The aim of the present prospective, randomized study was to investigate and compare the safety and efficacy of dexmedetomidine versus midazolam in providing sedation for gastroscopy. A total of 50 adult patients (25 patients receiving dexmedetomidine and 25 patients receiving midazolam), 18 to 60 years of age, and rated I and II on the American Society of Anesthesiologists physical status classification system were included. A brief questionnaire was used to collect demographic data; patients were asked to rate anxiety, satisfaction with care to date and expected discomfort on a visual analogue scale. The following parameters were measured continuously and recorded every minute: heart rate, mean arterial pressure, hemoglobin oxygen saturation and respiratory rate. The two groups were similar with regard to age, body mass index, sex, education, duration of endoscopy, and ethanol or tobacco use. After the procedure, full recovery time, mean arterial pressure, heart rate, respiratory rate and hemoglobin oxygen saturation levels were similar in both groups. Both groups also had low levels of perceived procedural gagging, discomfort and anxiety scores (P > 0.05), and high satisfaction levels (90.1+/-3.0 for dexmedetomidine versus 84.9+/-4.5 for midazolam; P > 0.05). Retching and endoscopist satisfaction were significantly different in patients receiving dexmedetomidine versus those receiving midazolam (88.8+/-6.5 versus 73.5+/-16.4, P < 0.05; and 20.6+/-4.4 versus 45.2+/-6.0; P < 0.001). In the midazolam group, the number of patients who had adverse effects was higher than the dexmedetomidine group (P < 0.05). As a result, dexmedetomidine performed as effectively and safely as midazolam when used as a sedative in upper gastroscopy; it was superior to midazolam with regard to retching, rate of side effects and endoscopist satisfaction. It was concluded that dexmedetomidine may be a good alternative to midazolam to sedate patients for upper endoscopy.
Familial mediterranean fever (FMF) is an autosomal recessive autoinflammatory disorder (MIM# 249100), particularly common in populations of Mediterranean extraction. MEFV gene, responsible for FMF, encoding pyrin has recently been mapped to chromosome 16p13.3. In the present study, 3,341 unrelated patients with the suspicion of FMF in south-east part of Turkey between the years 2009 and 2013 were enrolled and genomic sequences of exon 2 and exon 10 of the MEFV gene were scanned for mutations by direct sequencing. We identified 43 different type of mutations and 9 of them were novel. DNA was amplified by PCR and subjected to direct sequencing for the detection of MEFV gene mutations. Among the 3,341 patients, 1,598 (47.8 %) were males and 1,743 (52.1 %) were females. The mutations were heterozygous in 806 (62.3 %), compound heterozygous in 188 (14.5 %), homozygous in 281 (21.8 %) and mutations had complex genotype in 17 (1.32 %) patients. No mutation was detected in 2,051 (61.4 %) patients. The most frequent mutations were M694V, E148Q, M680I(G/C) and V726A. We could not find any significant differences between the two common mutations according to the gender. Molecular diagnosis of MEFV is a useful tool in clinical practice, thus a future study relating to genotype/phenotype correlation of FMF in more and larger group in Turkish population involving the whole MEFV gene mutations is necessary.
BIS is a reliable method to evaluate volume status in PD patients. BIS performed after peritoneal equilibration test with an empty abdomen, better reflects overhydration and is related to echocardiographic parameters.
Objective: To evaluate the relationship of vitamin D status and vitamin D replacement therapy with glycemic control, serum uric acid (SUA) levels, and microalbuminuria (MAU) in patients with type 2 diabetes (T2DM) and chronic kidney disease (CKD). Subjectsand Methods: A total of 1,463 patients with T2DM and CKD (aged 14-88 years), 927 females and 536 males, were included in this study. The serum data of 25-hydroxyvitamin D, i.e., 25(OH)D, level, SUA, hemoglobin (Hb)A1c, creatinine, estimated glomerular filtration rate, and urine albumin-to-creatinine ratio (UACR) were obtained from the medical records. The Mann-Whitney U test, the χ2 test, the Mantel-Haenszel test, and linear regression models were used for data analysis. Results: Vitamin D deficiency and insufficiency were evident in 770 (52.0%) and 357 (24.0%) patients, respectively. Median HbA1c levels (7.3 [IQR 3.9] vs. 6.5 [IQR 2.3]%; p < 0.01) were significantly higher in patients deficient in vitamin D than in those with a normal vitamin D status. A significantly low level of vitamin D was noted with a high UACR (β −0.01; 95% CI −0.01 to −0.001; p = 0.017) and HbA1c (β −1.1; 95% CI −1.6 to −0.6; p < 0.001), but with low levels of SUA (β 1.3; 95% CI 0.5-2.2; p = 0.002). Vitamin D replacement was associated with a significantly low level of HbA1c (7.4 [2.7] vs. 6.7 [1.9]%; p < 0.001]. Conclusion: In this study, there was a high prevalence of hypovitaminosis D among T2DM patients with CKD, with a higher UACR, higher HbA1c, and lower SUA being noted as playing a role in predicting a decrease in vitamin D levels and potential benefits of vitamin D replacement therapy on glycemic control in T2DM management.
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