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Biomedical subjects

P A Arndt

Publications and source records attributed to P A Arndt.

At least 19 recordsLinked to original sources
PubMed2005

Late onset neonatal anaemia due to maternal anti-Ge: possible association with destruction of eythroid progenitors.

There have been no reports of severe haemolytic disease of the newborn (HDN) due to Gerbich (Ge) antibodies. Two babies with HDN due to anti-Ge3, both born to the same mother, are described. The anti-Ge appeared in the first pregnancy and was not detectable in the first trimester, the babies' reticulocyte and bilirubin values were not greatly elevated (similar to HDN due to Kell antibodies), and the anaemia in both cases was either not apparent or not severe until 2 to 4 weeks after birth. Ge antigens are found on glycophorins (GPs) C and D; GPC, like Kell, has been shown to be expressed early on erythroid progenitor cells. The maternal anti-Ge3 was shown to promote phagocytosis of Ge+ early erythroid progenitors by monocytes (similar to what has been reported with anti-K and K+ progenitor cells). Thus, anti-Ge3 may cause immune destruction of erythroid progenitors and possibly suppression of erythropoiesis (which would explain the reticulocyte and bilirubin values seen in both cases). Anti-Ge3 appears to be capable of causing severe HDN. We suggest that babies born to mothers with anti-Ge should have their haemoglobin concentrations monitored for signs of anaemia for several weeks after birth. Functional assays may prove useful.

Anemia, Hemolytic↗
PubMed2002

Two cases of immune haemolytic anaemia, associated with anti-piperacillin, detected by the 'immune complex' method.

BACKGROUND AND OBJECTIVES: Sera containing antibodies to penicillin and penicillin-related drugs are typically thought to react with drug-coated red blood cells (RBCs) (drug adsorption method), but not when the sera are added to drug and RBCs in the same tube ('immune complex' method). Two cases of immune haemolytic anaemia caused by anti-piperacillin have been previously described. Serological details were given in only one patient. In that subject, the antibody was immunoglobulin (Ig)M + IgG and reacted by both the drug adsorption and 'immune complex' methods. MATERIALS AND METHODS: Two patients with cystic fibrosis developed positive direct antiglobulin tests (DATs) and haemolytic anaemia after 11-12 days of piperacillin therapy. Serological studies were performed with piperacillin, Zosyn (piperacillin + tazobactam) and penicillin by using the drug adsorption and 'immune complex' methods. RESULTS: The first patient's serum contained an IgG, complement-activating anti-piperacillin that reacted by the 'immune complex' method only. The second patient's IgM + IgG, complement-activating anti-piperacillin reacted by the 'immune complex' method and agglutinated piperacillin-treated RBCs. An eluate from the patient's RBCs reacted weakly with all RBCs tested without the presence of drug. This patient had evidence of intravascular haemolysis and died. CONCLUSIONS: We describe the third and fourth examples of immune haemolytic anaemia caused by anti-piperacillin; one was associated with fatal haemolytic anaemia. As piperacillin is commonly used in the treatment of cystic fibrosis, anti-piperacillin should be considered whenever patients with cystic fibrosis develop haemolytic anaemia and/or positive DATs.

Adult↗
PubMed2002

Practical aspects of investigating drug-induced immune hemolytic anemia due to cefotetan or ceftriaxone-a case study approach.

In the 1970s, the most common causes of drug-induced immune hemolytic anemia were methyldopa and penicillin. Since 1990, the most common causes of drug-induced immune hemolytic anemia have been the second- and third-generation cephalosporins, cefotetan and ceftriaxone. Three case histories illustrate the common findings in the serologic investigation of immune hemolytic anemias due to these two drugs.

Journal Article↗
PubMed2001

Countermanding saccades with auditory stop signals: testing the race model.

In a stop signal paradigm to investigate the control of human saccades subjects were instructed to make a saccade to a visual target appearing suddenly l5 degrees to the left or to the right of the fixation point. In 25% of the trials an auditory stop signal was presented after a variable delay that required the subject to inhibit the saccade. The stop signal was presented randomly at the target position, at the opposite side, or at fixation. Using different estimation techniques the average time needed to inhibit a saccade (stop signal processing time, or SSPT) was estimated on the basis of the race model. The SSPT estimates ranging from 50 to 100 ms (depending on subject) are shorter than those from previous studies with visual stop signals. Position of the auditory stop signal did not show an effect on countermanding effectiveness. We found saccadic response times consistent with the race model predictions for two subjects, while a third subject showed small but consistent violations. Moreover, all subjects showed a tendency towards hypometric saccades for responses that could not be inhibited. These findings are discussed with respect to recent neurophysiological results.

