A Case of Endocarditis Secondary to Bacteremia Caused by Obstructive Pyelonephritis From Infective Nephrolithiasis in the Setting of Untreated Hyperparathyroidism.

Hyperparathyroidism is known to be associated with nephrolithiasis but has less frequently been reported to contribute to infective endocarditis. We report a case of a 56-year-old woman with a past medical history of parathyroid adenoma, hyperparathyroidism, hypercalcemia, nephrolithiasis requiring bilateral nephrostomy, multiple episodes of complicated urinary tract infection (UTI), pulmonary and cardiac sarcoidosis treated with steroids previously, and intermittent complete heart block with implantable cardioverter-defibrillator (ICD), who presented to the ED with septic shock. She was found to have Enterococcus faecalis bacteremia complicated by large vegetations on her right ventricle ICD lead and tricuspid valve. Urinalysis was positive for leukocyte esterase, WBC, RBC, and bacteria. Transabdominal ultrasound and CT abdomen/pelvis showed multiple renal stones in bilateral kidneys. Nephrolithiasis secondary to untreated primary hyperparathyroidism had likely caused acute obstructive pyelonephritis in the patient, which had progressed to bacteremia and septic shock eventually leading to infective endocarditis. The patient was started on a six-week course of IV ceftriaxone and ampicillin, had her ICD removed, her blood cultures cleared, and was then referred to ENT and Endocrinology for parathyroidectomy. Prompt identification and treatment of hyperparathyroidism including parathyroidectomy can reduce the risk of nephrolithiasis and serious infections.

Post-Myocardial Infarction Ventricular Septal Defect: A Comprehensive Review.

Post-myocardial infarction (MI) ventricular septal defect (VSD) is a rare but potentially catastrophic mechanical complication that occurs in <1% of patients following a myocardial infarction and it is associated with a high morbidity and mortality despite improvements in medical and surgical therapies. Post-MI VSD is a medical emergency and outcome is very poor in medically treated patients. Treatment of choice remains surgical closure of defect and transcatheter defect closure less so. We performed a comprehensive review of the clinical presentation and management options of post-MI VSD.

Aortic Stenosis in African Americans: Focus On Disparities in Treatment and Outcomes.

Aortic stenosis (AS) is the third most common type of cardiovascular disease after hypertension and coronary artery disease, and it carries a high mortality rate when left untreated. Risk factors include male sex, hypertension, tobacco use, advanced age, elevated LDL cholesterol, and coronary atherosclerosis. Definitive treatment for AS includes valve repair, either percutaneously or surgically; however, in aging populations corrective surgery carries increased risk. While research suggests that patients of some non-White ethnic groups, including African-Americans, are less likely than their Caucasian counterparts to have AS, these minority patients may experience may experience differences in the way they receive and accept care. This paper seeks to explicate the mechanisms of racial disparities among the African-Americans affected by aortic stenosis as they pertain to healthcare utilization, referral for valve replacement, acceptance of therapy, and overall treatment outcomes.

Snapin mediates incretin action and augments glucose-dependent insulin secretion.

Impaired insulin secretion contributes to the pathogenesis of type 2 diabetes mellitus (T2DM). Treatment with the incretin hormone glucagon-like peptide-1 (GLP-1) potentiates insulin secretion and improves metabolic control in humans with T2DM. GLP-1 receptor-mediated signaling leading to insulin secretion occurs via cyclic AMP stimulated protein kinase A (PKA)- as well as guanine nucleotide exchange factor-mediated pathways. However, how these two pathways integrate and coordinate insulin secretion remains poorly understood. Here we show that these incretin-stimulated pathways converge at the level of snapin, and that PKA-dependent phosphorylation of snapin increases interaction among insulin secretory vesicle-associated proteins, thereby potentiating glucose-stimulated insulin secretion (GSIS). In diabetic islets with impaired GSIS, snapin phosphorylation is reduced, and expression of a snapin mutant, which mimics site-specific phosphorylation, restores GSIS. Thus, snapin is a critical node in GSIS regulation and provides a potential therapeutic target to improve ß cell function in T2DM.