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Sailer CO, Wiedemann SJ, Strauss K, et al. Markers of systemic inflammation in response to osmotic stimulus in healthy volunteers. Endocr Connect. 2019;8(9):1282-1287doi: 10.1530/EC-19-0280.
Sailer, C. O., Wiedemann, S. J., Strauss, K., Schnyder, I., Fenske, W. K., & Christ-Crain, M. (2019). Markers of systemic inflammation in response to osmotic stimulus in healthy volunteers. Endocrine connections, 8(9), 1282-1287. https://doi.org/10.1530/EC-19-0280
Sailer, Clara Odilia, et al. "Markers of systemic inflammation in response to osmotic stimulus in healthy volunteers." Endocrine connections vol. 8,9 (2019): 1282-1287. doi: https://doi.org/10.1530/EC-19-0280
Sailer CO, Wiedemann SJ, Strauss K, Schnyder I, Fenske WK, Christ-Crain M. Markers of systemic inflammation in response to osmotic stimulus in healthy volunteers. Endocr Connect. 2019 Sep;8(9):1282-1287. doi: 10.1530/EC-19-0280. PMID: 31434055; PMCID: PMC6765321.
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Endocr Connect. 2019 Sep;8(9):1282-1287. doi: 10.1530/EC-19-0280.

Markers of systemic inflammation in response to osmotic stimulus in healthy volunteers.

Endocrine connections

Clara Odilia Sailer, Sophia Julia Wiedemann, Konrad Strauss, Ingeborg Schnyder, Wiebke Kristin Fenske, Mirjam Christ-Crain

Affiliations

  1. Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
  2. Department of Clinical Research, University of Basel, Basel, Switzerland.
  3. Department of Biomedicine, University of Basel, Basel, Switzerland.
  4. Division of Endocrinology and Diabetes, Department of Internal Medicine I, University Hospital, University of Würzburg, Würzburg, Germany.
  5. Leipzig University Medical Center, Integrated Center for Research and Treatment Adiposity Diseases, Leipzig, Germany.
  6. Medical Department III, Endocrinology, Nephrology, Rheumatology, University Hospital of Leipzig, Leipzig, Germany.

PMID: 31434055 PMCID: PMC6765321 DOI: 10.1530/EC-19-0280

Abstract

Osmotic stimulus or stress results in vasopressin release. Animal and human in vitro studies have shown that inflammatory parameters, such as interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α), increase in parallel in the central nervous system and bronchial, corneal or intestinal epithelial cell lines in response to osmotic stimulus. Whether osmotic stimulus directly causes a systemic inflammatory response in humans is unknown. We therefore investigated the influence of osmotic stimulus on circulatory markers of systemic inflammation in healthy volunteers. In this prospective cohort study, 44 healthy volunteers underwent a standardized test protocol with an osmotic stimulus leading into the hyperosmotic/hypernatremic range (serum sodium ≥150 mmol/L) by hypertonic saline infusion. Copeptin - a marker indicating vasopressin activity - serum sodium and osmolality, plasma IL-8 and TNF-α were measured at baseline and directly after osmotic stimulus. Median (range) serum sodium increased from 141 mmol/L (136, 147) to 151 mmol/L (145, 154) (P < 0.01), serum osmolality increased from 295 mmol/L (281, 306) to 315 mmol/L (304, 325) (P < 0.01). Median (range) copeptin increased from 4.3 pg/L (1.1, 21.4) to 28.8 pg/L (19.9, 43.4) (P < 0.01). Median (range) IL-8 levels showed a trend to decrease from 0.79 pg/mL (0.37, 1.6) to 0.7 pg/mL (0.4, 1.9) (P < 0.09) and TNF-α levels decreased from 0.53 pg/mL (0.11, 1.1) to 0.45 pg/mL (0.12, 0.97) (P < 0.036). Contrary to data obtained in vitro, circulating proinflammatory cytokines tend to or decrease in human plasma after osmotic stimulus. In this study, osmotic stimulus does not increase circulating markers of systemic inflammation.

Keywords: TNF-α; copeptin; hyperosmolality; interleukin-6; interleukin-8

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