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P Lalezari

Publications and source records attributed to P Lalezari.

At least 37 records · Page 2Linked to original sources
PubMed1983

Inhibition of cold insolubility of an IgA cryoglobulin by decanedicarboxylic acid and related compounds.

Cold insolubility of a serum IgA cryoimmunoglobulin was found to be inhibited by the addition of 1.5 mM sodium decanedicarboxylate in vitro. The patient with the cryoglobulin had advanced multiple myeloma complicated by severe hyperviscosity that caused lethargy and episodic loss of consciousness. Decanedicarboxylic acid administered orally resulted in transient relief of symptoms and the loss of cryoprecipitability of the paraprotein. Further in vitro studies revealed that sodium salts of long-chain monocarboxylic acids with a minimum of eight carbons, and dicarboxylic acids with a minimum of 12 carbons inhibited cryoprecipitation. Salts of short-chain carboxylic acids, by contrast, enhanced cryoprecipitation. Sodium phenolate and sodium salts of benzoic acid, 2,4-DNP, phenylpropionic acid, and salicylic acid were also inhibitory. These latter compounds, which have a ring structure, did not cause precipitation at any concentration. It was demonstrated that the presence of a free carboxylic group was required for these activities; conversion of carboxylic acid to amide resulted in the loss of both the inhibitory and cryoprecipitation-enhancing effects. Normal plasma, or plasma from five other patients who had IgG, IgM, or mixed-type cryoglobulinemia, were not affected by any of these compounds. It is suggested that in selected cases of hyperviscosity syndrome associated with cryoglobulinemia, some of these compounds, especially monocarboxylic acids with appropriate chain lengths, or those with a ring structure, may have therapeutic applications.

Acetamides↗
PubMed1983

Reversal of neutropenia with intravenous gammaglobulin in autoimmune neutropenia of infancy.

Intravenous gammaglobulin (IVIgG) was used to treat autoimmune neutropenia of infancy in two males with repeated infections. The neutrophil count increased significantly in both patients with the initial IVIgG therapy; 1 patient went into remission. The neutrophil count in the other remained above baseline for 3 wk, and a subsequent booster infusion also caused the neutrophil count to increase. The patients have remained clinically well since their treatment began. Serial studies of antineutrophil antibody and serum lysozyme, performed to elucidate the mechanism of action, suggested decreased neutrophil destruction, perhaps by Fc receptor blockade, as well as decreased synthesis of antineutrophil antibody. Neutrophil function was not impaired after the neutrophil count increased. Many patients with immune neutropenia have a benign course, but those who have significant infections could be treated, acutely or prophylactically, with intravenous gammaglobulin.

Agranulocytosis↗
PubMed1982

Ability of thrombocytes to acquire HLA specificity from plasma.

Thrombocytes from HLA-A1 and HLA-A2 negative donors were incubated with plasma obtained from respective HLA-positive donors. The plasma-treated thrombocytes were shown to acquire HLA specificity of the plasma as demonstrated by their ability to absorb lymphocytotoxic activity of monospecific anti-HLA sera. The data are consistent with the hypothesis that the expression of HLA antigens in cells of hematopoietic origin diminishes in the course of differentiation and maturation and that the expression of HLA antigens on thrombocytes is primarily due to absorption of these antigens from plasma.

Blood Platelets↗
PubMed1982

Serologic profile of alphamethyldopa-induced hemolytic anemia: correlation between cell-bound IgM and hemolysis.

