Prolactin but not ACTH increases during sodium lactate-induced panic attacks

Otte, Christian; Kellner, Michael; Arlt, Josef; Jahn, Holger; Holsboer, Florian; Wiedemann, Klaus

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Volume 109, Issue 2 , Pages 201-205, 15 March 2002

Prolactin but not ACTH increases during sodium lactate-induced panic attacks

Christian Otte
- University Hospital Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Martinistrasse 52, 20246 Hamburg, Germany
- Corresponding author. Tel.: +49-40-42803-3232; fax: +49-40-42803-5546
Michael Kellner
- University Hospital Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Martinistrasse 52, 20246 Hamburg, Germany
Josef Arlt
- University Hospital Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Martinistrasse 52, 20246 Hamburg, Germany
Holger Jahn
- University Hospital Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Martinistrasse 52, 20246 Hamburg, Germany
Florian Holsboer
- Max-Planck-Institute of Psychiatry, Kraepelinstrasse 10, 80804 Munich, Germany
Klaus Wiedemann
- University Hospital Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Martinistrasse 52, 20246 Hamburg, Germany

Received 9 May 2001; received in revised form 12 December 2001; accepted 22 January 2002.

Abstract

Paradoxically, the pituitary–adrenal axis is not activated during sodium lactate-induced panic. We measured the response of another stress-sensitive hormone, prolactin, to standard lactate and placebo infusion in a double-blind randomised design in eight patients with panic disorder and eight matched normal controls. Prolactin release was significantly elevated (P<0.05) in panickers compared with non-panickers, whereas ACTH secretion was not activated at all. This differential stress response needs further investigation.

Keywords: HPA axis, Anxiety, Neuroendocrinology, Pituitary, Panic disorder