Association between TSH Values and GFR Levels in Euthyroid Cases with Metabolic Syndrome.

BACKGROUND: Metabolic syndrome (MetS) is associated with the risk of developing chronic kidney disease. Although the negative effects of high thyroid-stimulating hormone (TSH) values on glomerular filtration rate (GFR) levels have been known for years, the negative effects of increased TSH on GFR in euthyroid cases have been reported in recent years. This study was aimed at investigating the association between the effect of increased TSH values and estimated-GFR (eGFR) levels in euthyroid cases with MetS. METHODS: For this hospital-based descriptive study, 191 MetS cases (123 females, 68 males) were evaluated. Those whose TSH was not within 0.5-4.5 uIU/mL, eGFR was <40 mL/min/1.73 m2, and/or reported any thyroid/kidney disease were excluded. Partial correlation coefficients were calculated to investigate the relationship between the eGFR values and several other numerical variables while controlling for age and BMI in addition to the adjusted gender effect. Thereafter, the multiple linear regression analysis with a stepwise variable selection approach was used to reveal the independent factors that could affect the logarithmically transformed eGFR. RESULTS: The median age was 52 (19-65) years, the median eGFR was 94.3 (41.3-194) mL/min/1.73 m2, and the median TSH was 1.58 (0.50-4.50) uIU/mL in the whole group. Increased TSH even in the normal range was associated with eGFR after adjusting for age and body mass index (BMI), especially in females. The high age (b = -0.160, p=0.005), high BMI (b = -0.134, p=0.020), high TSH (b = -0.380, p < 0.01), and high uric acid (b = -0.348, p < 0.01) were found as significant predictors of the eGFR in MetS patients. CONCLUSION: Independent of age and BMI, elevated TSH even in the euthyroid range showed an association with the eGFR in female MetS cases who had normal kidney functions. This correlation was stronger than the correlations between the eGFR and the MetS diagnostic parameters. These findings need further studies on the issue..

Polidocanol (Lauromacrogol 400) has anti-angiogenic effects in vitro and in vivo.

OBJECTIVE: Polidocanol is the most frequently used sclerosant for sclerotherapy all around the world. Our experimental research aims to find out the angiogenic effects of Polidocanol. MATERIALS AND METHODS: Angiogenic activity of polidocanol was examined in vivo in the chick chorioallantoic membrane (CAM) model, cell viability assay (human umbilical vein endothelial cells - HUVECs) and in vitro tube formation assay of HUVECs. RESULTS: In CAM assay, a significant decrease on CAM vessel growth was observed after the application of polidocanol solutions. Vessel growth inhibition was strongly dose-dependent. There was a cytotoxic effect on HUVECs in the presence of polidocanol observed with MTT assay (p < 0.05). In the tube formation assay, statistically significant decrease in tube formation was observed in polidocanol group. It was found that polidocanol had an anti-angiogenic effect (p < 0.05). The results provide evidence that polidocanol decreases angiogenesis and has a cytotoxic effect on ECs. CONCLUSIONS: These results provide evidence that Polidocanol (lauromacrogol 400) have strong anti-angiogenic effects in vitro and in vivo. Further researches needed to reveal early and long-term effects of polidocanol in the human vascular system and new treatment approach as an anti-angiogenic therapy.

Comparison of angiogenic and proliferative effects of three commonly used agents for pulmonary artery hypertension (sildenafil, iloprost, bosentan): is angiogenesis always beneficial?

OBJECTIVE: Pulmonary artery hypertension (PAH) is devastating disease that has very serious outcomes. Dysregulated angiogenesis is one of the main responsible courses in pathophysiology of disease. Our experimental research intends to find out and compare the angiogenic effects of medications used sildenafil, iloprost, and bosentan in the treatment of PAH. MATERIALS AND METHODS: This study was performed in Department of Biochemistry and Cancer and Stem Cell Research Laboratory of our institutes between August and October 2014. Angiogenic activity of sildenafil, iloprost, and bosentan were examined in vivo in chick chorioallantoic membrane (CAM) model and in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs). Proliferative activity of these three agents was also determined through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay on HUVECs. RESULTS: In CAM assay, when compared to the control and drug groups, treatment with sildenafil solutions resulted in a significant dose-dependent increase (budding, sprouting, extravasation) on CAM vessel growth. While there was no significant proliferative effect with iloprost and bosentan, presence of sildenafil caused a statistically significant proliferation on HUVECs following 24 and 48 h incubation (p < 0.05) compared to the control group. Comparing the tube length/area ratio values, there was statistically significant increase in sildenafil group with respect to the other 2 groups (p < 0.05). Iloprost and bosentan did not show a significant effect. CONCLUSIONS: The results provide evidence that sildenafil but not iloprost and bosentan induces angiogenesis in vitro and in vivo. Dysregulated angiogenesis, as an important pathophysiological part in the progression of PAH, may be triggered by the chronic ingestion of sildenafil in the long treatment period and may cause negative effects.

Aspartame induces angiogenesis in vitro and in vivo models.

Angiogenesis is the process of generating new blood vessels from preexisting vessels and is considered essential in many pathological conditions. The purpose of the present study is to evaluate the effect of aspartame on angiogenesis in vivo chick chorioallantoic membrane (CAM) and wound-healing models as well as in vitro 2,3-bis-2H-tetrazolium-5-carboxanilide (XTT) and tube formation assays. In CAM assay, aspartame increased angiogenesis in a concentration-dependent manner. Compared with the control group, aspartame has significantly increased vessel proliferation (p < 0.001). In addition, in vivo rat model of skin wound-healing study showed that aspartame group had better healing than control group, and this was statistically significant at p < 0.05. There was a slight proliferative effect of aspartame on human umbilical vein endothelial cells on XTT assay in vitro, but it was not statistically significant; and there was no antiangiogenic effect of aspartame on tube formation assay in vitro. These results provide evidence that aspartame induces angiogenesis in vitro and in vivo; so regular use may have undesirable effect on susceptible cases.