Appendix 2|Review Questions – PICOM Format Chapter 1

Total Page:16

File Type:pdf, Size:1020Kb

Appendix 2|Review Questions – PICOM Format Chapter 1 Appendix 2|Review Questions – PICOM Format Chapter 1. In patients with hypotonic hyponatraemia, how sensitive and or specific are various 'diagnostic strategies' in comparison with a gold reference standard of sodium challenge in differentiating hypovolemic from euvolaemic hyponatraemia? Patients In people with hypotonic hyponatraemia Children, adults, aged adults Intervention Clinical signs and symptoms of hypovolaemia Orthostatic hypotension Tachycardia Dry mouth Decreased skin turgor Prolonged capillary refill Flat jugular central venous pressure Urine sodium concentration Fractional sodium excretion Serum urea concentration Fractional urea excretion Serum uric acid concentration Fractional uric acid excretion Urine osmolality Serum urea/creatinine ratio Comparator Sodium challenge (2L saline/24h) Outcome Differentiating hypovolemic from euvolaemic hyponatraemia Methodology Systematic review Diagnostic test accuracy study Chapter 1. In patients with hypotonic hyponatraemia, how sensitive and or specific are various 'diagnostic strategies' in comparison with a gold reference standard of expert panel diagnosis in differentiating hypovolemic from euvolaemic hyponatraemia? Patients In people with hyponatraemia Children, adults, aged adults Intervention Urine sodium concentration Urine osmolality Fractional sodium excretion Fractional uric acid excretion Serum urea concentration Serum uric acid concentration serum urea/creatinine ratio Vasopressin / copeptin Plus Clinical signs and symptoms of hypovolaemia Orthostatic hypotension Tachycardia Dry mouth Decreased skin turgor Prolonged capillary refill Flat jugular central venous pressure Comparator Expert panel clinical diagnosis of 'type' of hyponatraemia Outcome Differentiating hypovolemic from euvolaemic hyponatraemia Methodology Systematic review Diagnostic test accuracy study Chapter 2. In patients with hypotonic hyponatraemia, which treatments are effective in improving outcomes? Patients In people with hyponatraemia Children, adults, aged adults Acute or chronic hyponatraemia Symptomatic or asymptomatic hyponatraemia Intervention Saline, NaCl, Sodium Chloride (normal, hypertonic, isotonic) Urea Demeclocycline Lithium Mannitol Loop diuretics, furosemide, bumetanide, ethacrinic acid, torasemide Desmopressin, DDAVP Phenytoin Tolvaptan, lixivaptan, mozavaptan, satavaptan, conivaptan Fludrocortisone, hydrocortisone, mineralocorticoids, glucocorticoids Fluid restriction, water restriction Comparator No treatment Placebo Outcome Survival Sodium increase Fall Bone fracture CNS Status Myelinolysis Osmotic demyelination syndrome (ODS) Respiratory arrest Coma Seizures, epilepsy Brain oedema, brain damage Length of hospital stay Quality of life Cost Methodology Systematic review RCT Cohort study Case‐control study Case reports No letters, editorials or letters Other information Head to head comparisons of all interventions Note: initially combined search, if yield too high (>600) separate search for interventions versus no treatment separately, all 'strategies' versus fluid restriction, all except fluid restriction head to head. Chapter 2. In patients with hypotonic hyponatraemia, does the rate of sodium correction influence the outcome? Patients In people with hyponatraemia Children, adults, aged adults Acute or chronic hyponatraemia Symptomatic or asymptomatic hyponatraemia Intervention 'Slow' "Correction rate" "Daily increase" "Daily increase" "Rate of increase" *per hour, per day, per 24 h, per 48 h, per 72 h Comparator 'Fast' correction Outcome Survival Sodium increase Fall Bone fracture CNS Status Myelinolysis Osmotic demyelination syndrome (ODS) Respiratory arrest Coma Seizures, epilepsy Brain edema, brain damage Length of hospital stay Quality of life Cost Methodology Systematic review RCT Cohort study Case‐control study Case reports No letters, editorials or letters Other information Head to head comparisons of all interventions .
