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Biomedical subjects

L D Petz

Publications and source records attributed to L D Petz.

At least 73 records · Page 4Linked to original sources
PubMed1981

Acute immune intravascular hemolysis due to hydrochlorothiazide.

Acute near-fatal intravascular hemolysis and renal failure developed in a patient after he had ingested 15 to 20 tablets of both methyldopa (Aldomet) nd hydrochlorothiazide (HydroDiuril). Serologic test results were inconsistent with those associated with methyldopa-induced hemolytic anemia and suggested that hemolysis was caused by hydrochlorothiazide antibodies reacting by an immune complex mechanism.

Acute Kidney Injury↗
PubMed1980

Complement activation by Coccidioides immitis: in vitro and clinical studies.

Mycelial- or spherule-phase derivatives of Coccidioides immitis caused a decrease in vitro of total hemolytic complement in serum from a nonsensitized person. Activation involved both classic and alternative pathways as shown by deprssion of hemolytic C4 and by generation of products of activation of components C3, C4, and factor B. In addition, functional complement activity or immunoreactive levels of complement components or both were measured in 23 patients with self-limited or disseminated coccidioidomycosis. Low total hemolytic complement was found in nine, usually during the early phase of primary illness, and was transient. Hemolytic C4 was low, and the effect of inulin to decrease complement levels was blunted, suggested both classic and alternative pathways may be deficient. However, associated depression of immunoreactive levels of components assayed (C3, C4, C5, factor B, and properdin) was not consistently found. This disparity raises the possibility of enhanced in vitro inactivation analogous to activation by immune complexes.

Coccidioides↗
PubMed1980

Possible gonadal mosaicism in a family with hemoglobin Köln.

A brother and sister were the first members of a family to possess hemoglobin Köln (alpha 2 beta 2(98) Val leads to Met). Studies of these siblings and their parents strongly indicated that the anomaly had arisen by spontaneous mutation. Gonadal mosaicism of one of the parents offers the best explanation for the appearance of a spontaneous mutation in multiple members of a sibship.

Adult↗
PubMed1979

Immune hemolytic anemia associated with anti-Kell and a carrier state for chronic granulomatous disease.

A patient presented with immune hemolytic anemia associated with a strongly positive direct antiglobulin test (IgG and complement). Anti-K was eluted from the patient's red cells, which were shown to be K negative. A powerful complement-binding anti-K was present in the serum together with another antibody(ies) showing characteristics resembling anti-Bg. Leukocyte antibodies were also present in the patient's serum. The anti-K could be adsorbed and eluted from K negative red cells in vitro. It is suggested that either non-specific adsorption of the anti-K may have occurred due to the Matuhasi-Ogata phenomenon; or, the antibody was an auto "minicking anti-K" capable of reacting with a broader specificity within the Kell system. A serendipitous finding was that the patient was a carrier for chronic granulomatous disease. The associations of immune hemolytic anemia, chronic granulomatous disease, and the Kell system are discussed.

Absorption↗
PubMed1979

[The radioactive antiglobulin (Coombs') test].

Weak red cell sensitization by hemolyzing antibodies may not be detected by the standard antiglobulin test. For the diagnosis of certain immune hemolytic anemias more sensitive methods are needed. Anti-IgG was purified as F(ab)2 by pepsin digestion and labelled with 125 I using the chloramine T method. 15 X 10(7) cells were washed and suspended in 0.1 ml of 6% albumin in saline. After incubation with 0.1 ml of 125 I-anti-IgG F(ab')2 for 30 minutes, the cells were washed and the uptake of radioactivity was counted using a gamma-counter. Standard cells were coated with a known concentration of an IgG anti-D preparation in the range of 50--1000 molecules per red cell. The sensitivity for the detection of red cell sensitization was at least 50 molecules per red cell. Because of varying binding ratios between the labelled anti-IgG reagent and different red cell antibodies the determination of the exact number of IgG molecules on the red cells is difficult. However, this very sensitive and reproducible method shows practical advantages in comparison with a complement fixation antibody consumption method with which corresponding results were obtained. Beside the evaluation of antiglobulin test negative autoimmune hemolytic anemias, this method may be applied for the determination of the specificity of weak red cell alloantibodies not detectable by standard blood bank procedures.