Acoustic Stimulation↗
PubMed2000

In vitro studies of the impact of transfusion on the detection of alloantibodies after autoadsorption.

BACKGROUND: In a patient with warm autoantibodies who has recently received a transfusion, it is not recommended to perform adsorptions using autologous RBCs to detect alloantibodies. Although not scientifically documented, this position is based on the theory that transfused RBCs in the patient's circulation would be capable of adsorbing alloantibodies that may be present. This in vitro study was designed to determine what percentage of transfused RBCs might completely remove alloantibodies in vivo. STUDY DESIGN AND METHODS: Selected D, E, K, Fy(a), and Jk(a) antibodies were adsorbed with mixtures of antigen-positive and antigen-negative RBCs to determine the lowest concentration of antigen-positive RBCs capable of removing all alloantibody reactivity. The percentage of antigen-positive RBCs in each mixture was determined by flow cytometry. RESULTS: Small amounts of antigen-positive RBCs (2-6%, as determined by flow cytometry) completely removed anti-D, -E, and -Fy(a) reactivity. Reactivity of two examples of anti-K was removed by 11 percent and 17 percent of K+ RBCs, respectively. Anti-Jk(a) reactivity was completely removed by 4 to 5 percent Jk(a+) RBCs using a PEG adsorption; the endpoint (>11%) was estimated, but complete adsorption with ZZAP-treated RBCs was not performed. CONCLUSION: Small amounts of antigen-positive RBCs are generally capable of removing all alloantibody reactivity. Thus, waiting for 3 months after transfusion before performing autologous adsorptions is a prudent policy.

Autoantibodies↗
PubMed1999

Severe immune hemolytic anemia associated with prophylactic use of cefotetan in obstetric and gynecologic procedures.

Second- and third-generation cephalosporins, especially cefotetan, are increasingly associated with severe, sometimes fatal immune hemolytic anemia. We noticed that 10 of our 35 cases of cefotetan-induced hemolytic anemias were in patients who had received cefotetan prophylactically for obstetric and gynecologic procedures. Eight of these cases of severe immune hemolytic anemia are described.

Anemia, Hemolytic, Autoimmune↗
PubMed1998

Positive direct antiglobulin tests and haemolytic anaemia following therapy with beta-lactamase inhibitor containing drugs may be associated with nonimmunologic adsorption of protein onto red blood cells.

A high incidence (39%) of positive direct antiglobulin tests (DATs) has been reported in patients taking Unasyn [ampicillin sodium plus sulbactam sodium (a beta-lactamase inhibitor)]. Three of four patients, with positive DATs, receiving Unasyn or Timentin [ticarcillin disodium plus clavulanate potassium (also a beta-lactamase inhibitor)] developed a haemolytic anaemia (HA) associated with a positive DAT, which resolved when drug therapy was stopped. The patients' sera did not react with red blood cells (RBCs) in the presence of Unasyn or Timentin, but when drug-treated RBCs were tested, patients' sera and normal sera reacted equally by indirect antiglobulin test. Following incubation in normal sera, RBCs treated with Unasyn, Timentin, Augmentin (amoxicillin + clavulanate), sulbactam and clavulanate reacted with anti-human globulin and anti-human albumin (an index of non-specific adsorption); RBCs treated with ampicillin and amoxicillin were nonreactive. The beta-lactamase inhibitors sulbactam and clavulanate seem to cause nonimmunologic adsorption of protein onto RBCs in vitro. This may explain the high incidence of positive DATs detected in patients taking Unasyn, which contains sulbactam. It was not possible to prove that there was a direct association between the nonspecific uptake of protein onto drug-treated RBCs in vitro with the positive DATs or the HA.

Adult↗
PubMed1998

An acute hemolytic transfusion reaction caused by an anti-P1 that reacted at 37 degrees C.

