Small intestine necrosis in catastrophic antiphospholipid syndrome: A rare and severe case.

Catastrophic antiphospholipid syndrome (CAPS) is a multisystem autoimmune disease with widespread thrombotic events. In this case report, we present a young man with primary antiphospholipid syndrome (PAPS) admitted to the hospital with abdominal pain and vomiting. Abdominal computed tomography showed pneumoperitoneum and acute explorative laparotomy revealed small intestinal necrosis indicating small vessel thrombosis without involvement of large intestine. "Triple therapy" was initiated after surgery and the patient was treated in an intensive care unit for 72 days before being discharged to a rehabilitation clinic. A review of the literature regarding CAPS affecting small intestine shows it is extremely rare and may be associated with higher mortality.

A Serological Biomarker of Laminin Gamma 1 Chain Degradation Reflects Altered Basement Membrane Remodeling in Crohn's Disease and DSS Colitis.

BACKGROUND: The laminin gamma 1 chain (LMγ1) is abundant along the crypt-villus axis in the intestinal basement membrane. AIMS: We investigated whether a serological biomarker of laminin degradation was associated with disease activity in patients with Crohn's disease (CD) and in rats with dextran sulfate sodium (DSS)-induced colitis. METHODS: Serum samples from CD patients (n = 43), healthy subjects (n = 19), and Sprague Dawley rats receiving 5-6% DSS water for five days and regular drinking water for 11 days were included in this study. The LG1M biomarker, a neo-epitope degradation fragment of the LMγ1 chain generated by matrix metalloproteinases-9 (MMP-9), was measured in serum to estimate the level of laminin degradation. RESULTS: Serum LG1M was elevated in CD patients with active and inactive disease compared to healthy subjects (p < 0.0001). LG1M distinguished CD patients from healthy subjects, with an area under the curve (AUC) of 0.81 (p < 0.0001). Serum LG1M was decreased in DSS rats compared to controls 2 days after DSS withdrawal, and increased upon reversal of the disease. CONCLUSIONS: Increased serum LG1M in active and inactive CD patients supports the evidence of altered LM expression in both inflamed and non-inflamed tissue. Moreover, lower LG1M levels in the early healing phase of DSS-induced colitis may reflect ongoing mucosal repair.

Incorporation of a Poly-ε-Caprolactone Scaffold in a ;Circular Stapled End-To-End Small Intestine Anastomosis Does Not Have Any Adverse Effects Within 30 days: A Study in Piglets.

Background. Incorporation of a poly-ε-caprolactone (PCL) scaffold in circular stapled anastomoses has been shown to increase the anastomotic tensile strength on postoperative day (POD) 5 in a pig model. The aim of this study was to investigate the effects of incorporation of a PCL scaffold in a circular stapled end-to-end small intestine anastomosis, with stricture formation and anastomotic histology as primary outcomes in a 30-day observation period. Methods. A total of 15 piglets were included. In each piglet, three circular stapled end-to-end anastomoses were made in the small intestines. Two were interventional and one was a control. On POD 10, 20, or 30, the anastomoses were subjected to in vivo intraluminal contrast study, and the index for anastomotic lumen was calculated. The anastomotic segment was resected and subjected to a tensile strength test and histological examination. Results. At POD 10, the mean ± SD value for anastomotic index was .749 ± .065 in control anastomoses and .637 ± .051 in interventional anastomosis (P = .0046), at POD 20, .541 ± .150 and .724 ± .07 (P = .051), and at POD 30, .645 ± .103 and .686 ± .057 (P = .341), respectively. No significant difference was observed in maximum tensile strength and histology at POD 30. Conclusions. The incorporation of a PCL scaffold in a circular stapled end-to-end small intestine anastomosis does not increase the risk of stricture or impair wound healing after 30 days.

FIBCD1 ameliorates weight loss in chemotherapy-induced murine mucositis.

PURPOSE: Chemotherapy-induced gastrointestinal toxicity is a common adverse event during chemotherapeutic treatment. No uniformly applicable strategies exist to predict, prevent, or treat gastrointestinal toxicity. Thus, a goal of mucositis research is to identify targets for therapeutic interventions and individualized risk prediction. Fibrinogen C domain containing 1 (FIBCD1) is a transmembrane protein expressed in human intestinal epithelial cells with functions in the innate immune system. Previous observations have shown that FIBCD1 ameliorates dextran sulfate sodium (DSS)-induced intestinal inflammation in vivo. We evaluated the effect of FIBCD1 in a murine model of chemotherapy-induced gastrointestinal toxicity and inflammation. METHODS: Transgenic (Tg) mice overexpressing FIBCD1 in the intestinal epithelium (Fibcd1Tg) and wild-type (WT) littermates (C57BL/6N) were randomized to receive an intraperitoneal injection of doxorubicin 20 mg/kg or saline and were terminated 2 or 7 days after the injection. Gastrointestinal toxicity was evaluated by weight change, intestinal length, villus height/crypt depth, and histological mucositis score. Expression of inflammatory markers (IL-6, IL-1ß, and Tnfα) was measured by quantitative real-time PCR in intestinal tissue samples. RESULTS: Following doxorubicin treatment, WT mice exhibited an increased weight loss compared with Tg littermates (p < 0.001). No differences between genotypes were seen in mucositis score, intestinal length, villus height/crypt depth, or IL-6, IL-1ß, and Tnfα expression. CONCLUSION: Our findings suggest that FIBCD1 could ameliorate chemotherapy-induced gastrointestinal toxicity by reducing weight loss; however, the mechanism of this possible protective effect remains to be defined warranting additional investigations.