Anemia, Hemolytic, Autoimmune↗
PubMed1978

Immunologic cross-reactivity between penicillins and cephalosporins: a review.

Several approaches have been undertaken in the study of possible immunologic cross-reactivity between cephalosporins and penicillins. Although the chemical structures of these compounds are similar in several respects, there are distinct differences in their degradation and transformation. Various degrees of cross-reactivity of antibodies produced in response to administration of these drugs have been demonstrated both with test systems that measure IgG and IgM antibodies and with those that measure IgE antibodies. The clinical significance of immune responses to cephalosporins is best understood in regard to immunohematologic abnormalities: positive direct antiglobulin (Coombs') tests occur in only approximately 3% of patients receiving cephalosporins; however, several cases of cephalosporin-induced immune hemolytic anemia have been reported. Clinical studies of the cephalosporins indicated that patients with a history of penicillin allergy have increased incidence of reactivity to cephalosporins, but it is impossible to determine to what extent this finding is due to immunologic cross-reactivity because penicillin-allergic patients have an increased incidence of hypersensitivity reactions to drugs immunologically unrelated to penicillins. In addition, there is evidence of specific immune response to cephalosporins that indicates independently acquired hypersensitivity rather than cross-reactivity in some patients.

Anemia, Hemolytic, Autoimmune↗
PubMed1977

The correlation of cold agglutinin titrations in saline and albumin with haemolytic anaemia.

Cold agglutinin syndrome (CAS) is usually associated with IgM cold agglutinins with titres exceeding 1000 at 4 degrees C and a thermal amplitude of 30-32 degrees C. Occasionally patients are encountered who although having clinical and laboratory findings compatible with CAS do not have the characteristic serological findings. Thirty-two patients with a positive direct antiglobulin test due to complement sensitization were studied. Thirty-one of these patients had cold agglutinin titres greater than 64. Twenty-eight had haemolytic anaemia, including one patient with a cold agglutinin titre of only 8 against saline-suspended red cells. 53.6% of sera from patients with haemolytic anaemia reacted at 30 degrees C and 7.1% at 37 degrees C when albumin was not present, whereas in the presence of albumin all of the sera reacted at 30 degrees C and 67.9% reacted at 37 degrees C. None of the four patients without haemolytic anaemia reacted at 30 degrees C or 37 degrees C in the presence of albumin, even though one serum reacted to a titre of 1280 at 4 degrees C. Cold agglutinin titres and thermal amplitudes in the presence of bovine albumin were found to correlate better with haemolytic anaemia than reactions without albumin. If bovine albumin is utilized in compatibility testing, multiple cold autoabsorptions may be necessary before alloantibody activity at 37 degrees C can be excluded.

Agglutinins↗
PubMed1976

Immunologic reactions in penicillin factory workers.

One hundred sixty-nine employees of a synthetic penicillin plant participated in this study to correlate immunologic reactions, allergic symptomatology and dustiness of the work area. Statistically significant positive correlations existed among the following: (1)presence or absence of symptomatology and increasing dustiness of the work area; (2)presence or absence of symptoms and the presence or absence of benzyl-penicilloyl specific hemagglutinating antibody (BPO-specific antibody); (3)the absence, presence and level of titer of BPO-specific antibody with the dustiness of the work area. Because synthetic penicillin dust in the workroom air is able to evoke immunologic responses and produce symptoms among workers exposed to high levels, it is recommended that a reasonable air level for penicillin in factories be in the range of those demonstrated in the least symptomatic group in the study with measurements below 0.1 mg/m3.

Agglutination Tests↗
PubMed1975

Penicillin-induced immune hemolytic anemia. Occurrence of massive intravascular hemolysis.

