Body perception treatment, a possible way to treat body image disturbance in eating disorders: a case-control efficacy study.

BACKGROUND: The body image disturbance (BID) is a common symptom in eating disorders, often observed and described in anorexia nervosa (AN) and bulimia nervosa (BN). Recently, this symptom has also been observed in binge eating disorder (BED). The research underlines that the BID presents three different altered components: affective, cognitive, and perceptual one. Current treatments for BID have mainly focused on the affective and cognitive components. Nowadays, the need emerges for treatments focused also on the perceptual component of the BID. In this paper, we present the results of an efficacy study on the body perception treatment (BPT), a new treatment for BID focused on the perceptual component of the disorder. OBJECTIVE: We looked for an additional treatment effect on a protocol for ED inpatients to evaluate the efficacy of BPT. We performed the study through statistical analysis of admission and discharge scores. METHODS: We conducted a case-control study in a hospital ward specialized in eating disorders. Two groups were identified: the control group (TAU; N = 91) and the experimental group (TAU + BPT; N = 91). The experimental group performed BTP activities in addition to the treatment at usual. All patients in both groups had an eating disorder diagnosis (AN, BN, BED and EDNOS/OSFED). Sampling occurred on a time basis and not by randomization. Moreover, all patients admitted in the ED hospital ward in the time frame considered (from end-2009 to mid-2017) were included in the study. BPT activities were introduced in mid-2013 and three psychometric instruments upon entry and discharge were used: Symptom Check List-90 (SCL-90) to measure the general psychopathological state; the Eating Disorder Inventory-3 (EDI-3) to estimate the incidence of personality traits strongly correlated to eating disorders; the body uneasiness test (BUT) to measure the body uneasiness. We performed a pre/post analysis for both groups; we studied the additional effect of the treatment through deltas analysis of the three questionnaires (Δ = assessment at discharge - assessment at the entrance). Data were analyzed using the Student T and the Wilcoxon rank-sum test. RESULTS: The pre/post analysis showed statistically significant improvement in both conditions (TAU and TAU + BPT) in the general psychopathological state (SCL-90) and in the incidence of personality traits (EDI-3). Improvements in body uneasiness (BUT) were observed only in the experimental group (TAU + BPT). Furthermore, the analysis of the deltas shows more significant improvements in TAU + BPT compared to TAU in all the variables considered. CONCLUSION: We found an additional effect of the BPT on TAU. The usual ED protocol added with BPT activities showed significantly better clinical results. We have interpreted these results in light of recent developments in the neuroscientific field of body image. LEVEL OF EVIDENCE: Level II: controlled trial without randomization.

The role of diagnostic hysteroscopy and endometrial biopsy in assisted reproductive technologies.

OBJECTIVE: To study the incidence of unsuspected endouterine abnormalities in patients for whom IVF-ET repeatedly fails. DESIGN: Prospective study. SETTING: Infertility Unit of the Department of Obstetrics and Gynecology, Arcispedale Santa Maria Nuova, Reggio Emilia, Italy. PATIENT(S): One hundred patients for whom two IVF-ET cycles failed in which > or =2 good-quality embryos were transferred. INTERVENTION(S): In-office diagnostic hysteroscopy and endometrial biopsy. MAIN OUTCOME MEASURE(S): Relation between IVF-ET failure and unsuspected endouterine abnormalities. RESULT(S): In 18 patients, hysteroscopy showed an important unsuspected endouterine abnormality. Fifteen of these patients did not become pregnant after IVF-ET, and 3 became pregnant but had a spontaneous abortion. Histologic examination of the endometrium revealed chronic endometritis in 1 patient and tuberculous endometritis in another. CONCLUSION(S): Previous studies have reported that the incidence of endouterine abnormalities is high in patients undergoing IVF-ET. Our data confirm the previous reports and lead us to conclude that diagnostic hysteroscopy should be performed on all patients before they undergo IVF-ET.

Altered neuroendocrine control of GH secretion in normal women of advanced reproductive age.

