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שלום אני בהריון בשבוע ה- 12 בבדיקת דם עלה כי סוג דמי - מינוסA וכי יש לי נוגדן בשם CW בערך של titer 1:16 מהו הנוגדן הנ"ל? תודה רבה

Cw הוא אנטיגן (חלבון) מקבוצת RH. שכיחותו קטנה והוא מצוי אצל אוכלוסיות נורדיות בכ- 8% מהאוכלוסיה בלבד ואצל אמריקאים /אירופאים / לבנים רק בכ- 2.5% מהאוכלוסיה. אצלך אין אנטיגן זה כנראה ויש לך נוגדנים נגדו בכייל נמוך. אם קיבלת דם בעבר - אולי זו תוצאה של העירוי ואם לא קיבלת דם בעבר, הנוגדן הזה יכול להופיע בצורה ספונטנית או בעקבות הריון קודם. המשמעות תלויה בסוג הדם של העובר. אם יש לו את האנטיגן Cw עלולה להיות אצלו המוליזה בתגובה לנוגדנים שלך. לכן, קודם לכל יש לבדוק את סוג הדם של בעלך ולראות אם הוא Cw חיובי ואם יש אפשרות שהעובר יהיה Cw חיובי. אולי גם לבדוק סוג דם של ילדים קודמים, אם יש לך עוד ילדים. אם יש סיכוי שלעובר יש Cw חיובי צריך יהיה לנטר את ההריון ולעקוב אחר צלילות מי השפיר (כמדד להמוליזה אפשרית). Vox Sang 1993;64(4):226-30 Maternal CW alloimmunization. Bowman JM, Pollock J. Department of Pediatrics and Child Health, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. The Winnipeg Rh Laboratory has reviewed its experiences with maternal CW alloimmunization. From September 24, 1956, to March 31, 1992, 12 women with significant CW alloimmunization underwent 18 pregnancies. In 3 (4 pregnancies) the antibody, despite its strength, was 'naturally occurring' (i.e. there was no known exposure to CW-positive red cells). The remaining 9 women (14 pregnancies) had CW-positive husbands. Two had CW-negative babies and a third infant, probably CW negative, was stillborn and macerated at 43 weeks gestation. Eleven babies were CW positive and had hemolytic disease of the newborn (HDN), with antiglobulin-positive red cells. Five did not require treatment; 2 needed phototherapy only, and 4 (born between 1956 and 1963) required exchange transfusions. No anti-CW screening was carried out until 1977; thereafter it was sporadic, 11 of 51 screening red cells being CW positive in the 39-month period ending March 31st, 1992. From November 1, 1977, to March 31, 1992, 24 women (30 pregnancies, 31 conceptuses) with insignificant anti-CW alloantibodies were identified. Extrapolating these figures to the entire period from September 24, 1956, to March 31, 1992, we estimate that at least 430 women (at least 573 pregnancies) were CW alloimmunized, most of the antibodies being 'naturally occurring'. Only 2% of the conceptuses were CW positive and affected; none were severely affected. Anti-CW is relatively common, occurring in about 1 pregnant Manitoban woman in 1,100. On very rare occasions (11 times in Manitoba in 36 years and 5 months) anti-CW HDN occurs which, although not severe, may end in kernicterus with brain damage or neonatal death unless it is detected promptly and treated appropriately. ******************************************** Am J Perinatol 1999;16(6):277-81 Use of a PCR-based assay for fetal Cw antigen genotyping in a patient with a history of moderately severe hemolytic disease of the newborn due to anti-Cw. Reiner AP, Teramura G, Aramaki KM. Department of Medicine, University of Washington, Seattle 98195, USA. Anti-Cw is an uncommon cause of clinically significant hemolytic disease of the newborn (HDN). We report an unusually severe case of HDN due to anti-Cw that required phototherapy and exchange transfusion. We also describe a novel PCR-RFLP method for Cw typing of fetal genomic DNA that was used for prenatal diagnosis in a subsequent pregnancy. Following PCR amplification of a 163 bp segment of the RHCE gene containing the nucleotide 122 G to A substitution that corresponds to the Cw allele, Cw types were distinguished by TaqI digestion. PCR-RFLP analysis confirmed that the father and previously affected child were Cw-positive. The fetus was Cw-negative, thus excluding HDN in the current pregnancy and obviating the need for further invasive or noninvasive diagnostic procedures for the remainder of the pregnancy. This case illustrates the utility of PCR-based fetal genotype determination in pregnancies at risk of HDN due to uncommon red cell antibodies such as anti-Cw. *************************************

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