Exercise-induced hypertension (EIH) is defined as elevated blood pressure (BP) > 190mm Hg for females and > 210 mmHg for males during exercise. EIH is prevalent among athletes and healthy individuals with no cardiovascular (CV) risk factors. While previous data corroborates exercise in reducing hypertension and cardiovascular risk, the development of EIH and its attendant cardiovascular risk necessitates a review of the pathophysiological mechanisms resulting in EIH. To date, these mechanisms causing EIH are not fully understood, nor are there any established guidelines on the management of EIH. In this article, we discuss in detail the pathophysiological mechanisms, the prognostic value, clinical implications, possible treatment, and future directions in managing EIH.

Objective: This pilot study aimed to determine the correlation of metabolic syndrome (MetS), its components, and increased LDL (low-density lipoprotein) and total cholesterol levels with osteoarthritis (OA). In addition, our goal was to establish the association between MetS and the degree of handicap measured by the Lequesne index of functionality and severity of knee osteoarthritis. Materials and methods: The pilot study included 25 subjects with knee OA and 19 subjects without knee OA. All subjects were menopausal or premenopausal women. MetS was diagnosed according to the National Cholesterol Education Program, Adult Treatment Panel III. OA was diagnosed if Kellgren-Lawrence ≥ 2. Results: MetS was detected in 80% of subjects with OA. In the non-OA group, MetS was detected in 26% of subjects. The difference in MetS prevalence between the two groups was significant (p=0.000). The presence of each MetS component was significant in the OA group, except for central obesity, which presence was marginally significant (p=0.054). Prevalence of increased total (p=0.019) and LDL cholesterol (p=0.000) was also significant in the OA group. A significant difference between OA and the non-OA group was detected in the prevalence of all five MetS components (p=0.016). In the OA group, the Lequesne index of functionality and severity of knee osteoarthritis was not significantly altered between subjects with and without MetS. Conclusion: Metabolic syndrome, its components, increased LDL, and total cholesterol are correlated with osteoarthritis in premenopausal and menopausal women. MetS is not correlated with the degree of handicap in the knee joint measured by the Lequesne index.

Androgen receptor signaling primarily influences both the normal growth and proliferation of the prostate gland and the development of prostatic carcinoma. While localized prostate cancers are typically managed with definitive therapies like surgery and radiotherapy, many patients have recurrences in the form of metastatic disease. Androgen deprivation therapy, by way of castration via orchiectomy or with drugs like luteinizing hormone-releasing hormone (commonly called gonadotropin-releasing hormone) agonists and luteinizing hormone-releasing hormone antagonists, is the primary mode of therapy for advanced castration-sensitive prostate cancer. Castration resistance invariably develops in these patients. Further treatment has shifted to newer anti-androgen drugs like enzalutamide or abiraterone and taxane-based chemotherapy. Prolonged inhibition of the androgen receptor signaling pathway causes androgen receptor-independent clonal evolution which leads to the development of treatment-emergent neuroendocrine prostate cancer. All prostate cancers at the initial presentation should undergo evaluation for the markers of neuroendocrine differentiation. Detection of serum biomarkers of neuroendocrine differentiation and circulating tumor cells is a prospective non-invasive method of detecting neuroendocrine transdifferentiation in patients undergoing treatment with androgen receptor pathway inhibitors. It is essential to perform a biopsy in the presence of red flags of neuroendocrine differentiation. Alisertib, an Aurora kinase inhibitor, showed promising clinical benefit in a subgroup of patients with certain molecular alterations. A thorough understanding of the molecular and clinical programming of treatment-emergent neuroendocrine prostate cancer can potentially lead to the development of drugs to prevent the development of this lethal variant of prostate cancer.