Silibinin Effect on Methotrexate-Induced Hepatotoxicity in Rats.

OBJECTIVE: Hepatotoxicity is one of the major side effects of methotrexate and limits its use. In this study, we investigated the hepatoprotective effect of silibinin and the role of oxidative stress markers and cytokines on high-dose methotrexate-induced hepatotoxicity in rats. MATERIALS AND METHODS: In this study, rats were randomly divided into 5 groups (n=7). Methotrexate (20 mg/kg, intraperitoneally) was administered on the first day in all groups except control. Silibinin was injected for 5 days to methotrexate-silibinin25, methotrexate-silibinin50, and methotrexate-silibinin100 groups at a dose of 25, 50, and 100 mg/kg/day, respectively. On the sixth day, blood and liver samples were obtained and rats were sacrificed. Serum total antioxidant capacity, total oxidant status, total thiol, native thiol, alanine aminotransferase, aspartate transaminase, bilirubin, albumin, tumor necrosis factor-alpha, and interleukin-10 levels were measured. In addition, a histopathological evaluation of liver tissues was performed. RESULTS: Methotrexate reduced total antioxidant capacity and increased disulfide/total thiol ratio. Histopathologic examination revealed that methotrexate increased hepatic damage and 50 mg/kg/dose of silibinin prevented inflammatory cell infiltration in particular. CONCLUSION: Our results suggest that silibinin (50 mg/kg/day) may reduce the hepatic damage in methotrexate-induced hepatotoxicity in rats by increasing antioxidant capacity.

The effects of amantadine on lung tissue in lower limb ischemia/reperfusion injury model in rats.

BACKGROUND: This study aims to evaluate the effect of amantadine on lung tissue of after lower limb ischemia/reperfusion injury in rats. METHODS: A total of 24 Wistar rats were divided into four equal groups including six rats in each: sham group (Group S), amantadine group (Group A), ischemia/reperfusion group (Group I/R), and ischemia/reperfusion + amantadine group (Group I/R-A). All groups underwent a midline abdominal incision. In Groups I/R and I/R-A, the infrarenal abdominal aorta was clamped for 120 min and, then, reperfused for 120 min after removal of the clamp. Amantadine hydrochloride 45 mg/kg was administered intraperitoneally to the rats of Groups A and Group I/R-A 15 min before surgery. At the end of reperfusion period (240 min), all rats were sacrificed, and their lung tissues were obtained. Lung tissue catalase and superoxide dismutase activities and glutathione S-transferase and malondialdehyde levels were analyzed. Lung tissues were examined histopathologically. RESULTS: Catalase activity was lower in Groups A, I/R, and I/R-A compared to Group S. Superoxide dismutase activity was higher in Group I/R than Group S. Superoxide dismutase activity in Groups I/R-A and A decreased, compared to Groups S and I/R. Glutathione S-transferase levels decreased in Groups I/R and A, compared to Group S. Glutathione S-transferase levels in Group I/R-A were higher than Groups I/R and A. The highest level of malondialdehyde was found in Group I/R and the lowest level was found in Group I/R-A. According to histopathological examination, infiltration scores were significantly lower in Group S than Groups I/R and I/R-A (p=0.009 and p=0.011, respectively). The alveolar wall thickening scores in Group I/R were also significantly higher than Groups S and Group A (p=0.001 and p=0.001, respectively). CONCLUSION: Lung tissue can be affected histopathologically by ischemia/ reperfusion injury and this injury can be reversed by amantadine administration.

Dynamic thiol/disulphide homeostasis in patients with hypertrophic cardiomyopathy.

BACKGROUND: In addition to the genetic complexity of hypertrophic cardiomyopathy (HCM), there must be other disease-modifying factors that contribute to its highly variable clinical and phenotypic expression. The authors aimed to investigate serum thiol/disulphide homeostasis as a proxy for oxidative stress using a novel automated assay in patients with HCM. METHODS: This cross-sectional study was conducted on 119 patients with HCM and 52 without HCM. The methods used to measure dynamic thiol/disulphide homeostasis as calorimetric and duplex quantities were developed in 2014. RESULTS: Median serum native thiol levels were significantly lower in patients with HCM than in those without (312.5 µmol/L [285-370 µmol/L] vs 421 µmol/L [349-469.5 µmol/L]; p < 0.001). Serum total thiol levels and disulphide levels were considerably lower than those in the control group ([844.68 ± 195.99 µmol/L vs 1158.92 ± 243.97 µmol/L; p < 0.001], [259.13 ± 65.66 µmol/L vs 375.02 ± 79.99 µmol/L; p < 0.001], respectively). Serum disulphide/native thiol ratios and disulphide/total thiol ratios were significantly lower in HCM patients than in controls (0.80 ± 0.09 vs 0.92 ± 0.05; p < 0.001 and 0.31 [0.30-0.32] vs 0.32 [0.32-0.33]; p < 0.001). Finally, reduced thiol ratios were higher and oxidized thiol ratios were significantly lower in patients with HCM than in controls. CONCLUSIONS: Despite the fact that antioxidant capacity was impaired, the extracellular environment remained in a reducing state by keeping serum disulphide/native thiol ratios low. Therefore, the authors speculate that HCM may behave similarly to tumours with respect to serum thiol-disulphide levels.