Recommended publications
  • Therapeutic Potential of Vasopressin-Receptor Antagonists in Heart Failure
    J Pharmacol Sci 124, 1 – 6 (2014) Journal of Pharmacological Sciences © The Japanese Pharmacological Society Current Perspective Therapeutic Potential of Vasopressin-Receptor Antagonists in Heart Failure Yasukatsu Izumi1,*, Katsuyuki Miura2, and Hiroshi Iwao1 1Department of Pharmacology, 2Applied Pharmacology and Therapeutics, Osaka City University Medical School, Osaka 545-8585, Japan Received October 2, 2013; Accepted November 17, 2013 Abstract. Arginine vasopressin (AVP) is a 9-amino acid peptide that is secreted from the posterior pituitary in response to high plasma osmolality and hypotension. AVP has important roles in circulatory and water homoeostasis, which are mediated by oxytocin receptors and by AVP receptor subtypes: V1a (mainly vascular), V1b (pituitary), and V2 (renal). Vaptans are orally and intravenously active nonpeptide vasopressin-receptor antagonists. Recently, subtype-selective nonpeptide vasopressin-receptor agonists have been developed. A selective V1a-receptor antago- nist, relcovaptan, has shown initial positive results in the treatment of Raynaud’s disease, dysmen- orrhea, and tocolysis. A selective V1b-receptor antagonist, nelivaptan, has beneficial effects in the treatment of psychiatric disorders. Selective V2-receptor antagonists including mozavaptan, lixivaptan, satavaptan, and tolvaptan induce highly hypotonic diuresis without substantially affecting the excretion of electrolytes. A nonselective V1a/V2-receptor antagonist, conivaptan, is used in the treatment for euvolaemic or hypervolemic hyponatremia. Recent basic and clinical studies have shown that AVP-receptor antagonists, especially V2-receptor antagonists, may have therapeutic potential for heart failure. This review presents current information about AVP and its antagonists. Keywords: arginine vasopressin, diuretic, heart failure, vasopressin receptor antagonist 1. Introduction receptor blockers, diuretics, b-adrenoceptor blockers, digitalis glycosides, and inotropic agents (4).
    [Show full text]
  • Hypernatremia: 2 Months Back When He Had Progressive Decrease in Vision (Right > Left)
    Correspondence to increased intrathoracic pressure and central radiologist regarding vascular injury when there is venous pressure, decreased venous return from the refractory hypotension so that necessary steps can be brain and increased ICP[4] taken to identify and treat iatrogenic complications that • Patients with aneurysmal SAH have disturbed might compound the pre‑existing morbidity. autoregulation of cerebral blood flow. Hence, intraoperative hypotension of any cause has an REFERENCES adverse effect on the outcome of SAH[5,6] • Patients with poor grade SAH (Fischer III/IV) and 1. Young WL, Pile-Spellman J. Anesthetic considerations for interventional Neuroradiolgy (Review). Anesthesiology angiographic evidence of vasospasm which our 1994;80:427-56. patient had, are at risk for cerebral hypoperfusion 2. Varma MK, Price K, Jayakrishnan V, Manickam B, Kessell G. because of impaired cerebral autoregulation and Anaesthetic considerations for interventional neuroradiology. thus intraoperative hypotension and cerebral Br J Anaesth 2007;99:75-85. [6,7] 3. Kent KC, Moscucci M, Mansour KA, Dimattia S, Gallagher S, hypoperfusion compounds the poor outcome Kuntz R, et al. Retroperitoneal hematoma after cardiac • Blood loss leading to severe anaemia (Hb 3.8 g%) catheterization: Prevalence, risk factors, and optimal during the procedure might have lead to decreased management. J Vasc Surg 1994;20:905-10. oxygen‑carrying capacity of blood and further 4. De Laet I, Citerio G, Malbrain ML. The influence of exacerbate the hypoxic injury to brain. intraabdominal hypertension on the central nervous system: Current insights and clinical recommendations, is it all in the Thus a combination of age, poor grade SAH, diffuse head? Acta Clin Belg Suppl 2007;1:89-97.
