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Biomedical subjects

A Salama

Publications and source records attributed to A Salama.

At least 127 records · Page 7Linked to original sources
PubMed1986

Effect of IgG anti-Rho(D) in adult patients with chronic autoimmune thrombocytopenia.

Seventeen adult patients with chronic (15 cases) or acute (two cases) autoimmune thrombocytopenia (ITP) were given intravenous and/or intramuscular injections of 0.75-4.5 mg of IgG anti-Rho(D) over a period of 1-5 days. Significant elevations of the platelet count (increments greater than 50 X 10(9)/liter) resulted in 13 of 15 Rh-positive patients but not in either of two Rh-negative patients. Heat-aggregated human albumin given to one of the Rh-negative patients also did not lead to a significant increase of the platelet count. The elevation of the platelet counts in Rh-positive patients after IgG anti-Rho(D) administration was often transient (less than 4 weeks), but long-term benefit (greater than 5 months) was achieved in five cases. The IgG concentration on RBC from five Rh-positive patients studied increased from a usually undetectable value before to approximately 700-1,700 IgG molecules/per RBC after anti-Rho(D) administration resulting in a strongly positive direct antiglobulin test. Nevertheless, an overt clinical hemolysis was seen in only one patient. The clearance of autologous 51Cr-labeled RBC was determined in four patients and was slightly enhanced in three and normal in one splenectomized patient. We conclude that the Fc receptor blockade involved in platelet sequestration was not associated with the induction of significant RBC clearance and that a reversible interaction of sensitized RBC with phagocytic cells and/or a low-grade destruction of these cells might be sufficient for the elevation of circulating platelets in the majority of patients with ITP.

Adult↗
PubMed1986

Treatment of childhood idiopathic thrombocytopenic purpura with Rhesus antibodies (anti-D).

We have recently reported that a rise of platelet numbers in ITP can be induced by blockade of the RES with antibody-coated red blood cells. We now present a collaborative study in which 15 Rhesus-positive children with ITP (nine boys and six girls aged 1-15 years) were treated with low-dose anti-D. Ten patients had chronic ITP (duration 6-47 months), five had acute ITP. Doses of 28-50 micrograms anti-D/kg bodyweight per course were given intravenously. In all patients clinical signs of bleeding ceased and platelet counts were elevated. An excellent, good or fair response with platelet increments of greater than 100, 50-100, or 20-50 X 10(9)/l, respectively, was observed in 19, 7, and 12 out of 45 courses in chronic ITP, and in 4, 1, and 2 out of 8 courses in acute ITP. The platelet increase (greater than 40 X 10(9)/l) persisted for 10 to over 360 days in chronic ITP. There were no untoward side reactions. Haemoglobin values remained stable in all patients but laboratory signs of mild, compensated haemolysis ensued. The direct antiglobulin test became positive in all cases due to anti-D IgG. Previous therapy of patients with chronic ITP included high-dose immunoglobulins and prednisone. These regimens were both effective but remissions were short. We conclude that anti-D therapy is an effective and safe form of treatment in childhood ITP.

Adolescent↗
PubMed1986

Two types of nomifensine-induced immune haemolytic anaemias: drug-dependent sensitization and/or autoimmunization.

Thirty-one patients who developed immune haemolytic anaemia while receiving nomifensine were studied. We provide evidence that nomifensine can cause two forms of immune haemolytic anaemia: one that is associated with an abrupt haemolytic episode due to drug-dependent antibodies, and a less acute form associated with IgG autoantibodies. The majority of patients' serum samples (23 cases) contained IgG and/or IgM antibodies reacting to a highly variable extent with red blood cells (RBC) only in the presence of the drug and/or its metabolites. Sera of six patients contained IgG autoantibodies which reacted, like those in warm autoimmune haemolytic anaemia, with RBC in the absence of drugs. Three patients had developed both types of antibodies. From a diagnostic viewpoint, nine of the drug-dependent antibodies could not be identified by using the drug itself, but by its known (three cases) or unknown urine-born metabolites (ex vivo antigens). We conclude that nomifensine can induce in vivo the production of RBC drug- and/or metabolite-dependent antibodies, autoantibodies, or both in the same patient.

Adult↗
PubMed1986

Rh blood group-specific antibodies in immune hemolytic anemia induced by nomifensine.

