American Journal zyxw of Hematology 46:151-167 (1994) z LETTERS AND CORRESPONDENCE Letters and correspondence submitted for possible publication must be identified as such. Text length must not exceed zyxwvuts 500 words and five bibliographic references. A single concise figure or table may be included if it is essential to support the communication. Letters not typed double-spaced will not be considered for publica- tion. Letters not meeting these specifications will not be returned to authors. Letters to the Editor are utilized to communicate a single novel observation or finding. Correspondence is to be used to zyxwvuts sup- plement or constructively comment on the contents of a publication in the journal and cannot exceed the restrictions for Letters to the Editor. The Editor reserves the right to shorten text, delete objec- tional comments and make other changes to comply with the style Of the journal. Permission for publication must be appended as a post- script. Submissions must be sent to Marcel E. Conrad, M.D., ASSO- ciate Editor, American Journal of Hematology, USA Cancer Center, Mobile, Alabama 36688 to permit rapid consideration for publica- zyxwvuts We have performed a retrospective study concerning 187 pregnancies from 68 women recently diagnosed of heterozygous deficiencies in AT-I11 (n = 12), PC zyxwvu (n = 21), PS (n = 21), plasminogen (n = 12), or heparin cofactor I1 (n = 2). The diagnostic criteria have been described in detail [4]. A group of 5 pregnancies (3 in AT-111, 1 in PC, and 1 in PS deficient women) was excluded because they received a prophylactic anticoagulant treatment during pregnancy or post-partum. Eight miscarriages were ob- served (7 in AT-I11 and 1 in PC deficiency), none of them associated to thrombosis. A total of 21 episodes of clinical thrombosis during pregnancy (n = zyxwvu 6) or post-partum (n = 15) were recorded: 3 superficial vein thrombo- sis, 16 deep vein thrombosis and/or pulmonary embolism, and 2 cerebral thrombosis. All the thrombotic episodes occurred within the second or third trimester of pregnancy or during the first month after delivery. Thirteen of the 68 women had antecedent of thromboemholic episode(s) non-related to pregnancies. The results of our study are shown in Table I. The global estimated risk tion. of clinical thrombosis in women with heterozygous hereditary thrombo- philia (symptomatic and asymtomatic), is clearly increased during preg- nancy and/or post-partum (1 1%). It should be noted that the risk of patients with previous antecedent of thromboembolic episodes (19%) is twice those without such antecedent (9%). Similarly to previous studies [1,2], we observe that incidence of thrombosis is higher in the post-partum than during pregnancy (15 vs. 6 cases) in AT-111, PC, and PS deficient women z (P < .01). The pregnancies from women with AT-I11 deficiency had three times higher risk of thromboembolic complications than PC and PS defi- Risk of Thrombosis During Pregnancy and Post-Partum in Hereditary Thrombophilia To the Editor: While it is generally believed that the combination of preg- nancy and hereditary thrombophilia predisposes to thrombosis, the magni- tude of the interaction is not clear. Only a few data have been published on this subject [I-31, and it should be kept in mind that the rates of throm- boembolic complications related to pregnancy or puerperium probably rep- resent overestimates, attributable to report biases in the literature for sub- jects from families with the most severe thrombotic diatheses. Accordingly, the real risk of thrombosis needs to be defined, as does the period of increased risk. Additionally, it is also unknown if the several causes involved in hereditary thromhophilia (antithrombin 111, protein C, protein S, heparin cofactor 11, and plasminogen deficiencies) are associated to the different risks of thromhoembolism during pregnancy or post-parturn. ciencies. Concerning women with protein C and S deficiencies, they ap- peared to have a similar risk of thrombosis during pregnancy and/or post- partum. On the other hand, no complications were seen in 26 pregnancies from 11 women with plasminogen defiency, and in 4 pregnancies from 2 heterozygous women for heparin cofactor 11. These data are not surprising, because heterozygozity for heparin cofactor I1 or plasminogen is unlikely to be in itself a clear risk factor for thrombosis [5]. In conclusion, this retrospective study suggests the existence of an im- portant risk of clinical thrombosis related to pregnancy and/or post-partum in heterozygous women (symptomatic and asymptomatic) for AT-111, PC, or PS deficiencies. As expected, antecedent of thromboembolism compli- cations increase the risk of thrombosis. These data support the prophylactic TABLE 1. Risk of Thrombosis During Pregnancy or Post-ParIum in Women With Hereditary Thrombophilia Total cases No antecedent of thrombosis Antecedent of thrombosis Thrombosisin Deficiency Women Pregnancies Thrombosis" Women Pregnancies Thrombosis" Women Pregnancies Thrombosis" Pregnancies Post-Darturn AT-I11 12 26 8 (31) 10 24 7 (29) 2 2 1 (50) 3 5 Pc 21 71 7 (10) 16 42 2 (5) 5 29 5 (17) 2 5 PS 21 55 6 (1 1) 17 46 4 (9) 4 9 2 (22) 1 5 Plasminogen 12 26 - 11 25 - 1 1 Heparin 11 2 4 - 1 2 - 1 2 - - - - - - cofactor Total cases 68 182 21 (11) 55 141 13 (9) 13 41 8 (19) 6 15 "Parentheses show percentage of thrombosis with respect to the number of pregnancies. zyxwvut 0 1994 Wiley-Liss, Inc.