Evaluation of cardiac parameters between survivors and nonsurvivors of COVID-19 patients

SUMMARY OBJECTIVE: The present study compares the cardiac parameters of the survivor and nonsurvivor patients with COVID-19 infection. METHODS: This study was conducted in 379 patients diagnosed with COVID-19 disease. Information of 21 nonsurvivor and 358 survivor patients with COVID-19 was obtained from the hospital information management system and analyzed retrospectively. Relationship between cardiac parameters in patients categorized into the mortal and immortal groups was investigated. RESULTS: Of the total 379 patients involved in this study, 155 (40.9%) were females and 224 (59.1%) were males. No statistically significant difference in mortality was found between females and males (p=0.249). The total median age was 70, the median age in the nonsurvivor group was 74 (35-89), and it was 69.5 (18-96) in the survivor group (p=0.249). The median values of high-sensitivity troponin (hs-Tn), creatine kinase MB form, and especially myoglobin in the survivor and nonsurvivor groups were 25/64.9 (p=0.028), 18/23 (p=0.02), and 105.5/322.4 (p<0.001), and the difference was statistically significant. Comparing mortality, while there was 1 (0.7%) nonsurvivor out of 134 patients in the service unit, there were 20 (8.2%) nonsurvivors out of 245 patients in the intensive care unit. This difference was statistically significant (p=0.003). The cutoff value of myoglobin, which may pose a risk of mortality, was found to be 191.4 µg/L, while it was 45.7 ng/l for hs-Tn and 60.1 U/L for creatine kinase MB. CONCLUSIONS: Advanced age and increased levels of high-sensitivity troponin, creatine kinase MB, and myoglobin were found to be associated with mortality.

The effects of povidone iodine (pH 4.2) on patients with adenoviral conjunctivitis.

OBJECTIVE: To compare the efficacy of classical treatment and povidone-iodine treatment for adenoviral conjunctivitis. METHODS: This retrospective study was conducted at the Centre of Marmara Eye Health, Sakarya, Turkey, between January 2011 and February 2014, and comprised adult patients suffering from adenoviral conjunctivitis. The participants were randomly divided into two groups. Group I was given povidone-iodine solution while Group II was given the classical treatment and was taken as control. Povidone-iodine treatment was administered as three drops three times per day. The classical treatment comprised three drops of trifluorothymidine three times per day. Treatment were continued for two weeks. The patients who had not recovered in this time frame were defined as 'late recovering' patients. SPSS 23 was used for data analysis. RESULTS: Of the 112 participants, there were 56(50%) in each group. In Group I, 54(96.4%) patients recovered in two weeks, while 2(3.6%) took more time. In Group II, 33(58.9%) patients recovered in two weeks while 23(41.1%) took more time (p<0.001). Overall, 92(82.1%) patients had familial transmission-contamination. CONCLUSIONS: A new treatment protocol of povidone-iodine was used safely in patients with adenoviral conjunctivitis. Familial transmission was found very important to adenoviral conjunctivitis infection.

Cushing's Syndrome Presenting with Hyponatremia.

We present a case of Cushing's syndrome that presented with hyponatremia. A 64-year-old obese woman presented to the hospital emergency service complaining of a high fever, hypertension, and generalized oedema. During the examination, the patient suddenly became confused and lost consciousness. She was admitted to the intensive care unit. In addition, blood was drawn to measure the cortisol and ACTH levels, and urine samples were sent for analysis. Adenoctomy was performed through unilateral surgical treatment. Postoperatively, many of the complications arising from Cushing's syndrome disappeared. She healed quickly, and her complaints over the last 10 years disappeared completely within a few months.

Diagnosis of vitamin B12 deficiency in patients with myeloproliferative disorders.

BACKGROUND: Myeloproliferative disorders are characterized by proliferation of 1 or more lineage of hematologic cells. Rapid proliferation of cells may lead to depletion of vitamin B12, which may be falsely elevated by conventional assays in these disorders. We evaluated vitamin B12 status with conventional vitamin B12 assay and levels of serum methylmalonic acid (MMA), serum holotranscobalamin (holoTC), and plasma homocysteine in myeloproliferative disorders. METHODS: In 58 patients who had myeloproliferative disorders and normal serum creatinine levels, we measured levels of vitamin B12, MMA, holoTC, and homocysteine. Correlations were evaluated between these tests, with MMA as the reference standard for vitamin B12 deficiency. RESULTS: Prevalence of vitamin B12 deficiency was 69%, despite high serum vitamin B12 levels. Levels of holoTC of 40.6 pmol/L or less and homocysteine of greater than 14 mol/L were the best cutoff levels with sensitivity values of 75% and 70%, specificity values of 80% and 68%, and positive predictive values of 88% and 80%. Logistic regression showed that cutoff values of holoTC of 40.6 pmol/L or less and homocysteine of greater than 14 mol/L resulted in odds ratio 15.5 for low versus high holoTC, and odds ratio 5.4 for high versus low homocysteine, to confirm vitamin B12 deficiency. CONCLUSIONS: Patients who had myeloproliferative disorders had a high prevalence of vitamin B12 deficiency, despite high serum vitamin B12 levels. Therefore, vitamin B12 status should be evaluated in patients with myeloproliferative disorders. Holotranscobalamin level may be the best initial test and may replace vitamin B12 assay to accompany MMA and homocysteine levels.