The effects of nitrous oxide on vitamin B12 and homocysteine levels in methyltetrahydrofolate reductase gene mutation.

BACKGROUND: We aimed to investigate the effects of nitrous oxide on plasma total homocysteine and vitamin B12 levels in patients with or without methyltetrahydrofolate reductase (MTHRF) gene mutation. METHODS: After obtaining the ethics committee approval and written informed consents of patients, 93 patients between 18-70 years of age scheduled for surgery anticipated to last 1-4 hours were enrolled in the study. Patients with contraindications for nitrous oxide use were excluded. Preoperatively, blood samples were obtained from all patients for the determination of MTHFR gene mutation. Anesthesia induction was achieved with 3 mg.kg-1 of propofol and 1 µg.kg-1 of fentanyl. Anesthesia maintenance was performed with sevoflurane and with a carrier gas composed of 40 % O2 and 60 % N2O. Venous blood samples were obtained after venous canulation, and 24 hours after extubation for the analysis of plasma total homocysteine, vitamin B12 levels. RESULTS: Eighty-one patients were included in the study. Postoperative vitamin B12 levels were found to be significantly lower when compared with their preoperative levels (p<0.05). It was found that MTHRF gene polymorphism had no significant effect on postoperative plasma total homocysteine and serum vitamin B12 levels (p>0.05). Postoperative plasma total homocysteine levels were found to be significantly different between patients with operation times under and over 3 hours (p=0.028). CONCLUSIONS: We conclude that MTHRF gene polymorphism had no significant effects on postoperative plasma total homocysteine levels. However, we found that homocysteine levels might rise in patients who received general anesthesia with nitrous oxide for longer than 3 hours (Tab. 7, Ref. 26).

Angiotensin-converting enzyme insertion/deletion polymorphism has no effect on the risk of atherosclerotic stroke or hypertension.

BACKGROUND AND PURPOSE: Stroke is a heterogeneous multifactorial disease. Hence, a large number of candidate genes are involved in stroke pathophysiology, such as blood pressure regulation and atherosclerosis. Although angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism is considered to have a role in hypertension, coronary artery disease, and myocardial infarction, its relationship with cerebrovascular disease and hypertension in stroke in different ethnic populations is still inconsistent. METHODS: ACE I/D polymorphism, detected by polymerase chain reaction (PCR), was studied in 97 patients with large-vessel and 60 patients with small-vessel atherosclerotic stroke (44 asymptomatic, 16 symptomatic lacunes) and 85 healthy subjects with normal brain imaging. The demographic data, lipid profile and risk factors of patients and controls were obtained retrospectively. RESULTS: ACE genotypes were in Hardy-Weinberg equilibrium in both patients and controls. Prevalences of DD, ID and II genotype were 41%, 40%, and 19%, respectively, in the stroke group. Differences in ACE I/D polymorphism distribution were statistically insignificant between the groups. This lack of association between stroke and ACE I/D polymorphism did not change in the presence of traditional risk factors (hypertension, diabetes mellitus, smoking, and dyslipidemia). Although hypertension was significantly more common in the patient groups, ACE I/D polymorphism showed no effect on hypertension risk. This lack of association also did not change according to groups or in the presence of diabetes mellitus, male gender or smoking. CONCLUSION: ACE I/D polymorphism did not predict the risk of stroke or hypertension in our population living in the western Black Sea region of Turkey.

Relationship of apoE polymorphism with lipoprotein(a), apoA, apoB and lipid levels in atherosclerotic infarct.

BACKGROUND AND PURPOSE: Apolipoprotein E (apoE) polymorphism is suggested to be a risk factor in stroke in some populations, either by affecting lipid parameters or independently. Its effect on lipoprotein(a) [Lp(a)] is not known. The roles of apoE polymorphism and of high Lp(a) levels in atherosclerotic stroke (AS) in the Turkish population are unclear. Our aim was to investigate the relationship of apoE alleles and Lp(a) level with AS and the relationship of apoE alleles with Lp(a) and other lipid parameters. METHODS: ApoE polymorphisms and lipid parameters were prospectively evaluated in 85 patients and 77 controls with normal brain imaging. RESULTS: Only hypertension, diabetes mellitus, associated vascular diseases and decreased high-density lipoprotein cholesterol levels were found to be independent risk factors for stroke. However, in the presence of apoE/E4 allele, increased low-density lipoprotein cholesterol (LDL-chol), apolipoprotein B (apoB) and Lp(a) levels and in the presence of apo E/E3 allele, only Lp(a) levels were determined as risk factors. CONCLUSION: This study showed that while apoE polymorphism was not a risk factor itself, high Lp(a), LDL-chol and apoB were determined to be risk factors in E3 or E4 carriers.

Effect of seminal plasma calcitonin levels on sperm mobility.

This study investigated the effect of the seminal and blood plasma calcitonin levels on the sperm motility in idiopathic infertile patients. The number of sperm cells and their motility were evaluated in the spermiograms of 52 idiopathic infertile patients. The levels of seminal plasma calcitonin were studied with double antibody technique using a DPC kit. Fifty-two patients were divided into 2 groups according to the motility rates of sperm and 20 healthy volunteers were assigned to a control group. The difference between the groups was evaluated by using Kruskall-Wallis and Mann-Whitney U tests, and the correlation of seminal and blood calcitonin levels with sperm motility were determined. The difference in motility rates between the 3 groups was statistically significant (p = .000, p < .05). Blood plasma calcitonin levels were in normal ranges in all cases and no significant difference was found among the 3 groups (chi2 = 2.7219, p = .2589, p > .05). While sperm motility was correlated with seminal calcitonin levels (r = .8581), blood calcitonin levels did not show a correlation with sperm motility rate (r = -.0265). Moreover, there was no correlation between seminal and blood plasma levels of calcitonin (r = -.0010). Motility rates decreased in the patients with low seminal calcitonin levels and seminal calcitonin levels had a significant effect on sperm motility.