Nomifensine (Merital, Alival; Hoechst, Frankfurt, FRG), an antidepressant drug, may cause immune hemolytic anemia (IHA) of the so-called immune complex type that is believed to occur by means of an innocent-bystander mechanism. In this report we describe findings that are not consistent with this mechanism in a patient with nomifensine-induced intravascular IHA associated with renal failure. In vitro studies showed a transitory positive direct antiglobulin test (DAT) due to IgG, IgM, and C3 fixation. The causative antibodies were found to be a drug-independent IgM antibody in the serum and eluate that reacted only with E-positive RBC, although the patient's RBC were E-negative; an IgG antibody in the serum and initial eluates that showed a stronger reaction with e-positive than with e-negative or Rhnull RBC, but only in the presence of ex vivo antigen (ie, urine containing the drug and all its metabolites); and an IgM antibody in the serum and initially also on the patient's RBC that, in the presence of ex vivo antigen as well as in the presence of known metabolites of the drug, agglutinated all RBC equally strongly, but was hemolytically more active against E-positive than E-negative cells. Within a few days of stopping the drug the hemolysis rapidly resolved without administration of prednisone, the DAT became negative with anti-IgG and anti-IgM, and the drug-independent anti-E disappeared, but both metabolite-dependent antibodies remained detectable in the patient's serum. We conclude that the production and specificity of the causative antibodies in this case were controlled by a larger antigenic site, presumably consisting of the drug and/or its metabolites plus RBC antigens, rather than by epitopes of the drug or metabolites alone.

Anemia, Hemolytic, Autoimmune↗
PubMed1986

Blood constituents in relation to the reproductive state in she-camel (Camelus dromedarius).

Progesterone, enzymes, minerals, trace elements, and total protein were determined in the blood serum of nine non-pregnant, early, mid-, and late pregnant as well as puerperal camels, and were assessed in their relation to the reproductive state. The progesterone level followed by the copper level reaches peak values at mid-pregnancy. The zinc level decreases with increasing pregnancy, alkaline phosphatase increases. Hypocalcaemia and hypomagnesaemia occur towards the end of pregnancy; the total protein content increases. Surprisingly, the manganese level remained more or less constant.

Alkaline Phosphatase↗
PubMed1985

The role of metabolite-specific antibodies in nomifensine-dependent immune hemolytic anemia.

Nomifensine is an antidepressant drug (widely used in Europe, but not yet available in the United States), which has been linked to intravascular hemolysis. We studied 19 patients (18 women and 1 man) with acute intravascular hemolysis due to nomifensine-dependent antibodies. Transitory renal insufficiency developed in at least seven patients, and four required temporary dialysis. To investigate the antibodies, we used nomifensine, its three main metabolites, and its ex vivo antigens (urine samples from a volunteer collected 1.5 to 16 hours after the ingestion of 100 mg of nomifensine). We found an extraordinary heterogeneity of antibody response. Only five antibodies appeared to be primarily reactive with nomifensine. The remaining antibodies reacted either optimally or exclusively in the presence of one or more of the metabolites. Three of the metabolite-specific antibodies were positive only in the presence of ex vivo antigens, indicating specificity for as-yet-unidentified early and late metabolites of nomifensine. All the antibodies were capable of activating complement and belonged to the IgG or IgM class or both. Two serum samples also contained weak IgA antibodies. In addition to a variable degree of cross-reactivity of the antibodies, at least one serum sample had two drug-dependent red-cell antibodies (IgG against nomifensine and IgM against metabolites), and one sample had a drug-dependent IgM red-cell antibody and an IgG platelet antibody. Despite their serologic heterogeneity, all the antibodies were strongly reactive with ex vivo antigens. We recommend the use of ex vivo antigens as the technique of choice for the detection of nomifensine-dependent (and probably other drug-dependent) antibodies.

Acute Disease↗
PubMed1985

A two-stage immunoradiometric assay with 125I-staphylococcal protein A for the detection of antibodies and complement on human blood cells.

A sensitive two-stage immunoradiometric assay (IRMA) using unlabeled specific antiglobulin sera followed by binding of radiolabeled staphylococcal protein A has been developed for detection of human IgG, IgM, IgA and complement C3 on human blood cells. In an experimental model system, purified human immunoglobulins (Ig) were coupled onto red blood cells, platelets, and leukocytes. The Ig-coated red blood cells were analyzed in parallel by three methods: the radioimmune antiglobulin test with radiolabeled anti-Ig; the radiolabeled staphyloccal protein A test, and the IRMA. Of the three methods evaluated, the latter was found to be sensitive and the easiest to perform. The applicability of the IRMA was established by investigating a group of 14 selected patients with autoimmune warm type hemolytic anemia. We observed that the IRMA detected cell-bound antibodies (IgG and/or IgM) in several cases where conventional assays yielded negative results.