BACKGROUND: Previous studies have suggested that the neuroendocrine control of growth hormone (GH) secretion changes with increasing age in women with normal menstrual cycles and sex steroid levels. METHODS: In order to verify this hypothesis, 8 younger (22-32 years) and 8 older (41-45 years) women with normal menstrual function and gonadal steroid levels were tested with the serotonergic agent sumatriptan (6 mg in a subcutaneous bolus), the GABAergic agonist sodium valproate (800 mg orally), the dopaminergic compound L-Dopa (500 mg orally) and placebos. Furthermore, all women were tested with GH-releasing hormone (GH-RH 1 microgram/kg body weight in an intravenous (i.v.) bolus) to determine whether GH secretion in response to its specific releasing factor was preserved. Serum GH levels were recorded over 2 hours in all tests and IGF-I levels in basal samples. RESULTS: Plasma IGF-I concentrations and the GH responses to sumatriptan, sodium valproate and L-Dopa were significantly lower in older than in younger women. Also, the GH-RH-induced GH response was significantly lower in older than in younger subjects. When peak GH responses to releasing stimuli were compared with age, significant negative correlations were found in all tests. CONCLUSIONS: These data did not show a specific neurotransmitter change underlying defective GH secretion in older aged reproductive women. On the other hand, the results indicated that age-related changes in the secretory machinery of GH, such as a reduced pituitary sensitivity to GH-RH and/or a reduction in the pituitary GH secretory capacity, affect women during the last years of the reproductive period.

Age-related decrease in the opioid control of LH secretion during reproductive years in normal women.

UNLABELLED: Our previous studies showed that naloxone is unable to stimulate LH secretion in elderly men, suggesting a loss in the endogenous opioid inhibitory control of LH in senescence. METHODS: In the present study, we examined whether increasing age during the reproductive period in women is associated with alterations in the LH-releasing effect of naloxone. Studies were performed in younger (age 20-28 years, n = 8) and older (age 40-48 years, n = 8) subjects with normal menstrual cycles and normal gonadal steroid levels to avoid the interference of premenopause or menopause on gonadotropin secretion. The LH response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h) was tested not only in normal conditions, but also after chronic dopaminergic stimulation with bromocriptine (5 mg/day for 7 days), because this treatment has been found able to restore normal LH responses to naloxone in elderly men. All tests were performed on the 22nd day of normal menstrual cycles. RESULTS: Naloxone induced a 100% increase in plasma LH levels in the younger group. In contrast, naloxone enhanced only by 50% LH secretion in the older subjects. When experiments were repeated after bromocriptine treatment, the effect of naloxone did not change in the younger subjects, whereas it was significantly higher in the older group. In the presence of bromocriptine, naloxone-induced LH increment in the older group was indistinguishable from that observed in the younger group. These data suggest that during the reproductive period, increasing age is associated with an impairment in the endogenous opioid control of LH secretion. In addition, age-related dopaminergic alterations independent of circulating gonadal steroid levels appear to underlie the defective endogenous opioid control of LH secretion in normally cycling women.

Effect of substance P on basal and thyrotropin-releasing hormone-stimulated thyrotropin release in humans.

To test the possible effects of intravenous administration of substance P (SP) on basal and thyrotropin-releasing hormone (TRH)-stimulated thyrotropin (TSH) release, SP was infused alone (0.5 or 1.5 pmol/kg-1/min-1 for 60 minutes) or after TRH (20 or 400 micrograms in an intravenous bolus) in 21 normal male subjects (aged 26 to 36 years) and in 18 normal women (aged 25 to 32 years). Women were studied during follicular (day 6 to 8) and luteal (day 21 to 23) phases of following regular menstrual cycles. In addition, plasma cortisol levels during SP infusion were measured. In agreement with previous findings, significant increments in plasma cortisol levels were observed in men and women when the higher (1.5 pmol/kg-1/min-1) but not the lower (0.5 pmol/kg-1/min-1) amount of SP was administered. In contrast, in both men and women basal and TRH (20 or 400 mg)-induced TSH releases were not modified by SP at any tested amount. Results in the follicular and luteal phase were similar. These data suggest that in normal men and women plasma SP is not involved in the control of TSH release, at least not outside the blood-brain barrier.

