Endoscopic retrograde cholangiopancreatography (ERCP) is often complex and involves long fluoroscopic times, with significant radiation exposure to medical staff. We investigated protective effects of an additional attached lead shielding device. The lead shielding device covered with the X-ray tube table (0.125 mm lead equivalent) during ERCP procedures. Fluoroscopy scatter radiation, with or without the lead shielding device, was measured using an acrylic phantom and a radiation survey meter. Measurements (25 points) were made at 50 cm intervals, at both 90 and 150 cm above the floor. We created radiation maps, with and without the additional lead shielding device. Moreover, we monitored annual staff exposure to radiation, before and after inclusion of the shielding device. Without additional shielding, exposure doses at the physician’s position, 90 and 150 cm above the floor, were 1940 and 4040 (μSv/h) respectively. In contrast, with the shielding device, corresponding exposures were 270 and 450 (μSv/h) at 90 and 150 cm, respectively. Scattered radiation was decreased by 86.1% at 90 cm or 88.9% at 150 cm. However, with additional lead shielding in the middle, rather than hung over the operating table, scattered radiation was decreased by only ~10%. The staff’s annual dose equivalents (DEs) were 12.2–29.8 mSv/year without and 3.8–8.4 mSv/year with lead shielding. With lead shielding, dose equivalent values for the staff were decreased by 41.0–76.5%. Thus, with additional lead shielding, properly used, scattered radiation would be decreased by ~90%, thus decreasing exposure doses to medical staff during ERCPs.
<b><i>Introduction:</i></b> Predictive biomarkers for the therapeutic outcome of induction therapy with systemic corticosteroid for active ulcerative colitis (UC) have not been established. This study aimed to investigate whether neutrophil-to-lymphocyte ratio (NLR) and/or platelet-to-lymphocyte ratio (PLR) can be predictive biomarkers for the therapeutic outcomes of systemic corticosteroid therapy in UC. <b><i>Methods:</i></b> This was a single-center retrospective cohort study. In total, 48 patients with UC who received induction therapy with systemic corticosteroid were enrolled. Based on the achievement of clinical remission after 8 weeks of treatment, the patients were divided into the remission group (<i>n</i> = 28) and the nonremission group (<i>n</i> = 20). Clinical characteristics, NLR, and PLR at baseline between the remission and nonremission groups were compared via a univariate analysis. The independent risk factors of nonremission were identified via a multivariate analysis. <b><i>Results:</i></b> The baseline Mayo score, platelet count, lymphocyte count, C-reactive protein (CRP) levels, NLR, and PLR between the 2 groups significantly differed. The nonremission group had higher NLR and PLR than the remission group (4.70 [3.04–11.3] vs. 3.10 [1.36–16.42]; <i>p</i> < 0.05, and 353.6 [220.3–499.8] vs. 207.2 [174.4–243.6]; <i>p</i> < 0.001, respectively). A multivariate analysis revealed that a Mayo score of ≥9, CRP level of ≥1.26 mg/dL, and PLR of ≥262 (hazard ratio: 23.1, 95% confidence interval: 1.29–413.7, <i>p</i> = 0.033) were considered independent risk factors for nonremission. <b><i>Conclusion:</i></b> This report first identified the efficacy of NLR and PLR as candidate biomarkers for predicting the therapeutic outcomes of systemic corticosteroid therapy in UC.
The histopathological findings of immune checkpoint inhibitor (ICI)-induced pancreatitis have rarely been reported. A 56-year-old man with squamous cell carcinoma of the lung with bone metastasis was being treated with pembrolizumab, an anti-programmed cell death protein-1 antibody. After 13 doses, he was referred to our department due to pancreatitis. Despite characteristic symptoms of acute pancreatitis, imaging findings were similar to those of autoimmune pancreatitis. However, a histological examination showed neutrophil-based inflammatory cell infiltration and acinar-ductal metaplasia. Immunostaining showed CD8positive T lymphocyte infiltration. This case revealed the characteristic histopathology of pembrolizumabinduced pancreatitis, which was previously poorly understood.
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