesterona em resposta ao estresse esteja preservada, a capacidade da adrenal em secretar corticosterona está reduzida. Esta redução parece não estar associada à deficiência central no funcionamento do eixo HPA (PVN) ou do sistema simpático central (LC), mas sim, a disfunções na esteroidogênese adrenal, que foram parcialmente corrigidas pela progesterona exógena. A diminuição da atividade neuronial do LC pelos esteróides ovarianos sugere uma possível atenuação do tônus simpático por estes hormônios. Ainda, a capacidade de recuperação pós-estresse da secreção de corticosterona e de progesterona se mostrou preservada neste modelo experimental. / Perimenopause is characterized as the period of transition from reproductive to nonreproductive life in women, and begins with the onset of clinical symptoms, lasting up to one year after the last menstrual period. This phase is characterized by irregular menstrual cycles, alterations in hormonal production, as well as by behavioral, neuroendocrine and metabolic changes, and increased vulnerability to affective disorders when compared to other phases of life. Despite the various studies on the manifestations of these symptoms during perimenopause, little is known about the changes in hypothalamic-pituitary-adrenal (HPA) axis activity and the response to stress. The chemical reagent diepoxide 4-vinylcyclohexene (VCD) accelerates the natural process of follicular atresia, enabling studies of this phase of reproductive life. Therefore, its application in rodents constitutes an excellent experimental model capable of simulating in animals what occurs during perimenopause. Thus, the objective of this study was to evaluate, in an animal model of perimenopause: 1) the endocrine responses (corticosterone and progesterone) as well as the neuronal response (parvocellular subdivisions of PVN, medial- PaMP) and posterior-PaPO and locus coeruleus - LC) to restraint stress and 2) the influence of hormonal therapy on these responses. Female Wistar rats received subcutaneous injections of Oil or VCD for 15 consecutive days, from the 28th day of life. Around the 56th to 66th day of the onset of Oil or VCD administration, the rats of the groups to be stressed received subcutaneous implants of a pellet containing placebo (PL), estradiol (E2), progesterone (P4) or estradiol + progesterone (E2P4 ). Restraint stress was applied for 30 minutes between 09:00 and 10:00 in the diestrus phase, or 20 days after the onset of hormonal therapy (VCD + E2, VCD + P4 and VCD + E2P4 groups), from 75 to 85 days after starting VCD / Oil administration. The blood was collected immediately (0min) and 60min after the end of stress, when the animals were anesthetized and perfused to take the brain for immunohistochemistry of PVN and LC. Basal corticosterone concentrations were similar between the non-stressed Oil and VCD groups. However, corticosterone secretion in response to stress was 72% lower than that of the control group. The basal progesterone concentrations of periestropausal rats were lower than those of the control rats, but the increase in the secretion of this hormone induced by stress was not different between thegroups. Centrally, in the PaMP and PaPO subdivisions of PVN as well as LC, the number of c-Fos positive neurons expressed was not different between VCD and Oil rats and the stress increased similarly the number of activated neurons in both groups. Corticosterone secretion from estradiol-treated periestropause rats, associated or not with progesterone, was further attenuated. On the other hand, in rats treated with progesterone, post-stress corticosterone concentrations were higher than those in the stressed VCD group without hormonal treatment. All groups treated with hormones increased progesterone secretion in response to stress, however this response was amplified by estradiol. None of the hormone treatments modified neuronal activity after stress in PaMP, although all hormone treatment attenuated this response in PaPo. In the LC, all treatments blocked the increase of neuronal activity induced by stress. One hour after the end of stress, corticosterone and progesterone concentrations returned to the baseline levels observed in the non-stressed rats. However, in the estradioltreated groups, progesterone levels did not return to the basal levels, these levels being significantly higher after the end of the stimulus. Taken together, our results demonstrate that in periestropause, although progesterone secretion in response to stress is preserved, the ability of the adrenal to secrete corticosterone is reduced. This reduction appears not to be associated with a central deficiency in HPA axis (PVN) or central sympathetic (LC) function, but rather to dysfunctions in adrenal steroidogenesis, which have been partially corrected by exogenous progesterone. The reduction of neuronal LC activity by ovarian steroids suggests a possible attenuation of sympathetic tone by these hormones. Furthermore, the post-stress recovery capacity of corticosterone and progesterone secretion seems to be preserved in this experimental model.

