Epidural anesthesia in pregnant patients with low platelet counts.

A number of patients demonstrate thrombocytopenia in the peripartum period. One hundred four patients with unexplained transient periparturient thrombocytopenia were found over a nine-month period. Sixty-one of them received epidural anesthesia without neurologic sequelae. Epidural anesthesia is safe if the platelet count exceeds 100 x 10(9)/L in otherwise healthy women.

Unexplained periparturient thrombocytopenia.

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.

Autoimmune hemolytic anemia with concurrence of warm and cold red cell autoantibodies and a warm hemolysin.

This report describes the laboratory findings and clinical course of a patient with thrombophlebitis, venous gangrene, and autoimmune hemolytic anemia. Three concomitant red cell autoantibody activities were detected: a low-titer, high-thermal-amplitude, IgM anti-I cold agglutinin; an IgG warm 'incomplete' panagglutinating autoantibody; and an IgM warm hemolysin.

Bacteriocin and flow cytometry in laboratory diagnosis of leukemic peripheral blood lymphocytes and bone marrow cells.

The bacteriocin, colicin HSC10, produced by Escherichia coli HSC10, was studied as a laboratory tool for detection and differentiation of leukemic from normal lymphocytes in human peripheral blood. Flow cytometry studies detected DNA loss in bacteriocin-affected cells by computerized histograms. Differential analysis is given for the peripheral blood of 26 individuals using bacteriocin, cytochemistry and surface markers. Sensitivity to colicin was detected in 10 (83%) of the 12 patients with chronic lymphocytic leukemias and other leukemias with morphologically immature lymphocytes. Cells were lost from the G0/G1 phase and accumulated in the 'pre-G1' channels of the histogram, indicative of cells with reduced DNA content. The lymphocytes of 14 normals, however, were not or only slightly affected by the bacteriocin (P less than 0.001). Similarly, normal bone marrow cells exposed to bacteriocin remained unaffected (P greater than 0.2). Thus, immaturity per se was not recognized by bacteriocin. The bacteriocin effect was more discriminatory than other laboratory tests reported here and in most cases differentiated malignant from normal cells.

Variants of an interspecies hybridoma with altered tumorigenicity and protective ability against mouse myeloma tumors.

Recent isolates of RX54-3 hybridoma cells (new cells) protect BALB/c mice against subsequent challenge with the tumorigenic myeloma parent cells used to construct this hybridoma. In contrast, hybridoma cells which have been maintained in tissue culture for long periods of time (old cells) are not protective. In the present study, we compared a number of properties of the new and old hybridoma cells and determined which line was more similar to the parent myeloma. We found that new hybridoma cells resembled myeloma cells in: (a) possessing A- and C-type viral particles on transmission electron microscopy and a relatively smooth surface on scanning electron microscopy; (b) being sensitive to a hypotonic solution containing the dye propidium iodide; (c) having similar DNA histograms on flow cytometric analysis; (d) being sensitive to the bacteriocin colicin HSC 10; and (e) being tumorigenic in nude mice. In contrast, old hybridoma cells differed in all of these characteristics from new hybridoma and myeloma cells. Therefore, in order to protect against challenge with the tumorigenic myeloma parent, hybridoma cells must retain properties of that parent.