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Published on: May 28, 2019
Association between posttraumatic stress disorder following myocardial infarction and liver enzyme levels: a
Roland von Känel1, Chiara C Abbas, Stefan Begré
1Department of General Internal Medicine, Division of Psychosomatic Medicine, Inselspital, Bern University Hospital, and University of Bern, 3010, Bern, Switzerland. roland.vonkaenel@insel.ch
Background:
Research in rodents demonstrated that psychological stress increases circulating levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase reflecting liver injury. Moreover, chronic posttraumatic stress disorder and transaminases predicted coronary heart disease.
Aims:
To investigate the hypothesis that severity of posttraumatic stress disorder following myocardial infarction would prospectively relate to liver enzymes.
Methods:
Study participants were 24 patients (mean 59+/-7 years, 79% men) with an interviewer-rated diagnosis of posttraumatic stress disorder caused by an index myocardial infarction 3+/-3 months before. After a mean follow-up of 26+/-6 months, patients had a clinical interview to reassess posttraumatic stress disorder severity, a medical history, and blood collected to determine liver enzymes.
Results:
Total posttraumatic stress disorder symptoms assessed at study entry prospectively predicted plasma levels of alanine transaminase (r=.47, p=.031) and alkaline phosphatase (r=.57, p=.004), but not of aspartate transaminase (p=.15), controlling for follow-up duration and antidepressant use. Total posttraumatic stress disorder symptoms assessed at follow-up were associated with alanine transaminase (r=.72, p=.004), aspartate transaminase (r=.60, p=.018), and alkaline phosphatase (r=.64, p=.001) in the 16 patients who had maintained diagnostic posttraumatic stress disorder, but not in all 24 patients.
Conclusions:
The severity of posttraumatic stress disorder following myocardial infarction was associated with mild increase in liver enzyme levels, suggesting that chronic psychological stress relates to hepatic damage in humans. This might help to explain the previously observed increased cardiovascular risk in chronically traumatized individuals.
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