Electrolyte disturbances in patients hospitalized for COVID-19 infection: An observational study.

There are multiple mechanisms by which The Coronavirus-19 (COVID-19) infection can cause electrolyte abnormalities, which may not be the case for bacterial causes of pneumonia. This study aimed to assess the differences in electrolyte levels between patients suffering from COVID-19 and bacterial pneumonia. This is an original, retrospective study. Two cohorts of hospitalized patients were included, 1 suffering from COVID-19 and the other from bacterial pneumonia. Their day 1 and day 3 levels of sodium, potassium, magnesium, and phosphorus, as well as their outcomes, were extracted from the charts. Statistical analysis was subsequently performed. Mean admission levels of sodium, potassium, phosphorus, and magnesium were 135.64 ±â€…6.13, 4.38 ±â€…0.69, 3.53 ±â€…0.69, and 2.03 ±â€…0.51, respectively. The mean day 3 levels of these electrolytes were 138.3 ±â€…5.06, 4.18 ±â€…0.59, 3.578 ±â€…0.59, and 2.11 ±â€…0.64, respectively. Patients suffering from bacterial pneumonia were significantly older (N = 219, mean = 64.88 ±â€…15.99) than patients with COVID-19 pneumonia (N = 240, mean = 57.63 ±â€…17.87). Bacterial pneumonia group had significantly higher serum potassium (N = 211, mean = 4.51 ±â€…0.76), and magnesium (N = 115, mean = 2.12 ±â€…0.60) levels compared to COVID-19 group (N = 227, mean = 4.254 ±â€…0.60 for potassium and N = 118, mean = 1.933 ±â€…0.38 for magnesium). Only magnesium was significantly higher among day 3 electrolytes in the bacterial pneumonia group. No significant association between electrolyte levels and outcomes was seen. We found that COVID-19 patients had lower potassium and magnesium levels on admission, possibly due to the effect of COVID-19 on the renin-angiotensin-aldosterone system as well as patient characteristics and management. We did not find enough evidence to recommend using electrolyte levels as a determinator of prognosis, but more research is needed.

Atrial Fibrillation and Cognitive Disorders.

The prevalence of atrial fibrillation among older adults is increasing. Research has indicated that atrial fibrillation is linked to cognitive impairment disorders such as Alzheimer and vascular dementia, as well as Parkinson disease. Various mechanisms are believed to be shared between atrial fibrillation and cognitive impairment disorders. The specific pathologies and mechanisms of different cognitive disorders are still being studied. Potential mechanisms include cerebral hypoperfusion, ischemic or hemorrhagic infarction, and cerebrovascular reactivity to carbon dioxide. Additionally, circulatory biomarkers and certain infectious organisms appear to be involved. This review offers an examination of the overlapping epidemiology between atrial fibrillation and cognitive disorders, explores different cognitive disorders and their connections with this arrhythmia, and discusses trials and guidelines for preventing and treating atrial fibrillation in patients with cognitive disorders. It synthesizes existing knowledge on the management of atrial fibrillation and identifies areas that require further investigation to bridge the gap in understanding the complex relationship between dementia and atrial fibrillation.

A Case of Diabetic Ketoacidosis Presented With Severe Rhabdomyolysis-Induced Acute Kidney Injury.

We present a patient who presented with diabetic ketoacidosis and severe rhabdomyolysis-induced acute kidney injury. The patient developed generalized edema, nausea, and vomiting, and his kidney function deteriorated, necessitating renal replacement therapy, despite the successful treatment of his initial conditions. A comprehensive evaluation was conducted to determine the underlying cause of the severe rhabdomyolysis, including autoimmune myopathies, viral infections, and metabolic disorders. A muscle biopsy revealed necrosis and myophagocytosis but no significant inflammation or myositis. The patient's clinical and laboratory results improved with appropriate treatment, including temporary dialysis and erythropoietin therapy, and he was discharged to continue his rehabilitation with home health care.

Gastrointestinal Stromal Tumor With a Rare Associated Meningioma: A Case Report.