Naloxone enhances angiotensin II-induced increase in serum luteinizing hormone concentrations in normal women.

The present study was carried out in order to establish whether the stimulatory effect of angiotensin II (ANG II) on serum concentration of LH in women is under control by endogenous opioid peptides. For this purpose, the effect of ANG II (infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg/min; each dose for 20 min) on serum LH levels was evaluated during administration of saline or the opioid antagonist naloxone (4 mg in an i.v. bolus followed by 10 mg over 2 h) in 7 normal women in both follicular and luteal phase. In all subjects, tests with saline alone (control test) or naloxone alone were performed. No significant changes in LH levels were observed in any test performed in the follicular phase and in the control test performed in the luteal phase. In contrast, in the luteal phase, both ANG II and naloxone induced significant increments in LH levels (23% increase vs. baseline by ANG II and 54% by naloxone). When naloxone and ANG II were given together stimulated LH increase was greatly enhanced. The mean peak was 154% higher than baseline and was higher than the sum of the individual peaks produced by naloxone and ANG II alone. These findings suggest inhibition by endogenous opioids of the stimulating action of ANG II on LH secretion during the luteal phase.

Endogenous opioid mediation of the inhibitory effect of ethanol on the prolactin response to breast stimulation in normal women.

The effect of ethanol on the prolactin (PRL) response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the PRL response to breast stimulation and ethanol action was also examined. Eleven normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 mg in an iv bolus plus 10 mg over 75 min. or 4 mg in an iv bolus plus 20 mg over 75 min.), ethanol (50 ml in 110 ml of whiskey p.o.) or the combination of ethanol and naloxone. Serum PRL levels rose significantly after breast stimulation, with a mean peak response (71.4% higher than baseline at 20 min). The PRL response to breast stimulation was not changed by the treatment with the lower (2 plus 10 mg) or the higher (4 plus 20 mg) dose of naloxone, whereas it was strikingly decreased by ethanol (mean peak was 25% higher than baseline). However, when ethanol was given together with naloxone, the peak rise induced by breast stimulation was only partially inhibited by ethanol (the mean PRL peak was 46.2% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the PRL response to breast stimulation. Naloxone-sensitive endogenous opioids do not appear to be involved in the control of the PRL rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

Inhibition by ethanol of the oxytocin response to breast stimulation in normal women and the role of endogenous opioids.

The possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110 ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

Oxytocin does not modify the prolactin response to metoclopramide in normal women.

The present study was undertaken in order to establish whether oxytocin (OT) affects the dopaminergic control of PRL secretion in normal women during follicular, periovulatory and luteal phase of their menstrual cycle. For this purpose, 22 normal women were tested with a lower (1 mg) or higher (10 mg) dose of the dopaminergic antagonist metoclopramide (MCP) with or without the concurrent treatment with OT (2 IU injected plus 0.033 IU/min infused for 2 h). Since OT was found unable to modify the effect of either 1 or 10 mg MCP, in additional experiments the same doses of MCP and OT were administered after dopamine (0.04 micrograms/kg/min for 2 h) infusion. Also in these experimental conditions OT failed to modify the PRL response to MCP. These data argue against a role of OT in modulation of the dopaminergic control of PRL secretion in normal women.

Relationship between plasma profiles of oxytocin and adrenocorticotropic hormone during suckling or breast stimulation in women.

Oxytocin (OT) administration has been shown to inhibit adrenocorticotropic hormone (ACTH)/cortisol secretion in several experimental conditions. In the present study, the plasma OT responses to suckling in 7 lactating women or to mechanical breast stimulation in 6 normally menstruating women (experimental tests) or to sham stimuli in the same subjects (control tests) were measured and correlated with the simultaneous changes in plasma ACTH/cortisol levels. All women showed similar basal levels of OT, ACTH and cortisol, which remained unmodified after sham stimulation. In contrast, both suckling and breast stimulation produced a significant increase in plasma OT levels and a significant decrease in plasma ACTH concentrations. When OT and ACTH data were considered together, a significant negative correlation was found between the OT increase and the simultaneous ACTH decline. Plasma cortisol levels were lower during suckling or breast stimulation than in control conditions. These data show an inverse relationship between plasma OT and ACTH levels during suckling and breast stimulation in humans, suggesting an inhibitory influence of OT on ACTH/cortisol secretion in a physiological condition.

