[Diagnosis of hematuria in children].
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Child↗
Biomedical subjects
P Mahieu
Publications and source records attributed to P Mahieu.
Anti-alpha-galactosyl antibodies and immune complexes in children with Henoch-Schönlein purpura or IgA nephropathy.
Episodes of hematuria in IgA nephropathy or Henoch-Schönlein purpura are frequently associated with microbial infections. Some of those infectious agents bear alpha-galactosyl residues on their cell surface. These observations prompted us to determine, by passive hemagglutination, the titers of natural anti-galactosyl antibodies in the serum of children presenting with Henoch-Schönlein purpura (10 cases) or IgA nephropathy (7 cases). Antibody titers of normal subjects (103 cases), children with a pharyngitis of unknown etiology (7 cases), and children exhibiting mesangial IgA deposits but no hematuria at the time of testing (6 cases) ranged from 1:20 to 1:80. Elevated titers (greater than 1:80) were observed in nine of 11 patients with mesangial IgA deposits and micro- or macroscopic hematuria, in nine of 19 children with other evolutive glomerular diseases (5 cases of acute glomerulonephritis and 4 cases of minimal change disease), and in most subjects presenting with a M. pneumoniae (4/5 cases) or a E. Coli (4/5 cases) infection. Antibody titers decreased after incubation of normal and pathological sera with D-galactose (10 mM) or with alpha-galactosyl-glucoside (10 mM), but not with D-glucose (10 mM). The anti-alpha-galactosyl antibodies purified, by affinity chromatography, from sera of 10 normal children, 10 pathological controls and four children with mesangial IgA deposits without hematuria belonged to IgG class. In contrast, both IgG and IgA anti-alpha-galactosyl antibodies were detected in six of six patients with mesangial IgA deposits and hematuria. The IgA content of immune complexes detected in those patients decreased after incubation of sera with alpha-galactosyl-glucoside, but not with D-glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
In-vivo studies on Haemaccel-fibronectin interaction in man.
An enzyme-linked immunoassay has been recently set up for direct measurement of the binding capacity of plasma fibronectin to gelatin. This binding capacity could be completely inhibited in vitro by an eight-fold excess of gelatin, of Haemaccel, but not of Geloplasma. On the contrary, the levels of immunoreactive fibronectin measured by laser nephelometry did not change, in presence of 10 to 1000 micrograms ml-1 of gelatin, of Haemaccel or of Geloplasma. When infused into normal volunteers, Haemaccel provoked a strong and immediate inhibition of the plasma fibronectin binding capacity to gelatin. This inhibition was dose-dependent and maximal after infusion of 500 ml of Haemaccel. Twenty-four hours after this infusion, there was a progressive recovery of the gelatin-binding capacity, which was almost completely achieved 96 h later. The formation of complexes between Haemaccel and fibronectin was demonstrated by gel filtration chromatography and by affinity chromatography. Immunoreactive plasma fibronectin levels remained unchanged up to 24 h after infusion of 500 ml of Haemaccel. A transient decline to 50% of its initial value then occurred the second day after the infusion. Therefore, a delay existed between the formation of fibronectin-Haemaccel complexes and their elimination from the bloodstream. This delay decreased when smaller volumes of Haemaccel were infused, which strongly suggests that plasma fibronectin is cleared by means of Haemaccel and does not seem to play a role of opsonin in these conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Chromatography, Affinity↗
Elevated anti-alpha-galactosyl antibody titres. A marker of progression in autoimmune thyroid disorders and in endocrine ophthalmopathy?
The titres of anti-alpha-galactosyl antibodies were measured by passive haemagglutination in 50 control subjects and in 128 patients presenting with various thyroid disorders. Titres of control subjects ranged from 1/10 to 1/80, regardless of age and blood group. Elevated titres (greater than 1/80) were constantly noted in 6/6 patients with progressive exophthalmos, in 5/5 patients with untreated Graves' disease, and in 11/12 patients with progressive nontoxic goitre. By contrast, the titres were within the normal range in primary myxoedema (17 patients) and in residual exophthalmos (11 patients), whereas they were only erratically increased in 1/31 patients with treated or cured Graves' disease and in 5/36 patients with nonprogressive nontoxic goitre. Finally, elevated titres were also found in 3/7 patients presenting with autoimmune thyroiditis. No correlations could be established between elevated titres and the thyrotropin binding inhibiting immunoglobulin activity, the antithyroglobulin antibody titres or the antimicrosomal antibody titres. As in the control subjects, the anti-alpha-galactosyl antibodies mainly belonged to the IgG class. Affinity purified anti-alpha-galactosyl antibodies were capable of binding to trypsinized human and porcine thyroid cells in culture, as shown by indirect immunofluorescence. On the other hand, they were not able to react with untreated thyroid cells. The data show that the measurement of anti-alpha-galactosyl antibody titres could represent an easy and useful tool to determine whether an autoimmune thyroid disorder is in progression. Besides, they suggest that some of the antigenic determinants implicated in the enhanced production of anti-alpha-galactosyl antibodies are present, but normally hidden, within the cell surface of thyroid cells.