BACKGROUND: Hemolytic transfusion reactions (HTRs) due to anti-P1 have rarely been reported. There is only one report (from 1945) of an acute HTR due to anti-P1. CASE REPORT: A 74-year-old woman with anti-P1 was given blood that had been found to be compatible by the use of prewarmed serum and saline-suspended red cells (RBCs) and of an antiglobulin test with anti-IgG. The test mixtures were not centrifuged or inspected for agglutination after the 37 degrees C incubation phase. After transfusion of 50 mL of P1 + blood, the patient had an acute HTR (hemoglobinemia, hemoglobinuria, and increased blood pressure, temperature, and respiration). RESULTS: When studied by a reference laboratory, the anti-P1 was shown to be easily detectable (3+ agglutination) by a prewarming technique (saline or low-ionic-strength saline [LISS]), which included centrifugation at 37 degrees C, but only weak reactions were observed when centrifugation after 37 degrees C incubation was omitted. The indirect antiglobulin test was weakly positive (1+) with anti-IgG, but polyspecific anti-human globulin reacted 2+. The anti-P1 agglutinin was IgM, and its titer was 16 at 37 degrees C (prewarmed) and 256 at 23 degrees C; it caused hemolysis of RBCs at 37 degrees C under conditions known to enhance hemolysis. An indirect monocyte monolayer assay gave results of 11.2 and 22 percent in testing of P1 + RBCs incubated with the patient's serum alone and with patient's serum plus fresh normal serum (as a source of complement), respectively (normal < or = 3%). CONCLUSION: An acute HTR was caused by a hemolytic anti-P1 that reacted at 37 degrees C. This antibody was not detected by the hospital in a prewarmed crossmatch that omitted 1) the addition of LISS, 2) the reading for agglutination after the 37 degrees C incubation, and 3) the use of antiglobulin sera containing anti-complement.

Acute Disease↗
PubMed1998

False-positive eluate reactivity due to the low-ionic wash solution used with commercial acid-elution kits.

BACKGROUND: During the use of commercial red cell (RBC) acid-elution kits for adsorption and elution (adsorption/elution) studies with anti-D, unexpected reactive eluates (anti-D) were obtained from D- RBCs. Such results were not obtained with a parallel xylene method or, historically, with heat and ether methods. STUDY DESIGN AND METHODS: Single-donor and commercial polyclonal anti-D samples were incubated with D+ and D- RBCs. Acid eluates were prepared by the manufacturers' directions. Variations in the wash step of the eluate preparation included the use of commercial kit wash solution versus phosphate-buffered saline versus solutions of various ionic strengths. RESULTS: Anti-D was eluted from 20 of 22 samples of D- RBCs after incubation with commercial polyclonal anti-D (titer 512) and from 2 of 3 samples of D- RBCs incubated with single-donor anti-D (titer 256). With a low-titer (16) single-donor anti-D, 0 of 4 eluates from D- RBCs reacted. When phosphate-buffered saline was substituted for the commercial wash solution, 0 of 11 D- RBC eluates reacted, as compared with 9 of 11 D- RBCs that yielded positive 1+(-)2+ eluates with the commercial wash solution. If the recommended initial phosphate-buffered saline wash was omitted before the use of the commercial wash solution, the eluate reactivity was stronger (2+(-)3+). When low-ionic-strength (< 0.03 M) saline was substituted, anti-D was eluted from D- RBCs. All last washes were nonreactive. Antiglobulin tests on all adsorbing D- were negative. CONCLUSION: Commercial wash solutions used for acid elution are at low ionic strength and commonly yield superior eluates, but in the presence of high-titer antibodies, false-positive eluates can result. It is our belief that the low-ionic-strength wash solution caused aggregation of IgG and nonspecific attachment of IgG on RBCs. Aggregates will contain IgG serum antibodies in proportion to the titer of the antibody. It is this nonspecifically bound antibody that is eluted from antigen-negative RBCs.

Acids↗
PubMed1998

Warm autoimmune hemolytic anemia associated with an IgM autoanti-Ge.

