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Anti-phospholipid antibodies, neuroleptic treatment and cardiovascular morbidity

Published online by Cambridge University Press:  02 January 2018

E. Leuci
Affiliation:
Psychiatry Department, Parma, Fidenza, Italy
L. Manenti
Affiliation:
Psychiatry Department, Fidenza District, ASL Parma, Via Berenini 151, Fidenza (PR), 43100 Italy Email: lucio.manenti@aod.it
C. Maggini
Affiliation:
Psychiatry Department, Parma, Fidenza, Italy
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Abstract

Type
Columns
Copyright
Copyright © Royal College of Psychiatrists, 2007 

Joukamaa et al (Reference Joukamaa, Heliovaara and Knekt2006) reported a clear relationship between the number of neuroleptic drugs prescribed and mortality of people with schizophrenia. The more important causes of death were cardiovascular disease and unspecified respiratory disease. Moreover, the authors postulated that overlooked venous thrombosis or pulmonary embolism accounted for some respiratory deaths.

Oomen et al (Reference Oomen, Wekking and de Jong1995) documented increased vascular morbidity at 2-year follow-up in patients with anti-phospholipid antibodies who were newly admitted for psychiatric treatment. These patients showed a range of cardiovascular accidents (arterial or venous thrombosis, pulmonary embolism and myocardial infarction). The negative control group without anti-phospholipid antibodies had no vascular complications during follow-up.

Vascular events associated with such autoantibodies range from superficial to life-threatening multiple organ thrombosis developing over a short period (‘catastrophic’ anti-phospholipid syndrome). Thrombosis in anti-phospholipid syndrome appears to be a ‘two-hit’ phenomenon. Autoantibodies (the first ‘hit’) are continually present in the circulation, yet a local trigger (the second ‘hit’) is required to induce thrombus formation. Erkan & Lockshin (Reference Erkan and Lockshin2006) recently suggested the elimination of reversible thrombosis risk factors and heparin prophylaxis during high-risk periods in people with persistent anti-phospholipid antibodies. Chengappa et al (Reference Chengappa, Carpenter and Keshavan1991) and Schwartz et al (Reference Schwartz, Rochas and Weller1998) demonstrated a high prevalence of anti-phospholipid antibodies (about 30%) in patients. A prospective study is ongoing in our departments to confirm the prevalence of anti-phospholipid antibodies with a first episode of acute psychosis before and after neuroleptic treatment. If historical data are confirmed, more attention should be paid to the fact that up to one-third of patients presenting with psychosis have anti-phospholipid antibodies and are at risk of cardiovascular or respiratory morbidity/mortality when neuroleptic treatment or physical restraint are used.

References

Chengappa, K. N., Carpenter, A. B., Keshavan, M. S. et al (1991) Elevated IGG and IGM anticardiolipin antibodies in a subgroup of medicated and unmedicated shizophrenic patients. Biological Psychiatry 30, 731735.Google Scholar
Erkan, D. & Lockshin, M. D. (2006) Antiphospholipid syndrome. Current Opinion in Rheumatology, 18, 242248.Google Scholar
Joukamaa, M., Heliovaara, M., Knekt, P., et al (2006) Schizophrenia, neuroleptic medication and mortality British Journal of Psychiatry 188, 122127.Google Scholar
Oomen, H. A., Wekking, F. M., de Jong, J., et al (1995) Screening psychiatric admissions for anticardiolipin antibody. Psychiatry Research, 58, 8388.Google Scholar
Schwartz, M. D., Rochas, M., Weller, B. et al (1998) High association of anticardiolipin antibodies with psychosis. Journal of Clinical Psychiatry 59, 2023.Google Scholar
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