Activity

Gynecomastia is a common incidental finding on thoracic computed tomography (CT). This study aimed to retrospectively determine the prevalence, imaging characteristics, and possible causes of incidental gynecomastia on thoracic CT. Records of male patients who underwent thoracic CT in 2015 were reviewed. The size and morphologic types (nodular, dendritic, and diffuse) were recorded for patients with breast glandular tissue larger than 1 cm, and the cutoff value of gynecomastia was defined as 2 cm. Additionally, the possible causes of gynecomastia obtained by reviewing patients’ charts were recorded. CT-depicted gynecomastia was identified in 12.7% (650 of 5,501) of patients. The median size of the breast glandular tissue was 2.5 cm (interquartile range 2.2-3.1), and 36.8% of patients (239 of 650) had unilateral gynecomastia. The age distribution provided a bimodal pattern with two peaks in the age groups from 20 to 29 years old and greater than 70 years old. Chronic liver disease (CLD; p less then .001), all stages of chronic kidney disease (CKD; p less then .001), and medications (p = .002) were significantly associated with gynecomastia. Gynecomastia did not correlate with body mass index (p = .962). The size of breast glandular tissue was identified to be correlated with the morphologic type of breast tissue and the severity of CLD or CKD. The prevalence of incidental gynecomastia seen on thoracic CT was 12.7%. CT-depicted gynecomastia is not associated with obesity but with CLD, CKD, and medications. When gynecomastia is detected on CT, further evaluations and management might be required for patients with a treatable cause.Background There is an open Centers for Medicare and Medicaid Services National Coverage Decision for Transcatheter Mitral Valve Repair (TMVr) and a recent multisociety consensus document suggesting that TMVr centers should achieve prespecified mitral valve replacement or repair (MVRr). Yet, little is known about the MVRr volume-TMVr outcome relationship. Methods and Results Using Centers for Medicare and Medicaid Services administrative claims from January 1, 2016 to December 31, 2018, we computed the Pearson correlation coefficient and performed multivariable hierarchical modeling to estimate the MVRr volume to TMVr outcome relationship for mortality and heart failure hospitalization. Additionally, we assessed the impact of the consensus recommendations on geographic access to care by hospital referral region. Total annualized MVRr volume was less then 11 to 1552 (median 96, interquartile range 53, 167). One-year survival, 1-year heart failure hospitalization after TMVr were not correlated with MVRr volume. After patient risk-adjustment for age, sex, and significant Elixhauser Comorbidities, there remained no significant correlation between institutional MVRr volume and 1-year mortality (estimate -0.010, SE 0.047, P=0.834) or heart failure hospitalization (estimate -0.011, SE 0.045, P=0.808) after TMVr. Raising the restriction on TMVr from 20 to 40 MVRr/y results in ≈30 million individuals having to travel outside of their hospital referral region to undergo TMVr, with a disproportionate impact in the Midwest and Southeast. Conclusions There is no relationship between MVRr volumes and TMVr outcomes. Additionally, adoption of an annual MVRr volume ≥40 for performance of TMVr disproportionately impacts geographic access in the Midwest and Southeast and their large black and Hispanic populations.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the coronavirus disease in 2019 (COVID-19) which rapidly evolved from an outbreak in Wuhan, China into a pandemic that has resulted in over millions of infections and over hundreds of thousands of mortalities worldwide. Various coagulopathies have been reported in association with COVID-19, including disseminated intravascular coagulation (DIC), sepsis-induced coagulopathy (SIC), local microthrombi, venous thromboembolism (VTE), arterial thrombotic complications, and thrombo-inflammation. There is a plethora of publications and conflicting data on hematological and hemostatic derangements in COVID-19 with some data suggesting the link to disease progress, severity and/or mortality. There is also growing evidence of potentially useful clinical biomarkers to predict COVID-19 progression and disease outcomes. Of those, a link between thrombocytopenia and COVID-19 severity or mortality was suggested. In this opinion report, we examine the published evidence of hematological and hemostatic laboratory derangements in COVID-19 and the interrelated SARS-CoV-2 induced inflammation, with a focussed discussion on platelet count alterations. We explore whether thrombocytopenia could be a potential disease biomarker and we provide recommendations for future studies in this regard.Objective Conceptualizations of delusion formation implicate deficits in feedforward information updating across the posterior to prefrontal cortices, resulting in dysfunctional integration of new information about contexts in working memory and, ultimately, failure to update overfamiliar prior beliefs. The authors used functional MRI and machine learning models to address individual variability in feedforward parietal-prefrontal information updating in patients with schizophrenia. They examined relationships between feedforward connectivity, and delusional thinking and polygenic risk for schizophrenia. Methods The authors studied 66 schizophrenia patients and 143 healthy control subjects during performance of context updating in working memory. Dynamic causal models of effective connectivity were focused on regions of the prefrontal and parietal cortex potentially implicated in delusion processes. EGFR targets The effect of polygenic risk for schizophrenia on connectivity was examined in healthy individuals. The authors cits in delusional psychopathology and in genetic risk for schizophrenia.Major depressive disorder is a common psychiatric disorder associated with marked suffering, morbidity, mortality, and cost. The World Health Organization projects that by 2030, major depression will be the leading cause of disease burden worldwide. While numerous treatments for major depression exist, many patients do not respond adequately to traditional antidepressants. Thus, more effective treatments for major depression are needed, and targeting certain hormonal systems is a conceptually based approach that has shown promise in the treatment of this disorder. A number of hormones and hormone-manipulating compounds have been evaluated as monotherapies or adjunctive treatments for major depression, with therapeutic actions attributable not only to the modulation of endocrine systems in the periphery but also to the CNS effects of hormones on non-endocrine brain circuitry. The authors describe the physiology of the hypothalamic-pituitary-adrenal (HPA), hypothalamic-pituitary thyroid (HPT), and hypothalamic-pituitary-gonadal (HPG) axes and review the evidence for selected hormone-based interventions for the treatment of depression in order to provide an update on the state of this field for clinicians and researchers.