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Dive into the research topics where Ulku Saritas is active.

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Featured researches published by Ulku Saritas.


Journal of Gastroenterology and Hepatology | 2004

Intralesional steroid injection in benign esophageal strictures resistant to bougie dilation

Engin Altintas; Sabite Kacar; Bilge Tunç; Orhan Sezgin; Erkan Parlak; Emin Altiparmak; Ulku Saritas; Burhan Sahin

Objective:  Some benign esophageal strictures are highly resistant to bougie dilation. The aim of this study was to determine whether intralesional steroid injection had additional benefit to Savary‐Gilliards bougie dilation therapy (SGBD).


Gastrointestinal Endoscopy | 2003

Endoscopic Management of Biliary Obstruction Caused by Cavernous Transformation of the Portal Vein

Orhan Sezgin; Dilek Oguz; Engin Altintas; Ulku Saritas; Burhan Şahin

BACKGROUND Symptomatic biliary obstruction caused by cavernous transformation of the portal vein is an extremely rare disorder for which there is no consensus as to optimal treatment. The results of endoscopic treatments in a small group of patients is reviewed. METHODS A total of 10 patients (5 men, 5 women; mean age 36.1 years, range 17-48 years) with severe biliary strictures were treated between 1995 and 2001. Biliary sphincterotomy was performed in all patients. Four patients also underwent balloon dilation, nasobiliary drainage, and stone or sludge extraction by using a balloon. All patients had stent insertion. OBSERVATIONS The mean duration of therapy was 3.3 years (range 1-7 years). There was no complication directly related to the endoscopic procedures except for hemobilia that occurred in one patient during stent removal. Cholangitis developed in 5 patients during the therapy period and was treated endoscopically. In 4 patients, significant improvement in the biliary stricture was observed and stents were removed in 3. These patients were followed without stent insertion for one year. CONCLUSIONS Endoscopic management of biliary stricture caused by cavernous transformation of the portal vein appears to be effective and safe.


Journal of Clinical Gastroenterology | 2004

Hepatobiliary fascioliasis: clinical and radiologic features and endoscopic management.

Orhan Sezgin; Engin Altintas; Selçuk Dişibeyaz; Ulku Saritas; Burhan Sahin

Fasciola hepatica is a zoonotic liver fluke that can cause disease in humans. Fascioliasis is an uncommon disease. We retrospectively analyzed 9 cases of fascioliasis and reviewed the relevant literature. A high index of suspicion and specific ultrasonographic findings are very helpful in the diagnosis of the disease. However, serological studies and endoscopic retrograde cholangiopancreatography confirm the diagnosis. The disease has 2 stages: hepatic stage and biliary stage. While several drugs are used during the hepatic stage, endoscopic retrograde cholangiopancreatography is particularly effective in the biliary stage.


The American Journal of Gastroenterology | 2001

Chronic pancreatitis and aortic pseudoaneurysm in Behçet's disease.

Huseyin Alkim; Gönül Gürkaynak; Orhan Sezgin; Dilek Oguz; Ulku Saritas; Burhan Sahin

Behçets disease is a chronic, recurrent, systemic disease characterized by orogenital ulcers and oculocutaneous inflammatory lesions. Cardiovascular, pulmonary, neurological, articular, and GI involvement are common features, but pancreatic involvement is very rare. We present a case of Behçets disease with both chronic pancreatitis and abdominal aorta pseudoaneurysm.


Journal of Clinical Gastroenterology | 2001

Endoscopic management of a duodenal duplication cyst associated with biliary obstruction in an adult.

Orhan Sezgin; Emin Altiparmak; Ugur Yilmaz; Ulku Saritas; Burhan Sahin

Duodenal duplication cysts are distinctly uncommon and most often present in infancy or early childhood. The clinical presentation is generally duodenal obstruction, hemorrhage, or pancreatitis. Duodenal duplication cysts rarely cause biliary obstruction in adults. So far, duodenal duplication cysts have been almost exclusively treated by surgical intervention. This report describes both endoscopic diagnosis and treatment of a large periampullary duodenal duplication cyst associated with biliary obstruction in an adult patient.


