Prevalence of glucose-6-phosphate dehydrogenase and thyroid hormones deficiency in neonatal jaundice

G6PD deficiency is the most common inherited metabolic disorder and clinically significant red cell enzyme defect in man. Severe neonatal jaundice proved to be the most common clinical manifestation and a globally important most dangerous consequence of G6PD deficiency. Prolonged jaundice is sometimes associated with congenital hypothyroidism. So the early characterization of G6PD activity and thyroid hormone levels provides an etiological diagnosis for neonatal jaundice as well as the opportunity to give the newborn's family information concerning hemolytic crisis prevention and an early management in case of hypothyroidism. This study was conducted in an attempt to evaluate the prevalence of G6PD deficiency and hypothyroidism in relation to neonatal physiological hyperbilirubinemia. The study included 50 neonates aged between 6 hr - 5 days, forty infants had jaundice and the other ten [control], were healthy neonates, matching the same age. All infants of the study were subjected to C-RP test, routine hematological evaluation, and serum total bilirubin levels, quantitative red blood cells G6PD assay and thyroid hormone levels. All the fifty cases of both jaundiced and healthy neonates were negative for C-RP test indicating that the 40 cases had physiological jaundice .The study revealed that G6PD enzyme was lower than normal level in 2 cases [5%]. TSH level was found to be higher than normal in 13 jaundiced neonates out of 40 [33%]. Seven jaundiced neonates [18%] had T4 hormone lower than normal while all the 40 jaundiced cases had normal T3 level. Correlation of the total bilirubin was significant with TSH and T3 at 0.05 levels, while there was no significance with both T4 and G6PD. statistically there was no correlation between bilirubin and both G6PD enzyme and thyroid hormones, but the incidence of hypothyroidism in this study was high [18%] and the incidence of G6PD deficiency was [5%]. This indicates a role of G6PD deficiency and hypothyroidism in developing neonatal jaundice among neonates. So, early neonatal screening program is recommended for early management

Oxidative damage in embryo and placenta of streptozotocin-induced diabetic rats

Maternal type 1 diabetes is associated with an increased risk for fetal malformations. The mechanism by which diabetes caused teratogenic disorders is not fully known. Previous studies have demonstrated that many teratogenic diabetic cases were related to free radical oxygen species. This study was conducted to evaluate the effect of maternal diabetes on both embryo and placenta by estimating the oxidative and DNA damage in embryo and placenta of diabetic mellitus- induced rats. The possible role of olive leaves extract of Olea europaea [O. europaea] plant in repairing the damage was also assessed. Diabetes mellitus was induced by streptozotocin [STZ] by a single intraperitoneal injection [35 mg/kg b wt]. O.europaea leaves water extract was administered orally [550 mg/ l00g b wt/ day] for 5days before pregnancy and 18 days after. Malondealdehyde [MDA] level, glutathione peroxidase [Gpx] and superoxide dismutase [SOD] activities and glycogen concentration were measured in term embryo and placenta homogenates of diabetic and control rats. Moreover, the evaluation of DNA damage was carried out by the Alkaline Comet Assay using embryos and placentas taken from STZ-induced diabetic and control pregnant rats. the results showed an elevation in MDA level of the diabetic groups of both embryo and placenta compared to that of the control. This was accompanied by reduction in Gpx and SOD activities indicating oxidative damage. Glycogen level was reduced in diabetic groups of embryo and placenta. Both oxidative and hyperglycemic status were improved in the groups treated with olive leaves water extract. The percentage of tail DNA and tail moment values were also higher in both embryo and placenta of the diabetic -induced rats. DNA damage seems to be partly ameliorated in groups treated with O. europaea leaves water extract. This study indicated that maternal hyperglycemic condition in diabetic- induced pregnant rats could generate oxidative and DNA damage to embryo and placenta that could be ameliorated by oral doses of olive leaves water extract

Effect of hypothyroid status on lipid peroxidation, antioxidant defences and susceptibility to oxidative stress under amiodarone therapy in female rats

The effect of free radicals on human beings has attracted considerable attention due to their close relation to health and disease. This study was carried out to investigate the antioxidant status in thyroid and liver due to treatment with amiodarone [AM] and the relationship between AM treatment and thyroid function in case of pre-existence of hypothyroidism. The present study comprised of two experiments, each of them extended for 2 months. The first one was designed to induce hypothyroidism and the second for treatment with AM. Serum malondialdehyde [MDA] and reduced glutathione [GSH] levels were measured as indicators of redox status. The levels of serum triiodothyronine [T3], thyroxine [T4] levels and thyroid stimulating hormone [TSH] were measured the agonist/antagonist interactions between the drug and thyroid hormones. Liver enzymes-Alanine aminotransaminase [ALT] and Aspartate aminotransaminase [AST] activities-and lipid parameters were measured in serum as well. In addition, hisopathological examinations for thyroid and liver tissues were done. The results showed that: 1] serum T3 and T4 levels were increased, while TSH levels were decreased in hypothyroid AM treated group, whereas in euthyroid AM treated group, serum T3 was decreased but serum T4 and TSH levels increased. 2] total cholesterol and LDL increased in both AM treated groups showing a state of hyperlipidemia. 3] serum MDA level was increased while serum GSH was decreased in AM treated hypothyroid group and in euthyroid AM treated one as well, inducing a state of oxidative stress. Serum MDA levels were decreased while serum GSH were increased in Hypo+. 4] ALT and AST increased in all AM treated groups. 5] hisopathological examination of thyroid and liver tissues showed some structural abnormalities due to AM treatment. Based on these results, patients with hypothyroidism should be monitored periodically their thyroid and liver functions during AM therapy due to its stimulation for the formation of reactive oxygen species, causing oxidative damage in both liver and thyroid functions and their tissues. These findings suggested that a state of hypothyroidism may exert beneficial protective and curative effects on this situation by decreasing T3, T4, ALT and AST levels, attenuating the endogenous antioxidant levels and decreasing lipid peroxidation