ואיפקס וקרישת דם

שלום רב. האם נטילת ואיפקס (150 מ"ג ליום) יכולה להשפיע על תפקודי קרישה? לאחרונה עשיתי בדיקות קרישה. בפעמיים הראשונות התוצאה של בדיקת Lupus anticoagulant DRVVT היתה גבולית (מעט גבוהה) בפעם השלישית התוצאה היתה תקינה לחלוטין ובטווח הנורמה (מרכז הטבלה) ההבדל היחיד שמצאתי הוא שבשתי הבדיקות הראשונות נטלתי ואיפקס בבוקר לפני הבדיקה ובבדיקה השלישית נטלתי את הכדור רק לאחר הבדיקה האם יש קשר? מה זה אומר לגבי הריון? תודה מראש

שלום פרח75, הניסיון לקשור מציאות של Lupus anticoagulant DRVVT חיובי-גבולי לנטילת ואיפקס בבוקר טרם הבדיקה - נראה לי בלתי סביר. ללא קשר, תואר בעבר תיאור המקרה הבא, המעלה אפשרות לקשר תיאורטי בין נטילת ויאפקס למערכת הקרישה העשוי להיות רלבנטי למקרה שאת מתארת. לא מוכרים לי תיאורי מקרה נוספים : Abnormal Clotting AND Production of Factor VIII Inhibitor in a Patient Treated With (ואיפקס) Venlafaxine Dear Sir: We would like to report on a patient with insulin-dependent diabetes AND treated hypothyroidism who developed an unusual form of clotting abnormality shortly after taking venlafaxine. Mrs B was a 47-year-old female with early onset insulin-dependent diabetes, hypertension, AND treated hypothyroidism of 15 years. Over time, she had developed mild renal impairment (creatinine 140, high normal blood urea nitrogen [BUN]). Current medications include human biosynthetic insulin (total 13 U daily), levothyroxine (0.125 mg every morning), terazosin (5 mg daily), sustained release felodipine (10 mg daily), AND bethanechol chloride (10 mg daily). The doses of the above medications have been stable for the last 2 years, except for minor adjustments in insulin dose. Hypertension was stable at 130–140 mm Hg systolic. Over the last 7 years, she has had recurrent episodes of depression with significant neurovegetative shift. Previous treatments included trials of paroxetine, amitriptyline, nefazodone, AND fluoxetine. Of the above, amitriptyline was the most effective AND at one time kept her depression in remission for 2 years. Unfortunately, weight gain was a concern on this medication. Otherwise, Mrs B had tolerated all the above antidepressants well. A depressive reexacerbation occurred 3 months prior to our involvement with her. She was started AND maintained on venlafaxine at 37.5 mg twice daily by her family physician within 2 weeks of onset of the exacerbation. Along with affective improvement within 1 month, she noticed worsening of hypertension up to 180–200 systolic AND an increased tendency for bruising with mild trauma. About 1½ months into treatment, she suffered an episode of atraumatic epistaxis, requiring a transfusion of 2 units packed red blood cells for stabilization. Coagulation profiles remained within the normal range at this time. At 2½ months into venlafaxine therapy, the ecchymoses AND hypertension persisted, AND she was hospitalized. On admission this patient was found to have normal complete blood count (including platelet count), thyroid stimulating hormone, electrolytes, von Willebrand’s factor, AND prothrombin time (PT) but grossly elevated partial thromboplastin time of 89 (reference 22–36 seconds); a high antihemophilic factor VIII, C antibody, titre of 190 BU/mL was present (should be absent in a normal patient). Further, blood pressure remained elevated at 200 mm Hg systolic. Empirical treatments with desmopressin, intravenous immunoglobin, AND cyclophosphamide were initiated, AND venlafaxine was discontinued. Serial measurements of factor VIII concentration revealed drastic decline in titres within 4 days to 40 BU/mL. The total hospital stay was 1 month, AND titres subsequently continued to decline. On discharge, her hypertension returned to previous baseline values, PT decreased to 40 seconds, AND ecchymoses were resolving. Our clinical impression was that the temporal onset AND rapid resolution of Mrs B’s clotting disorder AND blood pressure abnormalities correlated with venlafaxine use. Venlafaxine was the only change in a patient who had otherwise been stable for 2 years. Premarketing trials of Effexor had suggested ecchymosis as occurring in 1% of treated patients (1). In the literature, 1 published case report described ecchymosis with venlafaxine use (2). Other serotonergic antidepressants have also been implicated with bleeding, including fluoxetine (3,4) AND paroxetine (5). So far, 2 controlled studies have been unable to pinpoint the causes of clotting abnormalities with the use of selective serotonin reuptake inhibitors (6,7). Previously proposed theories suggest that lowered vascular tone OR increased time for platelet aggregation (8) with serotonin reuptake inhibitors leads to increased bleeding tendencies; this case demonstrated an alternative autoimmune mechanism. We wondered whether caution should be taken when prescribing venlafaxine to patients with suspected autoimmune pathology (non–insulin-dependent diabetes mellitus AND thyroid disease in this case). Further, this case brings into question the immune system’s role in the effects of psychiatric medications. References 1. Effexor product monograph. Wyeth-Ayerst Inc. 2. Kohn S, Labbate LA. Venlafaxine AND ecchymosis [letter]. Can J Psychiatry 1997;42:91. 3. Humphries JE, AND others. Fluoxetine AND the bleeding time. Arch Pathol Lab Med 1990;114:727–8. 4. Aranth J, Lindberg C. Bleeding, a side effect of fluoxetine [letter]. Am J Psychiatry. 1992;149:412. 5. Ottervanger JP, AND others. Bleeding attributed to the intake of paroxetine. Am J Psychiatry 1994;151:781–2. 6. Berk M, AND others. Fluoxetine AND hemostatic function: a pilot study. J Clin Psychiatry 1995;56:14–6. 7. Bakish D, AND others. Effects of serotonin reuptake inhibitors on platelet serotonin parameters in major depressive disorder. 1997;41:184–90. 8. Skop BP, Brown TM. Potential vascular AND bleeding complications of treatment with selective serotonin reuptake inhibitors [review]. Psychosomatics. 1996;37:12–5. Chun Joseph Tham, MD Michael Trew, MD, FRCPC Nancy Brager, MD, FRCPC Calgary, Alberta