Koro Syndrome: Epidemiology, Psychiatric and Physical Risk Factors, Clinical Presentation, Diagnosis, and Treatment Options.

Koro syndrome is a multi-tiered disease presenting as an overwhelming belief that one's sex organs are shrinking into their body. Moderate to severe anxiety attacks are associated with the condition, along with a fear of imminent death. Koro is often culturally related and is most seen as an epidemic form in East and Southeast Asia, although it can present anywhere worldwide in its sporadic form. The condition typically affects young males who believe in sex-related myths, and many individuals can co-present with anxiety, depression, or even psychosis. Although most presentations of Koro are self-limiting, the condition is harmful for one's self-esteem and quality of life, and some individuals may go through extreme, physically injurious measures to prevent genital retraction. Treatments include the use of psychotherapy that has a sex education component, especially if the patient believes in culturally rooted myths. In sporadic Koro, it is believed that if the primary psychiatric disorder is treated with anxiolytics, antidepressants, sedatives, or psychotics, the secondary Koro-like symptoms will also fade. Additional investigation on the prevalence, pathogenesis, factors that correlate with treatment efficacy are needed to fully understand Koro syndrome.

Ketamine-Induced Cystitis: A Comprehensive Review of the Urologic Effects of This Psychoactive Drug.

Ketamine is a common medical anesthetic and analgesic but is becoming more widely used as a recreational drug. Significant side effects on the urinary tract are associated with frequent recreational ketamine use most notably ketamine-induced cystitis (KIC). Regular ketamine consumption has been shown to increase the risk of cystitis symptoms by 3- to 4-fold, and cessation of ketamine use is usually associated with improvement of symptoms. Common KIC-related problems are urinary pain and discomfort, bladder epithelial barrier damage, reduced bladder storage and increased pressure, ureter stenosis, and kidney failure, all of which significantly impact patients' quality of life. Furthermore, it becomes a vicious cycle when KIC patients attempt to manage their urinary pain with increased ketamine use. The precise pathophysiology of KIC is still unknown but several theories exist, most of which highlight the inflammatory signaling pathways leading to bladder epithelium damage due to presence of ketamine in the urine. Empirical treatment options for KIC are available and consist of ketamine cessation, noninvasive therapies, and surgery, and should be decided upon based on the time course and severity of the disease. Of note, cessation of use is strongly recommended for all KIC patients, and should be supplemented with motivational interviews and psychological and social support. It is crucial for clinicians to be familiar with KIC diagnosis and treatment, and to be prepared to have informed discussions with ketamine-using patients about the potential health consequences of ketamine.

Insulin and glucose responses to hypoxia in male and female neonatal rats: Effects of the androgen receptor antagonist flutamide.

Hypoxia is common with preterm birth and may lead to long-term effects on adult pancreatic endocrine function and insulin sensitivity. This phenomenon may be sexually dimorphic due to the hypoxia-induced augmentation of the neonatal androgen surge in male newborns. We evaluated this phenomenon by pretreating neonatal rats on postnatal days (PD) 1, 6, 13, or 20 with flutamide (a nonsteroidal androgen receptor antagonist) at a standard or a high dose (10 or 50 mg/kg) compared to vehicle control. One day later, neonatal rats were exposed to either acute normoxic or hypoxic separation (fasting) for 90 min, and blood was sampled for the measurement of insulin and glucose and the calculation of HOMA-IR as an index of insulin resistance. During normoxic and hypoxic separation (fasting), flutamide increased insulin secretion in PD2, PD7, and PD14 pups, high dose flutamide attenuated insulin secretion, and high dose flutamide attenuated the increase in HOMA-IR due to hypoxia. Our studies suggest a unique role of the androgen receptor in the control of neonatal pancreatic function, possibly by blocking a direct effect of neonatal testosterone or in response to indirect regulatory effects of androgens on insulin sensitivity.

The effects of flutamide on the neonatal rat hypothalamic-pituitary-adrenal and gonadal axes in response to hypoxia.

Hypoxia is common with preterm birth and may lead to long-term effects on the adult hypothalamic-pituitary-adrenal (HPA) axis that are sexually dimorphic due to neonatal androgens. Although the adult rat adrenal does not express appreciable CYP17 activity, the neonatal rat adrenal may synthesize androgens that could be a critical local factor in the development of adrenal function. We evaluated these phenomena by pretreating the neonatal rats on postnatal days (PD) 1, 6, 13, 20 with flutamide (a nonsteroidal androgen receptor antagonist) at a standard or a high dose (10 mg/kg or 50 mg/kg) compared to vehicle control. One day later, neonatal rats were exposed to acute hypoxia and blood was sampled. We found that (a) in PD2 pups, flutamide augmented corticosterone responses in a sexually dimorphic pattern and without an increase in ACTH, (b) PD7 and PD14 pups had the smallest corticosterone response to hypoxia (c) PD21 pups had an adult-like corticosterone response to hypoxia that was sexually dimorphic, (d) flutamide attenuated ACTH responses in PD7 hypoxic pups, and (e) high-dose flutamide suppressed the HPA axis, FSH, and estradiol. Flutamide demonstrated mixed antagonist and agonist effects that changed during the first three weeks of neonatal life. We conclude that the use of flutamide in neonatal rats to evaluate androgen-induced programming of subsequent adult behavior is not optimal. However, our studies suggest neonatal androgens play a role in regulation of adrenal function that is sexually dimorphic and changes during early development.