Corrigendum to "Amiodarone Induced Hyponatremia Masquerading as Syndrome of Inappropriate Antidiuretic Hormone Secretion by Anaplastic Carcinoma of Prostate".
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ABSTRACT:
SUBMITTER: Dutta P
PROVIDER: S-EPMC6211146 | biostudies-other | 2018
REPOSITORIES: biostudies-other
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Corrigendum to "Amiodarone Induced Hyponatremia Masquerading as Syndrome of Inappropriate Antidiuretic Hormone Secretion by Anaplastic Carcinoma of Prostate".
Dutta Pinaki P Parthan Girish G Aggarwal Anuradha A Kumar Santosh S Kakkar Nandita N Bhansali Anil A Rotondo Fabio F Kovacs Kalman K
Case reports in urology 20181018
[This corrects the article DOI: 10.1155/2014/136984.]. ...[more]
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Project description:BACKGROUND:Tolvaptan effectively corrects hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but undesired overcorrection can occur. We hypothesized that pretherapy parameters can predict the rapidity of response to tolvaptan in SIADH. STUDY DESIGN:Multicenter historical cohort study. SETTING & PARTICIPANTS:Adults with SIADH or congestive heart failure (CHF) treated with tolvaptan for a serum sodium concentration ? 130 mEq/L at 5 US hospitals. PREDICTORS:Demographic and laboratory parameters. OUTCOMES:Rate of change in serum sodium concentration. MEASUREMENTS:Spearman correlations, analysis of variance, and multivariable linear mixed-effects models. RESULTS:28 patients with SIADH and 39 patients with CHF treated with tolvaptan (mean baseline serum sodium, 120.6 and 122.4 mEq/L, respectively) were studied. Correction of serum sodium concentration > 12 mEq/L/d occurred in 25% of patients with SIADH compared to 3% of those with CHF (P<0.001). Among patients with SIADH, the increase in serum sodium over 24 hours was correlated with baseline serum sodium concentration (r=-0.78; P<0.001), serum urea nitrogen concentration (SUN; r=-0.76; P<0.001), and estimated glomerular filtration rate (r=0.58; P=0.01). Baseline serum sodium and SUN concentrations were identified as independent predictors of change in serum sodium concentration in multivariable analyses. When patients were grouped into 4 categories according to baseline serum sodium and SUN median values, those with both low baseline serum sodium (?121 mEq/L) and low baseline SUN concentrations (?10mg/dL) exhibited a significantly greater rate of increase in serum sodium concentration (mean 24-hour increase of 15.4 mEq/L) than the other 3 categories (P<0.05). Among patients with CHF, only baseline SUN concentration was identified as an independent predictor of change in serum sodium concentration over time. LIMITATIONS:Lack of uniformity in serial serum sodium concentration determinations and documentation of water intake. CONCLUSIONS:Baseline serum sodium and SUN values are predictive of the rapidity of hyponatremia correction following tolvaptan use in SIADH. We advise caution when dosing tolvaptan in patients with both low serum sodium and SUN concentrations.
| S-EPMC5970971 | biostudies-literature
Project description:Tolvaptan (TLV) is indicated to treat hyponatremia due to syndrome of inappropriate diuretic hormone (SIADH) in Europe. Treatment is to be initiated at 15 mg QD but post-approval reporting indicates increasing use of 7.5 mg as the starting dose. Physicians believe 7.5 mg is effective and has a lower incidence of overly rapid correction of serum sodium.Single TLV doses of 3.75, 7.5, and 15 mg were administered to 14 healthy adults in a crossover design and to 29 subjects ?18 years with SIADH and serum sodium between 120 and 133 mmol/L in a parallel-group design. Pharmacodynamics and TLV plasma concentrations were assessed for 24 h post-dose.In SIADH subjects, corrections of serum sodium (? of ?8 mmol/L in the first 8 h or ?12 mmol/L in the first 24 h) were observed in one, one, and two subjects in the 3.75-, 7.5-, and 15-mg dose groups. Fluid balance (FB) for 0-6 h post-dose was correlated (r 2 = 0.37) with maximum increases in serum sodium; subjects with large corrections had large (~1 L) negative FB. Compared to healthy adults, subjects with SIADH did not drink in response to their negative FB and had larger increases in serum sodium at 24 h. Median time of maximum increase in healthy adults was 6 h, with no rapid corrections, and FB was near 0 mL by 24 h.Starting titration with 7.5 mg TLV will not eliminate the risk of rapid corrections in serum sodium. Monitoring FB may indicate that a subject is at risk for over correction.
