Muhlise Alvur

Magnesium, zinc and iron levels in pre-eclampsia

Objective: To determine the change in erythrocyte and plasma magnesium, plasma zinc and serum iron concentrations in pre-eclampsia. Methods: Twenty women with pre-eclampsia and 20 control subjects matched for gestational age were examined. The levels of magnesium, zinc and iron in all subjects were measured by flame atomic absorption spectrometry. In the pre-eclamptic women, who were supplemented with magnesium salts, these measurements were repeated after delivery. Results: The intraerythrocytic magnesium levels before supplementation were significantly lower in the pre-eclamptic patients than in the healthy pregnant women (0.98 - 0.15 vs. 1.35 - 0.30 mmol/l; p < 0.001) and increased (to 1.25 - 0.25 mmol/l) after treatment with magnesium. The plasma magnesium and zinc, and the serum iron concentrations were not significantly different between the pre-eclamptic and the healthy pregnant women. Conclusions: Our results suggest that low cellular magnesium levels in women with pre-eclampsia may contribute to the development of hypertension in these patients, and that the measurements of plasma zinc and serum iron concentrations are of doubtful clinical value in the management of pre-eclampsia.

Levels of stable metabolites of prostacyclin and thromboxane A2 and their ratio in normotensive and preeclamptic pregnant women during the antepartum and postpartum periods

OBJECTIVE To measure the levels of the circulating metabolites of prostacyclin and thromboxane A2 during the antepartum and postpartum periods in severe preeclamptic and eclamptic patients as well as in normotensive pregnant women. METHODS 6-Keto-prostaglandin F1alpha (6-keto-PGF1alpha) and thromboxane B2 (TxB2) were measured in the plasma of 15 severe preeclamptic, 15 eclamptic, and 15 normotensive pregnant women during the antepartum and postpartum (5th day) periods. At the same time blood pressure measurements were obtained. Kruskal-Wallis, Wilcoxon rank-sum, and Wilcoxons signed-rank tests were used for statistical analysis. RESULTS 1) There was no significant difference in the levels of 6-keto-PGF1alpha and TxB2 of the normotensive pregnant women between the antepartum and the postpartum (5th day) periods. 2) In the severe preeclamptic and eclamptic groups, 6-keto-PGF1alpha levels showed significant increase after the delivery (P < 0.01, and P < 0.001, respectively). 3) In the severe preeclamptic and eclamptic groups TxB2 levels showed significant decrease after delivery (P < 0.01, and P < 0.001, respectively). 4) The 6-keto-PGF1alpha/TxB2 ratio both during the antepartum and the postpartum (5th day) periods showed significant differences between the severe preeclamptic and normotensive, and between the eclamptic and normotensive groups (P < 0.001, and P < 0.001 respectively). 5) No correlation was observed between the mean arterial pressure and the antepartum levels of 6-keto-PGF1alpha TxB2 or their ratios. CONCLUSIONS Our study was able to demonstrate a significant difference in circulating metabolites of prostacyclin and TxA2 between normotensive pregnant women and those with severe preeclampsia and eclampsia. But no correlation was observed between the blood pressure and the antepartum 6-keto-PGF1alpha, TxB2 levels or their ratios. 6-keto-PGF1alpha levels increased and TxB2 levels decreased in the postpartum period (5th day). However, the 6-keto-PGF1alpha/TxB2 ratio was still low in the severe preeclamptic and eclamptic patients when compared with the control group. This situation shows that the pathophysiologic mechanism does not improve completely within a few days after delivery.

Assessment of Genotoxicity in Rats Treated With the Antidiabetic Agent, Pioglitazone

Pioglitazone (PIO), a member of the thiazolidinedione class of antidiabetic agents, specifically targets insulin resistance. Drugs of this class act as ligands for the gamma subtype of the peroxisome proliferator‐activated receptor. Although troglitazone, another drug in this class, displayed unacceptable hepatotoxicity, PIO was approved for human use by the U.S. Food and Drug Administration. To our knowledge, there are no published reports on the genotoxicity of PIO; however, the package insert indicates that it has minimal genotoxicity. In this study, we used the comet assay to investigate the DNA damage in the peripheral blood and liver cells of rats treated with PIO. Sixteen male Sprague‐Dawley rats were randomly distributed into four groups, and dosed daily for 14 days by oral gavage with 0, 10, 20, and 40 mg/kg/day PIO. A dose‐dependent increase in DNA damage, as assessed by % tail DNA, was observed in both hepatocytes and blood lymphocytes of the PIO‐treated groups, with significant increases detected between the rats treated with all the doses of PIO and the control, and between the rats treated with different PIO doses (P < 0.005 to P < 0.0001). Treating nuclei from the exposed animals with an enzyme cocktail containing Fpg and Endonuclease III prior to performing the comet assay increased the level of DNA damage, which reflects oxidized purine and pyrimidine. Taken together, our data indicate that PIO is able to dose‐dependently induce DNA damage in both the liver and blood lymphocytes of rats, which is partially due to the generation of oxidative lesions. Environ. Mol. Mutagen., 2008.

Leptin levels in Henoch–Schönlein purpura

The objective of this paper is to assess the possible role of nitric oxide (NO) and leptin in Henoch–Schönlein purpura (HSP). We investigated the serum leptin and total nitrite levels in 22 children with HSP in the acute phase and after remission and in 20 age- and sex-matched healthy control. Serum leptin levels (nanograms per milliliter; median, min–max) were statistically higher in the acute phase (12.9, 9.1–19.5) than those in the remission phase (6.1, 3.7–10.5, p<0.001) and in the control group (4.9, 3.8–7.5, p<0.001). Also, serum nitrite levels (micromole per liter; median, min–max) were higher in children in the acute phase (45.0, 32.0–60.0) compared to those in remission phase (30.5, 23.0–48.0) and in the control group (29.5, 18.0–38.0) (p<0.001, p<0.001, respectively). There was a positive correlation between serum leptin and total nitrite levels (r=0.65, p<0.001). We have demonstrated that serum leptin and NO levels were increased during the acute phase in children with HSP, and returned to normal levels in remission. We suggest that leptin and NO may have a role in the immunoinflammatory process of HSP, especially in the acute phase. Further studies are needed to clearly establish the roles of leptin and NO in the pathogenesis of HSP.