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Carmine Nappi - One of the best experts on this subject based on the ideXlab platform.

  • Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone.
    Clinical endocrinology, 2003
    Co-Authors: Giovanni A. Tommaselli, Costantino Di Carlo, Giuseppe Bifulco, Attilio Di Spiezio Sardo, Massimiliano Pellicano, Carmine Nappi
    Abstract:

    Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced Hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of Hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels. Prospective, randomized study. Twenty-eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3.75 mg intramuscularly) plus tibolone (2.5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms. Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months' pretreament period and after 2 months of therapy. No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology. Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.

  • Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone.
    Clinical endocrinology, 2003
    Co-Authors: Giovanni A. Tommaselli, Costantino Di Carlo, Giuseppe Bifulco, Attilio Di Spiezio Sardo, Massimiliano Pellicano, Carmine Nappi
    Abstract:

    OBJECTIVE Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced Hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of Hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels. DESIGN Prospective, randomized study. PATIENTS Twenty-eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3.75 mg intramuscularly) plus tibolone (2.5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms. MEASUREMENTS Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months' pretreament period and after 2 months of therapy. RESULTS No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology. CONCLUSIONS Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.

  • Effects of postmenopausal Hypoestrogenism on skin collagen.
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Giuseppe Bifulco, Maria Paola Arienzo, Carmine Nappi
    Abstract:

    The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Thirty-two women (mean age 48.78 +/- 9.86; year +/- S.D., range 28-68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. In the postmenopausal patients, a significant (P < 0.01) decrease of percentage of skin collagen type I, type III and type III/type I ratio was observed in comparison to premenopausal women. The percentages of collagen type I, type III and type III/I ratio of all patients studied was significantly (P < 0.01) correlated with chronological age (r = 0.88, 0.89 and 0.61, respectively). Considering only postmenopausal subjects, the correlation with chronological age was significant (P < 0.01) for collagen type I and type III of postmenopausal women (r = 0.59, r = 0.64, respectively), but not for the type III/I ratio (r = 0.37, P = 0.131). The percentages of collagen type I, type III and type III/I ratio of postmenopausal women showed a significant (P < 0.01) inverse correlation with years of postmenopause (r = 0.76, 0.73 and 0.73, respectively). Our data suggest that the decrease of skin collagen is an estrogen-related phenomenon.

  • effects of postmenopausal Hypoestrogenism on skin collagen
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Giuseppe Bifulco, Maria Paola Arienzo, Carmine Nappi
    Abstract:

    Objective: The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Methods: Thirty-two women (mean age 48.78±9.86; year±S.D., range 28–68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. Results: In the postmenopausal patients, a significant (P<0.01) decrease of percentage of skin collagen type I, type III and type III/type I ratio was observed in comparison to premenopausal women. The percentages of collagen type I, type III and type III/I ratio of all patients studied was significantly (P<0.01) correlated with chronological age (r=0.88, 0.89 and 0.61, respectively). Considering only postmenopausal subjects, the correlation with chronological age was significant (P<0.01) for collagen type I and type III of postmenopausal women (r=0.59, r=0.64, respectively), but not for the type III/I ratio (r=0.37, P=0.131). The percentages of collagen type I, type III and type III/I ratio of postmenopausal women showed a significant (P<0.01) inverse correlation with years of postmenopause (r=0.76, 0.73 and 0.73, respectively). Conclusions: Our data suggest that the decrease of skin collagen is an estrogen-related phenomenon.

  • Effects of postmenopausal Hypoestrogenism on skin collagen.
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Maria Paola Arienzo, Bifulco G, Carmine Nappi
    Abstract:

    Objective: The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Methods: Thirty-two women (mean age 48.78±9.86; year±S.D., range 28–68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. Results: In the postmenopausal patients, a significant (P

Costantino Di Carlo - One of the best experts on this subject based on the ideXlab platform.

  • Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone.
    Clinical endocrinology, 2003
    Co-Authors: Giovanni A. Tommaselli, Costantino Di Carlo, Giuseppe Bifulco, Attilio Di Spiezio Sardo, Massimiliano Pellicano, Carmine Nappi
    Abstract:

    Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced Hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of Hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels. Prospective, randomized study. Twenty-eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3.75 mg intramuscularly) plus tibolone (2.5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms. Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months' pretreament period and after 2 months of therapy. No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology. Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.

  • Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone.
    Clinical endocrinology, 2003
    Co-Authors: Giovanni A. Tommaselli, Costantino Di Carlo, Giuseppe Bifulco, Attilio Di Spiezio Sardo, Massimiliano Pellicano, Carmine Nappi
    Abstract:

    OBJECTIVE Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced Hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of Hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels. DESIGN Prospective, randomized study. PATIENTS Twenty-eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3.75 mg intramuscularly) plus tibolone (2.5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms. MEASUREMENTS Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months' pretreament period and after 2 months of therapy. RESULTS No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology. CONCLUSIONS Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.

  • Effects of postmenopausal Hypoestrogenism on skin collagen.
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Giuseppe Bifulco, Maria Paola Arienzo, Carmine Nappi
    Abstract:

    The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Thirty-two women (mean age 48.78 +/- 9.86; year +/- S.D., range 28-68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. In the postmenopausal patients, a significant (P < 0.01) decrease of percentage of skin collagen type I, type III and type III/type I ratio was observed in comparison to premenopausal women. The percentages of collagen type I, type III and type III/I ratio of all patients studied was significantly (P < 0.01) correlated with chronological age (r = 0.88, 0.89 and 0.61, respectively). Considering only postmenopausal subjects, the correlation with chronological age was significant (P < 0.01) for collagen type I and type III of postmenopausal women (r = 0.59, r = 0.64, respectively), but not for the type III/I ratio (r = 0.37, P = 0.131). The percentages of collagen type I, type III and type III/I ratio of postmenopausal women showed a significant (P < 0.01) inverse correlation with years of postmenopause (r = 0.76, 0.73 and 0.73, respectively). Our data suggest that the decrease of skin collagen is an estrogen-related phenomenon.

  • effects of postmenopausal Hypoestrogenism on skin collagen
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Giuseppe Bifulco, Maria Paola Arienzo, Carmine Nappi
    Abstract:

    Objective: The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Methods: Thirty-two women (mean age 48.78±9.86; year±S.D., range 28–68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. Results: In the postmenopausal patients, a significant (P<0.01) decrease of percentage of skin collagen type I, type III and type III/type I ratio was observed in comparison to premenopausal women. The percentages of collagen type I, type III and type III/I ratio of all patients studied was significantly (P<0.01) correlated with chronological age (r=0.88, 0.89 and 0.61, respectively). Considering only postmenopausal subjects, the correlation with chronological age was significant (P<0.01) for collagen type I and type III of postmenopausal women (r=0.59, r=0.64, respectively), but not for the type III/I ratio (r=0.37, P=0.131). The percentages of collagen type I, type III and type III/I ratio of postmenopausal women showed a significant (P<0.01) inverse correlation with years of postmenopause (r=0.76, 0.73 and 0.73, respectively). Conclusions: Our data suggest that the decrease of skin collagen is an estrogen-related phenomenon.

  • Effects of postmenopausal Hypoestrogenism on skin collagen.
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Maria Paola Arienzo, Bifulco G, Carmine Nappi
    Abstract:

    Objective: The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Methods: Thirty-two women (mean age 48.78±9.86; year±S.D., range 28–68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. Results: In the postmenopausal patients, a significant (P

Giuseppe Bifulco - One of the best experts on this subject based on the ideXlab platform.

  • Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone.
    Clinical endocrinology, 2003
    Co-Authors: Giovanni A. Tommaselli, Costantino Di Carlo, Giuseppe Bifulco, Attilio Di Spiezio Sardo, Massimiliano Pellicano, Carmine Nappi
    Abstract:

    Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced Hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of Hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels. Prospective, randomized study. Twenty-eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3.75 mg intramuscularly) plus tibolone (2.5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms. Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months' pretreament period and after 2 months of therapy. No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology. Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.

  • Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone.
    Clinical endocrinology, 2003
    Co-Authors: Giovanni A. Tommaselli, Costantino Di Carlo, Giuseppe Bifulco, Attilio Di Spiezio Sardo, Massimiliano Pellicano, Carmine Nappi
    Abstract:

    OBJECTIVE Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced Hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of Hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels. DESIGN Prospective, randomized study. PATIENTS Twenty-eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3.75 mg intramuscularly) plus tibolone (2.5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms. MEASUREMENTS Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months' pretreament period and after 2 months of therapy. RESULTS No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology. CONCLUSIONS Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.