Arginine vasopressin secretion in non-obese women with polycystic ovary syndrome.

Arginine vasopressin responses to osmotic (0.1 ml.kg-1.min-1 NaCl), orthostatic (standing upright and maintenance of orthostatic position for 20 min), and hypoglycemic (0.15 IU/kg insulin) stimuli were evaluated in women with polycystic ovaries and in normal subjects. Blood dehydroepiandrosterone, dehydroepiandrosterone sulphate, androstenedione, testosterone, cortisol, and endogenous insulin levels were significantly higher in women with polycystic ovaries than in controls, whereas estrone, estradiol-17 beta, progesterone and 17OH-progesterone concentrations were normal in all subjects. Arginine vasopressin basal levels (mean +/- SEM of 3 test days; women with polycystic ovaries: 2.8 +/- 0.2 pmol/l; controls: 2.7 +/- 0.2 pmol/l) and secretory responses to orthostatic (mean peaks 100% higher than baseline values) and to hypertonic (130% increments) stimuli were similar in the two groups. Arginine vasopressin responses to hypoglycemia were lower in women with polycystic ovaries (50% increment) than in controls (150% increment), although comparable blood glucose decrements and GH or cortisol increments were found in the two groups. Arginine vasopressin peak responses to hypoglycemia were negatively correlated to testosterone, androstenedione, and endogenous insulin levels, but did not correlate with basal and hypoglycemia-induced peak cortisol concentrations or with circulating levels of other steroids. These data indicate a hypothalamic posterior pituitary disorder affecting arginine vasopressin response to insulin-induced hypoglycemia in women with polycystic ovaries syndrome associated with elevated blood androgen and insulin concentrations.

Lysine-vasopressin does not affect basal and LH-RH-stimulated LH and FSH release during the menstrual cycle of normal women.

In order to test possible effects of lysine-vasopressin (LVP) on basal and LH-RH-stimulated LH and FSH release, an intravenous bolus of LVP (0.06 IU/kg body weight) was injected alone or 10 min before LH-RH (100 micrograms i.v.) in 33 normal women in the follicular, periovulatory and luteal phase of their menstrual cycle. The administration of LVP modified neither the basal secretion of the gonadotropins nor the LH-RH-induced LH and FSH release. These data suggest that in humans, vasopressin is not involved in the control of gonadotropin release at the level of the anterior pituitary.

Hysterosalpingography versus chromosalpingolaparoscopy: comparison of results in 174 patients with sterility problems.

The comparison of results of hysterosalpingography and chromosalpingolaparoscopy to which 174 patients with sterility problems were subjected confirmed that chromosalpingolaparoscopy is an altogether more accurate and reliable test than hysterosalpingography. However, it also showed that chromosalpingolaparoscopy can give false positives in the study of tubal accessibility. The Authors consider hysterosalpingography a fundamental test when studying sterile women, since it is the only examination enabling the observation of tubal passages and also because it is able to show the above-mentioned possible false positives of chromosalpingolaparoscopy. In agreement with most experts in gynecological endoscopy, the Authors consider hysterosalpingography and chromosalpingolaparoscopy two complementary examinations when studying the uterotubal approach while chromosalpingolaparoscopy is a balance test to be used, with rare exceptions, at the end of the diagnostic iter.

Inhibition by somatostatin of LH-RH-induced LH release in normal menstruating women.

The present study was carried out in order to establish whether the concomitant treatment with somatostatin (SRIH) is capable of modifying gonadotrophin release in response to LH-RH administration in normal women during follicular, periovulatory, and luteal phases. SRIH was administered in a dose of 5.55 micrograms/min over 180 min and LH-RH (100 micrograms) was injected as a bolus at 90 min after the beginning of SRIH infusion. Within the dose used, SRIH significantly reduced LH response to LH-RH, whereas it did not alter FSH response to LH-RH. These results suggest that SRIH may play a part in the regulation of LH secretion in normal women.