| S-EPMC5662662 | biostudies-literature
Project description:Hyponatremia, defined as serum sodium concentration <135 mEq/l, is the most common electrolyte balance disorder in clinical practice. Many causes are listed, but syndrome of inappropriate antidiuretic hormone secretion (SIADH) is certainly the most relevant, mainly in oncological and hospitalized patients. In this review, the pathophysiological and clinical aspects are described in detail. Patients' extensive medical history and structured physical and biochemical tests are considered the milestones marking the way of the SIADH management as to provide early detection and proper correction. We focused our attention on the poor prognostic role and negative effect on patient's quality of life of SIADH-induced hyponatremia in both malignant and non-malignant settings, stressing how optimal management of this electrolyte imbalance can result in improved outcomes and lower health costs.
| S-EPMC7386802 | biostudies-literature
Project description:The syndrome of inappropriate antidiuretic hormone secretion (SIADH) accounts for an important part of hyponatremia cases. The causes of SIADH can be detected almost always. As a rare disorder, Morvan Syndrome can be defined by the sum of peripheral nerve hyperexcitability, autonomic instability and neuropsychiatric features. Antibodies to voltage-gated potassium channels (Anti - VGKC-Ab) including contactin associated protein-like 2 antibodies (CASPR2-Ab) and leucine-rich glioma inactivated protein 1 antibodies (LGI1-Ab) were previously known for the potential association with this condition. We present a Morvan Syndrome in a patient who presented with various neuropsychiatric symptoms and SIADH.
| S-EPMC5536216 | biostudies-other
Project description:ObjectiveVarious studies have shown that a number of infectious disease causes syndrome of inappropriate antidiuretic hormone (SIADH). However, the relationship between infectious disease and SIADH is not yet fully known. In this prospective study, we aimed to assess the presence of SIADH in patients with brucellosis.Patients and methodsThirty-five patients with acute brucellosis were retrospectively reviewed. The diagnosis of brucellosis was performed using the Wright test in connection with blood culture. SIADH was defined by euvolemic hyponatremia (serum sodium level lower than 135 mEq/l) with increased urinary sodium excretion (urinary sodium higher than 40 mmol/l).ResultsOf the 35 patients, 19 (54%) had SIADH; 20 (57%) also had hypouricemia (uric acid level lower than 4 mg/dl). Additionally, all of the studied patients had a high mean urinary sodium excretion rate (mean 132 mmol/l; range 40-224). Most importantly, the hyponatremic patients were more likely to have a lower albumin level (P < 0.01).ConclusionsSIADH is a major complication of brucellosis. The presence of SIADH could be a diagnostic tool for diagnosing brucellosis. Further larger randomized studies may confirm these findings.
| S-EPMC6806686 | biostudies-literature
Project description:Hyponatremia is a common electrolyte disorder in cancer patients and has been associated with poor prognosis. A frequent cause of cancer-related hyponatremia is the syndrome of inappropriate antidiuretic hormone (SIADH). This study was a post hoc subgroup analysis of the SALT-1 (Study of Ascending Levels of Tolvaptan in Hyponatremia) and SALT-2 clinical trials. Hyponatremic subjects with SIADH and cancer received the oral selective vasopressin V2-receptor antagonist tolvaptan (n = 12) or matching placebo (n = 16) once-daily for 30 days. The initial tolvaptan dose (15 mg) was titrated over 4 days to 30 or 60 mg per day, as needed, according to serum sodium level and tolerability. Baseline serum sodium levels in the SIADH/cancer cohort of the SALT trials was 130 and 128 mEq/L for tolvaptan and placebo, respectively. Mean change from baseline in average daily serum sodium AUC for tolvaptan relative to placebo was 5.0 versus -0.3 mEq/L (P < 0.0001) at day 4, and 6.9 versus 1.0 mEq/L (P < 0.0001) at day 30; the observed treatment effects were similar to those in the overall SIADH population (i.e., with and without cancer) at both time points. Serum sodium normalization was observed in 6/12 and 0/13 subjects at day 4 and 7/8 and 2/6 subjects at day 30 in the tolvaptan and placebo groups, respectively (P < 0.05 for both). Common treatment-emergent AEs for tolvaptan were consistent with previously reported results. In this post hoc study of the SALT trial population, oral tolvaptan was an effective and safe therapy for the treatment of hyponatremia in subjects with SIADH and cancer.