Erythrocyte-bound immunoglobulins have been characterized by a PVP-potentiated antiglobulin test in 11 patients who had developed antibodies after treatment with alpha-methyldopa. Serologic profiles were recognized that could distinguish between the hemolyzing and nonhemolyzing patients: IgM antibodies together with the first component of complement (C1q) were demonstrated on erythrocytes of all eight hemolyzing patients. By contrast, these immunoproteins were absent from the cells of nonhemolyzing patients and became undetectable when the hemolyzing patients recovered. IgG and its subclasses were variably present on erythrocytes of all patients regardless of hemolytic activity. Eluates prepared from erythrocytes of the hemolyzing patients were shown to contain both IgG and IgM, and fixes C1q, C3, and C4. Eluates from the nonhemolyzing patients contained only IgG. The IgM antibodies differed from the commonly occurring cold agglutinins in that they were warm-reactive and were mainly concentrated on the patients' cells rather than being free in the serum. Because of their nonagglutinating property, it is suggested that they are monomeric IgM. It is concluded that the high affinity, warm-reactive IgM and not the IgG antibodies are primarily responsible for clinically manifest anemia in patients receiving alphamethyldopa and that the hemolytic activity is probably mediated by the classic pathway of complement activation.

Adult↗
PubMed1980

Inhibtion of cold insolubility of serum cryoglobulin by epsilon aminocaproic acid.

Cold-induced insolubility of serum cryoglobulins can be inhibited by various carbohydrates and aminocarboxylic acids. Among the inhibitors, Epsilon amino caproic acid (EACA) was found to be effective at therapeutic levels in a patient who had mixed-type cryoglobulinemia. In vivo administration of EACA completely prevented cryoprecipitation; the inhibition being accompanied by a parallel decrease in the viscosity of the precooled serum. The data along with kinetics of serum EACA levels suggest specific binding of the drug to the cryoglobulins in this patient. This binding may be the basis for the observed inhibitory activity. The in vivo use of specific inhibitors of cryoglobulin precipitation may prove to have therapeutic application in the management of cryoglobulinemic patients.

Aged↗
PubMed1980

Neutrophil kinetics in Felty's syndrome.

In 19 patients with Felty's syndrome, marrow production of neutrophils and neutrophil distribution were studied. Despite accelerated marrow release and disappearance of mature blood neutrophils, there was little or no increase in the marrow mitotic pool or in vitro progenitor cells. Only two patients had an increase in marrow neutrophils and precursors. Antineutrophil antibody was detected in seven of nine patients studied. Neither abnormal margination of blood neutrophils nor impaired marrow release of cells was detected. Skin exudate cellularity tended to correspond to prior history of infections, asymptomatic patients having more cellular exudates. Sustained neutrophil increments were observed in six of 10 patients following splenectomy, but in no patient did neutrophil kinetics return completely to normal. Three of four patients who failed to respond to splenectomy with sustained increments in blood neutrophils had a reduced mass of marrow neutrophils and neutrophil precursors when studied prior to splenectomy. No diminution in neutropenia was observed in any of five patients treated with lithium carbonate. This study indicates that multiple factors are involved in the pathogenesis of neutropenia in Felty's syndrome. In particular, neutropenia was associated with inadequate marrow granulocytopoiesis. The severity of the impairment, as determined by the mass of marrow neutrophils and precursor cells, may be useful in predicting response to splenectomy.

Aged↗
PubMed1980

Transient autoimmune neutropenia due to anti-NA1 antibody.

A 6-month-old girl developed severe, but transient neutropenia due to an antibody against a neutrophil-specific antigen, NA1. The mean absolute neutrophil count was 380/microliter for 2 months and spontaneously returned to normal as the anti-NA1 antibody disappeared. After recovery, the NA1 antigen was demonstrated on the patient's neutrophils. No etiology was found. There was no therapy directed at suppressing the antibody or increasing the neutrophil count. Life-threatening infection did not occur during the neutropenia.

Agglutination↗
PubMed1977

Neutrophil antigens: immunology and clinical implications.

