[Small fugal enteritis manifestation with intestinal obstruction and hematochezia: a case report].

Fungal enteritis was rarely reported. A case of fungal enteritis manifestation with jejunum multiple ulcers and obstruction was treated by Department of Gastroenterology, Third Xiangya Hospital, Central South University. After antifungal treatment, the clinical symptoms were relieved, and the ulcers in jejunal and upper gastrointestinal tract were healed completely. Clinical manifestation for small fungal enteritis is special, and the small intestine ulcer is easily to be misdiagnosed. It is helpful to prevent the misdiagnose for small fungal enteritis if we can tell the clinical features for this disease.

Classification of intestinal lymphangiectasia with protein-losing enteropathy: white villi type and non-white villi type.

BACKGROUND/AIMS: We classified intestinal lymphangiectasia (IL) into two categories, the white and non-white villi types, and evaluated their clinical characteristics and therapeutic responses. METHODS: Of the 988 patients who underwent double-balloon enteroscopy, 14 consecutive patients (7 men and 7 women, median age at onset 34 years) were enrolled with immunohistochemically confirmed IL with protein-losing enteropathy. RESULTS: Enteroscopically the white villi type (n = 8) showed white plaques and white-tipped villi were scattered in the small bowel, while non-white villi type (n = 6) showed that apparently normal but under more detailed observation, low and round villi with a normal color were diffused. The serum albumin levels and fecal α1-antitrypsin clearance before treatment were significantly worse in the non-white villi type (p = 0.017 and 0.039, respectively), whereas the serum immunoglobulin A and M levels were significantly lower in the white villi type (p = 0.010 and 0.046, respectively). At gastroscopy, a non-cirrhotic snakeskin appearance was significantly observed in the non-white villi type (p = 0.015). The corticosteroid response was better in the non-white villi type (p = 0.015). CONCLUSION: Two distinct subgroups were found in IL. This classification was useful in pathophysiological clustering and in predicting the therapeutic response.

Is L-glutathione more effective than L-glutamine in preventing enteric diabetic neuropathy?

BACKGROUND: Diabetes and its complications appear to be multifactorial. Substances with antioxidant potential have been used to protect enteric neurons in experimental diabetes. AIM: This study evaluated the effects of supplementation with L-glutamine and L-glutathione on enteric neurons in the jejunum in diabetic rats. METHODS: Rats at 90 days of age were distributed into six groups: normoglycemic, normoglycemic supplemented with 2 % L-glutamine, normoglycemic supplemented with 1 % L-glutathione, diabetic (D), diabetic supplemented with 2 % L-glutamine (DG), and diabetic supplemented with 1 % L-glutathione (DGT). After 120 days, the jejunums were immunohistochemically stained for HuC/D+ neuronal nitric oxide synthase (nNOS) and vasoactive intestinal polypeptide (VIP). Western blot was performed to evaluate nNOS and VIP. Submucosal and myenteric neurons were quantitatively and morphometrically analyzed. RESULTS: Diabetic neuropathy was observed in myenteric HuC/D, nNOS, and VIP neurons (p < 0.05). In the submucosal plexus, diabetes did not change nitrergic innervation but increased VIPergic neuronal density and body size (p < 0.05). Supplementation with L-glutathione prevented changes in HuC/D neurons in the enteric plexus (p < 0.05), showing that supplementation with L-glutathione was more effective than with L-glutamine. Myenteric nNOS neurons in the DGT group exhibited a reduced density (34.5 %) and reduced area (p < 0.05). Submucosal neurons did not exhibit changes. The increase in VIP-expressing neurons was prevented in the submucosal plexus in the DG and DGT groups (p < 0.05). CONCLUSION: Supplementation with L-glutathione exerted a better neuroprotective effect than L-glutamine and may prevent the development of enteric diabetic neuropathy.

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death.

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson's trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

Hydrogen sulfide attenuates intestinal ischemia-reperfusion injury when delivered in the post-ischemic period.

BACKGROUND AND AIM: To investigate whether pharmacologic post-conditioning of intestinal tissue with hydrogen sulfide (HS) protects against ischemia reperfusion injury (IRI). METHODS: In vitro, enterocytes were made hypoxic for 1, 2, or 3 h, treated with media containing between 0 and 100 µM HS 20 min prior to the end of the hypoxic period, then returned to normoxia for 3 h. An apoptotic index (AI) was determined for each time point and (HS). In vivo, jejunal ischemia was induced in male Sprague-Dawley rats for 1, 2, or 3 h; 20 min prior to the end of the ischemic period animals were given an intravenous injection of NaHS sufficient to raise the bloodstream concentration to 0, 10 µM, or 100 µM HS. This was followed by jejunal reperfusion for 3 h, histologic processing, and measurement of villus height. RESULTS: In vitro, there was a significant decrease in AI compared with non-HS-treated control at all time points after treatment with 10 µM HS, and at the 2 h time point with 100 µM HS (P < 0.017). In vivo, after 1 h ischemia, qualitative reduction of injury was noted with 10 µM and 100 µM; after 2 h ischemia, reduction was noted with 10 µM but not 100 µM; and after 3 h ischemia, there was no injury reduction. HS treatment resulted in significant quantitative preservation (P < 0.05) of villus height at all time points and doses, except for 3 h ischemia and delivery of 100 µM (P = 0.129). CONCLUSIONS: Hydrogen sulfide provides significant protection to intestinal tissues in vitro and in vivo when delivered after the onset of ischemia.

