Fatih Tekin

We thank Drs. Matsushita et al. for their letter and interest in our article [ 1 ]. Duodenal duplication cyst (DDC) is a benign congenital anomaly acquired during embryonic development of the digestive system [ 2 ]. Surgical resection is the standard therapy [ 3 ] [ 4 ]; however, the difficulty of the operative procedure owing to the close proximity of the major papilla has resulted in an interest in endoscopic therapies. Using the endoscopic needle-knife and sphincterotome to open the cyst into the duodenum [ 5 ] and endoscopic partial resection of the cyst [ 6 ] [ 7 ] are the favored endoscopic methods. A new endoscopic treatment method involving needle-knife sphincterotome incision, balloon dilation, and plastic stent implantation for a symptomatic duodenal cystic lesion was described in our article [ 1 ]. Our diagnosis for the duodenal cystic lesion was DDC; Matsushita et al. suggest a diagnosis of choledochocele rather than DDC. In fact, exact distinction between choledochocele and DDC is only possible at pathological examination. Matsushita et al. are justified in their suspicion since no biopsy from the cystic lesion was performed in our case. However, there were three findings which persuaded us to a diagnosis of DDC: (i) In general, DDC is a cystic lesion located distal to the orifice of the papilla, while a choledochocele is located proximal to the orifice of the papilla. In our case, the orifice of the papilla was found at the back side of and proximal to the cystic lesion, as seen in Fig. 1b in our article. (ii) Although the common bile duct and the pancreatic duct were opacified through the common channel, the cystic lesion showed no direct communication with the common bile duct, as may be seen in Fig. 1c,d. (iii) During the endoscopic therapeutic procedure, we observed drainage of a whitish viscous secretion, but not bile, from the cystic lesion. It has been speculated that a DDC might produce viscid mucous secretions [ 8 ]; on the other hand, a choledochocele would be expected to contain bile. When the above findings are considered, a diagnosis of DDC is more likely than one of choledochocele. We suggest that follow-up endoscopic biopsies should not be omitted in such cases, since there are several reported cases of malignancy arising inside a DDC [ 9 ] [ 10 ] [ 11 ]. Competing interests: None

A 56-year-old man with hepatitis B-related cirrhosis was admitted with massive hematemesis. Three months previously he had undergone upper endoscopy at another hospital and was diagnosed as having esophageal varices. However, no endoscopic therapy was carried out. On physical examination, the patient’s blood pressure was 76/40 mm Hg, his pulse rate was 136 bpm, and his respiratory rate was 26/min. Despite aggressive therapy with fluids and blood components the patient could not be stabilized, and a Sengstaken-Blakemore tube was inserted. Eleven hours after the insertion of the tube, the patient developed swelling over both his parotid glands ([ Fig. 1 ]), with local rise in temperature and tenderness. Fig. 1 Bilateral swelling of the parotid glands. Neck ultrasonography revealed bilateral generalized swelling of the parotid glands, without duct dilation. An otolaryngologist was consulted and bilateral acute parotitis was diagnosed. The patient was started on antibiotic therapy with ceftriaxone, the gastric and esophageal balloons were immediately deflated, and the Sengstaken-Blakemore tube was removed. There was no re-bleeding in the next 48 hours, and the patient was given terlipressin. The parotitis resolved completely after 72 hours of removal of the Sengstaken-Blakemore tube. While upper endoscopy was being considered, on the fifth day in hospital the patient again had massive hematemesis and died. Transient parotitis following the use of lidocaine spray [ 1 ] and midazolam [ 2 ] for upper endoscopy has been reported previously. In addition, upper endoscopy may also cause parotitis [ 3 ] [ 4 ]. Although the exact mechanism is unknown, venous congestion leading to straining, and parasympathetic stimulation during the procedure causing parotid vasodilation and transient enlargement, have been suggested as possible mechanisms [ 3 ]. Furthermore, recently, parotitis associated with double-balloon endoscopy has been reported in two cases [ 5 ] [ 6 ]. However, to our knowledge, parotitis associated with insertion of a Sengstaken-Blakemore tube has not been reported before. Although the reason for its occurrence is unclear, clinicians should be aware of this rare complication. Endoscopy_UCTN_Code_CPL_1AH_2AC