A 28-year-old male with a prior history of Hodgkin's disease and a recent upper respiratory tract infection presented with autoimmune hemolytic anemia (AIHA). The patient's red blood cells (RBCs) were spontaneously agglutinated after room temperature and 37 degrees C washes. Dithiothreitol-treated RBCs reacted strongly with anti-C3 and were nonreactive with anti-IgG, -IgM, and -IgA; they reacted with anti-IgM (kappa light chains only) by flow cytometry. The patient's serum was nonreactive. An acid eluate was only weakly reactive, but a 56 degrees C heat eluate strongly agglutinated untreated RBCs (3+). Ficin-treated RBCs were nonreactive. En(a-) RBCs were strongly reactive, but Ge- RBCs were nonreactive. The anti-Ge in the eluate was IgM. The patient's untreated RBCs were shown, by flow cytometry, to be weakly Ge+. This is the first report of IgM-mediated warm AIHA associated with autoanti-Ge.

Journal Article↗
PubMed1996

Is correspondence search in human stereo vision a coarse-to-fine process?

One possible strategy for the solution of the correspondence problem of stereo matching is the coarse-to-fine mechanism: The matching process starts with a lowpass-filtered version of the stereogram where only a few, high-contrast image features can be extracted and the probability of false matches is therefore low. In subsequent stages, information from higher spatial frequencies is used gradually to improve the correspondence data obtained on the coarser scales. Coarse-to-fine strategies predict that information from coarse scale is used to disambiguate matching information on finer scales. We have tested this prediction by means of the wallpaper illusion using periodic intensity-profiles with different matching ambiguities on different spatial scale. Our psychophysical experiments show (i) that unambiguous information at coarse scale is not always used to disambiguate finer scale information, (ii) that unambiguous fine-scale information can be used to disambiguate coarse-scale information and (iii) that low spatial frequency is more efficient for disambiguation than higher frequency. We conclude that the human stereo vision system does not always proceed from coarse to fine. As an alternative scheme for scale-space integration, we discuss more symmetric schemes such as maximum likelihood combinations of data from different channels.

Adult↗
PubMed1996

A psychophysical and computational analysis of intensity-based stereo.

We describe two psychophysical experiments testing predictions of the square difference mechanism we have previously proposed for intensity-based stereo. Experiment 1 assesses the relative contributions of disparity and contrast to intensity-based stereo by measuring detection thresholds. The product of disparity and contrast at threshold is shown to be constant. In experiment 2, we measure quantitatively the global depth position perceived in stereograms of curved, smoothly shaded surfaces. The results show that disparity averaging over the surface involves a contrast-dependent weighting function. The results from both experiments are consistent with predictions derived from the square difference mechanism. The relation of this mechanism to feature correspondence stereopsis and shape-from-shading is discussed and a general framework for assessing the modularity of stereopsis is presented.

Adult↗
PubMed1996

Disparity-evoked vergence is driven by interocular correlation.

Disparity-evoked vergence is studied in stereograms showing one or two depth planes which are defined by isolated dots of varying density and contrast. Vergence position immediately after stimulus presentation was measured using dichoptic nonius lines. Since the stimulus was not visible after the onset of the vergence movement, the experiment accesses the initiation of vergence rather than its eventual result. In the unequivocal stimuli (one depth plane), elicited vergence tends to reduce disparity. Disparities of 0.5-1 deg are most effective which is in accordance with earlier findings. If two depth planes are presented, elicited vergence lies between the two planes, approaching the plane with higher dot density and/or dot contrast. In quantitative measurements, we show that the depth-averaging mechanism uses signal power per depth plane as a weight. Therefore, the relative pulling strength of dot density compared with dot contrast follows a power law with exponent 2. We propose a population code for vergence control based on disparity-tuned pools of units.

Adult↗
PubMed1996

A second example of anti-Esa, an antibody to a high-incidence Cromer antigen.

A blood sample contained an antibody to a high-incidence antigen that reacted with all red blood cells (RBCs) tested by the indirect antiglobulin test (IAT). The antibody reacted with papain-, ficin-, and trypsin-treated RBCs, but not with a-chymotrypsin-treated RBCs. This pattern of reactivity suggested the possibility that the antibody was recognizing an antigen in the Cromer blood group system. Tests against RBCs deficient in decay-accelerating factor (which carries the Cromer antigens) were weakly positive. Tests with antibodies to high-incidence Cromer antigens and with RBCs lacking high-incidence Cromer antigens led to identification of the second example of anti-Esa in an Es(a-) person. The antibody was IgG1 and reacted by the IAT to a titer of 64. The monocyte monolayer assay indicated potential clinical significance of this antibody in relation to transfusion.

Journal Article↗