World Journal of Gastroenterology | 2013

Precut sphincterotomy: A reliable salvage for difficult biliary cannulation

Ulku Saritas; Yucel Ustundag; Ferda Harmandar

Even experienced endoscopists have 90% success in achieving deep biliary cannulation with standard methods. Biliary cannulation may become difficult in 10%-15% of patients with biliary obstruction and precut (access) sphincterotomy is frequently chosen as a rescue treatment in these cases. Generally, precut sphincterotomy ensures a rate of 90%-100% successful deep biliary cannulation. The precut technique has been performed as either a fistulotomy with a needle knife sphincterotome or as a transpapillary septotomy with a standard sphincterotome. Both methods have similar efficacy and complication rates when administered to the proper patient. Although precut sphincterotomy ensures over 90% success of biliary cannulation, it has been characterized as an independent risk factor for pancreatitis. The complications of the precut technique are not limited to pancreatitis. Two more important ones, bleeding and perforation, are also reported in some publications as being observed more commonly than during standard sphincterotomy. It is also reported that precut sphincterotomy increases morbidity when performed in patients without dilatation of their biliary tract. Nevertheless, precut sphincterotomy is a good alternative as a rescue method in the setting of a failed standard cannulation method. This paper discusses the technical details, timing, efficacy and potential complications of precut sphincterotomy.


Endoscopy | 2015

Per-rectal diclofenac decreases the risk of post-ERCP pancreatitis: What about intramuscular diclofenac?

Ulku Saritas; Yucel Ustundag

We read with interest the article by Park et al. [1] about the effect of intramuscular diclofenac for the prevention of postendoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP). In this prospective trial, the authors found that PEP developed in 11.8% (20/170) of the placebo group and in 12.7% (22/173) of the intramuscular diclofenac group.The difference was not significant, and the authors concluded that prophylactic intramuscular diclofenac does not have any beneficial preventive effect on PEP. To date, there have been eight randomized controlled trials and several meta-analyses published, which have all indicated a consistent beneficial role of per-rectal diclofenac administration in decreasing the incidence, and possibly the severity, of PEP [2]. Although the recent guideline issued by the European Society of Gastrointestinal Endoscopy suggests routine administration of diclofenac via the rectal route immediately before or after ERCP [3], there are some issues surrounding the routine use of per-rectal diclofenac for all patients undergoing ERCP. For example, per-rectal diclofenac is more expensive than its intramuscular formulation and it is not available in some countries. Furthermore, most patients do not prefer rectal suppository formulations and are more used to receiving the intramuscular or intravenous form of this drug. Therefore, it is reasonable to investigate other routes of diclofenac administration to scrutinize their effects on PEP development. To the best of our knowledge, apart from the Park et al. study, only one other study, which was conducted by our group, has investigated the role of intramuscular diclofenac on preventing PEP in averageand high-risk patients, including those with sphincter of Oddi dysfunction (SOD) [4]. Our study revealed a statistically significant difference in PEP rates between the 37 patients (3 with SOD excluded) who received intramuscular diclofenac prophylaxis and the 30 control patients (10 with SOD excluded) who received placebo (2.7% vs. 16.7%, respectively; P= 0.04). Our result was therefore not consistent with the Park paper. The Park paper includes some important details, which could explain the different results. In our study, we used vigorous fluid infusion just after the injection of intramuscular 75mg diclofenac. We believe that post-ERCP fluid infusion is necessary and important to achieve sufficient pancreatic microcirculation, which ensures that diclofenac reaches the pancreatic tissue. In the Park study, no post-ERCP fluid replacement protocol is mentioned. In addition, more than 50% of patients in each group in the Park studyhad pancreatic acinerization. Although there is controversy about the role of pancreatic acinerization in the development of PEP [5], we do not usually observe such a high percentage of acinerization in routine clinical practice, and in fact, in our study, no cases of pancreatic acinerization were observed [4]. Although Park et al. did not show a difference in the rate of PEP in cases with and without acinerization, acinerization may have limited the potential for preventive effects of intramuscular diclofenac administration in the study. Interestingly, the authors also revealed some findings that were contradictory to current literature, such as the risk of PEP being higher in the male sex andwith pancreatic stenting. Admittedly, we should accept that the small sample size was the main limitation in our study, and type II error due to adjustment of many confounding factors might be responsible for the lack of beneficial effect of intramuscular diclofenac on PEP in the Park study. Finally, we agree with the authors that larger, comparative, randomized, controlled trials are definitely needed to confirm the beneficial role of non-rectal administrations of diclofenac.