A patient with penicillin-induced immune hemolytic anemia had massive intravascular hemolysis with hemoglobinemia and hemoglobinuria. Substantial amounts of complement components C3 and C4 were detected on the patient's red blood cells (RBCs), in addition to the usual IgG antibody to penicillin. The patient's serum demonstrated a high titer of antibody to penicillin (8,000), which did not cause hemolysis in vitro, but did cause complement fixation when incubated with normal serum. The presence of complement components on the patient's RBCs, and the finding that the serum fixed complement in vitro suggests that penicillin-antipenicillin immune complexes may have been present in the serum. We attribute the severity of the hemolysis to participation of the complement system in the hemolytic process and to the high titer of antibody to pencillin.

Acute Disease↗
PubMed1975

Drug-induced immune hemolytic anemia.

Drug administration causes from 16 to 18 per cent of cases of acquired immune hemolytic anemia. The pathogenesis of erythrocyte sensitization by drug-related antibody with or without fixation of complement is variable, and there is a relationship between the responsible drug, the mechanism of red cell sensitization, clinical manifestations and laboratory methods of diagnosis. Drugs such as phenacetin and quinidine form a complex with the antidrug antibody, and the immune complex attaches to red cells usually fixing complement and causing acute intravascular hemolysis. Other drugs (e.g., penicillins), when given in large doses, coat normal red cells in vivo and in some patients a high titer IgG anti-drug antibody develops which reacts with the coated cells. Hemolytic anemia may develop with red cell destruction being primarily extravascular. Cephalosporins cause positive direct antiglobulin tests in a small percentage of patients either by the same mechanism as penicillins or by modification of the red cell membrane leading to nonimmunologic absorption of serum proteins. Hemolytic anemia has been reported only rarely. A few drugs (notably alpha methyldopa) cause the development of autoimmune hemolytic anemia. Knowledge of clinical manifestations and laboratory aids to diagnosis is necessary to distinguish immunohematologic abnormalities caused by drugs from other causes.

Adsorption↗
PubMed1975

The relationship between hemolytic and immunodiffusion methods for measurement of C4 in patients with immunologic disorders.

A comparison of radial immunodiffusion and functional (hemolytic) assays for C4 revealed a highly significant correlation between the two methods in patients with a variety of immunologic disorders. Immunodiffusion technics are more convenient than hemolytic assays for most clinical laboratories. C4 assays are useful for the presumptive diagnosis of hereditary angioneurotic edema, whereas C3 is usually normal in such patients. C4 is usually more sensitive than C3 in a variety of immunologic disorders, although in some patients the opposite is true, especially in hypocomplementemic nephritis.

Angioedema↗
PubMed1975

Drug-induced haemolytic anemia.

Drug administration causes 16 to 18 per cent of cases of acquired immune haemolytic anaemia. The pathogenesis of erythrocyte sensitisation by drug-related antibody with or without fixation of complement is variable and there is a relationship between the responsible drug, the mechanism of red cell sensitisation, clinical manifestations, and laboratory methods of diagnosis. Drugs such as phenacetin and quinidine form a complex with the antidrug antibody, and the immune complex attaches to red cells usually fixing complement and causing acute intravascular haemolysis. Other drugs (e.g. penicillins) when given in high doses coat normal red cells in vivo and some patients develop a high titre IgG antidrug antibody which reacts with the coated cells. Haemolytic anaemia may develop, with red cell destruction being primarily extravascular. Cephalosporins cause positive direct antiglobulin tests in a small percentage of patients either by the same mechanism as penicillins or by modification of the red cell membrane leading to non-immunological absorption of serum proteins. Haemolytic anaemia has been reported only rarely. A few drugs (notably alpha-methyldopa) cause the development of autoimmune haemolytic anaemia. A knowledge of clinical manifestations and laboratory aids to diagnosis are necessary to distinguish immunohaematological abnormalities caused by drugs fron other causes. Drugs may also cause haemolytic anaemia by nonimmunologic mechanisms as a result of oxidative denaturation of haemoglobin. Factors which make red cells particularly susceptible to the effects of oxidant drugs are intraerythrocytic metabolic abnormalities or the presence of unstable haemoglobins.

Anemia, Hemolytic↗