Biomedical subjects

I Iskander

Publications and source records attributed to I Iskander.

5 recordsLinked to original sources

PubMed1998

The acute effect of intravenously administered recombinant human erythropoietin on the immune response of uremic patients maintained on regular hemodialysis.

The uremic patient on regular hemodialysis (RHD) is subjected to a wide range of immune modulators including the uremic state per se, multiple transfusions and exposure to bioincompatible materials and endotoxins. Erythropoietin (EPO) therapy may raise concern about its potential influence on this complex scenario. To envisage this issue, 15 adequately selected patients, stable on RHD, were randomly assigned in a 2:1 ratio into EPO and placebo groups. After initial assessment and determination of baseline values, they received, in a double-blind manner, either EPO or normal saline as an intravenous bolus immediately after termination of dialysis for 30 successive sessions. Thirty minutes later, following sessions 1, 10, 20, and 30, samples were obtained for determination of blood counts, red cell indices, peripheral lymphocyte counts (PLC), CD4/CD8 ratios, blood EPO levels, and serum concentrations of interleukins (IL) IL-2r, IL-3, and IL-6, tumor necrosis factor (TNFs and TNFalpha), and neopterin (NPT). Blood EPO levels displayed the predicted rise in the EPO group, which correlated with partial improvement of red cell parameters. The mean total leukocyte count and PLCs was significantly increased in the EPO group (p < 0.05) but not in the placebo group. CD4/CD8 ratios were not significantly changed in either group. The serum concentrations of IL-2r, IL-3, and NPT remained fairly stable while that of IL-6 was widely variable in both study groups. The mean serum concentrations of TNF and particularly TNFalpha showed a steady and statistically significant increment in the EPO group from 6 to 41 pg/ml (p < 0.05) and 93 to 128 pg/ml (p < 0.03), respectively. No significant change was noticed in the control group. It is concluded that intravenous administration of EPO under the conditions of this study may have an immune stimulating effect. This is shown by the release of TNFs, which in turn may be responsible, through different potential mechanisms, for the increase in the mean peripheral neutrophil count and the blunting of erythroid responsiveness to EPO therapy.

Adjuvants, Immunologic↗

PubMed1996

Immunoglobulin-A and the pathogenesis of schistosomal glomerulopathy.

Several observations suggest that the evolution of schistosomal glomerulopathy into clinically overt and progressive disease may involve pathogenetic mechanisms other than simple glomerular deposition of parasitic antigens. In a previous study, IgA was suggested to be a mediator of late glomerular lesions in this disease. This issue is further addressed in this work. The study includes 32 patients with hepatosplenic schistosomiasis, of whom 16 had overt glomerular involvement, along with four control groups: (a) 15 healthy volunteers; (b) 15 patients with simple intestinal mansoniasis; (c) 17 patients with non-schistosomal chronic liver disease; and (d) 21 subjects with primary nephrotic syndrome not associated with schistosomiasis. Routine assessment was done for all subjects including confirmatory tests for schistosomal infection, liver and renal function tests, hepatitis viral markers and abdominal ultrasonography. The total serum concentrations of IgG, IgM, IgA were measured, as well as their respective circulating immune complexes, rheumatoid factors, anti-gliadin- and anti-DNA-antibodies. Liver and renal biopsies were obtained from the relevant groups and studied by light microscopy. Renal biopsies were also examined by immunofluorescence. Patients with simple intestinal schistosomiasis had a significant increase in IgM antigliadin antibodies. Those complicated with hepatosplenic involvement also had a significant increase in the mean IgG anti-gliadin antibodies, IgG rheumatoid factor and IgM anti-DNA activity. Cases further complicated by overt glomerular disease showed a distinct IgA predominance, mainly expressed in the serum anti-gliadin antibody pool and anti-DNA activity. This profile was essentially similar to that observed in control cirrhotics. There was a significant increase in the frequency of IgA glomerular deposits in renal biopsies obtained from patients with overt schistosomal glomerulopathy, in contrast to control nephrotics. The deposits were mainly mesangial, but were also encountered in subendothelial, subepithelial and peritubular locations. Their frequency was significantly higher with more advanced lesions as seen by light microscopy. The relevance of these data is discussed, leading to the following conclusions: (a) serum IgA-anti-gliadin and -anti-DNA antibodies, and glomerular IgA deposits are markers of significant renal involvement in patients with hepatosplenic schistosomiasis. (b) IgA may be involved in the pathogenesis of advanced glomerular pathology when superimposed on parasite-induced lesions. (c) There is a significant increase in serum auto-reactivity in hepatosplenic schistosomiasis, which may also have pathogentic implications. (d) Increased production by the inflammatory bowel lesions, impaired clearance by the fibrotic livers and probable switching of immunoglobulin synthesis are suggested to explain the observed IgA predominance in those who develop renal complications.

Adolescent↗

PubMed1985

Glycosylated proteins in diabetic nephropathy.

This study was carried out on 55 diabetic patients, 20 of whom had diabetic nephropathy, and 10 controls. Glycosylated haemoglobin, glycosylated serum protein, glucoprotein, serum protein electrophoresis, blood urea, serum creatinine and beta 2-microglobulin were measured. A significant increase of glucoprotein was observed in patients with diabetic nephropathy. No correlation was found between glycosylated serum protein and glycosylated haemoglobin and duration of diabetes. Glycosylated serum protein showed a positive correlation with beta 2-microglobulin, indicating a link between renal involvement and the rise in glycosylated serum protein. Whether there is a pathogenic relation between glycosylated serum protein and the development of nephropathy awaits further evidence.

Adult↗

PubMed1980

Altered cell mediated immunity in atrophic rhinitis.

Cellular immunity was studied in patients with atrophic rhinitis using the in vitro leucocyte migration and the spontaneous rosette tests. Cellular hypersensitivity to crude nasal homogenate was detected in 90 per cent of our cases as shown by inhibition of the leucocyte migration. The spontaneous rosette test showed a reduction in the number of T-cells forming rosettes which reflects a decrease in the absolute number of T-lymphocytes. This altered cellular reactivity or loss of tolerance to nasal tissues may be precipitated primarily by virus infection, malnutrition and/or immuno-deficiency which trigger a destructive auto-immune process with the release of antigen(s) of nasal mucosa into the circulation.

Adolescent↗

PubMedDate not supplied

Human leukocyte antigen in genodermatosis.

Tissue typing performed on the lymphocytes of 41 patients, including: 23 patients with ichthyosis (15 of autosomal dominant and 8 of the x-linked variety; 8 patients with tuberous sclerosis (epiloia); and 10 patients with acrodermatitis enteropathica (AEP). In addition, tissue typing was performed for a control group of 80 healthy unrelated subjects of the same ethnic origin as the patients. A significant increase of A2 antigen or its crossreacting antigen A28 was detected among the three diseases studied. A significant increase of HLA-A2 antigen was found in autosomal dominant ichthyosis, while the x-linked variety showed significant association with HLA-Cw2. A significant association with HLA-A28 antigen was noticed in both epiloia and AEP. The suggested mechanisms of such association may be referred to as incidental genetic linkage with mutants causing disease or deficiency.

Acrodermatitis↗