Adult↗
Assessment of urinary retinol-binding protein as an index of proximal tubular injury.
The urinary excretion of retinol-binding protein (RBP), beta 2-microglobulin (beta 2-m), and beta-N-acetyl-D-glucosaminidase was monitored in patients with renal tubular damage secondary to multiple injuries, rhabdomyolysis, antibiotic treatment, or poisoning by various chemicals such as solvents, heavy metals, or pesticides. In almost all cases, RBP proved to be a more sensitive index of renal tubular damage than was beta-N-acetyl-D-glucosaminidase and, being more stable in acid urine, a more practical analyte to measure than was beta 2-m. We corroborated this finding by studying the relationships between these three analytes in more than 150 patients. On the average, an increase in the urinary excretion of beta-N-acetyl-D-glucosaminidase becomes detectable when urinary RBP already exceeds the normal value by 50- to 100-fold. In urines with pH greater than 6, RBP and beta 2-m concentrations are well correlated (r = 0.93, n = 150), beta 2-m tending to be more frequently positive (i.e., greater than 311 micrograms/L). But in urines with pH less than 6 (about 30-40% of the samples), the RBP/beta 2-m concentration ratio increases as pH decreases, up to 500 in some patients with massive tubular injury. Because the renal uptake of proteins involves a saturable process, the urinary excretion of RBP, like that of beta 2-m, specifically reflects the reabsorption capacity of proximal tubules only when the glomerular filtration rate is normal or slightly impaired (i.e., serum creatinine less than 20 mg/L). Under these conditions the determination of RBP protein in urine appears the most appropriate test when early detection of tubular injury is desirable.
Acetylglucosaminidase↗
[Demonstration of anti-laminin antibodies in the serum of healthy subjects].
Antibodies directed against laminin, a glycoprotein of basement membranes, have been sought for in the sera of 347 healthy subjects by a method relying on the agglutination of laminin-coated latex particles. Fifty-five subjects (15.9%) hae been found to be positive, 37 with a titre of 2, 14 with a titre of 4 and 4 with a titer of 8. Applied to 106 patients whose a renal biopsy had been examined by immunofluorescence, the test yielded positive results in 91% of patients with linear deposits as compared to 10.3 and 15.4% respectively in patients presenting with and without granular deposits along the glomerular basement membrane. The titers in anti-laminin antibodies observed in these patients ranged from 2 to 8. The discovery of circulating anti-laminin antibodies in serum from subjects without clinical or subclinical sign of renal impairment rises several questions regarding the pathogenicity of these auto-antibodies and their possible association with genetic or environmental factors.
Anti-Glomerular Basement Membrane Disease↗
Human anti-alpha-galactosyl IgG reduces the lung colonization by murine MO4 cells.
The lung colonization of MO4 cells, a highly malignant murine cell line, is strongly reduced in syngeneic C3H/He mice by a prior incubation with anti-alpha-galactosyl antibody (alpha-Gal Ab), a natural IgG antibody present in high titers in all normal human sera and specifically recognizing Gal alpha(1----3) structures (alpha-D-galactopyranosyl; alpha-D-Galp). The protective effect is due to a binding of alpha-Gal Ab to alpha-D-Galp end groups of MO4 cells, inducing both an increase in their sequestration into the liver and the spleen and a decrease in their sequestration into the lung. The F(ab')2 fragments of this antibody also exhibit a protective effect by inhibiting the homing of MO4 cells into the lung, without modifying their accumulation into the spleen and the liver. Since both the antibody and the alpha-galactosidase pretreatments of MO4 cells block their subsequent attachment to murine laminin in vitro, we suggest that, in this model, the lung colonization may be dependent on the alpha-D-Galp end groups exposed on the surface of MO4 cells.
Animals↗
[Solitary lesions of the rectum caused by suppositories combining acetylsalicylic acid and paracetamol].
The reports of 8 female patients who, because of recurrent headache, were using analgesic suppositories containing acetylsalicylic acid and paracetamol (Perdolan) for more than two years are analyzed. Symptoms were nonspecific: anal pain, rectal tenesmus or bleeding. The lesions were located within 8 cm from the anal verge and consisted of superficial ulcerations, fibrotic scar tissue and rectal stenosis. Biopsies showed non-specific inflammation, limited to the rectum. Rectal prolapse or intussusception was not associated. By discontinuing the use of suppositories, symptoms usually resolved; rectal stenoses required anorectal dilatations and in 2 cases surgical resection. When solitary rectal lesions are observed in the absence of rectal prolapse, chemical aggression of the rectal mucosa by use of suppositories containing acetylsalicylic acid should be considered.
