ABSTRACT
Introduction Acute COVID-19 patients can suffer from chronic symptoms known as post-acute sequelae of SARS-CoV-2 infection (PASC). Point-of-care ultrasound (POCUS) is established in acute COVID, but its utility in PASC is unclear. We sought to determine the incidence of cardiac and pulmonary abnormalities with POCUS in patients with PASC in a COVID-19 recovery clinic. Methods This prospective cohort study included adults (>18 years old) presenting with cardiopulmonary symptoms to the COVID-19 recovery clinic. A lung ultrasound and standard bedside echocardiogram were performed by ultrasound-trained physicians. Images were interpreted in real time by the performing sonographer and independently by a blinded ultrasound faculty member. Discrepancies in interpretation were addressed by consensus review. A modified Soldati score was calculated by the sum of the scores in each of the 12 lung zones, with each zone score ranging from 0 to 3 (maximum score of 36). The score was then compared to clinical outcomes and outpatient testing. Results Between April and July 2021, 41 patients received POCUS examinations, with 24 of those included in the study. In all, 15 out of 24 (62.5%) had a normal lung ultrasound. Of the nine subjects with lung abnormalities, the median modified Soldati score was 2. Three patients had trivial pericardial effusions, and all had normal left and right ventricular size and function. Conclusion The majority (62.5%) of patients presenting to the PASC clinic had a normal pulmonary ultrasound, and the vast majority (87.5%) had normal cardiac ultrasounds. These findings suggest that cardiopulmonary symptoms in PASC may be from etiologies not well evaluated by POCUS.
Subject(s)
COVID-19 , SARS-CoV-2 , COVID-19/diagnosis , COVID-19/epidemiology , Hospitals , Humans , Incidence , Sensitivity and SpecificityABSTRACT
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.
ABSTRACT
Sarcoidosis is defined by granuloma formation in a multitude of organs. Despite its rare involvement in the nervous system, there are a number of cases that identify neurological symptoms to be the initial clinical manifestation of sarcoidosis. The involvement of the hypothalamic-pituitary (HP) axis presented most frequently with hormone deficiencies. Studies have reported that damage to the pituitary gland may be irreversible, and hormone abnormalities were generally permanent. Neurosarcoidosis has been described as the underlying cause of central diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. The pathological mechanism that can lead both to deficiency and excess of antidiuretic hormone (ADH) secretion is still not fully understood. It has been shown that diagnosis of neurosarcoidosis remains challenging, as symptoms can be inconclusive and diagnostic tools are not sufficiently sensitive and specific. Early treatment may potentially reverse pituitary deficiencies, although studies to confirm this hypothesis are minimal. This review article aims to increase knowledge about central DI and SIADH caused by neurosarcoidosis, identify possible difficulties in diagnosis, and discuss the importance of early management. Clinical trials investigating the long-term therapeutic response in patients with HP sarcoidosis are essential, as there are currently no established guidelines for the treatment of neurosarcoidosis.
ABSTRACT
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.
