Hyponatremia and anti-diuretic hormone in Legionnaires' disease

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 130-162-Neuroendocrinology
Clinical
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-162
Philipp Schuetz*1, Sebastian Haubitz2, Mirjam Jennifer Christ-Crain3, Werner Albrich2, Werner Zimmerli4 and Beat Mueller1
1Kantonsspital Aarau, Aarau, Switzerland, 2Kantonsspital Aarau, Switzerland, 3University Hospital Basel, Switzerland, 4Kantonsspital Liestal, Switzerland
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 community acquired pneumonia patients from a previous multicentre study with 31 patients having confirmed Legionnaires' disease by positive antigen tests for Legionella pneumophila. 

Results: Patients with Legionnaires' disease more frequently had low sodium levels (Na < 130 mmol/L) (43% versus 8%, p < 0.01), but similar median CT-ProVasopressin levels (pmol/l) (20 [12-26] versus 26 [13-53], p = 0.89) 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 (odds ratio per decile, 95% CI) (1.4, 1.2 - 1.6), and 30-day-mortality (1.3, 1.2 - 1.4).

Conclusion: While Legionnaires’ disease was associated with hyponatremia, no concurrent increase in CT-ProVasopressin levels was found, which argues against SIADH 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.

Nothing to Disclose: PS, SH, MJC, WA, WZ, BM

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

<< Previous Abstract | Next Abstract