    [Show full text]
  • "Hyponatremia"[Text Word]) OR "Hyponatremic"[Text Word]
    SYSTEMATIC MAPPING SEARCH STRATEGY PubMed "Hyponatremia"[Mesh] ("hyponatremia"[Text Word]) OR "hyponatremic"[Text Word] ("euvolemic"[Text Word]) OR "hypervolemic"[Text Word] "Inappropriate ADH Syndrome"[Mesh] "antidiuretic hormone"[Text Word] "Heart Failure"[Mesh] "heart failure"[Text Word] "Liver Cirrhosis"[Mesh] ("cirrhosis"[Text Word]) OR "ascites"[Text Word] "Receptors, Vasopressin"[Mesh] "Antidiuretic Hormone Receptor Antagonists"[Mesh] ("v2"[Text Word]) OR "v1a"[Text Word] (("vaptans"[Text Word]) OR "aquaretic"[Text Word]) OR "aquaresis"[Text Word] ("tolvaptan"[Text Word]) OR "opc 41061"[Text Word] ("conivaptan"[Text Word]) OR "ym087"[Text Word] ("satavaptan"[Text Word]) OR "sr121463b"[Text Word] ("lixivaptan"[Text Word]) OR "vpa 985"[Text Word] ("mozavaptan"[Text Word]) OR "opc 31260"[Text Word] "Clinical Trials as Topic"[Majr] "Controlled Clinical Trials as Topic"[Majr] "Randomized Controlled Trials as Topic"[Majr] "Clinical Trial" [Publication Type] "Controlled Clinical Trial" [Publication Type] "Randomized Controlled Trial" [Publication Type] "Random Allocation"[Majr] (("random"[Text Word]) OR "randomly"[Text Word]) OR "randomization"[Text Word] "trial"[Text Word] "Double-Blind Method"[Majr] "Single-Blind Method"[Majr] "double blind"[Text Word] "single blind"[Text Word] "open label"[Text Word] "Placebos"[Majr] "placebo"[Text Word] "post hoc"[Text Word] "subgroup"[Text Word] "extension"[Text Word] OvidMedline(R) Journals@Ovid (Sumarios y Resúmenes todas las Revistas Ovid), Revistas Subscritas a Texto Completo por Sacyl, OvidMEDLINE(R) Epub Ahead of Print, In-Process & Other Non-Indexed Citantions, Ovid MEDLINE(R) Daily, Ovid MEDLINE and Versions(R) exp Hyponatremia/ hyponatr$.tw. (euvolemic or hypervolemic).tw. exp Inappropriate ADH Syndrome/ (antidiuretic adj hormone).tw. exp Heart Failure/ (heart adj failure).tw. exp Liver Cirrhosis/ (cirrhosis or ascites).tw.
    [Show full text]
  • Vaptans and the Treatment of Water-Retaining Disorders Friedericke Quittnat and Peter Gross
    Vaptans and the Treatment of Water-Retaining Disorders Friedericke Quittnat and Peter Gross Hyponatremia is a frequent and symptomatic electrolyte disorder for which specific treat- ments have been lacking. Hyponatremia is attributable to nonosmotic vasopressin stimu- lation and continued increased fluid intake. In the past, peptidic derivatives of arginine vasopressin proved that blockade of vasopressin V-2 receptors served to improve hypo- natremia, however, these antagonists had intrinsic agonistic activity, too. In the past decade, random screening of molecules uncovered nonpeptide, orally available vasopres- sin antagonists without agonistic properties. The agents show competitive binding to the vasopressin V-2 receptor at an affinity comparable with that of arginine vasopressin. Four antagonists have undergone extensive study. Three of these agents—lixivaptan or VPA 985; SR 121 463 B; tolvaptan or OPC 41,061—are specific V-2 antagonists whereas conivaptan or YM 087 is a V-1/V-2 mixed antagonist. In animal and clinical studies all of the agents were able to correct water retention and hyponatremia in a dose-dependent manner. There was no tachyphylaxis, even when the agents were given over many weeks. It is expected that the clinical use of the agents will lead to a major improvement in the treatment of hyponatremia. Semin Nephrol 26:234-243 © 2006 Elsevier Inc. All rights reserved. KEYWORDS hyponatremia, vasopressin, vaptans, cardiac failure, syndrome of inappropriate antidiuretic hormone (SIADH) yponatremia is a water-retaining disorder that is de- in outpatients, especially when older patients are consid- Hfined by the presence of a plasma sodium concentration ered.3 of 136 mmol/L or less.
