Article

Sex hormones in psychotic men

Department of Clinical Psychiatry and Psychotherapy, Medical School of Hannover, Carl-Neuberg-Strasse 1, D-30623 Hannover, Germany.
Psychoneuroendocrinology (Impact Factor: 5.59). 02/2005; 30(1):111-4. DOI: 10.1016/j.psyneuen.2004.05.010
Source: PubMed

ABSTRACT For women at risk to develop schizophrenia, estradiol has been postulated to constitute a protective factor. Women suffering from psychotic disorders have accordingly been found to exhibit lower estradiol levels than controls. Our aim was to study gonadal function in psychotic men to determine the gender specificity of these observations, as available data in men are more scarce and conflicting and largely disregarded estradiol. Serum hormone levels were examined in 34 men admitted consecutively for an acute exacerbation or first onset of schizophrenia in a blinded prospective design. Subjects with current affective disorder including manic episode, concomitant substance abuse or severe medical illness were excluded. A control group of 34 healthy male blood donors was recruited. As compared to matched controls, acutely admitted men suffering from schizophrenia exhibited significantly lower serum levels of estradiol, oestrone, testosterone and free testosterone. Although results have to be regarded as preliminary, acute exacerbation of schizophrenia in men seems to be associated with low serum oestrogen and androgen levels. The oestrogen hypothesis postulating a protective action of estradiol concerning schizophrenia for women might well be valid for both genders. However, future research is needed before clinical applications are justified.

