Prof. Dr. Andreas E. Kremer

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Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 September 2010 in Gastroenterology

Journal Article

Lysophosphatidic Acid Is a Potential Mediator of Cholestatic Pruritus

Andreas E. Kremer

Job J.W.W. Martens

Wim Kulik

Franziska Ruëff

Edith M.M. Kuiper

Ronald P.J. Oude Elferink

1 October 2010 in Hepatology

Journal Article

The Biliary HCO3 − Umbrella: A Unifying Hypothesis on Pathogenetic and Therapeutic Aspects of Fibrosing Cholangiopathies

Ulrich Beuers

Simon Hohenester

Lucas J. Maillette de Buy Wenniger

Andreas E. Kremer

Peter L. M. Jansen

Ronald P. J. Oude Elferink

1 April 2015 in Kidney International

Journal Article

Uremic pruritus

Thomas Mettang

Andreas E. Kremer

2 April 2012 in Hepatology

Journal Article

Serum autotaxin is increased in pruritus of cholestasis, but not of other origin, and responds to therapeutic interventions

Andreas E. Kremer

Remco van Dijk

Pamela Leckie

Frank Schaap

Edith M.M. Kuiper

Ulrich Beuers

+10

Pruritus is a seriously disabling symptom accompanying many cholestatic liver disorders. Recent experimental evidence implicated the lysophospholipase, autotaxin (ATX), and its product, lysophosphatidic acid (LPA), as potential mediators of cholestatic pruritus. In this study, we highlight that increased serum ATX levels are specific for pruritus of cholestasis, but not pruritus of uremia, Hodgkin's disease, or atopic dermatitis. Treatment of patients with cholestasis with the bile salt sequestrant, colesevelam, but not placebo, effectively reduced total serum bile salts and fibroblast growth factor 19 levels, but only marginally altered pruritus intensity and ATX activity. Rifampicin (RMP) significantly reduced itch intensity and ATX activity in patients with pruritus not responding to bile salt sequestrants. In vitro , RMP inhibited ATX expression in human HepG2 hepatoma cells and hepatoma cells overexpressing the pregnane X receptor (PXR), but not in hepatoma cells in which PXR was knocked down. Treatment of severe, refractory pruritus by the molecular adsorbents recirculation system or nasobiliary drainage improved itch intensity, which, again, correlated with the reduction of ATX levels. Upon reoccurrence of pruritus, ATX activity returned to pretreatment values. Conclusion : Serum ATX activity is specifically increased in patients with cholestatic, but not other forms of, systemic pruritus and closely correlates with the effectiveness of therapeutic interventions. The beneficial antipruritic action of RMP may be explained, at least partly, by the PXR-dependent transcriptional inhibition of ATX expression. Thus, ATX likely represents a novel therapeutic target for pruritus of cholestasis. (Hepatology 2012)