Acetaminophen↗
An enzyme-linked immunoassay for direct measurement of the gelatin-binding capacity of human plasma fibronectin.
A new solid-phase enzyme immunoassay measuring the gelatin-binding capacity of plasma fibronectin has been developed. This assay is based on the direct and high-affinity interaction between fibronectin and gelatin coated to polyvinyl chloride plates. The amount of fibronectin bound to gelatin is then measured by sequential incubation with a specific rabbit anti-human fibronectin antiserum, with horseradish peroxidase-conjugated goat anti-rabbit IgG antibodies and with substrate. The final degradation of the substrate is read at 492-650 nm in an ELISA processor. The assay allows the accurate detection of fibronectin concentrations ranging from 1 to 20 micrograms/ml, is inhibited by the addition of gelatin to plasma, is highly reproducible (interplate CV less than 10%), requires 100 microliter of plasma only and has been fully automated. Significant linear correlations were noted between total antigenic fibronectin (measured by laser nephelometry) and fibronectin gelatin-binding capacity in plasma from 310 blood donors. Both parameters were higher in men than in women and significantly increased according to age. Dissociation between immunoreactive fibronectin and fibronectin gelatin-binding capacity was observed in two polytraumatized patients. This enzyme immunoassay therefore provides a new method to investigate functional alterations of the gelatin-binding domain of fibronectin in various pathological conditions.
Adult↗
Anti-basement-membrane antibodies in the serum of healthy subjects.
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Adult↗
C3b receptor (CR1) on erythrocytes and the HLA-DR3 antigen.
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Antibodies↗
Effects of ex-vivo plasma adsorption over protein A sepharose in acute leukemia.
Plasma adsorption over immobilized Staphylococcus aureus Cowan I has resulted in tumor regression in several animal and human trials. Protein A, because of its ability to bind IgGs has been considered as the effective component of Staphylococcus aureus. In 4 patients with acute leukemia, a plasma volume of 1500 cm3 was passed in an ex-vivo system over immobilized SpA-Sepharose and then reinfused. Almost all of the IgGs contained in the plasma volume could thus be removed. Toxic side-effects were mild. No significant clinical improvement could be obtained. Plasma incubation with SpA did not modify blast cell viability or leukemic progenitor cell growth. Along with others, this study shows that Protein A is probably not the mediator of the tumoricidal responses observed in studies using adsorption over Staphylococcus aureus Cowan I. The ex-vivo system prepared for this study could also be used for plasma IgG removal for the treatment of autoimmune or immune-complex related disorders.
Blood Cell Count↗
Glomerular mesangial cell contractility in vitro is controlled by an angiotensin-prostaglandin balance.
Rat renal mesangial cells possess morphological and functional features of smooth muscle cells in culture, such as intracellular myosin filaments, A II receptors and a contractile response to A II. Furthermore, they represent the main glomerular site of PGE2 synthesis. In the presence of A II (50 nM), their PGE2 production rate was significantly increased, this effect being potentiated by arachidonic acid (3 micrograms/ml). After a prior inhibition of arachidonic acid metabolism by cyclooxygenase inhibitors (indomethacin 1 microM or naproxen 0.02 microM) or by a cyclo- and lipoxygenase inhibitor (phenidone 670 microM), the percentage of cells contracting in response to various A II concentrations (10 pM to 10 nM) was significantly enhanced as compared to the basal conditions. On the contrary, the percentage of cells presenting a contractile response to A II in the presence of exogenous PGE2 (50 ng/ml) or of arachidonic acid (3 micrograms/ml) was significantly decreased. These modifications were not related to some changes in the A II receptor properties of the cells, i.e. the number of receptor sites and their affinity constant. The data demonstrate that the contractile response of glomerular mesangial cells is modulated by the PGE2 content of their incubation medium. Since their own PGE2 production rate is enhanced in the presence of A II, this cellular response may represent a local regulatory mechanism of their contractile properties.
Angiotensin II↗
Antibodies to laminin in preeclampsia.
Laminin is a large basement membrane glycoprotein localized in the trophoblast, glomerular basement membrane and in the mesangial matrix of human glomeruli. It promotes the attachment of epithelial cells to basement membrane collagen. We have found that 14 sera from 52 patients with severe preeclampsia or eclampsia contain IgG and IgM antibodies which react with placental and kidney basement membranes. These antibodies were specific for laminin and did not react with other basement membrane proteins. They were able to fix complement. They have been demonstrated by radial immunodiffusion, radioimmunoassay and immunofluorescence blocking studies. In primary cultures they were shown to impair the attachment of trophoblast cells to basement membrane collagen. High levels of circulating immune complexes were detected only in sera from preeclamptic patients with circulating antibodies to laminin. The auto-antibodies to laminin could play a major role in the pathogenesis of severe preeclampsia by impairing the attachment of trophoblast cells to placental basement membranes and by fixation to the glomerular basement membranes and mesangial matrix.
