Laparoscopic sleeve gastrectomy as a bridge to colorectal cancer surgery for obese patients: a case report.

BACKGROUND: Severe obesity greatly influences the difficulty of colorectal cancer surgery and has been reported to prolong operative time, increase the rate of laparotomy, and elevate increase postoperative complications. We investigated the efficacy of laparoscopic sleeve gastrectomy (LSG) for preoperative weight loss to ensure safe colorectal cancer surgery. CASE PRESENTATION: A 51 year-old female with a body mass index of 43.5 kg/m2 was referred to our hospital due to a positive fecal occult blood test. She was diagnosed as having a laterally spreading tumor of the cecum by colonoscopy. Endoscopic submucosal dissection was attempted but proved difficult due to the size of the lesion and its proximity to the appendiceal orifice. We planned bariatric surgery prior to colorectal surgery, and she underwent LSG without any complications. Seven months after the LSG, she had lost 30.7 kg, and her final preoperative body mass index was 27.8 kg/m2. Single-incision laparoscopic ileocecal resection was then performed safely. The pathological diagnosis was adenocarcinoma in adenoma of the cecum, TisN0M0. CONCLUSION: LSG was effective in reducing visceral fat and making it possible to perform safe surgery for colorectal cancer in a severely obese patient.

Polyclonal IgE induces mast cell survival and cytokine production.

BACKGROUND: Ag-dependent activation of IgE-bearing mast cells is a critical first step in immediate hypersensitivity and other allergic responses. Recent studies have revealed Ag-independent effects of monoclonal mouse IgE molecules on mast cell survival and activation. However, no studies have been performed on the effects of polyclonal IgE molecules. Here, we tested whether polyclonal mouse and human IgE molecules affect survival and cytokine production in mast cells. METHODS: Mast cells were cultured in the presence of polyclonal mouse and human IgE molecules, and cell survival and cytokine production were analyzed. RESULTS: Polyclonal mouse IgE molecules in sera from mice with atopic dermatitis-like allergic skin inflammation, enhanced survival and cytokine production in mast cell cultures. Similar to the effects of monoclonal IgE, the polyclonal IgE effects were mediated by the high-affinity IgE receptor, FcepsilonRI. Human polyclonal IgE molecules present in sera from atopic dermatitis patients were also capable of activating mast cells, and inducing IL-8 production in human cord blood-derived mast cells. CONCLUSIONS: These results imply that polyclonal IgE in atopic dermatitis and other atopic conditions might modulate mast cell number and function, thus amplifying the allergic response.

Hyperexpression of NOD2 in intestinal mast cells of Crohn's disease patients: preferential expression of inflammatory cell-recruiting molecules via NOD2 in mast cells.

NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP) has been implicated as a key player in intestinal immune health and disease. Mast cells (MCs) have been reported to be increased in the gut of patients with inflammatory bowel disease. However, NOD2 expression and its role in human primary MCs are unknown. The number of NOD2(+) intestinal MCs was significantly increased in the Crohn's disease (CD) specimens compared to Ulcerative colitis (UC) specimens and controls. IFN-gamma upregulated NOD2 expression in MCs. CXCL10 and urokinase-type plasminogen activator (uPA) upregulation was specific to MCs activated by MDP compared to MCs activated by LPS and IgE/anti-IgE. MDP-induced upregulation of ICAM-1, VCAM-1, and uPA was specific to MCs compared to mononuclear cells. The number of CXCL10(+)NOD2(+) intestinal MCs was significantly increased in the CD patients. Our results suggest that NOD2(+) MCs have specific pathogenic roles that involve the recruitment of inflammatory cells in CD.

Increased leukotriene E4 in the exhaled breath condensate of children with mild asthma.

BACKGROUND: Chronic airway inflammation is a feature of asthma. Increased levels of cysteinyl leukotrienes (cys-LTs; leukotriene [LT]C(4), LTD(4), LTE(4)) have been shown in the exhaled breath condensate (EBC) of children with moderate-to-severe asthma. The aim of this study was to examine the relationship between EBC cys-LTs (LTE(4)) levels and bronchial hyperreactivity in children with mild asthma in order to evaluate the clinical utility of measuring EBC cys-LTs levels. METHODS: We measured LTE(4) levels in the EBC of children aged 8 to 18 years, including healthy nonasthmatic children (n = 6) and children with mild asthma (n = 37). Patients with mild asthma were classified into the following three groups: group 1, participants who had been asymptomatic (no wheezing/symptoms of asthma) for > 6 months prior to examination (n = 12); group 2, participants who were asymptomatic but had had wheezing/symptoms of asthma within 6 months before examination (n = 18); and group 3, patients with current wheeze and/or mild symptoms of asthma exacerbation at the time of examination. RESULTS: Exhaled LTE(4) levels were increased in all children with mild asthma compared with nonasthmatic control subjects (5.69 +/- 9.62 pg/20 min vs 0.74 +/- 0.79 pg/20 min, p < 0.05) [mean +/- SD]. In particular, the EBC LTE(4) levels in group 2 (4.99 +/- 6.70 pg/20 min) and group 3 (14.66 +/- 17.11 pg/20 min) were increased compared with control subjects and group 1 (1.50 +/- 1.69 pg/20 min). The EBC LTE(4) levels negatively correlated with the provocative concentration of methacholine causing a 15% fall in FEV(1) (r = - 0.454, p = 0.012). CONCLUSION: EBC cys-LTs may be useful as a noninvasive marker assessing airway inflammation and hyperreactivity in children with asthma.