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INHIBITION OF SPECIFIC BINDING OF ANTIBODY TO THE RHO(D) FACTOR OF RED CELLS IN ANTIBODY EXCESS.

The uptake by red cells of I(131)-labeled nonagglutinating antibody to the Rh(0)(D) factor was dependent on the proportion of cells to antibody during sensitization. Inhibition of antibody binding by red cells in the region of antibody excess occurred with Rh(0)(D) positive red cells that were both papain modified and untreated; the inhibition was independent of the Rh phenotype.

Antibodies↗

Underutilization of Rh prophylaxis in the emergency department: a retrospective survey.

STUDY OBJECTIVE: To determine the practice of emergency physicians with regard to the issue of Rh isoimmunization. DESIGN: A retrospective chart review. SETTING: A university-affiliated tertiary care hospital emergency department. TYPE OF PARTICIPANTS: Pregnant women presenting with a risk factor for Rh sensitization. MEASUREMENTS AND MAIN RESULTS: One hundred thirty-eight patient encounters were analyzed descriptively as to whether they were candidates for Rh immune prophylaxis, and if so, whether it was given. Most (68%) were hospitalized. Of those, all were Rh typed, but two patients were not given Rh immune globulin (RhIG) when indicated. Of those discharged from the ED, most (86%) were not Rh typed, and none was administered RhIG. CONCLUSION: This study demonstrates a need for increased attention to the potential for Rh isoimmunization in patients presenting to the ED.

Abortion, Spontaneous↗

Effect of recombinant tumor necrosis factor on tumoricidal activation of murine macrophages: synergism between tumor necrosis factor and gamma-interferon.

The activation of tumoricidal murine macrophages by recombinant human tumor necrosis factor (rH-TNF) alone or in combination with recombinant murine gamma-interferon (rM-IFN-gamma) was examined. When used alone, rH-TNF (10(-1)-10(5) units/ml) did not induce macrophage tumoricidal activity against TNF-insensitive P815 mastocytoma cells. Combining rH-TNF with rM-IFN-gamma resulted in the synergistic induction of tumoricidal activity in resident peritoneal macrophages. This synergistic effect was not due to contaminating bacterial lipopolysaccharide. A comparative study using recombinant murine tumor necrosis factor (rM-TNF) showed that rM-TNF alone also could not stimulate murine macrophages and there was no significant difference between effects of rM-TNF and rH-TNF on macrophage activation in the presence of rM-IFN-gamma. In experiments comparing sequential to simultaneous exposure of macrophages to rH-TNF and rM-IFN-gamma, it was found that: (a) when macrophages are primed with rM-IFN-gamma, rH-TNF serves only as a very weak triggering signal for tumoricidal activation; and (b) marked activation is obtained only when macrophages are exposed to the two cytokines simultaneously. These results suggest that TNF has an autocrine regulatory function in concert with lymphokines in macrophage-mediated host defense against tumors.

Animals↗

Randomized comparison between antibiotics alone and antibiotics plus granulocyte-macrophage colony-stimulating factor (Escherichia coli-derived in cancer patients with fever and neutropenia.

PURPOSE: A prospective, randomized study was conducted to determine if recombinant human granulocyte-macrophage colony-stimulating factor (rh-GMCSF) (Escherichia coli-derived) could improve response rates to antibiotic therapy and shorten the duration of neutropenia in cancer patients. PATIENTS AND METHODS: A total of 107 febrile neutropenic cancer patients were randomly assigned to empiric therapy with ticarcillin-clavulanate (4 g ticarcillin + 0.1 g clavulanate i.v. every 4 hours) plus netilmicin (2 mg/kg i.v. every 8 hours) with or without rh-GMCSF (3 micrograms/kg per day i.v.). Clinical improvement, duration of neutropenia, and toxicity were monitored. RESULTS: Addition of rh-GMCSF to the antibiotics significantly improved the response rate (96% versus 82%, P = 0.03), but not the survival rate (93% versus 93%), in the evaluable patients. This difference in response rate was not significant when considering all patients in an intent-to-treat analysis. The number of patients who recovered from severe neutropenia ( < 100 cells/microliter) during the period of observation in the study was significantly greater among patients receiving the colony-stimulating factor, although the median duration of neutropenia was not affected. Superinfections and subsequent infections were not significantly different among the two treatment regimens. Side effects were more common among patients treated with the colony-stimulating factor. CONCLUSIONS: Our data do not support the routine administration of rh-GMCSF with antibiotics for patients with fever and neutropenia. Further studies should be conducted to identify those patients most likely to benefit from rh-GMCSF therapy, such as patients with persistent profound neutropenia and refractory infections.

Adolescent↗

Ovenstone Factor in the management of Rh sensitization.

Several methods have been developed for analyzing amniotic fluid to aid in the management of rhesus isoimmunization. Because all methods attempt to predict the severity of fetal hemolysis based on the original findings of Bevis and on the amount of unconjugated bilirubin in amniotic fluid as measured by its optical density at 450 millimicron, they share two possible sources of error: calculation of exact gestational age and accurately reading bloody or contaminated amniotic fluid. The Ovenstone Factor measures the derivative of the bilirubin curve against wavelength and thereby avoids some of the contaminating pigments at 450 millimicron. This paper compares the predictive accuracy of two methods, Liley versus Ovenstone Factor, in 78 samples of fluid from 46 patients. Predictions were correct in 80% of infants using Ovenstone Factor and 67% using the Liley curve, and incorrect in only 7% and 13%, respectively. The Ovenstone Factor, with its simplicity and high predictive accuracy, is an excellent additional tool in the management of Rh-sensitized pregnancies.

Amniotic Fluid↗