No description available.

Este estudo teve por objetivo avaliar a influência da terapia hormonal sobre a pressão ocular de mulheres na pós-menopausa. A amostra foi constituída por 58 olhos de 58 pacientes no período da pós-menopausa, com indicação de terapia hormonal, com idade entre 41 e 65 anos, que não tenham utilizado hormônio nos últimos três meses. As pacientes foram randomizadas (por sorteio) em dois grupos: terapia hormonal contínua (n=32) com comprimidos de estradiol 2 mg e acetato de noretisterona 1 mg, diário durante três meses e grupo controle placebo (n=26). O estudo foi realizado de forma cega pela investigadora principal. As pacientes foram avaliadas quanto à pressão ocular, paquimetria, ceratometria e dosagens dos hormônios sexuais pré e pós-tratamento. A média de idade foi de 54,21 anos ± 4,95, sendo 53,66 anos ± 5,60 no grupo com terapia hormonal e de 54,88 anos ± 4,01 no grupo placebo. Não houve diferença significativa entre os grupos com relação a idade (p= 0,352), índice de massa corporal (p= 0,818), pressão ocular (p=0,697), ceratometria (p > 0,05), paquimetria central (p=0,580), e dosagens dos hormônios sexuais (p>0,05) no pré-tratamento. A pressão ocular média pré-tratamento foi de 14,08 mmHg ± 1,96 no grupo terapia hormonal e de 13,81 mmHg ± 3,28 no grupo placebo. Houve redução significativa da pressão ocular média entre o pré e o pós-tratamento (p=0,0009) no grupo terapia hormonal e redução não significativa no grupo placebo (p=0,108). Na avaliação entre os grupos, não houve diferença estatística nos valores de pressão ocular média no pós-tratamento. Na avaliação entre os grupos, não houve diferença estatisticamente significativa para os valores de paquimetria e ceratometria. O grupo com terapia hormonal apresentou aumento significativo dos níveis hormonais de estradiol e redução significativa nas dosagens hormonais médias de LH e FSH no pós-tratamento com 30, 60 e 90 dias (p=0,000). As dosagens hormonais no grupo placebo não apresentaram variação estatisticamente significante. No grupo terapia hormonal, houve correlação diretamente proporcional entre as pressões oculares médias e níveis hormonais de LH e FSH, e correlação inversamente proporcional com níveis hormonais de estradiol. Em resumo, houve redução da pressão ocular média no grupo terapia hormonal entre o pré e o pós-tratamento e os níveis pressóricos neste grupo se correlacionaram com os níveis hormonais de LH, FSH e estradiol / This trial aimed to assess the influence of hormonal therapy on intraocular pressure in post-menopausal women. The sample had 58 eyes of 58 patients during menopause period, indicated for hormonal therapy, they were between the age of 41 and 65 years, who have not taken hormone in the past three months. Patients were randomized (raffle) in two groups: continuous hormonal therapy (n=32) with 2 mg of estradiol and 1 mg daily of norethisterone acetate for three months and controlled placebo group (n=26). It was a blind study carried out by the main investigator. Patients were assessed regarding ocular pressure, pachymetry, keratometry and sex hormone\'s dosages, pre and post treatment. The average was 54.21 years old ± 4.95, where 53.66 years old ± 5.60 in the group with hormonal therapy and 54.88 years old ± 4.01 in the placebo group. There was no significant difference between the groups regarding age (p= 0.352), body mass index (p= 0.818), ocular pressure (p=0.697), keratometry (p > 0.05), central pachymetry (p=0.580), and sex hormone dosages (p>0.05) during pre treatment. The average pre treatment pressure was 14.08 mmHg ± 1.96 in the hormonal therapy group and 13.81 mmHg ± 3.28 in the placebo group. There was a significant reduction in the average ocular pressure between the pre and post treatment (p=0.0009) in the hormonal therapy group and not a significant reduction in the placebo group, (p=0.108). There was no statistically difference between the groups in the average ocular pressure values after treatment. There were no statistically significant differences between the two groups in the values of pachymetry and keratometry. The hormonal therapy group showed a significant increase in estradiol hormonal levels and a significant reduction in the average hormonal dosages of LH e FSH in the post treatment after 30, 60 and 90 days (p=0.000). The hormonal dosages in the placebo group no showed significant changed. In the hormonal group, there was a direct and proportional relation between the average ocular pressure and LH and FSH hormonal levels and a proportional contrariwise correlation with estradiol hormonal levels. In summary, there was a reduction in the ocular pressure average in the hormonal therapy group between the pre and post treatment and the pressure levels in this group were correlated with the hormonal levels of LH, FSH and estradiol

