Iron overload is considered to be associated with various complications in patients who undergo both allogeneic (allo) and autologous hematopoietic stem cell transplantation (HSCT). A total of 23 alloHSCT recipients who started deferasirox treatment due to hyperferritinemia (ferritin ≥1,000 ng/mL) were analyzed retrospectively. The demographic characteristics, data about deferasirox treatment, and history of phlebotomy were obtained from the patients' files. The reduction in posttreatment ferritin levels was found statistically significant compared with pretreatment ferritin levels in both def+phlebotomy and def+nonphlebotomy groups (p = 0.025 and 0.017, respectively). The liver enzymes, especially ALT and bilirubins, were significantly reduced after the treatment (p < 0.05). The deferasirox treatment reduced pretreatment ferritin levels below the level of 1,000 ng/mL in a median period of 94 days, and these data were found to be statistically significant (p < 0.05). The median treatment duration time with deferasirox was 94 days (72-122). The most common adverse effects were nausea and vomiting, which occurred in three of the patients (13%). In conclusion, our data suggest that oral deferasirox treatment may be used as a safe and effective alternative method for reducing iron overload in alloHSCT recipients, whether combined with or without phlebotomy.
Central venous catheterization is frequently performed for perioperative management and long-term intravenous access. Although complications associated with central venous catheter insertion have been widely reported, there are few reports of carotid-jugular arteriovenous fistula formation. Endovascular procedures are associated with a risk of immediate and delayed thromboembolic and ischemic complications. We describe a case of a carotid-jugular arteriovenous fistula and a cerebrovascular infarct following the insertion of a double-lumen catheter for hemodialysis access. We provide recommendations for the prevention and the early detection of this iatrogenic complication.
Peritoneal dialysis (PD)-related peritonitis is a common morbid complication of PD. Culture-negative peritonitis should not represent more than 20% of episodes (1). In our hospital, the ratio of culture-negative peritonitis has been declining in recent years. Here, we discuss the reasons for that improvement.
ObjectivesTo evaluate the clinical results of insulin degludec/aspart (IDEgAsp) therapy and its effect on the fear of hypoglycemia.MethodsA prospective observational study has been conducted through surveys of 36 patients using insulin because of type 2 diabetes mellitus who initiated treatment with IDegAsp switching from other insulins. Patients, 18–75 years old, were recruited to the study, consecutively. Participants’ age, gender, height, weight, body mass index (BMI), daily insulin dose, glycated hemoglobin (HbA1c), hypoglycemia rate, hypoglycemia fear survey (HFS) were recorded at the beginning of the study. By the end of 12th month, data was re-measured and compared with each other.ResultsHbA1c was declined by mean of −1.59% (95% CI −1.06 to −2.12, p<0.001). There was also a significant decrease in mean, daily insulin dose, weight and BMI values of patients via IDegAsp. While there was an increase in the amount of dipeptidyl peptidase 4-inhibitors (DPP4-i) and sodium-glucose co-transporter 2-inhibitors (SGLT2-i), there was a decrease in daily injection frequency. There was also a significant decrease in the median values of monthly hypoglycemia rate (from 2.0 to 1.0, p<0.001) and the entire HFS scores (HFS-T: from 1.09 to 0.73, p<0.001; HFS-B: from 0.83 to 0.60, p<0.001; HFS-W: from 1.33 to 0.88, p<0.001). There was a strong positive correlation between ΔHFS-B and daily injection frequency (Rho: 0.398; P: 0.016).ConclusionsIDegAsp co-formulation, combined with DPP4-i and/or SGLT2-i, can provide usefulness in terms of rates of hypoglycemia, reduced HbA1c, less injection administration, and decreased the fear of hypoglycemia in diabetics.
<p class="abstract"><strong>Background:</strong> Hepatic encephalopathy is a serious neuropsychiatric complication of cirrhosis. Changes in the oxidative and anti-oxidative system and nitric oxide levels in brain tissue contribute to the development of symptoms related to HE and HE. Purpose of the study to reveal the alterations in oxidative, anti-oxidative system and nitric oxide levels in cirrhotic patients during and after hepatic encephalopathy periods.</p><p class="abstract"><strong>Methods:</strong> This was a randomized controlled double-blind study conducted in Erciyes University Hospital between 3 July 2010 and 30 March 2011. We investigated the oxidative and anti-oxidative stress parameters by quantification of total antioxidant capacity (TAC), total oxidant capacity (TOC), nitric oxide (NO), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), total thiol and xanthine oxidase (XO) levels in serum. We compared the group of patients with hepatic encephalopathy, post-hepatic encephalopathy (clinically recovered) and control groups (healthy control). </p><p class="abstract"><strong>Results:</strong> Thirty hepatic encephalopathy patients were studied. Serum levels of nitric oxide and xanthine oxidase were statistically significantly high in the hepatic encephalopathy group according to control group (p<0.031, and p<0.001, respectively). Serum thiol levels were significantly low in hepatic encephalopathy patients than the controls (p<0.001). Total oxidant capacity, total antioxidant capacity, glutathione peroxidase and superoxide dismutase levels were not significantly different in hepatic encephalopathy group than the controls. Serum thiol levels were low and serum NO levels were high in recovered clinically from hepatic encephalopathy group according to control group currently (p<0.001, p<0.001, respectively). Total antioxidant capacity, total oxidant capacity, glutathione peroxidase, superoxide dismutase and xanthine oxidase levels were similar in both groups (p>0.05). Total antioxidant capacity and especially xanthine oxidase levels were significantly decreased in recovered clinically from hepatic encephalopathy group compared to hepatic encephalopathy group (p<0.05, p<0.001, respectively).</p><p class="abstract"><strong>Conclusions:</strong> Oxidative system, in systemic circulation, is activated during hepatic encephalopathy and changes in XO level during and after hepatic encephalopathy is very different. This parameter may be a potential marker in differential diagnosis of hepatic encephalopathy from other coma causes. Further investigation is needed.</p>
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