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Background/Aims@#Post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common and serious complication of endoscopic retrograde cholangiopancreatography. To prevent this event, a unique precutting method, termed opening window fistulotomy, was performed in patients with a large infundibulum as the primary procedure for biliary cannulation, whereby a suprapapillary laid-down H-shaped incision was made without touching the orifice. This study aimed to assess the safety and feasibility of this novel technique. @*Methods@#One hundred and ten patients were prospectively enrolled in this study. Patients with a papillary roof size ≥10 mm underwent opening window fistulotomy for primary biliary access. In addition, the incidence of complications and success rate of biliary cannulation were evaluated. @*Results@#The median size of the papillary roof was 6 mm (range, 3–20 mm). Opening window fistulotomy was performed in 30 patients (27.3%), none of whom displayed PEP. Duodenal perforation was recorded in one patient (3.3%), which was resolved by conservative treatment. The cannulation rate was high (96.7%, 29/30 patients). The median duration of biliary access was 8 minutes (range, 3–15 minutes). @*Conclusions@#Opening window fistulotomy demonstrated its feasibility for primary biliary access by achieving great safety with no PEP complications and a high success rate for biliary cannulation.
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Objective: In late 1970s, occupational exposure to antineoplastic agents was reported. Various countries, including Japan, have published guidelines for handling antineoplastic agents. Surveys are still being conducted to determine the levels of environmental exposure to antineoplastic agents at individual hospitals, and incidents of contamination are often reported. This study provides details regarding a literature survey conducted to evaluate the actual state of environmental contamination by antineoplastic agents and identify the related issues in order to promote environmental monitoring.Methods: The literature search was carried out from January 1, 1990 to July 31, 2017. PubMed and Ichushi-Web were searched with the following keywords: “antineoplastic agents,” “occupational exposure,” “surface contamination,” and “environmental monitoring.”Results: Following the literature search, 117 papers were included in the analysis. The findings showed that contamination by antineoplastic agents was widely reported in hospitals and places where antineoplastic drugs were not handled. The findings of this study regarding the actual state of environmental exposure are partial, as there is a lack of information on retail pharmacies and homes of outpatients who have received chemotherapy.Discussion: Therefore, further investigation is warranted. In addition, according to the current Japanese guidelines, published in 2015, environmental surveillance is not required to reduce contamination by antineoplastic agents. To promote environmental monitoring, we feel that it is necessary to determine a new survey method and the clarify optimum interval of environmental monitoring.
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Antineoplastic drugs play an important role in cancer therapy. A growing number of patients and new fields of application have resulted in an increasing use of these agents. Most antineoplastic drugs are classified as carcinogenic, mutagenic, or teratogenic for humans. Antineoplastic drugs also cause adverse effects in health care workers who handle them. In the late 1960s, acute symptoms by exposure to antineoplastic drugs were first reported. In 1979, Falck reported a small increase in urine mutagenicity of nurse who handled antineoplastic drugs. Thereafter several studies showed that association of occupational exposure to antineoplastic drugs with health effects such as DNA damage, chromosomal abnormalities, adverse reproductive outcomes, possibly leukemia and other cancers. To prevent them, many guidelines for safe handling were published in various countries in 1980s, they are revised periodically afterward. In 1990s, despite recommended safe handling procedures, environmental contamination with antineoplastic drugs was still observed in hospital and health care workers were still exposed. In 2004, the National Institute for Occupational Safety and Health (NIOSH) published an Alert on hazardous drugs used in health care settings. One recommendation was to consider the use of closed system drug transfer devices (CSTD) in addition to ventilated cabinets. The effectiveness of CSTDs in reduction of environmental contamination and exposure of health care workers has been reported. Here this report briefly reviews the history of the health effects of exposure to antineoplastic drugs and of safe handling.
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Objectives: Mucosal immunity plays a pivotal role for body defense against infection and allergy. The aim of this study was to clarify the effects of 2,3,7,8-tetraclorodibenzo-p-dioxin (TCDD) on mucosal immunity in the gut. Methods: Fecal IgA level and oral tolerance induction were examined in TCDD-treated mice. Flow cytometric and histological analyses were also performed. Results: Single oral administration of low dose 2,3,7,8-TCDD resulted in a marked decrease in IgA secretion in the gut without any effects on the cellular components of gut-associated lymphoid tissues (GALT) including Peyer’s patches (PPs) and mesenteric lymph nodes (LNs). Decreased IgA secretion by TCDD was not observed in aryl hydrocarbon receptor (AhR)-deficient mice. Flow cytometric analysis revealed that IgA+ B cells in PPs and the mesenteric LNs remained unchanged in the TCDD-treated mice. An immunofluorescence study also demonstrated that a significant number of cytoplasmic IgA+ cells were present in the lamina propria of the gut in the TCDD-treated mice. Furthermore, oral tolerance induction by ovalbumin (OVA) was impaired in the TCDD-treated mice and OVA-specific T cell proliferation occurred in the peripheral lymphoid tissues including the spleen and LNs. Conclusions: These results suggest that a relatively low dose of TCDD impairs mucosal immunity in the gut and induces systemic sensitization by oral antigens.
Subject(s)
Polychlorinated Dibenzodioxins , Mice , Immunity, MucosalABSTRACT
<p><b>OBJECTIVES</b>Mucosal immunity plays a pivotal role for body defense against infection and allergy. The aim of this study was to clarify the effects of 2,3,7,8-tetraclorodibenzo-p-dioxin (TCDD) on mucosal immunity in the gut.</p><p><b>METHODS</b>Fecal IgA level and oral tolerance induction were examined in TCDD-treated mice. Flow cytometric and histological analyses were also performed.</p><p><b>RESULTS</b>Single oral administration of low dose 2,3,7,8-TCDD resulted in a marked decrease in IgA secretion in the gut without any effects on the cellular components of gut-associated lymphoid tissues (GALT) including Peyer's patches (PPs) and mesenteric lymph nodes (LNs). Decressed IgA secretion by TCDD was not observed in aryl hydrocarbon receptor (AhR)-deficient mice. Flow cytometric analysis revealed that IgA B cells in PPs and the mesenteric LNs remained unchanged in the TCDD-treated mice. An immunofluorescence study also demonstrated that a significant number of cytoplasmic IgA cells were present in the lamina propria of the gut in the TCDD-treated mice. Furthermore, oral tolerance induction by ovalbumin (OVA) was impaired in the TCDD-treated mice and OVA-specific T cell proliferation occurred in the peripheral lymphoid tissues including the spleen and LNs.</p><p><b>CONCLUSIONS</b>These results suggest that a relatively low dose of TCDD impairs mucosal immunity in the gut and induces systemic sensitization by oral antigens.</p>