Este estudo teve por objetivo avaliar a influência da terapia hormonal sobre a pressão ocular de mulheres na pós-menopausa. A amostra foi constituída por 58 olhos de 58 pacientes no período da pós-menopausa, com indicação de terapia hormonal, com idade entre 41 e 65 anos, que não tenham utilizado hormônio nos últimos três meses. As pacientes foram randomizadas (por sorteio) em dois grupos: terapia hormonal contínua (n=32) com comprimidos de estradiol 2 mg e acetato de noretisterona 1 mg, diário durante três meses e grupo controle placebo (n=26). O estudo foi realizado de forma cega pela investigadora principal. As pacientes foram avaliadas quanto à pressão ocular, paquimetria, ceratometria e dosagens dos hormônios sexuais pré e pós-tratamento. A média de idade foi de 54,21 anos ± 4,95, sendo 53,66 anos ± 5,60 no grupo com terapia hormonal e de 54,88 anos ± 4,01 no grupo placebo. Não houve diferença significativa entre os grupos com relação a idade (p= 0,352), índice de massa corporal (p= 0,818), pressão ocular (p=0,697), ceratometria (p > 0,05), paquimetria central (p=0,580), e dosagens dos hormônios sexuais (p>0,05) no pré-tratamento. A pressão ocular média pré-tratamento foi de 14,08 mmHg ± 1,96 no grupo terapia hormonal e de 13,81 mmHg ± 3,28 no grupo placebo. Houve redução significativa da pressão ocular média entre o pré e o pós-tratamento (p=0,0009) no grupo terapia hormonal e redução não significativa no grupo placebo (p=0,108). Na avaliação entre os grupos, não houve diferença estatística nos valores de pressão ocular média no pós-tratamento. Na avaliação entre os grupos, não houve diferença estatisticamente significativa para os valores de paquimetria e ceratometria. O grupo com terapia hormonal apresentou aumento significativo dos níveis hormonais de estradiol e redução significativa nas dosagens hormonais médias de LH e FSH no pós-tratamento com 30, 60 e 90 dias (p=0,000). As dosagens hormonais no grupo placebo não apresentaram variação estatisticamente significante. No grupo terapia hormonal, houve correlação diretamente proporcional entre as pressões oculares médias e níveis hormonais de LH e FSH, e correlação inversamente proporcional com níveis hormonais de estradiol. Em resumo, houve redução da pressão ocular média no grupo terapia hormonal entre o pré e o pós-tratamento e os níveis pressóricos neste grupo se correlacionaram com os níveis hormonais de LH, FSH e estradiol / This trial aimed to assess the influence of hormonal therapy on intraocular pressure in post-menopausal women. The sample had 58 eyes of 58 patients during menopause period, indicated for hormonal therapy, they were between the age of 41 and 65 years, who have not taken hormone in the past three months. Patients were randomized (raffle) in two groups: continuous hormonal therapy (n=32) with 2 mg of estradiol and 1 mg daily of norethisterone acetate for three months and controlled placebo group (n=26). It was a blind study carried out by the main investigator. Patients were assessed regarding ocular pressure, pachymetry, keratometry and sex hormone\'s dosages, pre and post treatment. The average was 54.21 years old ± 4.95, where 53.66 years old ± 5.60 in the group with hormonal therapy and 54.88 years old ± 4.01 in the placebo group. There was no significant difference between the groups regarding age (p= 0.352), body mass index (p= 0.818), ocular pressure (p=0.697), keratometry (p > 0.05), central pachymetry (p=0.580), and sex hormone dosages (p>0.05) during pre treatment. The average pre treatment pressure was 14.08 mmHg ± 1.96 in the hormonal therapy group and 13.81 mmHg ± 3.28 