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AIMS: Hyponatremia is associated with poorer outcomes and diuretic response in patients hospitalized for heart failure. This study compared a tolvaptan-based vs. furosemide-based diuretic regimen on short-term clinical responses in hyponatremic acute heart failure. METHODS AND RESULTS: Prospective, randomized, open-label, parallel-group, single-centre study comparing oral tolvaptan vs. continuous infusion furosemide. Thirty-three subjects requiring hospitalization for acute congestive heart failure, and a serum sodium < 135 mmol/L, were randomized to tolvaptan 30 mg orally daily or furosemide 5 mg/h intravenously for initial 24 h, after which treatments could be escalated. Median daily dose throughout was tolvaptan 30 mg and furosemide 120 mg, with four subjects in each group requiring dose escalation. Urine output and net fluid balance were not different between groups at 24 h or subsequent time points up to 96 h. Changes in estimated glomerular filtration rate were comparable. Cystatin C improved at 24 h with tolvaptan compared with furosemide (-6.4 ± 11.8 vs. 4.1 ± 17.2% change, P = 0.036), but the effect was transient. No significant between group differences were seen for NT-proBNP, plasma renin activity, or urinary neutrophil gelatinase-associated lipocalin:Cr. Serum sodium, as well as copeptin levels, increased with tolvaptan compared with furosemide. CONCLUSIONS: Oral tolvaptan was associated with similar, but not superior, diuresis compared with intravenous furosemide for acute heart failure with concomitant hyponatremia.

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OBJECTIVE: We aimed to determine factors related to avoidability of 30-day readmissions at our public, safety net hospital in the United States (US). METHODS: We prospectively reviewed medical records of adult internal medicine patients with scheduled and unscheduled 30-day readmissions. We also interviewed patients if they were available. An independent panel used pre-specified, objective criteria to adjudicate potential avoidability. RESULTS: Of 153 readmissions evaluated, 68% were unscheduled. Among these, 67% were unavoidable, primarily due to disease progression and development of new diagnoses. Scheduled readmissions accounted for 32% of readmissions and most (69%) were clinically appropriate and unavoidable. The scheduled but avoidable readmissions (31%) were attributed largely to limited resources in our healthcare system. CONCLUSIONS: Most readmissions at our public, safety net hospital were unavoidable, even among our unscheduled readmissions. Surprisingly, one-third of our overall readmissions were scheduled, the majority reflecting appropriate management strategies designed to reduce unnecessary hospital days. The scheduled but avoidable readmissions were due to constrained access to non-emergent, expensive procedures that are typically not reimbursed given our system's payor mix, a problem which likely plague other safety net systems. These findings suggest that readmissions do not necessarily reflect inadequate medical care, may reflect resource constraints that are unlikely to be addressable in systems caring for a large burden of uninsured patients, and merit individualized review.

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Hemophagocytic lymphohistiocytosis (HLH), while uncommon, may be a devastating complication of lymphoma and/or human immunodeficiency virus (HIV) infection. While several of the diagnostic criteria for HLH are relatively nonspecific, particularly in the setting of a systemic inflammatory response, more diagnostic specificity may be achieved with marked elevations in serum ferritin (e.g., >100,000 ng/mL). Increased suspicion of HLH, particularly in the setting of persistent, unexplained fevers, pancytopenia, and transaminitis, should prompt consideration of HLH. Earlier diagnosis and initiation of therapy have the potential to alter the natural history and poor prognosis of this disorder. We present a patient with HIV infection who developed relapsed T-cell lymphoma complicated by hemophagocytic lymphohistiocytosis.

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Cardiovascular disease (CVD) remains the leading cause of death in the United States. There is evidence that shows a direct relationship between an elevated uric acid level and an increased risk of cardiovascular (CV) events, which has set the foundation for the investigation of uric acid-lowering drugs for the treatment of CVD. Although traditionally the cornerstone therapy for gout, allopurinol's ability to be a competitive inhibitor of the key enzyme, xanthine oxidase, needed for uric acid formation, has prompted recent clinical research evaluating allopurinol as a CV drug. Epidemiologic and biochemical studies on uric acid formation have shown that it is not only uric acid itself that leads to worsening prognosis and increased CV events, but also the free radicals and superoxides formed during xanthine oxidase activity. The combination of uric acid formation and formed free radicals could ultimately lead to coronary endothelial dysfunction and worsening of myocardial oxidative stress. Along with preventing uric acid formation, allopurinol also has the ability to behave as a free radical scavenger of the superoxide anions and free radicals released during uric acid formation.Clinical studies have shown that allopurinol improves endothelial dysfunction and subsequently improves the exercise capacity in patients diagnosed with angina pectoris. Allopurinol has also been shown to decrease oxidative stress and ameliorate the morbidity and mortality of congestive heart failure patients by possibly improving mechanoenergetic uncoupling, with the enhancement of myocardial contractility and the left ventricular ejection fraction. This review presents the pharmacologic action of allopurinol on the CV system and describes the effectiveness of allopurinol as a potential drug to treat 2 CVD morbidities: ischemic heart disease and congestive heart failure.

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Yeast replicative aging is a process resembling replicative aging in mammalian cells. During aging, wild-type haploid yeast cells enlarge, become sterile, and undergo nucleolar enlargement and fragmentation; we sought gene expression changes during the time of these phenotypic changes. Gene expression studied via microarrays and quantitative real-time reverse-transcription polymerase chain reaction (qPCR) has shown reproducible, statistically significant changes in messenger RNA (mRNA) of genes at 12 and 18-20 generations. Our findings support previously described changes towards aerobic metabolism, decreased ribosome gene expression, and a partial environmental stress response. Our findings include a pseudostationary phase, downregulation of methylation-related metabolism, increased nucleotide excision repair-related mRNA, and a strong upregulation of many of the regulatory subunits of protein phosphatase I (Glc7). These findings are correlated with aging changes in higher organisms as well as with the known involvement of protein phosphorylation states during yeast aging.

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