  • Effects of postmenopausal Hypoestrogenism on skin collagen.
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Giuseppe Bifulco, Maria Paola Arienzo, Carmine Nappi
    Abstract:

    The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Thirty-two women (mean age 48.78 +/- 9.86; year +/- S.D., range 28-68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. In the postmenopausal patients, a significant (P < 0.01) decrease of percentage of skin collagen type I, type III and type III/type I ratio was observed in comparison to premenopausal women. The percentages of collagen type I, type III and type III/I ratio of all patients studied was significantly (P < 0.01) correlated with chronological age (r = 0.88, 0.89 and 0.61, respectively). Considering only postmenopausal subjects, the correlation with chronological age was significant (P < 0.01) for collagen type I and type III of postmenopausal women (r = 0.59, r = 0.64, respectively), but not for the type III/I ratio (r = 0.37, P = 0.131). The percentages of collagen type I, type III and type III/I ratio of postmenopausal women showed a significant (P < 0.01) inverse correlation with years of postmenopause (r = 0.76, 0.73 and 0.73, respectively). Our data suggest that the decrease of skin collagen is an estrogen-related phenomenon.

  • effects of postmenopausal Hypoestrogenism on skin collagen
    Maturitas, 1999
    Co-Authors: P. Affinito, Stefano Palomba, C. Sorrentino, Costantino Di Carlo, Giuseppe Bifulco, Maria Paola Arienzo, Carmine Nappi
    Abstract:

    Objective: The aim of our study was to evaluate the effect of aging and postmenopausal Hypoestrogenism on skin collagen content. Methods: Thirty-two women (mean age 48.78±9.86; year±S.D., range 28–68), 14 in premenopause and 18 in postmenopause, underwent skin biopsies performed during laparotomic operation. The amount of collagen type I, III and type III/type I ratio was evaluated by immunohistochemistry and computerised image analysis, and was related to age and years of postmenopause. Results: In the postmenopausal patients, a significant (P<0.01) decrease of percentage of skin collagen type I, type III and type III/type I ratio was observed in comparison to premenopausal women. The percentages of collagen type I, type III and type III/I ratio of all patients studied was significantly (P<0.01) correlated with chronological age (r=0.88, 0.89 and 0.61, respectively). Considering only postmenopausal subjects, the correlation with chronological age was significant (P<0.01) for collagen type I and type III of postmenopausal women (r=0.59, r=0.64, respectively), but not for the type III/I ratio (r=0.37, P=0.131). The percentages of collagen type I, type III and type III/I ratio of postmenopausal women showed a significant (P<0.01) inverse correlation with years of postmenopause (r=0.76, 0.73 and 0.73, respectively). Conclusions: Our data suggest that the decrease of skin collagen is an estrogen-related phenomenon.

Franz Resch - One of the best experts on this subject based on the ideXlab platform.

  • Plasma concentrations of estradiol in women suffering from schizophrenia treated with conventional versus atypical antipsychotics.
    Schizophrenia research, 2005
    Co-Authors: Niels Bergemann, Christoph Mundt, Peter Parzer, Iris Jannakos, Ines Nagl, Birgit Salbach, Klaus Klinga, Benno Runnebaum, Franz Resch
    Abstract:

    Low estrogen levels leading to an elevated rate of menstrual dysfunctions such as amenorrhea and irregular menstruation have been described in women with schizophrenia and have often been attributed to antipsychotic-induced hyperprolactinemia. However, there is some evidence that "Hypoestrogenism" in schizophrenic women does not occur exclusively under medication with hyperprolactinemia-inducing antipsychotics. While the precise mechanism of low estrogen levels in schizophrenic women has not been elucidated yet, "Hypoestrogenism" is of clinical relevance because estrogen seems to endow an antipsychotic-like effect in schizophrenia and thus positively affect the course of illness in schizophrenic women. In addition, low levels of estrogen might have a negative effect on bone mineral density and on the cardiovascular system. To test the "Hypoestrogenism hypothesis", hormone levels in 75 women with schizophrenia diagnosed according to DSM-IV and ICD-10 were determined in the follicular, periovulatory, and luteal phases of the menstrual cycle. Levels of estradiol, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and testosterone were assessed. The serum levels of estradiol were generally reduced during the entire menstrual cycle compared to normal reference values. With low levels of LH over the entire cycle and of progesterone in the luteal phase, anovulatory cycles were assumed. Hypoestrogenism was found in about 60% of the patients in accordance with a strict definition (estradiol serum level below 30 pg/ml in the follicular phase and below 100 pg/ml in the periovulatory phase). To rule out a possible effect of hyperprolactinemia on the gonadal axis and a subsequent effect on estradiol levels from treatment with conventional ("typical") antipsychotics, serum estradiol levels of patients treated with certain atypical antipsychotics known to induce only a mild increase in prolactin, or no increase at all, were compared with those from patients treated with conventional antipsychotics. The data clearly indicate high prolactin levels in the latter, but low levels in the group treated with atypical antipsychotics. In both groups, however, low levels of estradiol compared to normal reference values were measured. The present findings provide evidence that Hypoestrogenism in schizophrenia occurs in women with and without antipsychotic-induced hyperprolactinemia. Further research should be conducted to clarify the cause of Hypoestrogenism in schizophrenic women and focus on possible clinical implications.

