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      Hyponatremia and anti-diuretic hormone in Legionnaires’ disease

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          Abstract

          Background

          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.

          Methods

          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.

          Results

          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).

          Conclusion

          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.

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          Most cited references42

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          A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone.

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            Hyponatremia and Inflammation: The Emerging Role of Interleukin-6 in Osmoregulation

            Although hyponatremia is a recognized complication of several inflammatory diseases, its pathophysiology in this setting has remained elusive until recently. A growing body of evidence now points to an important role for interleukin-6 in the non-osmotic release of vasopressin. Here, we review this evidence by exploring the immuno-neuroendocrine pathways connecting interleukin-6 with vasopressin. The importance of these connections extends to several clinical scenarios of hyponatremia and inflammation, including hospital-acquired hyponatremia, postoperative hyponatremia, exercise-associated hyponatremia, and hyponatremia in the elderly. Besides insights in pathophysiology, the recognition of the propensity for antidiuresis during inflammation is also important with regard to monitoring patients and selecting the appropriate intravenous fluid regimen, for which recommendations are provided.
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              C-terminal provasopressin (copeptin) as a novel and prognostic marker in acute myocardial infarction: Leicester Acute Myocardial Infarction Peptide (LAMP) study.

              The role of the vasopressin system after acute myocardial infarction is unclear. Copeptin, the C-terminal part of the vasopressin prohormone, is secreted stoichiometrically with vasopressin. We compared the prognostic value of copeptin and an established marker, N-terminal pro-B-type natriuretic peptide (NTproBNP), after acute myocardial infarction. In this prospective single-hospital study, we recruited 980 consecutive post-acute myocardial infarction patients (718 men, median [range] age 66 [24 to 95] years), with follow-up over 342 (range 0 to 764) days. Plasma copeptin was highest on admission (n=132, P<0.001, day 1 versus days 2 to 5) and reached a plateau at days 3 to 5. In the 980 patients, copeptin (measured at days 3 to 5) was elevated in patients who died (n=101) or were readmitted with heart failure (n=49) compared with survivors (median [range] 18.5 [0.6 to 441.0] versus 6.5 [0.3 to 267.0] pmol/L, P<0.0005). With logistic regression analysis, copeptin (odds ratio, 4.14, P<0.0005) and NTproBNP (odds ratio, 2.26, P<0.003) were significant independent predictors of death or heart failure at 60 days. The area under the receiver operating characteristic curves for copeptin (0.75) and NTproBNP (0.76) were similar. The logistic model with both markers yielded a larger area under the curve (0.84) than for NTproBNP (P<0.013) or copeptin (P<0.003) alone, respectively. Cox modeling predicted death or heart failure with both biomarkers (log copeptin [hazard ratio, 2.33], log NTproBNP [hazard ratio, 2.70]). In patients stratified by NTproBNP (above the median of approximately 900 pmol/L), copeptin above the median (approximately 7 pmol/L) was associated with poorer outcome (P<0.0005). Findings were similar for death and heart failure as individual end points. The vasopressin system is activated after acute myocardial infarction. Copeptin may predict adverse outcome, especially in those with an elevated NTproBNP (more than approximately 900 pmol/L).
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                Author and article information

                Journal
                BMC Infect Dis
                BMC Infect. Dis
                BMC Infectious Diseases
                BioMed Central
                1471-2334
                2013
                11 December 2013
                : 13
                : 585
                Affiliations
                [1 ]Medical University Clinic, Kantonsspital Aarau, Aarau, Switzerland
                [2 ]Department of Internal Medicine, Division of Endocrinology, Diabetes and Clinical Nutrition, University Hospital Basel, Basel, Switzerland
                [3 ]Medical University Clinic, Kantonsspital Liestal, Liestal, Switzerland
                Author notes
                the ProHOSP Study Group
                Article
                1471-2334-13-585
                10.1186/1471-2334-13-585
                3880094
                24330484
                0f7f1d10-d09d-46e2-ab7c-2d3a463c617a
                Copyright © 2013 Schuetz et al.; licensee BioMed Central Ltd.

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 May 2013
                : 9 December 2013
                Categories
                Research Article

                Infectious disease & Microbiology
                low sodium levels,community-acquired pneumonia,siadh,legionella,hyponatremia

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