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The placenta is often viewed as an immunologically passive organ either “camouflauged” to avoid immune surveillance or acting as a “sponge” to clear maternal anti-fetal antibodies. We and others have previously isolated low molecular weight lymphokines from human placental explant culture supernatants which would suggest a more active role of the placenta in modulating maternal immune responses (Lala et al., 1984). These include a 70–78 Kilodalton (KD) suppressor of IL-2 dependent cell proliferation (Main et al., 1985), and a 15–17 KD protein which on partial purification (by gel filtration and isoelectric focusing) and by biological activity is identical to adult monocyte-derived Interleukin-1 (IL-1) (Flynn et al., 1982). IL-1 is a key mediator of inflammatory responses leading to lymphocyte activation, systemic metabolic changes, elevated body temperature, local production of collagenase, and stimulation of fibroblast proliferation (Dinarello, 1984; Lachman, 1983). It is now known to be produced by a variety of cell types including monocytes, tissue fixed macrophages, keratinocytes, corneal epithelial cells, astrocytes, and renal mesangial cells. IL-1 is extraordinary potent, with biologic activity demonstrated in the 10-10M concentration range. This high specific activity has facilitated its detection in bioassays but because it is produced in such small quantities, purification and production of monoclonal antibodies has been difficult. We have measured placental IL-1 using both the mouse thymocyte assay and the newer, more sensitive IL-1 dependent tumor line assay. In this report, we address three issues: (1) Can villous tissue from early in gestation produce Interleukin-1? (2) Of the various cell types present in a human term placenta which are capable of producing IL-1? (3) How does the level of IL-1 production by placental cells compare to that produced by human peripheral blood monocytes?

We prospectively studied 40 women with preeclampsia and 26 women with normal pregnancy for the presence of platelet-bound and circulating platelet-bindable immunoglobulin and complement. Although only 12 patients with preeclampsia had a platelet count less than 150,000/mm3, 36 of 40 demonstrated an abnormal direct antiglobulin test, compared with only three of 26 control subjects (p less than 10(-8]. An abnormal indirect test was also detected in 30 of 40 patients with preeclampsia compared with five of 26 healthy pregnant control women (p = 9.3 X 10(-6]. Abnormal antiglobulin tests persisted for 2 to 6 weeks after delivery. Although each neonate had a platelet count greater than 200,000/mm3 at the time of delivery, 10 of 18 had an abnormal direct antiglobulin test compared with one of 14 control subjects (p = 0.0049). The high frequency of abnormal platelet antiglobulin tests in women with preeclampsia and their neonates may indicate an immune cause of certain aspects of the syndrome or may reflect the extent of platelet activation.

Serum iron was measured in 30 patients with pregnancy-induced hypertension and 24 normal pregnant women. The mean iron concentration was significantly higher in the group with pregnancy-induced hypertension (111 ± 26 μg/ml) than in the controls (69 ± 17 μg/ml) (p

A pregnant 36-year-old Vietnamese refugee with chloroquine-resistant Plasmodium falciparum infection was treated with pyrimethamine and a sulfonamide. This treatment produced rapid clearance of the patient's parasitemia and was associated with a resumption of normal fetal and uterine growth. Because the other drugs effective against chloroquine-resistant P falciparum may produce uterine stimulation (quinine sulfate) or damage the fetal skeleton (tetracyclines), the pyrimethamine-sulfonamide combination (with folinic acid supplementation) may be the best available choice for the treatment and prophylaxis of chloroquine-resistant P falciparum infection in pregnancy, despite its theoretical risk of teratogenicity. ( JAMA 1983;249:3207-3209)