| S-EPMC5387121 | biostudies-literature
Project description:Rationale & Objective:Euvolemic hyponatremia often occurs due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Vasopressin 2 receptor antagonists may be used to treat SIADH. Several of the major trials used 15 mg of tolvaptan as the lowest effective dose in euvolemic and hypervolemic hyponatremia. However, a recent observational study suggested an elevated risk for serum sodium level overcorrection with 15 mg of tolvaptan in patients with SIADH. Study Design:A retrospective chart review study comparing outcomes in patients with SIADH treated with 15 versus 7.5 mg of tolvaptan. Settings & Participants:Patients with SIADH who were treated with a very low dose of tolvaptan (7.5 mg) at a single center compared with patients using a 15-mg dose from patient-level data from the observational study described previously. Predictors:Tolvaptan dose of 7.5 versus 15 mg daily. Outcomes:Appropriate response to tolvaptan, defined as an initial increase in serum sodium level > 3 mEq/L, and overcorrection of serum sodium level (>8 mEq/L per day, and >10 mEq/L per day in sensitivity analyses). Analytical Approach:Descriptive study with additional outcomes compared using t tests and F-tests (Fischer's Exact ?2 Test). Results:Among 18 patients receiving 7.5 mg of tolvaptan, the mean rate of correction was 5.6 ± 3.1 mEq/L per day and 2 (11.1%) patients corrected their serum sodium levels by >8 mEq/L per day, with 1 of these increasing by >12 mEq/L per day. Of those receiving tolvaptan 7.5 mg, 14 had efficacy, with increases ? 3 mEq/L; similar results were seen with the 15-mg dose (21 of 28). There was a statistically significant higher chance of overcorrection with the use of 15 versus 7.5 mg of tolvaptan (11 of 28 vs 2 of 18; P = 0.05; and 10 of 28 vs 1 of 18; P = 0.03, for >8 mEq/L per day and >10 mEq/L per day, respectively). Limitations:Small sample size, retrospective, and nonrandomized. Conclusions:Tolvaptan, 7.5 mg, daily corrects hyponatremia with similar efficacy and less risk for overcorrection in patients with SIADH versus 15 mg of tolvaptan.
| S-EPMC7380356 | biostudies-literature
Project description:Diamond Blackfan anemia is a congenital bone marrow failure syndrome characterized by hypoproliferative anemia, often with associated physical abnormalities. Perturbations of the ribosome appear critically important to the development of DBA, as alterations in 9 different ribosomal protein genes have been identified in multiple unrelated families, along with rarer abnormalities of additional ribosomal proteins. However, presently only 50-60% of patients have an identifiable genetic lesion by ribosomal protein gene sequencing. Using genome-wide SNP array to evaluate for regions of recurrent copy variation, we identified 2 patients with mosaic loss in the region of the the chromosome 5-deleted region involved in somatically-acquired 5q- myelodysplastic syndrome.
2013-11-05 | GSE42570 | GEO
Project description:A 60-year-old man with a history of smoking was transferred to our hospital for consciousness disorder. A diagnosis of ALK-rearranged lung adenocarcinoma associated with a paraneoplastic electrolytic disorder was made following a cutaneous needle biopsy. Both the primary lung lesion and multiple metastases shrunk and his electrolytic disorder resolved after the introduction of a first-line molecular-targeted drug chemotherapy with crizotinib. We herein report a case of ALK-rearranged lung adenocarcinoma accompanied by SIADH, successfully treated with crizotinib.
| S-EPMC7322342 | biostudies-literature
Project description:Medical textbooks often list Legionnaires' disease as a differential diagnosis of the syndrome of inappropriate secretion of anti-diuretic hormone (ADH) (SIADH), but evidence supporting this association is largely lacking. We tested the hypothesis whether hyponatremia in patients with Legionnaires' disease would be caused by increased CT-ProVasopressin.We measured CT-ProVasopressin and sodium levels in a prospective cohort of 873 pneumonia patients from a previous multicentre study with 27 patients having positive antigen tests for Legionella pneumophila.Patients with Legionnaires' disease more frequently had low sodium levels (Na?<?130 mmol/L) (44.4% vs 8.2%, p?<?0.01), but similar mean CT-ProVasopressin levels (pmol/l) (39.4 [±7] vs 51.2 [±2.7], p?=?0.43) as compared to patients with pneumonia of other etiologies. In patients with Legionnaires' disease, CT-ProVasopressin levels showed a positive correlation with sodium (r?=?0.42, p?<?0.05). Independent of pneumonia etiology, CT-ProVasopressin correlated significantly with the pneumonia severity index (r?=?0.56, p?<?0.05), ICU admission (adjusted odds ratio per decile, 95% CI) (1.6, 1.2 - 2.0), and 30-day-mortality (1.8, 1.3 - 2.4).While Legionnaires' disease was associated with hyponatremia, no concurrent increase in CT-ProVasopressin levels was found, which argues against elevated ADH levels as the causal pathway to hyponatremia. Rather, Vasopressin precursors were upregulated as response to stress in severe disease, which seems to overrule the osmoregulatory regulation of ADH.
| S-EPMC3880094 | biostudies-literature