Journal of Hepatology | 2016

Non-selective beta-blockers for the patients with acute on chronic liver failure

Yucel Ustundag; Ulku Saritas

To the Editor: We read with great interest the article by Mookerjee et al. [1], about the beneficial effects of non-selective beta blockers (NSBBs) in patients with acute on chronic liver failure (ACLF). The authors indicated that 164 of patients on NSBBs had lower grades of ACLF than those not on NSBBs. Furthermore, 24.4% of the patients on NSBBs died while 34.1% of the patients not on NSBBs died. As an explanation for improved short term survival, they reported that NSBBs reduce systemic inflammation by reducing gut motility and bacterial translocation if the patients develop ACLF. ACLF is a highly prevalent syndrome that can occur in 30% of cirrhosis leading to acute decompensation, organ failure and high mortality [2]. This syndrome is dominated by a systemic inflammatory reaction like tabloid which is accepted as an independent predictor of mortality in these patients. Thus, we agree with the authors that treatment or modulation of this inflammatory response on ACLF is very important goal for the clinicians. Remarkably, the authors believe that other than beneficial effects on hemodynamic parameters, NSBBs decrease gut motility and reduce bacterial translocation which would reduce systemic inflammation in patients with ACLF. However, if we look at Table 1, we see that the rates of spontaneous bacterial peritonitis which arises from bacterial translocation from the gut were same in patients on NSBBs and those not being on NSBBs. The rates of bacterial infection, though statistically insignificant, were also noted to be higher in patients on NSBBs than those that are not on NSBBs. Another flaw with their hypothetical explanation is that plasma C-reactive protein levels were very similar in both groups of patients on or not on NSBBs. However, the authors believe that significantly lower white blood cell counts in patients on NSBBs reflect the anti-inflammatory effects of NSBBs. Nevertheless, we do not agree with the authors since the white blood cell counts may be affected from other reasons in this cohort of patients. One of them may be active alcohol use (significantly higher alcohol use/alcoholic hepatitis as a cause of decompensation in patients not on NSBBs in Table 1) (p = 0.02). It is very well known that alcoholic hepatitis is commonly associated with elevated level of blood white cell counts. Another reason may be the different degree of hypersplenism in patients on NSBBs. The group on NSBBs had lower platelet counts (p = 0.04) and had higher rates of previous decompensation events such as gastrointestinal bleeding (p = 0.0001) in the present article. Thus, this group of patients may have higher rates of hypersplenism due to severer portal hypertension and may have lower levels of white blood cell counts. Another important point is that CLIF C ACLF scores do not seem to be different in patients on or not on NSBBs. As far as we know CLIF A ACLF score (includes white cell counts) is the best predictor of short term mortality in ACLF


Journal of Hepato-biliary-pancreatic Sciences | 2015

Re: Management strategy for biliary stricture following laparoscopic cholecystectomy

