The physiological range indicated by the measurements was close to the reference limits for adults (1-7 pmol/l; 9.4-66 pg/ml). PTH level above this range can be considered as hyperparathyroidism in preterm neonates.
BackgroundThe mechanism underlying aortic dilatation is still unknown. Vascular dilatation is thought to be the result of progressive aortic media degeneration caused by defective vascular matrix hemostasis, including TGF-β1 dysregulation. The goal of this study is to draw attention to the potential utility of TGF-β1 as a diagnostic marker in non-syndromic patients with aortic dilatation.MethodsTGF-β1 levels in plasma were measured in 50 patients who had undergone surgery and had a tricuspid or bicuspid aortic valve as well as a normal or dilated ascending aorta. A pathologist also examined thirty resected aorta samples. To specify the reference range of TGF-β1, a control group of 40 volunteers was enrolled in this study.ResultsWe discovered a significant difference in TGF-β1 levels between patients with aortic dilatation and the control group (32.5 vs. 63.92; P < 0.001), as well as between patients with non-dilated aorta but with aortic valve disease, and the control group (27.68 vs. 63.92; P < 0.001). There was no difference between the dilated ascending aorta group and the non-dilated ascending aorta group. We found a poor correlation between TGF-β1 levels and ascending aorta diameter as well as the grade of ascending aorta histopathological abnormalities.ConclusionTGF-β1 concentration does not meet the criteria to be a specific marker of aortic dilatation, but it is sensitive to aortic valvulopathy-aortopathy. A larger patient cohort study is needed to confirm these findings.
Goeckerman therapy (GT) of psoriasis vulgaris is based on the application of crude coal tar and ultraviolet radiation. We investigated DNA damage by the number of micronucleated binucleated cells (MNBC) in lymphocytes, serum homocysteine, vitamin B12, folic acid, and two polymorphisms (C677T and A1298C) in the MTHFR gene in 35 patients with exacerbated psoriasis vulgaris classified according to the psoriasis area and severity index (PASI) score and treated by GT. The median of PASI score decreased from nineteen to five, and MNBC increased from 10 to 18‰ after GT (p < 0.001 in both cases). Correlations of MNBC with homocysteine (Spearman’s rho = 0.420, p = 0.012) and vitamin B12 (rho = −0.389, p = 0.021) before the therapy were observed. Hyperhomocysteinemia was an independent predictor of genotoxicity (OR 9.91; 95% CI, 2.09–55.67; p = 0.003). Homocysteine was higher in females than in males (13 vs. 12 µmol/L, p = 0.045). In contrast, vitamin B12 levels in the females were lower than in the males (160 vs. 192 pmol/L, p = 0.047). Vitamin B12 in the females were negatively influenced by smoking status (160 pmol/L in smokers vs. 192 pmol/L in non-smokers, p = 0.025). A significantly higher MNBC was found in CC homozygous patients (A1298C polymorphism) than in AC heterozygotes (32 vs. 16‰, p = 0.005) and AA homozygotes (32 vs. 18‰, p = 0.036). Our data showed that homocysteine participates in the pathogenesis of psoriasis. Its serum levels correlated with MNBC and allowed the prediction of DNA damage to appear within GT. Both micronutrients status and homocysteine metabolic pathway contribute to the genotoxicity of GT.
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