Gastrointestinal stromal tumors (GISTs) tend to be associated with other tumors. In certain familial cancer syndromes, GIST has been associated with breast cancer or other endocrine tumors. Multiple endocrine neoplasia syndrome along with certain other genomic mutations such as succinate dehydrogenase complex mutations described GIST as one of the potential tumors of the syndrome. There has not yet been a definite association between GIST and meningioma. We present a case of a patient with a GIST who was later found to have a meningioma on incidental brain imaging. Despite being a benign tumor not requiring additional intervention, it is quite apparent that providers need to have a low threshold to scan for other tumors if suspicious symptoms arise.

Disseminated Intravascular Coagulation With Excessive Fibrinolysis Following Diagnostic Prostatic Biopsy for Prostate Cancer.

The most common hematological disorder associated with prostate cancer is disseminated intravascular coagulation (DIC). In most cases, cancer patients with DIC have compensated fibrinolysis with a low incidence of bleeding. However, DIC with excessive fibrinolysis is a rare albeit life-threatening variant that can present with massive bleeding and is thought to occur due to the unique properties of neoplastic cells of prostate cancer that activate both procoagulant and anticoagulant pathways simultaneously. Depending on the shift of the intricate balance between the two forces, the net result can be either systemic micro- (DIC) or macro-thrombi, deep venous thrombosis (DVT) or pulmonary embolism, or a bleeding syndrome from excessive vicious activation of fibrinolysis. Here, we present a unique case of suspected prostate cancer who underwent a diagnostic prostatic biopsy. Subsequently, he developed massive hematuria requiring intensive care unit admission with multiple supportive blood products. Additionally, he was administered epsilon-aminocaproic acid with a prophylactic dose of heparin, with prompt resolution of bleeding. After stabilization, he was discharged with planned outpatient chemotherapy. However, he subsequently presented with lower extremity DVT within a week, which led to a stroke in the setting of a patent foramen ovale. This unique case report highlights how a change in the intricate balance of the coagulation cascade causes a polar shift in clinical presentation and complications.

Cardiovascular benefits from SGLT2 inhibition in type 2 diabetes mellitus patients is not impaired with phosphate flux related to pharmacotherapy.

The beneficial cardiorenal outcomes of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in patients with type 2 diabetes mellitus (T2DM) have been substantiated by multiple clinical trials, resulting in increased interest in the multifarious pathways by which their mechanisms act. The principal effect of SGLT2i (-flozin drugs) can be appreciated in their ability to block the SGLT2 protein within the kidneys, inhibiting glucose reabsorption, and causing an associated osmotic diuresis. This ameliorates plasma glucose elevations and the negative cardiorenal sequelae associated with the latter. These include aberrant mitochondrial metabolism and oxidative stress burden, endothelial cell dysfunction, pernicious neurohormonal activation, and the development of inimical hemodynamics. Positive outcomes within these domains have been validated with SGLT2i administration. However, by modulating the sodium-glucose cotransporter in the proximal tubule (PT), SGLT2i consequently promotes sodium-phosphate cotransporter activity with phosphate retention. Phosphatemia, even at physiologic levels, poses a risk in cardiovascular disease burden, more so in patients with type 2 diabetes mellitus (T2DM). There also exists an association between phosphatemia and renal impairment, the latter hampering cardiovascular function through an array of physiologic roles, such as fluid regulation, hormonal tone, and neuromodulation. Moreover, increased phosphate flux is associated with an associated increase in fibroblast growth factor 23 levels, also detrimental to homeostatic cardiometabolic function. A contemporary commentary concerning this notion unifying cardiovascular outcome trial data with the translational biology of phosphate is scant within the literature. Given the apparent beneficial outcomes associated with SGLT2i administration notwithstanding negative effects of phosphatemia, we discuss in this review the effects of phosphate on the cardiometabolic status in patients with T2DM and cardiorenal disease, as well as the mechanisms by which SGLT2i counteract or overcome them to achieve their net effects. Content drawn to develop this conversation begins with proceedings in the basic sciences and works towards clinical trial data.