  • Plasma concentrations of estradiol in women suffering from schizophrenia treated with conventional versus atypical antipsychotics
    Schizophrenia Research, 2004
    Co-Authors: Niels Bergemann, Christoph Mundt, Peter Parzer, Iris Jannakos, Ines Nagl, Birgit Salbach, Klaus Klinga, Benno Runnebaum, Franz Resch
    Abstract:

    Abstract Background Low estrogen levels leading to an elevated rate of menstrual dysfunctions such as amenorrhea and irregular menstruation have been described in women with schizophrenia and have often been attributed to antipsychotic-induced hyperprolactinemia. However, there is some evidence that “Hypoestrogenism” in schizophrenic women does not occur exclusively under medication with hyperprolactinemia-inducing antipsychotics. While the precise mechanism of low estrogen levels in schizophrenic women has not been elucidated yet, “Hypoestrogenism” is of clinical relevance because estrogen seems to endow an antipsychotic-like effect in schizophrenia and thus positively affect the course of illness in schizophrenic women. In addition, low levels of estrogen might have a negative effect on bone mineral density and on the cardiovascular system. Methods To test the “Hypoestrogenism hypothesis”, hormone levels in 75 women with schizophrenia diagnosed according to DSM-IV and ICD-10 were determined in the follicular, periovulatory, and luteal phases of the menstrual cycle. Levels of estradiol, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and testosterone were assessed. Results The serum levels of estradiol were generally reduced during the entire menstrual cycle compared to normal reference values. With low levels of LH over the entire cycle and of progesterone in the luteal phase, anovulatory cycles were assumed. Hypoestrogenism was found in about 60% of the patients in accordance with a strict definition (estradiol serum level below 30 pg/ml in the follicular phase and below 100 pg/ml in the periovulatory phase). To rule out a possible effect of hyperprolactinemia on the gonadal axis and a subsequent effect on estradiol levels from treatment with conventional (“typical”) antipsychotics, serum estradiol levels of patients treated with certain atypical antipsychotics known to induce only a mild increase in prolactin, or no increase at all, were compared with those from patients treated with conventional antipsychotics. The data clearly indicate high prolactin levels in the latter, but low levels in the group treated with atypical antipsychotics. In both groups, however, low levels of estradiol compared to normal reference values were measured. Conclusions The present findings provide evidence that Hypoestrogenism in schizophrenia occurs in women with and without antipsychotic-induced hyperprolactinemia. Further research should be conducted to clarify the cause of Hypoestrogenism in schizophrenic women and focus on possible clinical implications.

  • Hypoestrogenism and Estrogen Replacement Therapy in Women Suffering from Schizophrenia
    Estrogen Effects in Psychiatric Disorders, 1
    Co-Authors: Niels Bergemann, Christoph Mundt, Peter Parzer, Benno Runnebaum, Franz Resch
    Abstract:

    functions in the gonadal axis. In the past it could be demonstrated that estrogens have an influence on major neurotransmitter systems and brain regions affecting cognitive, emotional, and vegetative functions (e.g., Fink et al. 1996; 1998; Halbreich 1995; Morisette and DiPaolo 1993; DiPaolo 1994; Gordon et al. 1980). Estrogens also exert neurotrophic and neuroprotective effects which are mediated by nongenomic as well as by direct and indirect genomic pathways (for review, see McEwen and Alves 1999; Lee and McEwen 2001; GarciaSegura 2001; Behl 2001). How estrogen influences the course of various diseases of the nervous system has been the focus of research in the neural sciences in the past few years. These diseases include stroke, Parkinson’s disease, Alzheimer’s disease, depression, and schizophrenia. Generally, gender differences in the incidence and in recovery from neurological damage and mental disorders were an important starting point of research in these fields. In schizophrenia research, the estrogen protection hypothesis has been investigated over the last 20 years. It assumes a protective effect of estrogen in women vulnerable to schizophrenia. Evidence for this hypothesis is based on epidemiologic, neurochemical, animal, and clinical data (cf. chap. 2 and 3 of this volume by RiecherRossler and/or Hafner; Seeman 1996). As early as 1909, Kraepelin reported that first-time hospitalization in men with schizophrenia occurs earlier than in women. However, the peak age of onset of schizophrenia is significantly later for women than for men, regardless of whether one investigates age at first hospitalization, first treatment, or age when psychotic symptoms are first noted (DeLisi et al. 1989; Seeman 1982; 1985; Tsuang

David A. Eschenbach - One of the best experts on this subject based on the ideXlab platform.

  • Depomedroxyprogesterone-induced Hypoestrogenism and changes in vaginal flora and epithelium.
    Obstetrics and gynecology, 2000
    Co-Authors: Leslie Miller, Dorothy L. Patton, Amalia Meier, Soe Soe Thwin, Thomas M. Hooton, David A. Eschenbach
    Abstract:

    Objective: To identify the effects of depomedroxyprogesterone acetate (DMPA) on vaginal microbial flora and epithelium. Methods: Women who desired DMPA for contraception were evaluated before and at 3 and 6 months after initiation of 150-mg DMPA injections every 3 months. At each visit we assessed genital symptoms vaginal signs vaginal microflora and histopathology by vaginal biopsies. Results: Among 38 women observed for 6 months there was significant reduction in mean serum estradiol level (99.9 +or- 9.3 pg/mL to 26.6 +or- 1.6 pg/mL P < .001). The number of subjects with any Lactobacillus did not change but the number with hydrogen peroxide (H2O2)-positive Lactobacillus decreased from 20% before to 12% after 6 months of DMPA (P = .005). The log concentration in colony-forming units per milliliter of vaginal fluid of H2O2-positive Lactobacillus decreased in a linear manner from 4.0 +or- 0.6 at baseline to 2.5 +or- 0.6 after 6 months of DMPA use (P = .006). The mean number of cell layers in the epithelium was reduced slightly from 28.1 +or- 0.7 to 25.9 +or- 0.9 (P = .05) epithelial thickness decreased from 1.02 +or- 0.04 mm to 0.89 +or- 0.05 mm (P = .005) and the glycogen-positive thickness decreased from 0.81 +or- 0.04 mm at baseline to 0.66 +or- 0.05 after 6 months of DMPA use (P = .005). Conclusion: Depomedroxyprogesterone acetate produced a systemic hypoestrogenic state associated with decreased H2O2-positive Lactobacillus colonization and slight thinning of the glycogen vaginal epithelial layer. Such changes possibly compromise the vaginal barrier to infection.

  • depomedroxyprogesterone induced Hypoestrogenism and changes in vaginal flora and epithelium
    Obstetrics & Gynecology, 2000
    Co-Authors: Leslie Miller, Dorothy L. Patton, Amalia Meier, Soe Soe Thwin, Thomas M. Hooton, David A. Eschenbach
    Abstract:

    Abstract Objective: To identify the effects of depomedroxyprogesterone acetate (DMPA) on vaginal microbial flora and epithelium. Methods: Women who desired DMPA for contraception were evaluated before and at 3 and 6 months after initiation of 150-mg DMPA injections every 3 months. At each visit, we assessed genital symptoms, vaginal signs, vaginal microflora, and histopathology by vaginal biopsies. Results: Among 38 women observed for 6 months, there was significant reduction in mean serum estradiol level (99.9 ± 9.3 pg/mL to 26.6 ± 1.6 pg/mL, P Conclusion: Depomedroxyprogesterone acetate produced a systemic hypoestrogenic state associated with decreased H2O2–positive Lactobacillus colonization and slight thinning of the glycogen vaginal epithelial layer. Such changes possibly compromise the vaginal barrier to infection.