Antibody Specificity↗
[Acute poisoning by chlorinated solvents: apropos of 3 case reports].
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Acute Kidney Injury↗
Ex vivo perfusion of plasma over protein A columns in human mammary adenocarcinoma. Evidence for a protein A leaking by radioimmunoassay.
A solid phase radioimmunoassay (RIA) has been developed for detection of protein A in human serum or plasma using plates coated with specific goat anti-protein A IgG and affinity-purified anti-protein A F (ab')2 fragments labelled with 125Iodine as a tracer. This RIA detected 25 ng of protein A per ml of serum or plasma. The 'intra-plate' coefficient of variation (CV) was 4.26%, whereas the 'inter-plate' CV was 5.86%, even in the presence of aggregated IgG. The presence of protein A was searched for by this RIA in samples collected during ex vivo perfusion of the plasma of patients suffering from a metastatic mammary adenocarcinoma either over columns of 'native' protein A (seven patients; group A) or over columns of protein A in which the Fc-binding capacity was destroyed (five patients; group B). A protein A leaking occurred with the same incidence (about 20% of the sessions) in both groups. However, major acute side effects (hypotension, chills, mild fever, etc.) and necrolytic responses were seen only in some patients from group A. In these cases, the incidence of side effects, but not of tumoricidal responses, increased with the protein A serum concentrations reached 1 h after the end of the sessions (25-150 ng ml-1). The data suggest that the therapeutic efficacy of ex vivo protein A immunoadsorption in breast cancer is related to the Fc-binding capacity of the columns rather than to a leakage of 'native' protein A into the blood stream.
Adenocarcinoma↗
Ex vivo perfusion of plasma over protein A columns in human mammary adenocarcinoma. Role of the Fc-binding capacity of protein A in the side effects and the tumoricidal response.
Plasma of twelve patients presenting with a metastic mammary adenocarcinoma was perfused ex vivo over columns of protein A covalently linked to crystalline silica. The plasma of seven patients (group A) was perfused over columns of protein A exhibiting a normal Fc-binding capacity and the plasma of five (group B) over columns of protein A in which the Fc-binding capacity was destroyed. In group A, all patients experienced acute, easily manageable, side effects (hypotension, chills, mild fever, leucocytosis and pain in tumour sites) during or immediately after the immunoadsorption procedures, and three exhibited an objective partial regression after two to five sessions. In contrast, none of the patients from group B developed any acute side effects and all showed evident progression of their disease during the treatment. Tumour cells in all stages of destruction, sometimes surrounded by extensive fibrosis, were seen in biopsies of patients A. However, focal areas of active tumour proliferation were always present in these patients. These data confirm that ex vivo perfusion over protein A columns of plasma from patients with cancer can induce a tumoricidal response in some instances and show that the Fc-binding capacity of protein A is most probably responsible for the necrolytic response and the side effects.
Adenocarcinoma↗
Beneficial effects of intensive plasma exchange followed by immunosuppressive therapy in severe Graves' ophthalmopathy.
Nine patients with severe Graves' ophthalmopathy were treated by intensive plasma exchange, followed by immunosuppression. Severity of ocular involvement and response to therapy were evaluated clinically by numerical scoring (ophthalmopathy index). Serum thyroid stimulating immunoglobulins (TSI) and urinary excretion of glycosaminoglycans (GAG) were measured immediately before and immediately after plasmapheresis. Plasma exchange was rapidly accompanied by marked clinical improvement in 8/9 patients. The most marked effects were on soft tissue involvement, proptosis, intraocular pressure, and visual acuity. The ophthalmopathy index decreased from 9.7 +/- 4.1 to 5.7 +/- 2.2 (P less than 0.001) after plasmapheresis. Serum TSI levels were initially elevated in 6 patients and remained positive in 3 patients after treatment. Urinary GAG excretion was initially 2- to 12-fold normal levels and was decreased by 60%. After plasmapheresis, patients received immunosuppressive drugs for 3-6 months. The follow-up period, after withdrawal of drugs, ranged from 5 to 38 months with a median of 17 months. The ocular condition remained stable in 6 patients. Three patients had a relapse 1 year after plasmapheresis: they were treated a second time by plasma exchange with subsequent improvement. In conclusion, intensive plasma exchange provided prompt and effective improvement in patients with severe progressive Graves' ophthalmopathy. This therapeutic procedure, followed by immunosuppression, gave long lasting results. Relapses were responsive to plasmapheresis therapy. The data suggest that plasma exchange may represent the best primary treatment for severe progressive Graves' ophthalmopathy.
Adult↗