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Albert N.M.,Cleveland Clinic | Chase S.,Otsuka America Pharmaceutical Inc.
Journal of Cardiovascular Nursing | Year: 2013

BACKGROUND:: Asymptomatic or clinically mild hyponatremia commonly occurs in the setting of heart failure, especially among elderly and severely decompensated, fluid-overloaded patients, and is associated with increased morbidity and mortality. Successful detection and treatment of hyponatremia by cardiovascular and advanced practice nurses caring for patients with heart failure are part of multidisciplinary team care. Nurses should be able to detect signs and symptoms of hyponatremia and, even when patients are asymptomatic, initiate appropriate treatment promptly to prevent complications. PURPOSE:: In this review, the epidemiology and pathophysiology of hyponatremia in heart failure, and signs and symptoms are described. In patients with heart failure, challenges involved in determining the type of hyponatremia (hypervolemic, hypovolemic, or euvolemic) and in correctly managing hyponatremia to prevent serious complications are presented. Conventional treatment options and their limitations are reviewed, and the vasopressin-receptor antagonist tolvaptan, an emerging oral therapy option, is introduced and discussed. CONCLUSIONS:: Hyponatremia is a marker of morbidity and mortality in patients with heart failure. Nurses working collaboratively with other healthcare providers must be able to recognize the condition and understand treatment options, including potential adverse effects of current and emerging therapies. One emerging therapy - tolvaptan - can be used in hypervolemic and euvolemic hyponatremic patients with heart failure to correct serum sodium level without negatively affecting renal function. CLINICAL IMPLICATIONS:: Improved nurse understanding of hyponatremia in patients with heart failure may promote nurse-initiated or nurse-facilitated detection and management, which could decrease mortality and morbidity. Copyright © 2013 Lippincott Williams & Wilkins. Source


Castillo J.J.,Brown University | Vincent M.,Otsuka America Pharmaceutical Inc. | Justice E.,BioScience Communications
Oncologist | Year: 2012

Hyponatremia, a common electrolyte abnormality in oncology practice, may be a negative prognostic factor in cancer patients based on a systematic analysis of published studies. The largest body of evidence comes from small-cell lung cancer (SCLC), for which hyponatremia was identified as an independent risk factor for poor outcome in six of 13 studies. Hyponatremia in the cancer patient is usually caused by the syndrome of inappropriate antidiuretic hormone (SIADH), which develops more frequently with SCLC than with other malignancies. SIADH may be driven by ectopic production of arginine vasopressin (AVP) by tumors or by effects of anticancer and palliative medications on AVP production or action. Other factors may cause hypovolemic hyponatremia, including diarrhea and vomiting caused by cancer therapy. Hyponatremia may be detected on routine laboratory testing before or during cancer treatment or may be suggested by the presence of mostly neurological symptoms. Treatment depends on several factors, including symptom severity, onset timing, and extracellular volume status. Appropriate diagnosis is important because treatment differs by etiology, and choosing the wrong approach can worsen the electrolyte abnormality. When hyponatremia is caused by SIADH, hypertonic saline is indicated for acute, symptomatic cases, whereas fluid restriction is recommended to achieve a slower rate of correction for chronic asymptomatic hyponatremia. Pharmacological therapy may be necessary when fluid restriction is insufficient. The orally active, selective AVP receptor 2 (V 2)-receptor antagonist tolvaptan provides a mechanism-based option for correcting hyponatremia caused by SIADH or other conditions with inappropriate AVP elevations. By blocking AVP effects in the renal collecting duct, tolvaptan promotes aquaresis, leading to a controlled increase in serum sodium levels. © AlphaMed Press. Source


Pocoski J.,Bayer AG | Ma A.,University of North Carolina at Chapel Hill | Kessler C.M.,Georgetown University | Boklage S.,Otsuka America Pharmaceutical Inc. | Humphries T.J.,Bayer AG
Haemophilia | Year: 2014

There is conflicting evidence in the literature on whether individuals with haemophilia in the USA have greater, reduced, or similar risks for cardiovascular disease as the general population. This study evaluated the prevalence of cardiovascular comorbidities among USA males with haemophilia A, relative to an unaffected general male population with similar characteristics. Males with haemophilia A and continuous insurance coverage were identified by ICD-9-CM code 286.0 (1 January 2007-31 December 2009) using the MarketScan® Commercial and Medicare Research Databases. Individuals with haemophilia A were exact matched 1:3 with males without a diagnosis of haemophilia A. The prevalence of cardiovascular comorbidities identified by ICD-9-CM code was determined for matched cohorts. Of the study population, 2506 were grouped in the haemophilia A cohort and 7518 in the general cohort. Proportions of individuals with haemorrhagic stroke (2.0% vs. 0.5%, P < 0.001), ischemic stroke (4.7% vs. 2.7%, P < 0.001), coronary artery disease (10.7% vs. 5.8%, P < 0.001), myocardial infarction (0.8% vs. 0.3%, P = 0.003), hypertension (22.6% vs. 15.5%, P < 0.001), hyperlipidaemia (15.9% vs. 11.9%, P < 0.001), arterial thrombosis (12.1% vs. 5.9%, P < 0.001), and venous thrombosis (4.4% vs. 1.1%, P < 0.001) were significantly greater for the haemophilia A cohort. Results were consistent across most age groups, and comorbidities appeared at an earlier age in those with haemophilia A than in the general population. Among the USA haemophilia A population cardiovascular comorbidities are more prevalent and they appear earlier in life in comparison to the general male population, suggesting the need for earlier, enhanced screening for age-related comorbidities in the haemophilia community. © 2013 John Wiley & Sons Ltd. Source


