There is a lack of consensus regarding the risk of postoperative hemorrhage in patients on antithrombotic therapy who undergo endoscopic submucosal dissection (ESD).

Objectives: Although drug treatment is the usual first-line therapy for gastroesophageal reflux disease (GERD), not all patients receive satisfactory relief from drug therapy, alone. We developed an endoscopic fundoplication technique using endoscopic submucosal dissection (ESD); the technique is referred to as ESD for GERD (ESD-G). This study investigated the safety and efficacy of this novel technique in patients with drug-refractory GERD. Patients and methods: ESD-G narrows the hiatal opening through ESD of the esophagogastric junction (EGJ) mucosa. For safety reasons, the range of mucosal resection was limited to half (1/2 or 1/4 +1/4) of the circumference of the EGJ lumen. ESD-G was performed on 13 patients with proton pump inhibitor (PPI)-refractory GERD. GERD symptoms, PPI dose, and 24-h esophageal pH monitoring results were compared before and 6 months after the procedure. Results. In 12 cases, symptoms significantly improved after ESD-G. Five patients demonstrated improved esophagitis, three were able to discontinue PPI therapy, and three were able to reduce their PPI dosage following surgery. The esophageal pH <4 holding time ratio was also decreased after ESD-G. Conclusions. ESD-G may be useful for PPI-refractory GERD patients.

As a first step in the development of a future wearable artificial kidney, we conducted three forms of treatment with continuous haemofiltration (CHF) on a group of 10 patients in an attempt to determine what plasma values of small molecules and β ₂ -microglobulin (β ₂ -M) could be maintained. In the first system, one ordinary 4-h haemodialysis, followed by 7-day CHF with 51 exchange per day, was repeated. The second system consisted of CHF with 51 exchange/day and thrice weekly slow nocturnal dialysis. The third system used CHF with 101 exchange per day. The first, second and third systems were used with three, four and four patients, respectively, for at least 4 weeks each. PAN-DX and FH-66 haemofilters were used eight and three times, respectively, with continuous infusion of heparin at 500–700 units/h. In the first system, the pre-CHF plasma β ₂ -M was 45.5±3.1 mg/l, against a much lower 18.8±1.0 mg/l 4 weeks later. With the second system, this decrease was from 43.5±5.7 mg/l to 18.1±1.1 mg/l with 4 weeks treatment, and from 44.7±3.4 mg/l to 18.1±1.4 mg/l with 3 weeks treatment. Pre-haemodialysis treatment levels of urea nitrogen, plasma creatinine and uric acid in the first system were greater than ordinary prehaemodialysis levels. On the second system, these were kept at −54±8.3%, −52.2±6.7% and −47.6±4.4% of the ordinary pre-haemodialysis levels, respectively. After 4 weeks on the third system, these same levels were maintained at -32.1±3.1%, −56.7±2.1% and −59.2±5.4%, respectively. Although with the first system the serum Na, Cl and Ca were within the normal range, the pre-dialysis plasma K concentration was high. Plasma P ₁ was greater than normal in the first and second systems, but was maintained within the normal range in the third system.

Background and Aims: The calcineurin inhibitor tacrolimus is reportedly effective for moderate/severe ulcerative colitis (UC); however, it is also reportedly associated with nephrotoxicity. We investigated the risk factors for tacrolimus-induced nephrotoxicity and whether renal impairment adversely affected the outcomes of tacrolimus treatment in patients with UC. Methods: We conducted a retrospective study of 93 patients with UC who were administered tacrolimus leading to high trough levels (10–15 ng/mL) for 2 weeks and low trough levels (5–10 ng/mL) for 3 months. Results: Acute kidney injury (AKI) occurred in 44 patients (47.3%) during tacrolimus treatment. Of these patients, 34 (36.6%) developed AKI during the high trough phase and 17 (18.3%) developed AKI when the trough value exceeded the original target value of 15 ng/mL. Multivariate logistic regression analysis revealed that the male sex was significantly associated with AKI (p = 0.002, AOR = 4.38, 95% CI [1.69–11.3]). Clinical remission rate after 4, 8, 12, and 24 weeks of tacrolimus treatment in patients with AKI was lower than that in patients without AKI. Six patients (6.5%) had chronic kidney disease (CKD) after tacrolimus treatment completion, and all patients with CKD developed AKI during treatment. The median duration of treatment with no improvement in AKI was significantly longer in patients with CKD than in those without CKD (p = 0.016). Conclusion: We revealed the risk factors for tacrolimus-induced nephrotoxicity. Renal impairment occurrence adversely affected the tacrolimus treatment outcome; therefore, it is important to carefully administer tacrolimus to prevent renal impairment.