in the placebo group. There was a significant reduction in the average ocular pressure between the pre and post treatment (p=0.0009) in the hormonal therapy group and not a significant reduction in the placebo group, (p=0.108). There was no statistically difference between the groups in the average ocular pressure values after treatment. There were no statistically significant differences between the two groups in the values of pachymetry and keratometry. The hormonal therapy group showed a significant increase in estradiol hormonal levels and a significant reduction in the average hormonal dosages of LH e FSH in the post treatment after 30, 60 and 90 days (p=0.000). The hormonal dosages in the placebo group no showed significant changed. In the hormonal group, there was a direct and proportional relation between the average ocular pressure and LH and FSH hormonal levels and a proportional contrariwise correlation with estradiol hormonal levels. In summary, there was a reduction in the ocular pressure average in the hormonal therapy group between the pre and post treatment and the pressure levels in this group were correlated with the hormonal levels of LH, FSH and estradiol

No description available.

Advances in breast cancer detection and oncology treatment modalities have prolonged the survival time for the cancer population, which is officially the largest group of cancer survivors among women in the western world, including South Africa (Brem & Kumar, 2011; Fisher, Dolbeault, Sultan & Bredart, 2014; Herbst, 2011; Reyes-Gibby, et al., 2012). In the light of shocking statistics and ever rising numbers of cancer, especially breast cancer, the time is ripe for further research in the domain of psycho-oncology and has motivated the researcher, due to her interest and involvement in breast cancer, to make this her field of research. Despite the need for a bio-psycho-social approach when treating cancer patients there is little literature available on the psychological interventions in South Africa where the majority of research studies previously conducted in South Africa have generally focused on the bio-medical aspects of cancer (Albrecht, 2009; Venter, 2014). To comprehend the paradigm of psycho-oncology, which is the backbone of this study, a theoretical framework was attained from Engel’s humanistic or psychological model (caring) and Pasteur’s biomedical model (curing) (Borrel-Carrio, Suchman, & Epstein, 2004). The primary aim of this study was to explore the lived experiences of breast cancer patients concerning their diagnosis, treatment and survivorship and unique needs for psycho-oncological interventions through their own “voices”. The research was conducted within a qualitative framework with a case study method of inquiry employing open-ended style interviews and psychotherapeutic sessions with five purposely sampled breast cancer patients. Two qualitative questionnaires were also used for triangulation purposes. Transcripts of all the therapeutic sessions were analysed using interpretive analysis where categories and themes were developed and described in full. Findings indicated that in spite the extensive proof that breast cancer causes numerous sexual and psychological complications during active treatment and afterwards, patients still feel that they have no “platform” to express their emotions and sexual issues within the oncology framework, or that there is enough and sufficient assistance to attend to their needs. e The researcher hopes that this study will make a valuable contribution to research in the field of psycho-oncology in South Africa and to indicate new realities of the chronicity of breast cancer and treatment complications that demand psychotherapeutic interventions in cancer care and that the study will initiate new ways of understanding the role of psychology and the psychologist in the medical world of cancer. The researcher hopes that by offering an understanding of participants’ unique experiences of this process, practitioners will have insight when working therapeutically with this population and empower them to have a quality of life, even within the boundaries of their illness. / Psychology / D. Litt. et Phil. (Psychology)