Antibodies↗
PubMed1985

A new red blood cell cold autoantibody (anti-Me)

A new red blood cell (RBC) cold autoantibody (anti-Me) is presented which was detected in a patient with autoimmune hemolytic anemia of 'cold type' associated with Waldenström's macroglobulinemia. The autoantibody was of the IgM (Kappa) class, had a moderate titer, and reacted with cord as well as with adult RBC. Its hemagglutinating activity against RBC was markedly increased in the presence of preheated human milk, but not in the presence of simple sugars or preheated casein. The data suggest that the antibody is directed against a new (glycolipid) antigen common to human RBC termed Me antigen ('milk enhanced').

Anemia, Hemolytic, Autoimmune↗
PubMed1985

Lack of efficacy of high-dose intravenous immunoglobulin in autoimmune haemolytic anaemia: a clue to its mechanism.

5 patients with autoimmune haemolytic anaemia (AIHA) of warm type (4 idiopathic, 1 associated with systemic lupus erythematosus and thrombocytopenia) were treated with high doses of i.v. immunoglobulin (IgG; Sandoglobulin; 2.0 g/kg body weight). IgG therapy was ineffective in all 5 cases as indicated by a lack of clinical improvement, continuous signs of accelerated red blood cell (RBC) destruction, and an unchanged survival rate of 51Cr-labelled autologous RBC in 4 patients studied. IgG infused at equivalent doses into 5 healthy volunteers led to an increase of IgG coating of autologous RBC (irrespective of the ABO blood groups) without concomitant changes of haemoglobin, haematocrit or reticulocytes, increase of serum IgM in 3/5, a decrease of serum C4 in 5/5, and a decrease of serum haptoglobin in 2/5 individuals. We conclude that IgG at a dose of 2.0 g/kg body weight is ineffective in AIHA. This may be caused by an increased, though clinically inapparent, interaction of IgG-coated autologous RBC with the mononuclear phagocyte system.

ABO Blood-Group System↗
PubMed1984

IgG therapy in autoimmune haemolytic anaemia of warm type.

Three patients with autoimmune haemolytic anaemia of warm type were treated with high doses of intravenous immunoglobulin (Sandoglobulin). The therapy was ineffective in all three cases. The possible reasons for this therapeutic failure are discussed.

Adolescent↗
PubMed1984

Treatment of autoimmune thrombocytopenic purpura with rhesus antibodies (anti-Rh0(D).

There is evidence that blockade of the reticuloendothelial system (RES) by sequestration of autologous red blood cells (RBC) leads to an elevation of platelet counts in immune thrombocytopenia. To substantiate this hypothesis, 10 Rh0(D)-positive adult patients (9 female, 1 male) with chronic autoimmune thrombocytopenic purpura (ITP) (1 to 21 years duration) were treated with low doses of intravenous IgG-anti-Rh0(D) (200 to 1,000 micrograms per dose; 300 to 3,600 micrograms per course; administration within 1 to 5 days). All patients improved clinically as indicated by cessation of bleeding. In eight out of ten patients there was a rise in platelet count. Platelet increments were excellent (greater than 100 X 10(9)/l) in one, good (50-100 X 10(9)/l) in three, fair (20-50 X 10(9)/1) in two and low (10-20 X 10(9)/1) in two patients. Splenectomized patients (N = 4) had a poorer response than non-splenectomized patients (N = 6) with mean increments of 16 X 10(9)/l (range 5-43 X 10(9)/l) versus 60 X 10(9)/l (range 10-110 X 10(9)/l). The increase in platelet counts persisted for seven to over 150 days. Transient and slight signs of haemolysis developed in seven out of ten patients (haemoglobin remained stable; increase of lactate dehydrogenase (greater than 250 IU/l) in four, decrease of haptoglobin (less than 60 mg/dl) in five patients). The direct antiglobulin test became positive in all cases due to IgG1 without complement fixation. We conclude that the interaction of antibody-coated RBC with macrophages (and, probably, other means of RBC alteration) is a feasible therapeutic approach in selected cases of ITP and related conditions.

