Hemostatic alterations in patients with acute, unilateral vestibular paresis.
OBJECTIVE
The etiopathogenesis of acute unilateral peripheral vestibulopathy (APV) still remains a matter of debate; ischemic changes in the circulation of the labyrinth may play a role. We consequently looked for possible hemostasis alterations in a group of patients with APV of an unknown nature.


METHODS
We evaluated blood parameters known to be involved in circulation disorders, including total and HDL cholesterol, triglycerides, apolipoprotein A and B, lipoprotein(a), homocysteine, folate, prothrombin time, activated partial thromboplastin time, fibrinogen, D-dimer, antithrombin III, protein C, protein S, activated protein C resistance, and anticardiolipin IgG and IgM antibodies. A series of 23 patients affected with APV were consecutively referred to our department, in the acute phase, before treatment, and in the follow-up phase after 4 to 6 weeks of pharmacologic washout. The aforementioned blood parameters were also measured in a series of 15 patients with Menière's disease.


RESULTS
The patients with APV in the acute phase compared with the patients with Menière's disease in the acute phase exhibited increased plasma levels of fibrinogen (mean, 338.3 +/- 135.9 SD vs 271.3 +/- 69.8 SD mg/dL, P = 0.05), increased plasma levels of D-dimer (mean, 320 +/- 207.8 SD vs 226.7 +/- 138.7 SD NG/mL), enhanced plasma levels of lipoprotein(a) (41.4 +/- 38.6 SD vs 16 +/- 18.2 SD mg/dL, F = 5.67, P = 0.02), high leukocyte count (9.1 +/- 2.7 SD vs 6.5 +/- 1.3 SD x 10(3)/microL; F = 8.42, P < 0.006), and low serum folate concentration (5.3 +/- 1.8 SD vs 7.1 +/- 2.7 NG/mg; F = 4.34, P = 0.04). During follow-up the prothrombin time was prolonged (F = 4.34, P = 0.04) and leukocyte count decreased (F = 7.39, P < 0.019) in the APV patients, whereas fibrinogen, D-dimer, lipoprotein(a), and folate were unchanged.


CONCLUSIONS
Our results provide evidence suggesting an involvement of the hemostatic system in APV.
Department of Neuroscience, ENT Unit, University of Pisa, Italy. bfattori@ent.med.unipi.it
B
B
Fattori
A
A
Nacci
A
A
Casani
R
R
Cristofani
A
A
Sagripanti
D000208:Acute Disease; D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000097:blood; D001053:Apolipoproteins / Q000097:blood; D002784:Cholesterol / Q000097:blood; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products; D005492:Folic Acid / Q000097:blood; D005500:Follow-Up Studies; D006487:Hemostasis / Q000502:physiology*; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007075:Immunoglobulin M / Q000097:blood*; D008297:Male; D008575:Meniere Disease / Q000097:blood / Q000453:epidemiology; D008875:Middle Aged; D010291:Paresis / Q000097:blood* / Q000453:epidemiology / Q000209:etiology; D015995:Prevalence; D011517:Prothrombin Time; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood; D014715:Vertebrobasilar Insufficiency / Q000150:complications; D014722:Vestibule, Labyrinth / Q000098:blood supply
D017153:Antibodies, Anticardiolipin; D001053:Apolipoproteins; D005338:Fibrin Fibrinogen Degradation Products; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D014280:Triglycerides; C036309:fibrin fragment D; D006710:Homocysteine; D005492:Folic Acid; D002784:Cholesterol