Unexplained periparturient thrombocytopenia

Abstract

Since the advent of routine automated platelet counting we have observed unexplained periparturient thrombocytopenia (PPT) in an unexpected number of periparturient women, ie, during labor or within 24 hr postpartum. Mean +/- SD platelet count in 686 random blood donors was 236 +/- 50 X 10(9)/L and 1.02% had a platelet count less than 136 X 10(9)/L; in 2,204 random prenatal and postpartum women mean count was significantly higher (275 +/- 86 X 10(9)/L; p less than 0.001). Of 1,621 periparturient women, 74 (4.6%) had unexplained PPT (mean +/- SD platelet count 122 +/- 24 X 10(9)/L, range 21-135 X 10(9)/L, N = 74). Platelet count in PPT usually rose to normal within 1 week of delivery; in 10% thrombocytopenia persisted greater than 6 months. PPT occurred in successive pregnancies with normal intervening platelet counts. Nine of 34 newborns of mothers with PPT were thrombocytopenic; there was no correlation between mother's and baby's platelet counts. In no case of PPT was there excessive bleeding in mother or infant. Positive indirect platelet radioactive antiglobulin tests (PRAT) were seen in 11% of normal postpartum women and in 90% of 22 women with PPT; 65% of the positive tests in PPT were due to reactions with anti-C3 only. In contrast, pregnant women with autoimmune thrombocytopenic purpura (AITP) had positive PRAT primarily because of anti-IgG (+/- anti-C3); only 10% were positive only with anti-C3. Results were concordant in all of eight women with PPT tested by both indirect and direct PRAT. Amount of C3 bound per platelet in direct or indirect PRAT was not predictive of degree of thrombocytopenia, but there was correlation of fg C3 per platelet detected by the two assays in individual patients (r = 0.8). Mean levels of serum C3, C4, and factor B in women with PPT did not differ from normal; individual patients had abnormal serum complements but no characteristic pattern was observed. Increased immune complexes were observed in 6% of normal subjects and 33% of women with PPT. Etiology and mechanism of PPT is unclear. Despite lack of clinical evidence in women with PPT of syndromes associated with increased platelet destruction, the presence of preeclampsia cannot be absolutely excluded. Similarly, although the pattern of antiglobulin sensitization in PPT differed markedly from that seen in AITP, autoimmune disorder cannot be excluded. Alloantibodies did not appear to be responsible for PPT. While PPT is usually benign, some patients had a markedly reduced platelet count. Recognition of the phenomenon may be important in obstetrics.

Relation between Gestational Thrombocytopenia and the Syndrome of Hemolysis, Elevated Liver Enzymes, and Low Platelet Count (HELLP Syndrome)

“…10 9 /l and ^135 ! 10 9 /l, respectively) in the peripartum phase [4,5], giving rise to a new clinical entity, 'gestational thrombocytopenia' [6]. In a recent longitu-dinal cohort study, we found that similar percentages of women exhibited similar and significant increases or decreases in the platelet count during the third trimester, which would explain why the mean platelet count reportedly shows no apparent change during normal pregnancy [7].…”

Obstetric prognosis of the gestational thrombocytopenia

“…Although the pathogenesis of GT has not yet been determined, accumulating clinical experience indicates that GT is of limited obstetric or hematologic signi cance, either to the mother or to the newborn. However, the basis for this perception is derived from studies using the standard cutoff value of 150,000/ mm 3 for de ning thrombocytopeni a [4,5,8,9,12,13]. Our study using a cutoff value of 100,000/ mm 3 showed GT was virtually asymptomatic during pregnancy and delivery, and there was no severe neonatal thrombocytopenia .…”

“…After exclusion of these cases, there remains a group of women who have persistent thrombocytopenia with no identi able cause. This condition has been called epidemic [8], periparturitiona l [9], incidental [4], gestational [10], asymptomatic [11], and pregnancy-associate d thrombocytopeni a [12].…”

“…We performed PUBS in the 7 women with GT and an emergency cesarean section in 1 case was done due to the complication of PUBS-induced severe fetal bradycardia. [9] 1986 < 135,000 14 / 34 0 Nagey [15] 1986 < 150,000 2/ 14 0 Burrows [4] 1988 < 150,000 12 / 300 0 Kaplan [11] 1990 < 150,000 4/ 31 1 Matthews [12] 1990 < 150,000 3/ 40 0 Samuels [16] 1990 < 150,000 3/ 74 0 Copplestone [6] 1992 < 120,000 0/ 14 0 Jaschevatzky [17] 1994 < 100,000 0/ 19 0 Anteby [18] 1994 Anteby and Shalev [18] reported that maternal thrombocytopenia resolved spontaneously to more than 150,000 / mm 3 in eighteen patients within 1 month postpartum, in ve within 3 months postpartum, and in two as late as 5 months after delivery among 26 pregnancies with GT. They also showed recurrence of thrombocytopenia in four patients in the same study: three in the context of a subsequent pregnancy and in one patient who developed ITP.…”

Platelet reactivity in twin pregnancies

“…This may explain why gestational thrombocytopenia is more likely to occur in twin than in singleton pregnancy. The 10 th percentile value (137×10 9 /l) of platelet count before delivery for twin pregnancies [6] corresponds to the 3 rd -4 th percentile value for singleton pregnancies [5,24,25]. Gestational thrombocytopenia of less than 100×10 9 /l was seen in 17% of twin pregnancies [26], while its rate was less than 1.0% of singleton pregnancies [27].…”