    [Show full text]
  • The Structure and Function of V1b Vasopressin Receptor
    The Structure and Function of V1b Vasopressin Receptors Yukie Goto A thesis submitted to the University of Birmingham for the degree of Doctor of Philosophy School of Biosciences University of Birmingham Edgbaston, Birmingham B15 2TT, United Kingdom September 2009 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. Acknowledgement Firstly I would like to thank my supervisor Professor Mark Wheatley for giving me this opportunity to participate in his research, and for his support and guidance throughout my study. I would also like to thank those who have worked in his research group: in particular John for providing us with molecular models of vasopressin receptors; Alex, Mattew, Denise, Cymone and Amelia, for equipping me with the laboratory techniques required for carrying out this study; and Rachel and Richard for their companies and supports in the research group for last few years. I am truly grateful to Dr. David Poyner and Prof. Ian Martin for their inspiring teachings on this subject area in my undergraduate years. My gratitude goes to Rosemary for her conscientious hard work in looking after laboratories, equipments, and students; and to Eva, David, Karthik, Prof.
    [Show full text]
  • Management of Hyponatremia
    E CMAJ M Review C Management of hyponatremia Jennifer Ji Young Lee BHSc, Kajiru Kilonzo MD, Amy Nistico MD, Karen Yeates MD yponatremia, defined as a decrease in How does the type of Competing interests: serum sodium below 136 mmol/L, is a Karen Yeates has received hyponatremia affect treatment? honoraria for a career H common occurrence in both inpatients mentorship talk from and outpatients and can be found in up to 15% Amgen and for a continuing of the general hospital populations. 1,2 Acute Although there are many approaches to the man - medical education event from Otsuka hyponatremia (duration < 48 h) and its manage - agement of hyponatremia, one of the most com - Pharmaceuticals. No other ment can be a cause of major morbidity and mon approaches used by nonexpert clinicians competing interests were mortality among patients in hospital. 3 Chronic begins with an assessment of extracellular fluid declared. hyponatremia (duration > 48 h), which is typi - (ECF) volume status. Because diabetes mellitus This article has been peer cally seen among older ( ≥ 65 yr) outpatients, is becoming more prevalent in the adult popula - reviewed. also contributes to morbidity because it is often tion, clinicians should be mindful of ruling out Correspondence to: unrecognized. 3,4 Typically, correction of serum hyperosmolar hyponatremia caused by hyper - Karen Yeates, sodium concentration in patients with acute glycemia as a potential cause of hyponatremia. [email protected] hyponatremia should occur at a more rapid rate The clinical history and physical examination CMAJ 2014. DOI:10.1503 than in patients with chronic hyponatremia provide important diagnostic clues that help to /cmaj.120887 because the symptoms are usually more severe classify the cause of hyponatremia as hypov - when serum sodium rapidly decreases over a olemic, euvolemic or hypervolemic.
    [Show full text]
  • (CRDAC) Meeting Date: 13 September 2012
    FDA Briefing Document for the Cardiovascular and Renal Drugs Advisory (CRDAC) Meeting Date: 13 September 2012 NDA: 203009 Sponsor: Cardiokine Biopharma, LLC Drug: Lixivaptan Proposed Indication for Use: The treatment of symptomatic hypervolemic and euvolemic hyponatremia associated with heart failure and syndrome of inappropriate antidiuretic hormone (SIADH), respectively. Important Limitations Patients requiring intervention to raise sodium concentration urgently to prevent or to treat serious neurological symptoms should not be treated with lixivaptan. DISCLAIMER STATEMENT The attached package contains background information prepared by the Food and Drug Administration (FDA) for the panel members of the advisory committee. The FDA background package often contains assessments and/or conclusions and recommendations written by individual FDA reviewers. Such conclusions and recommendations do not necessarily represent the final position of the individual reviewers, nor do they necessarily represent the final position of the Review Division or Office. We have brought the Lixivaptan NDA to this Advisory Committee in order to gain the Committee’s insights and opinions, and the background package may not include all issues relevant to the final regulatory recommendation and instead is intended to focus on issues identified by the Agency for discussion by the advisory committee. The FDA will not issue a final determination on the issues at hand until input from the advisory committee process has been considered and all reviews have been finalized. The final determination may be affected by issues not discussed at the advisory committee meeting. CLINICAL REVIEW Application Type NDA 203,009 Application Number(s) 000-000 Priority or Standard Standard Submit Date(s) December 29, 2011 Received Date(s) December 29, 2011 PDUFA Goal Date October 29, 2012 Division / Office Cardiovascular and Renal Products/ ODE1 Reviewer Name(s) Nancy N.
