Prevalence of Clinical and Laboratory Markers of Hypofibrinolysis in Psychotic Patients
|Study Design:||Observational Model: Case Control
Time Perspective: Cross-Sectional
|Official Title:||Prevalence of Clinical and Laboratory Markers of Hypofibrinolysis in Psychotic Patients|
- Prevalence of hypofibrinolysis markers in psychotic patients [ Time Frame: One year ] [ Designated as safety issue: No ]The investigators' hypothesis is that a high prevalence of hypofibrinolysis markers will be probably found in psychotic patients.
- Prevalence of Clinical and Laboratory Markers of Hypofibrinolysis in Patients who Need Electroconvulsive Therapy [ Time Frame: 2013-2014 ] [ Designated as safety issue: No ]The investigators are assessing clinical and laboratory markers of plasminogen activator imbalance in psychiatric patients who require electroconvulsive therapy, specifically patients with major depressive disorders and schizophrenia.
|Study Start Date:||January 2013|
|Study Completion Date:||May 2013|
|Primary Completion Date:||May 2013 (Final data collection date for primary outcome measure)|
Inpatients and outpatients followed at Instituto de Psiquiatria da Universidade Federal do Rio de Janeiro, Brazil
If the thrombotic tendency plays a significant role in the etiology of psychosis, one would expect to find ischemic brain injuries in neuroimaging studies, but it does not happen. Therefore, if there is a correlation between thrombotic tendency-hypofibrinolysis and psychosis it is likely to occur at the biochemical level, such as in neuronal transmission.
The investigators hypothesis is that mechanisms that inhibit tissue plasminogen activator (t-PA) and therefore promote hypofibrinolysis, are directly or indirectly involved in the genesis of psychosis, because t-PA participates in neuronal plasticity and low t-PA levels are related to dementia.
Hypofibrinolysis due to t-PA inhibition can be seen in:
- Insulin resistance, when the pancreas must produce large amounts of insulin and proinsulin by feedback. If pancreatic reserve is inadequate, the result is diabetes mellitus. If the response is adequate, proinsulin stimulates the production of PAI-1 (plasminogen activator inhibitor 1. PAI-1 inhibits the formation of plasmin, whose function is to dissolve fibrin which makes up the clot. Obesity, certain infections and inflammations potentiate insulin resistance.
- Antiphospholipid antibody syndrome.
- PAI-1 4G/5G or 4G/4G polymorphism.
Some hypofibrinolysis indicators are:
- severe dysmenorrhea, because strong uterine contractions are necessary to expel undissolved clots.
- PCOS because plasmin is required to activate some metalloproteinases involved in ovary remodelling.
- early pregnancy losses, as some metalloproteinases involved in placental angiogenesis are activated by plasmin,
- preeclampsia and eclampsia, as metalloproteinases that dissolve elastic fibers of the placental vessels, to create a low flow resistance, are activated by plasmin. Vascular endothelial growth factor (VEGF), a protein that restricts glomerular porosity, is also activated by plasmin,
- sudden death and heart attack before age 50 in first degree relatives.
On physical exam, acanthosis, high body mass index, and in women, hirsutism and acne are indirect indicators of insulin resistance. Livedo suggest antiphospholipid antibody syndrome.
This study intents to investigate the prevalence of hypofibrinolysis markers, such as PAI-1 4G/5G and 4G/4G, protein S deficiency, antiphospholipid antibodies and prothrombin G20210A, in psychotic patients.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01487291
|Institudo de Psiquiatria da UFRJ|
|Rio de Janeiro, Brazil, 22290-140|
|Study Chair:||Antonio E Nardi, MD, PhD||Universidade Federal do Rio de Janeiro, Brazil|