Neutrophil antigens may be classified into two major categories: antigens shared with other cells and antigens specific for neutrophils. The first category includes the ABH, I, i, 5a,b and HLA determinants. Additional antigens with special characteristics in this category are the blood-group U, Kx, JkaJkb, and Ge determinants which apparently neutrophils share only with erythrocytes. Neutrophil-specific antigens include the NA1, NA2, NB1 and 9a. These specificities are detected by the agglutination test and have been shown to be present on mature neutrophils. Independent allospecificities, detectable by the granulocytotoxicity test, may also exist. In addition, neutrophil antigens, which are species-specific, have been identified by the use of xenogeneic antibodies. The EDTA-dependent agglutination test remains a most reliable assay for the study of neutrophil-specific antigens. The lack of reproducibility known in the leukoagglutination reaction does not pertain to the modification used in the assay of neutrophil-specific antibodies. It does apply, however, to those tests that were performed in the absence of EDTA, and in connection to the study of HLA-related antigens. For every pathophysiological state involving the erythrocyte antigens a neutrophil analogue is observed, the difference being in symptomatology which is related to the structural and functional characteristics of the cells: febrile and pulmonary transfusion reactions result from incompatibility neutrophils. It is found that similarity in the HLA antigens and nonreactivity in the MLC test do not preclude immunization against neutrophil-specific antigens. Therefore, it is probable that febrile and pulmonary reactions will occur in the recipients of multiple granulocyte transfusions, even though donors and recipients may be considered "histocompatible" by the HLA assays. It has been shown that fetal-maternal incompatibility can cause neonatal neutropenia, and several forms of autoimmune neutropenia are described: in "idiopathic" neutropenia of infancy, autoantibodies have been found to have specificity against NA1 and NA2 and in one adult, autoimmune neutropenia due to anti-NA1 antibody has been observed. Neutropenia also occurs due to idiopathic, cold-reacting antileukocyte antibodies, and with cold agglutinins associated with lymphoma, infectious mononucleosis, and Mycoplasma pneumonia. Although the role of neutrophil antigens in bone marrow transplantation has not as yet been determined, these antigens are undoubtedly immunogenic and potentially play an important role in neutrophil compatibility. It is obvious that neutrophils cannot survive in the presence of antineutrophil antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1975

Chronic autoimmune neutropenia due to anti-NA2 antibody.

In exploring the immunologic causes of chronic neutropenia, we identified a persistent neutrophil-specific antibody with NA2 specificity in the blood of a nontransfused two-year-old girl with severe neutropenia. No such antibody was detected in the maternal blood. The antibody was first studied and identified when the patient was 11 months old, but she had had clinical manifestations since the age of one month. After a trial of steroid therapy, a marked but temporary reduction in the antibody titer occurred, accompanied by the rise of the neutrophils to normal level. Neutropenia reoccurred, however, when the antibody titer began to rise, despite continuation of steroid therapy. This transient response allowed the patient's neutrophils to become available and identified as NA2-positive. Although the cause of this disorder remains obscure, the data presented indicate that the anti-NA2 autoantibody is responsible for the neutropenia observed.

Agranulocytosis↗
PubMed1975

Role of amino groups in formation of human lymphocyte-xenogeneic erythrocyte rosettes; a proposed mechanism for antigen recognition.

Formation of coulombic and possible hydrogen bonds between amino groups on human lymphocytes and negatively charged sites on sheep erythrocytes is involved in rosette formation. Supportive evidence includes rosette inhibition by chemical binding of lymphocyte membrane amino groups, and the results of changing the pH, ionic concentration, and temperature of the reaction. Although the possibility has not been excluded that the amino group dependence of this reaction is related to the property of certain proteins attached to the T-cell (thymus processed) surface, it is suggested that this dependence may be related to a charge pattern recognition in the form of "codes" present on the T-cell membrane. It is speculated that this type of recognition may be a contributory mechanism in the initiation of the T-cell-dependent immune response.

Amines↗
PubMed1975

Development of direct antiglobulin reaction accompanying alloimmunization in a patient with Rhd (D, category III) phenotype.

New examples of the Rhd (D, category III) red cell phenotype are described in three siblings. One of these individuals who had previously been transfused, received three units of Rho(D) positive blood several years later and developed a high titer anti-RhD antibody. This anamnestic response was associated with the development of an autoantibody which persisted for a period of at least 8 months. This observation represents another example of autoimmunization which has rarely been observed to accompnay alloimmunization.

Adult↗