קרישיות יתר

דיון מתוך פורום  המטולוגיה

01/11/2002 | 00:41 | מאת: דורית

בעקבות אבחנה של קרישיות יתר אצל בתי, שנפתרה ע"י הפסקת גלולות למניעת הריון, התחלתי בברור קרישיות אצלי. אני בת 53 ומקבלת הורמונים (מדבקת אוורל 50מ"ג) עקב גלי חום קשים כ-6 שנים.(אין לי שחלות). בבדיקות התקבלו התוצאות הבאות: pt%=120 pt-sec=10.0 pt-inr=0.93 aptt-sec=31 antithrombin-3=93 protein c activity=136 apcr ratio=2.2 PROTEIN S ACTIVITY=46 prot-s-antigen free=66 prot-s antigen=88 lac screen fsl=1.21 אני עומדת לטוס לארה"ב בעוד שבועיים.האם אוכל לטוס?האם עלי להתחיל לקחת אספרין?האם להפסיק את ההורמונים? ברור לי שאני צריכה ברור יסודי ע"י המטולוג, אך שבועיים הם זמן קצר. אודה על תשובתך דורית

לקריאה נוספת והעמקה
01/11/2002 | 01:47 | מאת: תשובת מנהל הפורום

הרמה של פעילות פרוטאין S נמוכה ואולי גם הרמה של FREE פרוטאין S (תלוי בנורמה של המעבדה). אם זה נכון זה מהוה סיכון לקרישיות יתר. אבל, רמה נמוכה של פרוטאין S חופשי יכולה להיות בהריון וגם בעת נטילת הורמונים חליפיים (HRT). לכן נראה שאולי יש מקום לביצוע בדיקה חוזרת לאחר הפסקה של ההורמונים. מה לעשות לגבי הנסיעה ? איני יכול לייעץ לך בנושא זה מסיבות ברורות. עלייך לפנות לרופא ולקבל ממנו הנחיות מושכלות ומבוססות. http://www.psbc.org/medical/labs/coagulation/_frm/frm_thrombosis05.htm http://www.contemporaryobgyn.net/hostedfiles/features/low_dose_hrt/dt09.htm ***************************** Menopause September-October 2001 (Volume 8, Number 5) Comparison of Transdermal and Oral Estrogen-Progestin Replacement Therapy: Effects on Cardiovascular Risk Factors Chen FP, Lee N, Soong YK, Huang KE Menopause. 2001;8(5):347-352 This article assesses the associations between oral and transdermal combined hormone replacement therapy (HRT) and physiologic variables related to cardiovascular risk. Forty-one postmenopausal women volunteered for this study; their average age was 52 years. They were randomly assigned to 1 of 2 treatment groups. Group 1 (n = 20) received oral sequential combined formulation of estradiol (E2) valerate (2 mg/day for 21 days) plus cyproterone acetate (CPA) (1 mg/day for 10 days -- day 11 to day 21) and no medication for 7 days. Group 2 (n = 21) received transdermal 17-beta E2 combined with 5 mg of medroxyprogesterone acetate (MPA) from day 13 to day 24 followed by no medication for 7 days. All participants completed 12 cycles of HRT use. After 12 months of treatment, there was a reduction of total cholesterol and LDL-C concentration in both groups, and there were no differences between the 2 groups. HDL-C levels were significantly increased in group 1 (oral estradiol), and there were no significant changes with HDL-C in group 2 (transdermal estradiol). The between-group difference was statistically significant (P < .01). The reduction in the atherogenic indices (total cholesterol/HDL-C and LDL-C/HDL-C) was more pronounced in group 1 than in group 2 (P < .05). Triglycerides decreased in group 2 (P < .05) but did not change significantly in group 1, and the between-group differences in treatment effects on triglycerides were statistically significant (P < .01). There were also reduced levels of tissue plasminogen activator (TPA), plasminogen activator inhibitor-1 (PAI-1), antithrombin III, and protein S in both groups after 12 months of treatment, with no significant difference between the 2 groups. There was an increase in protein C levels in both groups, and factor VII was reduced in group 2. The between-group difference for factor VII was statistically significant. Clinical Commentary This article shows that both oral and transdermal HRT change lipoprotein metabolism and fibrinolytic activity toward a more beneficial profile. Whether HRT will reduce cardiovascular disease is still a subject of debate, and we await the outcomes of the long-term trials (ie, the Women's Health Initiative and WISDOM trials). Deficiencies of antithrombin III, protein C, and protein S do predispose persons to venous thromboembolism. Both oral and transdermal HRT showed a trend toward procoagulation in the first year of HRT use. The adverse effects of HRT on antithrombin III and protein C have been reported to subside after 12 months of treatment. It is suggested that transdermal HRT should be used for those women with defects in triglyceride metabolism and coagulation factors. When prescribing either oral or transdermal HRT, clinicians should consider the risk of venous thromboembolism, especially in the first year of treatment, and should measure levels of protein S and other antithrombotic factors. Of note is that this study is limited: there was no control group, the sample size was small, and both a different estrogen and a different progestogen were utilized in the oral and transdermal groups.

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