Beta2 Microgolbulin amyloidsis in uremic patients

Aim: The aim of this work was designed to study some parameters of uremic- oxidant stress and their impact on the pathogenesis of dialysis- related amyloidosis. Subjects and This study was carried on 40 uremic patients and 10 normal subjects as control group [group l]. Patients were divided into 4 groups according to the duration of hemodialysis. Group II: 10 uremic patients on conservative treatment. Group III: 10 patients on hemodialysis for 1-5 years. Group IV: 10 patients on hemodialysis for 5-10 years. Group V: 10 patients on hemodialysis for more than 10 years. AII patients were subjected to thorough history taking, clinical examination, routine and specific laboratory investigations [plasma and tissue malonyldialdhyde, plasma advanced oxidation protein products, vitamin C and E and beta2 microglobulin concentration]. Histopathological study was done by light and electron microscope and histochemical assay for beta2 microglobulin in the affected tissue. plasma and tissue concentration of MDA were significantly higher among uremic non-dialysed and HD patients than in controls. Plasma AOPP were significantly higher in uremic non-dialysed and HD patients as compared to the control group. Plasma vitamin C was significantly lower in patients than in controls, while its oxidized product [dehydroascorbate] was significantly higher among the same groups as compared to the control group. Plasnma vitamin E was normal among all groups. It was significanthy inversely correlated with plasma MDA. PIasma beta2 M was significantly higher in uremic non-dialysed and HD patient as compared to the control group. Light and electrcon microscopical studies showed no amyloid deposits in group I and II, but in groups III, IV and V the incidence amyloid deposits were 10%, 40% and 70°, respectively. The prevalence of beta2 M amyloid in H patients was positively and significantly correlated to the duration of HD. Immunohistochemical study showed beta2 M deposition in all tissue specimens but the intensity of deposition was higher in uremic patients as compared i the control group. Conclusions: Oxidant-stress is well documented and clearly expressed both at the plasma and tissue levels in uremic and HD patients. It may have an important role in the pathogenesis of DRA through creating a state of carbonyl stress that modifies beta2M increasing its amyloidogenic tendency

Oxidative stress and neonatal jaundice: an etiological study

This study aimed at investigating the role of oxidative stress in the development of neonatal jaundice. The enzyme activities of erythrocyte glucose-6-phosphate dehydrogenase [G6PD], plasma glutathione peroxidase [GSHPx] and glutathione-S-transferase [GST] were measured by quantitative determination of enzyme activity in 40 jaundiced full term newborns with different peak bilirubin levels [12.5 - 20 mg/dl] [not attributable to any known etiology] and 20 control newborns. The level of plasma advanced oxidation protein products [AOPP], an index of oxidative stress was also measured in these newborns. None of the jaundiced newborns needed phototherapy or exchange blood transfusion before the study. Plasma GSHPx activity was significantly lower in infants with hyperbilirubinaemia compared to control group. However, the enzyme activities of both plasma GST and erythrocyte G6PD as well as plasma AOPP concentrations were significantly higher in jaundiced newborn infants than in the control group. Plasma GSHPx activity demonstrated a significant negative correlation with GST activity, bilirubin concentration and AOPP levels. A significant positive correlation was also evident between serum bilirubin and plasma AOPP concentrations. The results of this study suggest that low GSHPx activity in jaundiced newborn infants might predispose these infants to oxidative stress. This may result in the development of mild oxidative hemolysis and jaundice