    [Show full text]
  • Olive Leaf Extract (OLE) Impaired Vasopressin-Induced Aquaporin-2
    www.nature.com/scientificreports OPEN Olive Leaf Extract (OLE) impaired vasopressin‑induced aquaporin‑2 trafcking through the activation of the calcium‑sensing receptor Marianna Ranieri1*, Annarita Di Mise1, Mariangela Centrone1, Mariagrazia D’Agostino1, Stine Julie Tingskov2, Maria Venneri1, Tommaso Pellegrino1, Graziana Difonzo3, Francesco Caponio3, Rikke Norregaard2, Giovanna Valenti1 & Grazia Tamma1* Vasopressin (AVP) increases water permeability in the renal collecting duct through the regulation of aquaporin‑2 (AQP2) trafcking. Several disorders, including hypertension and inappropriate antidiuretic hormone secretion (SIADH), are associated with abnormalities in water homeostasis. It has been shown that certain phytocompounds are benefcial to human health. Here, the efects of the Olive Leaf Extract (OLE) have been evaluated using in vitro and in vivo models. Confocal studies showed that OLE prevents the vasopressin induced AQP2 translocation to the plasma membrane in MCD4 cells and rat kidneys. Incubation with OLE decreases the AVP‑dependent increase of the osmotic water permeability coefcient (Pf). To elucidate the possible efectors of OLE, intracellular calcium was evaluated. OLE increases the intracellular calcium through the activation of the Calcium Sensing Receptor (CaSR). NPS2143, a selective CaSR inhibitor, abolished the inhibitory efect of OLE on AVP‑dependent water permeability. In vivo experiments revealed that treatment with OLE increases the expression of the CaSR mRNA and decreases AQP2 mRNA paralleled by an increase
    [Show full text]
  • Download Product Insert (PDF)
    PRODUCT INFORMATION Lixivaptan Item No. 21511 CAS Registry No.: 168079-32-1 O H Formal Name: N-[3-chloro-4-(5H-pyrrolo[2,1-c][1,4] N benzodiazepin-10(11H)-ylcarbonyl)phenyl]- 5-fluoro-2-methyl-benzamide Synonyms: VPA-985, WAY-VPA-985 F Cl MF: C27H21ClFN3O2 FW: 473.9 O Purity: ≥97% N N UV/Vis.: λmax: 268 nm Supplied as: A crystalline solid Storage: -20°C Stability: ≥2 years Information represents the product specifications. Batch specific analytical results are provided on each certificate of analysis. Laboratory Procedures Lixivaptan is supplied as a crystalline solid. A stock solution may be made by dissolving the lixivaptan in the solvent of choice. Lixivaptan is soluble in organic solvents such as ethanol, DMSO, and dimethyl formamide (DMF), which should be purged with an inert gas. The solubility of lixivaptan in ethanol is approximately 10 mg/ml and approximately 30 mg/ml in DMSO and DMF. Lixivaptan is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers, lixivaptan should first be dissolved in DMSO and then diluted with the aqueous buffer of choice. Lixivaptan has a solubility of approximately 0.33 mg/ml in a 1:2 solution of DMSO:PBS (pH 7.2) using this method. We do not recommend storing the aqueous solution for more than one day. Description 1 Lixivaptan is a nonpeptide antagonist of vasopressin V2 receptors (Ki = 2.3 nM). It is 100-fold selective 2 for V2 over V1a. Formulations containing lixivaptan decrease urinary excretion of aquaporin-2 in patients with chronic heart failure and increase serum sodium levels in patients with hyponatremia due to congestive heart failure.3,4 References 1.