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses.

BACKGROUND: Green tea has been shown to repair fasting-induced mucosal damage in rat intestine. The aim of this study was to elucidate the underlying mechanism. METHODS: Five groups of rats were used. Group 1 had free access to chow diet and water, and those in group 2 were fasted for 3 days. Animals in group 3 were fasted for 3 days, then were allowed drinking water for a further 7 days. Groups 4 and 5 were fasted for 3 days, then given drinking water containing green tea or vitamin E respectively for 7 days. Blood was collected for estimation of total plasma antioxidants, and jejunal samples were used for immunohistochemical analysis of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx), and for estimation of myeloperoxidase (MPO) activity. RESULTS: Use of green tea was associated with a significant increase in total plasma antioxidants (P < 0.001), and mucosal SOD (P < 0.001), catalase (P = 0.006) and GPx (P = 0.017), but a significant decrease in MPO activity (P < 0.001). Vitamin E produced similar changes, but the effects were smaller. CONCLUSION: Green tea reverses the fasting-induced damage to the intestinal mucosa by its antioxidant and anti-inflammatory effect.

Effect of firocoxib or flunixin meglumine on recovery of ischemic-injured equine jejunum.

OBJECTIVE: To determine whether treatment of horses with firocoxib affects recovery of ischemic-injured jejunum, while providing effective analgesia. ANIMALS: 18 horses. PROCEDURES: Horses (n = 6 horses/group) received saline (0.9% NaCl) solution (1 mL/50 kg, IV), flunixin meglumine (1.1 mg/kg, IV, q 12 h), or firocoxib (0.09 mg/kg, IV, q 24 h) before 2 hours of jejunal ischemia. Horses were monitored via pain scores and received butorphanol for analgesia. After 18 hours, ischemic-injured and control mucosa were placed in Ussing chambers for measurement of transepithelial resistance and permeability to lipopolysaccharide. Histomorphometry was used to determine denuded villus surface area. Western blots for cyclooxygenase (COX)-1 and COX-2 were performed. Plasma thromboxane B(2) and prostaglandin E(2) metabolite (PGEM) concentrations were determined. RESULTS: Pain scores did not significantly increase after surgery in horses receiving flunixin meglumine or firocoxib. Transepithelial resistance of ischemic-injured jejunum from horses treated with flunixin meglumine was significantly lower than in saline- or firocoxib-treated horses. Lipopolysaccharide permeability across ischemic-injured mucosa was significantly increased in horses treated with flunixin meglumine. Treatment did not affect epithelial restitution. Cyclooxygenase-1 was constitutively expressed and COX-2 was upregulated after 2 hours of ischemia. Thromboxane B(2) concentration decreased with flunixin meglumine treatment but increased with firocoxib or saline treatment. Flunixin meglumine and firocoxib prevented an increase in PGEM concentration after surgery. CONCLUSIONS AND CLINICAL RELEVANCE: Flunixin meglumine retarded mucosal recovery in ischemic-injured jejunum, whereas firocoxib did not. Flunixin meglumine and firocoxib were effective visceral analgesics. Firocoxib may be advantageous in horses recovering from ischemic intestinal injury.

Non-operatively managed case of contained jejunal diverticular perforation.

Jejunal diverticulosis is an underdiagnosed condition due to its relatively benign existence and uncharacteristic presentation. The complications can be very severe and, due to its often late diagnosis, patients may require urgent surgery. We present a woman who initially complained of non-specific abdominal symptoms but was diagnosed with a contained jejunal diverticular perforation relatively early. We managed her non-operatively with intravenous antibiotics from which she recovered well. She was discharged 2 days later and has remained completely well. Follow-up at 3 months showed no recurrence. Our case differs from most of the literature due to the early diagnosis and successful non-operative management of the patient. We conclude that, in cases of non-specific abdominal pain with diagnostic ambiguity, a diagnosis of small bowel diverticulosis should be considered. It should be managed non-operatively where possible.

Complications and survival associated with surgical compared with medical management of horses with duodenitis-proximal jejunitis.

