ABSTRACT
Objetivo: este artículo revisa el concepto de hipersexualidad, las condiciones asociadas a dicho comportamiento así como los tratamientos indicados para el mismo.Métodos: llevamos a cabo una búsqueda en internet de artículos en lenguaje inglés publicados en los últimos 20 años (hipersexualidad, sexualidad humana, comportamiento hipersexual, ninfomanía).Resultados: la hipersexualidad es un cambio en las formas e incremento en la frecuencia de los comportamientos sexuales. La etiología de la hipersexualidad es compleja e involucra una variedad de mecanismos fisiológicos y psicológicos. Puede ser idiopática o el resultado final de muchos procesos de enfermedad subyacentes. La disfunción del lóbulo frontal y de otras áreas cerebrales puede conducir a la desinhibición en el comportamiento sexual y a hipersexualidad; esta condición también puede ser el resultado de otros trastornos neurológicos, psiquiátricos o efectos secundarios de medicamentos. Cuando la causa subyacente puede ser tratada, el comportamiento sexual desinhibido cesa. Conclusión: la hipersexualidad puede ocasionar conductas de difícil manejo, pero los métodos farmacológicos pueden controlar de manera exitosa estos comportamientos en la mayoría de los pacientes.
Objective: This article reviews the concept of hypersexuality, the conditions attached to such behavior and the treatments prescribed for it. Methods: We conducted an internet search for English-language articles published over the past 20 years (Hypersexuality, human sexuality, hypersexual behavior, Nymphomania). Results: Hypersexuality is a change in the ways and an increase in the frequency of the sexual behaviors. The etiology of hypersexuality is complex and involves a variety of physiological and psychological mechanisms. It may be idiopathic or the final result of many underling disease processes. The dysfunction of the frontal lobe and other brain areas can lead to the disinhibition in the sexual behavior and hypersexuality; this condition can also be the result of other neurological and psychiatric disorders or an adverse effect of medications. When the underlying cause can be treated, the uninhibited sexual behavior ceases. Conclusion: Hypersexuality can cause unmanageable behavior, but pharmacological methods can successfully control this behavior in most patients.
Subject(s)
Humans , Clomipramine/pharmacokinetics , Sexual Dysfunction, Physiological/physiopathology , Gonadotropin-Releasing Hormone/pharmacokinetics , Selective Serotonin Reuptake Inhibitors/pharmacokinetics , Libido , Erotica/psychology , Frontal Lobe/pathology , Satiety Response , Social Behavior Disorders/psychologyABSTRACT
Background: Several studies suggest that leptin modulates the reproductive axis function. Leptin may stimulate release of GnRH from hypothalamus and of gonadotrophins from the pituitary. A synchronicity of LH and leptin pulses has been described in healthy women and in patients with polycystic ovarian syndrome (PCOS), suggesting a relationship between the episodic secretion of LH and leptin. In vitro experimental studies have demonstrated that leptin administration promotes GnRH-LH release. However it is not established whether GnRH promotes the episodic secretion of leptin. Aim: To assess the response of LH and leptin to the administration of a GnRH bolus in hyperandrogenic and healthy women. Patients and methods: Eleven hyperandrogenic and eleven healthy women of similar age and body mass index (BMI) were studied. Under basal conditions three blood samples were collected every 30 min before and after the administration of a GnRH bolus (100 µg). LH and leptin concentrations were measured in all samples. Testosterone, SHBG and estradiol were determined in the first sample. For data analysis, the increment of LH and leptin between 0-30 and 0-60 min. was calculated. The LH and leptin areas under the curve (AUC) before and after GnRH administration were also calculated in both groups. Results: After GnRH administration. an increment in LH concentrations was observed in both groups; however, leptin concentrations were not modified. In both groups LH area under the curve increased after GnRH administration; however, the leptin area was not modified. Conclusions: These results suggest that circulating leptin concentration is not modulated by GnRH-LH
Subject(s)
Humans , Female , Adult , Luteinizing Hormone/drug effects , Gonadotropin-Releasing Hormone/pharmacokinetics , Leptin , Polycystic Ovary Syndrome/drug therapy , Case-Control Studies , Hyperandrogenism/drug therapyABSTRACT
Nitric oxide (NO) plays a crucial role in reproduction at every level in the organism. In the brain, it activates the release of luteinizing hormone-releasing hormone (LHRH). The axons of the LHRH neurons project to the mating centers in the brain stem and by afferent pathways evoke the lordosis reflex in female rats. In males, there is activation of NOergic terminals that release NO in the corpora cavernosa penis to induce erection by generation of cyclic guanosine monophosphate (cGMP). NO also activates the release of LHRH which reaches the pituitary and activates the release of gonadotropins by activating neural NO synthase (nNOS) in the pituitary gland. In the gonad, NO plays an important role in inducing ovulation and in causing luteolysis, whereas in the reproductive tract, it relaxes uterine muscle via cGMP and constricts it via prostaglandins (PG).