Gaglio P.,Yeshiva University | Marfo K.,Yeshiva University | Joseph Chiodo III,Otsuka America Pharmaceutical Inc.
Digestive Diseases and Sciences | Year: 2012

Hyponatremia is common in patients with cirrhosis and portal hypertension, and is characterized by excessive renal retention of water relative to sodium due to reduced solute-free water clearance. The primary cause is increased release of arginine vasopressin. Hyponatremia is associated with increased mortality in cirrhotic patients, those with end-stage liver disease (ESLD) on transplant waiting lists, and, in some studies, posttransplantation patients. Clinical evidence suggests that adding serum sodium to model for ESLD (MELD) scoring identifies patients in greatest need of liver transplantation by improving waiting list mortality prediction. Hyponatremia is also associated with numerous complications in liver disease patients, including severe ascites, hepatic encephalopathy, infectious complications, renal impairment, increased severity of liver disease in cirrhosis, and increased hospital stay and neurologic/infectious complications posttransplant. Vasopressin receptor antagonists, which act to increase free water excretion (aquaresis) and thereby increase serum sodium concentration, have been evaluated in patients with hypervolemic hyponatremia (including cirrhosis and heart failure) and euvolemic hyponatremia (SIADH). Tolvaptan, a selective vasopressin V2-receptor antagonist, is the only oral agent in this class approved for raising sodium levels in hypervolemic and euvolemic hyponatremia. The SALT trials showed that tolvaptan treatment rapidly and effectively resolved hyponatremia in these settings, including cirrhosis, and it has been shown that this agent can be safely and effectively used in long-term treatment. Fluid restriction should be avoided during the first 24 h of treatment to prevent overly rapid correction of hyponatremia, and tolvaptan should not be used in patients who cannot sense/respond to thirst, anuric patients, hypovolemic patients, and/or those requiring urgent intervention to raise serum sodium acutely. © Springer Science+Business Media, LLC 2012. Source


Kirson N.Y.,Analysis Group Inc. | Weiden P.J.,University of Illinois at Chicago | Yermakov S.,Analysis Group Inc. | Huang W.,Analysis Group Inc. | And 4 more authors.
Journal of Clinical Psychiatry | Year: 2013

Objective: Nonadherence is a major challenge in schizophrenia treatment. While long-acting (depot) antipsychotic medications are often recommended to address adherence problems, evidence on the comparative effectiveness of depot versus oral antipsychotics is inconsistent. We hypothesize that this inconsistency could be due to systematic differences in study design. This review evaluates the effect of study design on the comparative effectiveness of antipsychotic formulations. The optimal use of different antipsychotic formulations in a general clinical setting depends on better understanding of the underlying reasons for differences in effectiveness across research designs. Data Sources: A PubMed literature review targeted English-language studies (2000-2011) with information on relapse, hospitalization, or allcause discontinuation for depot and oral antipsychotic treatment arms in schizophrenia. The time frame was chosen to reflect research focused on the newer generation of antipsychotic agents. The search required at least 1 term from each of the following categories: (1) schizophrenia; (2) inject, injection, injectable, injectables, injected, depot, long-acting; and (3) iloperidone, fluphenazine, haloperidol, paliperidone, risperidone, olanzapine, asenapine, flupentixol, flupenthixol, lurasidone, clopenthixol, fluspirilene, zuclopentixol, zuclopenthixol. Study Selection: Thirteen relevant studies were identified by 2 independent reviewers; these studies included information on 19 depot-oral comparisons. Data Extraction: Age- and gender-adjusted risk ratios (RRs) (depot/ oral) were calculated for the identified endpoints and pooled by study design (randomized controlled trial [RCT], prospective observational, and retrospective observational). Meta-analysis with random effects was used to estimate the pooled RRs, by study design. Average conversion factors between study designs were calculated as the ratios of pooled RRs. Results: Meta-analysis of adjusted endpoints showed no apparent benefit of depot over oral formulations in RCTs, with an RR of 0.89 (P = .416). In contrast, there was a significant advantage for depot formulations in other study designs (prospective RR = 0.62 [P < .001]; retrospective RR = 0.56 [P < .001]). These imply conversion factors of 1.43 and 1.59 between RCTs and prospective and retrospective designs, respectively. Conclusions: The comparative effectiveness of antipsychotic formulations is sensitive to research design. Depot formulations displayed significant advantages in nonrandomized observational studies, whereas in RCTs no difference was observed. The estimated conversion factors may facilitate comparison across studies. © 2013 Copyright Physicians Postgraduate Press, Inc. Source

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