    [Show full text]
  • Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines
    BRIEF REVIEW www.jasn.org Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines Ewout J. Hoorn and Robert Zietse Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus Medical Center, Rotterdam, The Netherlands ABSTRACT Hyponatremia is a common water balance disorder that often poses a diagnostic or approach to hyponatremia, two sets of therapeutic challenge. Therefore, guidelines were developed by professional orga- guidelines have been developed, one by nizations, one from within the United States (2013) and one from within Europe professional organizations from within (2014). This review discusses the diagnosis and treatment of hyponatremia, com- the United States (“United States guide- paring the two guidelines and highlighting recent developments. Diagnostically, the line”) and one from within Europe (“Eu- initial step is to differentiate hypotonic from nonhypotonic hyponatremia. Hypo- ropean guideline,” in which the authors tonic hyponatremia is further differentiated on the basis of urine osmolality, urine of this review participated).6–9 The pro- sodium level, and volume status. Recently identified parameters, including fractional fessional organizations involved in the uric acid excretion and plasma copeptin concentration, may further improve the United States guideline were Tufts Uni- diagnostic approach. The treatment for hyponatremiaischosenonthebasisof versity Office of Continuing Education duration and symptoms. For acute or severely symptomatic hyponatremia, both and In 2 MedEd; the initiative was guidelines adopted the approach of giving a bolus of hypertonic saline. Although also supported by an unrestricted edu- fluid restriction remains the first-line treatment for most forms of chronic hypona- cational grant from Otsuka America tremia, therapy to increase renal free water excretion is often necessary.
    [Show full text]
  • The Use of Stems in the Selection of International Nonproprietary Names (INN) for Pharmaceutical Substances" WHO/EMP/RHT/TSN/2013.1
    INN Working Document 17.406 20/01/2017 Addendum1 to "The use of stems in the selection of International Nonproprietary names (INN) for pharmaceutical substances" WHO/EMP/RHT/TSN/2013.1 Programme on International Nonproprietary Names (INN) Technologies Standards and Norms (TSN ) Regulation of Medicines and other health technologies (RHT) World Health Organization, Geneva © World Health Organization 2017 - All rights reserved. The contents of this document may not be reviewed, abstracted, quoted, referenced, reproduced, transmitted, distributed, translated or adapted, in part or in whole, in any form or by any means, without explicit prior authorization of the WHO INN Programme. This document contains the collective views of the INN Expert Group and does not necessarily represent the decisions or the stated policy of the World Health Organization. Addendum1 to "The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances" - WHO/EMP/RHT/TSN/2013.1 1 This addendum is a cumulative list of all new stems selected by the INN Expert Group since the publication of "The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances" 2013. ------------------------------------------------------------------------------------------------------------ -apt- aptamers, classical and mirror ones (a) avacincaptad pegol (113), egaptivon pegol (111), emapticap pegol (108), lexaptepid pegol (108), olaptesed pegol (109), pegaptanib (88) (b) -vaptan stem: conivaptan (82), lixivaptan
    [Show full text]
  • The Treatment of Vasopressin V2-Receptor Antagonists in Cirrhosis Patients with Ascites
    Yan et al. BMC Gastroenterology (2015) 15:65 DOI 10.1186/s12876-015-0297-z RESEARCH ARTICLE Open Access The treatment of vasopressin V2-receptor antagonists in cirrhosis patients with ascites: a meta-analysis of randomized controlled trials Long Yan1†, Feng Xie1†, Jiongjiong Lu1, Qingqiang Ni1, Changying Shi1, Caixi Tang2 and Jiamei Yang1* Abstract Background: Ascites is the most common complication of cirrhosis. It may lead to the consequence of poor prognosis and the deterioration of quality of life. Asopressin V2 receptor antagonists is a kind of vaptans, and it has been proved to be effective in hyponatremia patients. We conducted a meta-analysis about treatment of vaptans in cirrhosis patients with ascites. Methods: Following our selection criteria, we collected a total of 14 studies containing 16 randomized controlled trials (2620 patients) from a series of database about the treatment with vaptans for cirrhosis with ascites patients. The included studies compared the treatment effect of lixivaptan (VPA 985), or RMJ-351647, or satavaptan, or tolvaptan with placebo. Results: The included vaptans (asopressin V2 receptor antagonists) showed significant effect of increasing the serum sodium concentration for cirrhosis patients (WMD = 2.11 mmol/L, p < 0.00001). Patients also could acquire significant improvement of ascites, as this kind of aquaretics can significantly reduce ascites patients’ weight (WMD = −1.53, p < 0.00001), abdominal girth (WMD = −2.04, p < 0.00001), and the ratio of worsening ascites (RR = 0.51, p = 0.001). Though the drug did not produce more total adverse events (RR = 1.04, p = 0.09) and the total serious events (RR = 1.04, p = 0.42), the emergence of excessive correction of serum sodium concentrations (>145 mmol/L) was more frequently noted in patients under the employment of vaptans (RR = 2.14, 95 % CI [1.45, 3.16], p = 0.0001).
    [Show full text]