Reversible Posterior Leukoencephalopathy Syndrome Due to Carboplatin and Paclitaxel Therapy.

BACKGROUND: Reversible posterior leukoencephalopathy syndrome (RPLS) is a clinicoradiologic syndrome characterized by headache, decreased alertness, seizures, visual abnormalities, and white matter changes indicative of cerebral edema. Although the pathogenesis remains poorly understood, several etiological causes have been described. RPLS is a common complication of chemotherapeutics because of its toxic effect on the central nervous system. This syndrome is frequently associated with seizures but rarely seen with status epilepticus and periodic lateralized epileptiform discharges (PLEDs). CASE REPORT: We present a case with metastatic lung cancer that developed RPLS after carboplatin and paclitaxel therapy. Our case was admitted to the hospital with status epilepticus and her electroencephalography showed PLEDs. CONCLUSION: It is important to closely monitor blood pressure and electrolyte levels in patients who take chemotherapeutic agents, especially when there is no previous history of hypertension. It should be kept in mind that RPLS is a causative factor of status epilepticus and PLEDs.

The effect of 25-hydroxyvitamin D levels on QT interval duration and dispersion in type 2 diabetic patients.

AIM: To assess the relationship between corrected QT (QTc) interval and vitamin 25-hydroxyvitamin D levels (25-OHD) deficiency in type 2 diabetic patients. METHODS: The study included 253 patients with type 2 diabetes and 170 age-matched controls treated between October and December 2013. QTc duration and QTc dispersion were measured on ECG recordings and 25-OHD, calcium, phosphorus, and blood glucose levels were determined. RESULTS: Patients with diabetes had significantly longer QTc duration and QTc dispersion than controls (P<0.001 and P<0.001 respectively). Diabetic patients with prolonged QTc duration were older and had longer diabetes duration and higher HbA1c levels than patients with normal QTc interval. They significantly more frequently had 25-OHD deficiency (P<0.001), but had similar calcium and phosphorus levels. Diabetic patients with prolonged QTc dispersion were of similar age and had similar diabetes duration and HbA1c levels as patients with normal QTc dispersion. They significantly more frequently had 25-OHD deficiency (P=0.010), but had similar calcium and phosphorus levels. CONCLUSION: This study showed prolonged QTc duration and QTc dispersion in patients with type 2 diabetes, especially those with 25-OHD deficiency.

Ezetimibe effect on bone mineral density and markers of bone formation and resorption.

BACKGROUND: Ezetimibe, as a lipid-lowering agent, inhibits the intestinal absorption of cholesterol and decreases low-density lipoprotein cholesterol (LDL-C) level in serum. It also up-regulates hepatic cholesterol biosynthesis and, by contrast to statins, increases serum mevalonate levels. Statins and biphosphonates decrease osteoclastic activity through the same mechanisms by inhibiting the mevalonate pathway. We therefore tested the effect of ezetimibe on bone turnover in hypercholesterolemic patients. SUBJECT AND METHODS: In an open-label clinical trial, 54 hypercholesterolemic patients included in the study underwent 12 months of treatment with ezetimibe at a dosage of 10 mg/d. Before and after the 1-year ezetimibe treatment, bone mineral density (BMD) was measured by dual-energy x-ray absorptiometry and serum samples taken for measurements of levels of total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol and LDL-C, serum calcium (Ca), serum phosphate, total and bone alkaline phosphatases (ALPs), and carboxyterminal fragment of type 1 collagen in the serum. RESULTS: The hypercholesterolemic patients showed a significant reduction with respect to baseline TC and LDL-C serum levels: 20% for TC (270.18 [38.58]-214.46 [38] mg/dL) and 24% for LDL-C (189.57 [38.58]-144 [32.05] mg/dL). Biochemical markers of both bone formations (total ALP level, 65.50 [21.33]-66.27 [21.017] IU/L and bone ALP level, 55.93 [7.92]-56.25 [7.49] IU/L) and bone resorption (beta-CTx, 0.44 [0.24]-0.46 [0.21] ng/mL) increased but did not show any significant change for the whole study period. At the end of 1 year, both BMD-lumbar spine (0.90 [0.12]-0.89 [0.08] g/cm) and BMD-total femur (0.93 [0.12]-0.92 [0.12] g/cm) showed a negative trend but without reaching statistical significance. CONCLUSIONS: Our study results showed a negative trend but did not demonstrate statistically significant changes of BMD and metabolic markers with the treatment of ezetimibe.

Effects of captopril and losartan on lipid peroxidation, protein oxidation and nitric oxide release in diabetic rat kidney.

Increased oxidative stress has an important role in the pathogenesis of diabetic nephropathy. The aim of this study was to evaluate the effects of renin-anigiotensin system blockage, either by angiotensin-converting enzyme inhibition or angiotensin receptor blockage, on oxidative stress and nitric oxide release in diabetic rat kidneys. After induction of diabetes, six rats were given captopril, six rats were given losartan, and six rats served as diabetic controls. Six healthy rats were also included. At the end of an 8-week period nitric oxide release, lipid peroxidation and protein oxidation were measured in kidney cortices, and urinary albumin excretion (UAE) was determined in 24-h urine samples. Losartan- and captopril-treated diabetic rats had lower levels of UAE than diabetic controls. Diabetic rats had higher levels of lipid peroxidation and protein oxidation compared to healthy rats. NO release was significantly lower in diabetic groups than healthy controls. UAE levels showed a positive correlation with lipid peroxidation and a negative correlation with NO release. Inhibition of lipid peroxidation could be one of the protective mechanisms of renin-angiotensin axis inhibition in diabetic kidney tissues.

Effects of aminoguanidine on lipid and protein oxidation in diabetic rat kidneys.

Nonenzymatic glycation of tissue and plasma proteins may stimulate the production of oxidant and carbonyl stress in diabetes. The aim of this study was to evaluate the effects of aminoguanidine (AG) on lipid peroxidation, protein oxidation and nitric oxide (NO) release in diabetic rat kidneys. After induction of diabetes with streptozotocin, female Wistar rats were divided into 2 groups. Group DAG (n=9) rats were given AG hydrogen carbonate (1 g/L) in drinking water and group D (n=8) was diabetic control rats given only tap water. Group H (n=8) was followed as healthy controls. At the end of an 8 week period, NO release, lipid and protein oxidation were determined in kidney tissues. NO release was significantly lower in diabetic rats compared with healthy controls (p<0.05). Lipid peroxidation was significantly high in group D (3.9 +/- 0.3 nmol MDA/g tissue) compared with the group DAG (2.6 0.1 nmol MDA/g tissue, p<0.01) and group H (2.4 +/- 0.2 nmol MDA/g tissue). Protein oxidation was significantly higher in diabetics than healthy controls (563.8 +/- 23.9, 655.8 +/- 7.2, 431.5 +/- 8.8 mmol carbonyl / g tissue for group DAG, D and H, respectively, p< 0.05). A positive correlation between albuminuria and thiobarbituric acid reactive substance (TBARS) levels (r= 0.54,p<0.005) and carbonyl content (r=0.70, p<0.0005) in kidney homogenate were observed. Although AG treatment had no effect on NO release, it significantly decreased lipid peroxidation in diabetic rat cortices. Consequently increased lipid peroxidation -as well as- protein oxidation could be involved in the pathogenesis of diabetic albuminuria.