Adolescent↗
PubMed1984

Ex vivo antigen preparation for the serological detection of drug-dependent antibodies in immune haemolytic anaemias.

Two patients with severe, intravascular haemolysis due to drug-dependent antibodies are described. The antibodies were directed against presumptive metabolites of buthiazide (International Non-proprietary Name, butizide) and nomifensine. Their detection was possible only in the presence of ex vivo antigens (i.e. fresh serum of volunteers after ingestion of the drugs) while in vitro antigen preparations yielded inconclusive results. Both antibodies lysed normal red cells in the presence of ex vivo antigens and complement. The buthiazide-related antibody was IgG (subclass IgG1), the nomifensine-related antibody was IgM. We conclude that the use of ex vivo antigens is of great importance in the serological evaluation of cases with suspected drug-dependent immune haemolysis.

Anemia, Hemolytic↗
PubMed1984

Quantitative evaluation of elution methods for red cell antibodies.

Two recent techniques using xylene and chloroform for antibody elution from red blood cells (RBC) were compared with the most widely used ether and heat elution by means of a quantitative 125I-antiglobulin test. Free serum alloantibodies and cell-bound alloantibodies from in vivo sensitization of delayed hemolytic transfusion reactions and of hemolytic disease of the newborn as well as autoantibodies in autoimmune hemolytic disease were studied. With alloantibodies, xylene proved more efficient than chloroform (p less than 0.025), while both methods were superior to heat or ether elution (p less than 0.005). Autoantibody elution was equally effective with xylene and chloroform (p less than 0.1) but again better than heat or ether elution (p less than 0.02). However, no single method produced the strongest eluate with all antibodies studied. We conclude that xylene and/or chloroform elution are valuable implementations in RBC serology, but, in selected instances, the classical elution methods will retain their importance.

Autoantibodies↗
PubMed1983

Effect of intravenous immunoglobulin in immune thrombocytopenia.

The rapid rise in platelet count after immunoglobulin treatment in acute and chronic forms of idiopathic thrombocytopenic purpura (ITP), autoimmune neutropenia, and post-transfusion purpura is well documented. It is suggested that the rise in platelet count is due to competitive inhibition of the macrophage binding of platelets by preferential sequestration of immunoglobulin-coated red blood cells. Measurement of haptoglobin levels, a sensitive indicator of haemolysis, suggests that clinically inapparent haemolysis occurs during immunoglobulin therapy of ITP patients. In-vitro experiments confirm that there is immunoglobulin coating of red blood cells. The hypothesis is further supported by the findings that immunoglobulin treatment in autoimmune haemolytic anaemia is ineffective, and that platelet counts rise in some ITP patients after induction of a mild haemolytic syndrome by injection of anti-Rho (D).

Adolescent↗
PubMed1983

Deposition of the terminal C5b-9 complement complex on erythrocytes by human red cell autoantibodies.

A radioassay for the detection of complement activating autoantibodies (autohaemolysins) in patients with autoimmune haemolytic anaemia (AIHA) is described. The method is based on immunoradiometric quantitation of the cytolytic C5b-9 complement complex following its antibody-dependent deposition on red blood cells (RBC). The use of affinity-purified, radiolabelled antibodies directed against the neoantigens of the C5b-9 complex ensured specificity of the test which proved more sensitive than conventional haemolytic assays and was not subject to disturbances by haemolytic sera. The results obtained in 70 patients with various forms of AIHA (warm type N = 45); cold type (N = 22); Donath-Landsteiner type (N = 3] support the prevailing assumption that autohaemolysins can trigger the complement cascade to completion. Since intact RBC from patients with detectable autohaemolysins carried C3/C4 components but never C5b-9, it is inferred that regulatory mechanisms operate in vivo at the level of C4b/C3b inactivation to arrest the cascade and rescue the autologous cells.

Adolescent↗
PubMed1982

HLA-B7 on human red blood cells. Improved detection by a radioactive anti-IgG test.

By means of a sensitive radioimmune anti-IgG test (RIAT) HLA-B7 was demonstrated on RBC of all B7 positive individuals (N = 52). Most antigens of the B7 cross-reacting group (B8, 13, w22, 27, 40; N = 36) were also detected. Eluates from B7 positive RBC exhibited clear B7 specificity against RBC as well as lymphocytes.

Blood Platelets↗