Yucel Ustundag; Erkan Parlak; Ulku Saritas

We read with great interest the article by Sugawara et al. [1]. Their study included 14 patients and 11 of them had common hepatic duct injury and the remaining three had hepatic hilum injury during laparoscopic cholecystectomy (LC). All of these cases were reported to develop postoperative biliary strictures as type 4 or type 3 within 9 months. After referral, the authors reported eight percutaneous transhepatic biliary drainage (PTBD) procedures and four catheter exchanges for approximate positioning in patients without vascular injury. The authors also tried several PTBD catheter dilatations up to 12–16-Fr in eight patients and were successful only in six of them. Within 18-188 months after the catheter removal period, the authors indicated that these five cases were free of original biliary strictures. Major bile duct injuries after LC remain a constant problem for some of our patients. Although surgical reconstruction with duct to duct anastomosis at the time of operation or after a while is the treatment cornerstone, it will result in a recurrent biliary stricture inmost of these patients as notified in the present article. The authors in this article recommended that PTBD catheter dilatation should be the first choice for such patients. Although we believe the importance and the utility of multimodal treatment in this setting of complex biliary injuries due to LC, interventional radiology has some drawbacks such as the inconvenience of an existing one or two thick external catheters in each patient for long periods of time


Digestive Diseases and Sciences | 2013

Analysis of Adverse Events Associated with Endoscopic Papillary Large-Balloon Dilation

Yucel Ustundag; Galip Ersoz; Ulku Saritas

We read with great interest the article by Park et al. [1] entitled ‘‘Factors predictive of adverse events following endoscopic papillary large-balloon dilation: results from a multicenter series’’. In this multicenter study, the authors analyzed adverse events (AEs) after endoscopic papillary large-balloon dilation (EPLBD) in 946 patients and revealed that cirrhosis, stone size equal or larger than 16 mm, full endoscopic sphincterotomy (EST), continued balloon inflation despite persistent waist formation and distal common bile duct (CBD) stricture were predictors of significant AEs such as perforation and severe bleeding. Interestingly, the authors reported that the larger balloon size ([14 mm) is protective against the development of post-procedure pancreatitis. The paper by Park et al. nicely described those factors predictive of these AEs. However, we have some concerns with some of their findings. We know that EPBD is mostly suitable for patients with coagulopathy including those due to cirrhosis and EST is relatively contraindicated in them [2]. Indeed, it is not clear in the text that the 18 patients with cirrhosis in the present study had EST plus EPLBD or only EPLBD. If these cases had undergone combined approach, we also do not know how much of them had full EST which is the dominant factor for the intra or post procedure bleeding in these cases. In line with this, one of the patients with thrombocytopenia (probably due to cirrhosis) in this study developed severe bleeding after combined approach of full EST plus EPLBD and this patient died. We believe that such a combined approach in a thrombocytopenic patient must not be used at all and it should be accepted as contraindicated. Another point with this paper is that three patients developed post-procedure perforation and again it seems that two of them had full EST plus EPLBD therapy and the balloon sizes were noted to be larger than the size of distal CBD. Although it is not clear in the paper if the second case with post-procedure perforation had full EST as well, it is already known that patients with distal CBD stenosis or a narrow CBD are at risk of perforation, bleeding, and or bile duct injury [3]. Full EST also increases the risk of perforation itself and in daily practice; we always prefer partial EST and combine it with EPLBD since direct observation of the remaining intact papillary roof during gradual balloon inflation is possible during partial EST. This helps us to avoid perforation. The authors explained the reasons for perforation in these three cases only with over-inflation and rapid inflation of the balloon. We believe that full EST might also have contributed to perforation in these cases. Moreover, during the EPLBD procedure, it is a general rule to avoid excessive dilatation against a resistance and if the waist in the balloon decreases but not disappear completely, in such cases keeping the balloon in place for more than 45 s may be useful and secure rather than forcing it to disappear completely. Another flaw with this paper is that the authors indicated that a balloon size larger than 14 mm is protective against pancreatitis and it is not clear in the text if those cases had EST (partial or full?) or not. In cases undergoing EST plus EPLBD, EST separates pancreatic orifice from biliary orifice and this is believed to be protective for Y. Ustundag (&) Department of Internal Medicine, Gastroenterology Clinics, Bulent Ecevit University Hospital, Zonguldak Karaelmas University, 67600 Kozlu, Zonguldak, Turkey e-mail: [email protected]

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Yucel Ustundag

Zonguldak Karaelmas University

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Ferda Harmandar

Zonguldak Karaelmas University

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