High copper, cadmium and lead decreased iron absorption and negatively affected hematological parameters.

Children with TM are posed with an increased risk of psychopathology.

The basal cortisol level and cortisol response to ACTH stimulation test were assessed in patients with sepsis, the results being compared to a control group of 30 healthy persons. The study group included 49 patients with sepsis and 30 healthy subjects as a control group. The mean age in the study group was 42.6 +/- 18.7 years and 41.4 +/- 12.1 years in the control group. Fifteen of the 49 (30.6%) patients had hospital-acquired and 34 (69.4%) patients community-acquired sepsis. Etiological agent was isolated in 35 (71.4%) patients (57.1% gram negative bacteria and 34.3% gram positive bacteria, plus 8.6% polymicrobial). Fourteen of 49 (28.6%) patients died. Mean basal cortisol level was 597.1 +/- 304.6 nmol/l (range 217.8-1667.9) in the study group and 460.2 +/- 180.8 nmol/l (range 253.6-988.9) in the control group. Mean basal cortisol level in the study group was significantly higher than that of the control group (p < 0.05). Mean basal cortisol level was found to be 725.5 +/- 448.9 nmol/l in the patients who died and 545.8 +/- 210.9 nmol/l in the patients who recovered. The difference between the two groups was found to be significant (p < 0.05). ACTH stimulation test was performed in 43 of the patients and 30 healthy subjects. Cortisol response was significantly lower (mean 277.7 +/- 216.9 nmol/l) in the patients than that detected in the control group (mean 519.6 +/- 279.2) (p < 0.001). Mean cortisol response in the patients who died was 227.2 +/- 224.5 nmol/l and 302.1 +/- 212.7 nmol/l in the patients who recovered (p > 0.05). Adrenocortical insufficiency was detected in 16.3% of the patients and 42.9% of these patients died. In conclusion, sepsis is characterized by high basal cortisol level which may show a poor prognosis and a blunted cortisol response to ACTH stimulation. A small percentage of patients with sepsis may develop adrenocortical insufficiency.

Thyroid hormone supplementation in septic rats had a beneficial effect on the sepsis criteria and also resulted in a lower rate of mortality.

Endotoxaemia in obstructive jaundice may induce overproduction of nitric oxide that may lead to impairment of cGMP-associated vasodilatation and disrupt autoregulation of the renal vascular bed. This may contribute to renal failure in obstructive jaundice.

Although effects of stress on the stomach have been extensively investigated in children and adults, our knowledge about effects of fetal distress (FD) on the fetal stomach is quite limited. Therefore, an experimental study was planned to evaluate the effects of FD on fetal gastric physiology and histology. In this study, a model of FD was created by way of intermittent maternal aortic occlusion in pregnant rabbits. In total, 21 fetuses of 6 pregnant rabbits were available for surgical and laboratory procedures. Laboratory examinations showed that (1) fetal gastric acid secretion was 4.24 ± 2.68 (xEq/h in the control group and 18.08 ± 6.34 (xEq/h in the distress group (p < 0.01) and (2) fetal gastric PGE 2 level was 16.59 ± 6.15 mg/g wet weight in the control group and 9.86 ± 3.46 mg/g wet weight in the distress group (p < 0.05). Histopathologically, there were mild hemorrhagic and errosive changes in the distressed fetuses, but not in control fetuses. These findings support that FD adversely affects fetal gastric physiology through two mechanisms consisting of increased gastric acid secretion and decreased fetal gastric protection in rabbits. Consequently, gastric injury should be noted as a potential problem among hypoxia-associated abnormalities encountered in the distressed fetus.Although precise definition of the term "fetal distress" (FD) is not sufficiently clear, it is frequently used in perinatology to express fetal hypoxia. It is believed that fetal hypoxia shows close relation with increased perinatal morbidity and mortality. 1 Therefore, awareness in the context of hypoxia-induced problems has a critical importance in clinical practice.Because FD represents a generalized disorder in fetal oxygenation, it may compromise any tissue or organ. Acute respiratory distress syndrome is the best known entity related with FD. 2 Additionally, some studies on the subject suggest that FD causes neurological damage, neonatal sepsis, necrotizing enterocolitis, or acute renal failure. 34 Recently, it has been reported that a number of the newborns with esophagogastritis had the history of FD. 5 However, the effects of the FD on fetal gastric physiology and histology have not been investigated previously. In this study, we designed an FD model in maternal origin and investigated its effects on gastric acid secretion, PGE 2 levels, and histopathology of the fetal stomach.

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