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    • "In this context, the clinical relationship between prolactin elevation and changes in bone density appears to correlate with menstrual dysregulation in women. In studies of patients with prolactin elevation during chronic antipsychotic treatment, hypogonadism has also been observed [Smith et al. 2002; Kinon et al. 2003; Huber et al. 2005; O'Keane and Meaney, 2005; Kishimoto et al. 2008]. Studies in rodents and nonhuman primates also illustrate that chronic treatment with risperidone lowers BMD by increasing bone resorption [Kunimatsu et al. 2010; Sackett et al. 2010], and that this increase in resorption is related to prolactin elevation and reductions in estrogen. "
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    ABSTRACT: Prolactin elevation has been proposed as a risk factor for low bone density and potentially osteoporosis in patients on long-term treatment with prolactin-elevating antipsychotics. Our objective was to study the acute effects of prolactin elevation on serum markers of bone formation and resorption in patients treated with risperidone. Thirty participants meeting Diagnostic and Statistical Manual of Mental Disorders fourth edition criteria for schizophrenia, major depressive disorder with psychotic features, or bipolar disorder with psychosis were enrolled. At baseline, subjects were antipsychotic free. Subjects were evaluated before and after 4 weeks of risperidone treatment. Assessments included symptom ratings along with testosterone, estradiol, prolactin, osteocalcin (marker of bone formation), and n-telopeptide crosslinks (NTx marker of bone resorption). Primary analysis examined the impact of risperidone treatment on change in the bone markers and hormone levels from pre to post treatment. Prolactin levels significantly increased from 12.1 ± 1.9 ng/ml to 65.7 ± 12.2 ng/ml after treatment (p < 0.001). NTx markers of bone resorption significantly decreased from 18.31 ± 1.49 nM bone collagen equivalent (BCE) before treatment to 15.50 ± 1.22 nM BCE after treatment in the study sample as a whole (p < 0.05). A trend was observed indicating that NTx may increase in individuals who have the greatest increases in prolactin after treatment r = 0.33, p = 0.07). These findings suggest that prolactin elevation is associated with changes in bone physiology very early in the course of treatment with risperidone. Bone resorption decreased in many subjects but higher levels of bone resorption occurred in patients with the greatest increases in prolactin. This may have important implications for prolactin monitoring or the periodic assessment of osteoporosis-related outcomes in patients requiring extended treatment.
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    • "In this context, the clinical relationship between prolactin elevation and changes in bone density appears to correlate with menstrual dysregulation in women. In studies of patients with prolactin elevation during chronic antipsychotic treatment, hypogonadism has also been observed [Smith et al. 2002; Kinon et al. 2003; Huber et al. 2005; O'Keane and Meaney, 2005; Kishimoto et al. 2008]. Studies in rodents and nonhuman primates also illustrate that chronic treatment with risperidone lowers BMD by increasing bone resorption [Kunimatsu et al. 2010; Sackett et al. 2010], and that this increase in resorption is related to prolactin elevation and reductions in estrogen. "
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    ABSTRACT: Introduction A growing body of literature suggests that there may be an increased risk for low bone density and osteoporosis in patients receiving chronic therapy with antipsychotics associated with significant prolactin elevation [O'Keane, 2008]. This phe-nomenon was initially observed in patients with schizophrenia, where bone mineral density (BMD) values measured by dual-emission X-ray absorptiometry (DXA) scans were 14% lower than matched controls [Baastrup et al. 1980] with further research indicating that up to 44% of women treated with first-generation antipsychot-ics had BMD values at least 1 SD below age-and sex-matched controls [Halbreich et al. 1995]. To date the relationships between antipsychotics and changes in BMD or bone metabolism have pre-dominantly been investigated in cross-sectional Risperidone-associated prolactin elevation and markers of bone turnover during acute treatment
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    • "Several lines of evidence document that neuroactive steroids (NSs) play a critical role in the pathophysiology of psychotic disorders. While numerous studies have highlighted alterations in NS levels in schizophrenia (Goyal et al., 2004; Taherianfard and Shariaty, 2004; Huber et al., 2005; Marx et al., 2006), the functional significance of these changes remains elusive, in view of the pleiotropic activity of NSs in behavioral regulation. Sex hormones are posited to modulate the course of schizophrenia (Häfner, 2003; Halari et al., 2004; Elias and Kumar, 2007) and may account for the earlier onset and higher severity of this disorder in males (Andreasen et al., 1990; Tamminga, 1997; Gur et al., 2000; Goldstein et al., 2002; Häfner, 2003; Seeman, 2004). "
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    ABSTRACT: Cogent evidence highlights a key role of neurosteroids and androgens in schizophrenia. We recently reported that inhibition of steroid 5α-reductase (5αR), the rate-limiting enzyme in neurosteroid synthesis and androgen metabolism, elicits antipsychotic-like effects in humans and animal models, without inducing extrapyramidal side effects. To elucidate the anatomical substrates mediating these effects, we investigated the contribution of peripheral and neural structures to the behavioral effects of the 5αR inhibitor finasteride (FIN) on the prepulse inhibition (PPI) of the acoustic startle reflex (ASR), a rat paradigm that dependably simulates the sensorimotor gating impairments observed in schizophrenia and other neuropsychiatric disorders. The potential effect of drug-induced ASR modifications on PPI was excluded by measuring this index both as percent (%PPI) and absolute values (ΔPPI). In both orchidectomized and sham-operated rats, FIN prevented the %PPI deficits induced by the dopamine (DA) receptor agonists apomorphine (APO, 0.25mg/kg, SC) and d-amphetamine (AMPH, 2.5mg/kg, SC), although the latter effect was not corroborated by ΔPPI analysis. Conversely, APO-induced PPI deficits were countered by FIN infusions in the brain ventricles (10μg/1μl) and in the nucleus accumbens (NAc) shell and core (0.5μg/0.5μl/side). No significant PPI-ameliorating effect was observed following FIN injections in other brain regions, including dorsal caudate, basolateral amygdala, ventral hippocampus and medial prefrontal cortex, although a statistical trend was observed for the latter region. The efflux of DA in NAc was increased by systemic, but not intracerebral FIN administration. Taken together, these findings suggest that the role of 5αR in gating regulation is based on post-synaptic mechanisms in the NAc, and is not directly related to alterations in DA efflux in this region.
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