An 18-year-old woman was referred to our clinic for endoscopic retrograde cholangiopancreatography (ERCP) because of a history of recurrent abdominal pain and a previous episode of acute pancreatitis. No etiology was found except a duodenal cystic polypoid lesion detected at computed tomography. ERCP revealed a cystic lesion with a 3 × 2 cm diameter ([ Fig. 1 a ]), and the orifice of the papilla to be at the back side of the cystic lesion ([ Fig. 1 b ]). After the cannulation had been performed, the cystic lesion ([ Fig. 1 c ]), the common bile duct, and the pancreatic duct ([ Fig. 1 d ]) were opacified through the common channel. The gallbladder, common bile duct, and pancreatic duct were of normal size and shape. As the cystic lesion showed no communication with the common bile duct, a diagnosis of a duodenal duplication cyst (DDC) was established rather than a choledochocele. An incision was made with a needle-knife sphincterotome (Boston Scientific Microvasive, Indiana, USA) on the anterior portion of the cyst. After the cyst was cannulated, a guide wire was sent into the cystic cavity. Thereafter, dilation with an 8-mm diameter balloon ([ Fig. 2 ]) and a consecutive plastic stent implantation (10-Fr double-pigtail) were performed. Drainage of a whitish viscous secretion, but not the bile, was observed through the pigtail stent. The pigtail stent was endoscopically removed 1 month later, and the DDC cavity was found to be totally collapsed ([ Fig. 3 ]). Four months after discharge, the patient was well and symptom free. Although surgically complete resection of the DDC is the standard therapy, few endoscopic therapies have also been reported. Use of the endoscopic needle-knife and sphincterotome to open the cyst into the duodenum [ 1 ] and endoscopic partial resection of the cyst [ 2 ] [ 3 ] are the favored endoscopic methods. This is the first report of a DDC that has been successfully treated with needle-knife sphincterotome incision, balloon dilation, and a plastic stent implantation. Fig. 1  Duodenoscopy revealed a cystic polypoid lesion protruding inside the duodenal lumen. b The orifice of the papilla was found to be at the back side of the cystic lesion allowing cannulation. c Opacification of the cyst. Note the absence of the communication with the common bile duct. d The gallbladder, common bile duct (CBD) and the main pancreatic duct (MPD) were of normal size and shape. Fig. 2 After an incision on the cyst, balloon dilation through the guide wire was performed. Thereafter, a pigtail stent was implanted. Fig. 3 The cyst cavity was found to be totally collapsed after 1 month. Endoscopy_UCTN_Code_CPL_1AK_2AJ

Summary: Background  Pretransplantation clearance of hepatitis C virus (HCV)‐RNA reduces the risk of HCV recurrence after transplantation. Furthermore, a sustained virological response could reduce disease progression and slow clinical deterioration in nontransplanted patients.Aim  To evaluate the safety, tolerability and efficacy of pegylated‐interferon (PEG‐IFN) alfa‐2a plus ribavirin therapy in HCV‐related decompensated cirrhotics.Methods  Twenty HCV‐related decompensated cirrhotics (44–67 years, 12 males, six Child–Pugh score A, 14 Child–Pugh score B, all with genotype 1b) were enrolled into the study. Treatment with PEG‐IFN alfa‐2a (135 μg, once a week) plus ribavirin (1000–1200 mg/day) was commenced. A 48‐week treatment was planned in patients who had early virological response.Results  Treatment was stopped in 8 (40%) patients. The remaining 12 (60%) patients completed 48 weeks of therapy; nine (45%) of them obtained end‐of‐therapy virological response and six (30%) of them obtained sustained virological response. Living donor liver transplantation was performed in three (15%) patients. Eight (40%) and six (30%) patients needed to reduce PEG‐IFN alfa‐2a and ribavirin dosages, respectively. No patient died during the follow‐up period.Conclusion  PEG‐IFN alfa‐2a plus ribavirin therapy is safe, tolerable and efficacious in selected HCV‐related decompensated cirrhotics.