REASONS FOR PERFORMING STUDY: Based on clinical observation, it is hypothesised that horses with duodenitis-proximal jejunitis (DPJ) that are treated surgically have a shorter duration, smaller volume, and slower rate of nasogastric reflux (NGR) compared to horses treated medically, are more likely to develop diarrhoea than medically managed cases, and have a higher incisional infection rate than a sample population of horses undergoing abdominal exploration for gastrointestinal disease other than DPJ. OBJECTIVES: To compare: 1) duration, volume and rate of NGR and the percentage of horses with diarrhoea between medically and surgically treated DPJ cases; and 2) incisional infection rate in horses with DPJ undergoing abdominal exploration to a sample population of horses undergoing abdominal exploration for gastrointestinal disease other than DPJ. METHODS: Medical records of cases with DPJ diagnosed 1995-2006 were reviewed. Information obtained included subject details, presenting clinical findings, treatment category (medical/surgical), complications (diarrhoea, incisional infection), and outcome (survival/nonsurvival). Data were analysed using a Chi-squared test and a mixed model analysis of variance. Level of significance was P<0.05. RESULTS: Compared to medical cases, surgical cases had significantly decreased survival, a longer duration and larger total volume of NGR, and were more likely to develop diarrhoea. The incisional infection rate for horses with DPJ undergoing abdominal exploration was 16% compared to 7% for the sample population of horses. CONCLUSIONS: Surgical treatment of horses with DPJ did not lead to resolution of NGR faster than medical treatment. Surgical cases were more likely to develop diarrhoea and did not have a significantly higher incisional infection rate than the sample population.

Successful azathioprine treatment in an adolescent with chronic enteropathy associated with SLCO2A1 gene: A case report.

INTRODUCTION: Chronic nonspecific multiple ulcers of the small intestine (CNSU), an entity with female preponderance and manifestations including anemia and hypoproteinemia reflecting persistent gastrointestinal bleeding and intestinal protein loss, has been considered idiopathic. Umeno et al recently reported that CNSU is caused by loss-of-function mutations in the solute carrier organic anion transporter family member 2A1 gene (SLCO2A1) encoding a prostaglandin transporter, renaming the disorder "chronic enteropathy associated with SLCO2A1 gene mutation" (CEAS). Treatments for chronic enteropathies such as inflammatory bowel disease, including 5-aminosalicylic acid, corticosteroids, azathioprine, and anti-tumor necrosis factor-α antibody, often are ineffective in CEAS, which frequently requires surgery. CASE PRESENTATION: A 14-year-old girl had refractory anemia and hypoproteinemia for more than 2 years. Video capsule endoscopy showed nonspecific jejunal and ileal ulcers with varied sizes and shapes. She was diagnosed with CEAS resulting from compound heterozygous mutation of the SLCO2A1 gene. After corticosteroid treatment without improvement, azathioprine treatment improved her anemia and edema as hemoglobin and serum protein increased. Video capsule endoscopy 1 year after initiation of azathioprine showed improvement of small intestinal ulcers. CONCLUSION: Physicians should consider CEAS in patients with refractory anemia, hypoproteinemia, and multiple small intestinal ulcers. Why our patient responded to azathioprine but not to corticosteroids is unclear, but azathioprine might benefit some other patients with CEAS.

[A patient with repeated, life-threatening gastro-intestinal haemorrhages treated by means of medication, open surgery, endoscopic surgery, intervention radiology and conservative methods]. / Een patiënt met recidiverende levensbedreigende darmbloedingen behandeld met medicamenteuze, chirurgische, endoscopische, interventieradiologische en conservatieve methoden.

A 56-year-old man with Henoch Schönlein purpura vasculitis suffered from repeated and multiple life-threatening gastrointestinal haemorrhages. Over recent years a number of interventions for the treatment of gastrointestinal haemorrhaging have become available; choosing which option to use can present difficulties. The available interventions are carried out by different disciplines and include haemostatic drugs, endoscopic intervention, intervention radiology, and surgery. In this patient, following a severe drop in haemoglobin levels, CT and angiography revealed active bleeding in the distal jejunum. Transarterial embolization by means of a coiling procedure halted the bleeding. The patient was also given tranexamic acid, a fibrinolysis inhibitor. More episodes of bleeding subsequently followed which necessitated further coiling procedures, two bowel resections, the endoscopic clipping of a bleeding artery, treatment with the recombinant activated factor VII (rFVIIa) at a dosage of 90 microg/kg, as well as conservative treatment with multiple transfusions of filtered erythrocytes and fresh plasma. The patient eventually recovered.

Effect of lidocaine on inflammation in equine jejunum subjected to manipulation only and remote to intestinal segments subjected to ischemia.

OBJECTIVE To examine effects of continuous rate infusion of lidocaine on transmural neutrophil infiltration in equine intestine subjected to manipulation only and remote to ischemic intestine. ANIMALS 14 healthy horses. PROCEDURES Ventral midline celiotomy was performed (time 0). Mild ischemia was induced in segments of jejunum and large colon. A 1-m segment of jejunum was manipulated by massaging the jejunal wall 10 times. Horses received lidocaine (n = 7) or saline (0.9% NaCl) solution (7) throughout anesthesia. Biopsy specimens were collected and used to assess tissue injury, neutrophil influx, cyclooxygenase expression, and hypoxia-inducible factor 1α (HIF-1α) expression at 0, 1, and 4 hours after manipulation and ischemia. Transepithelial resistance (TER) and mannitol flux were measured by use of Ussing chambers. RESULTS Lidocaine did not consistently decrease neutrophil infiltration in ischemic, manipulated, or control tissues at 4 hours. Lidocaine significantly reduced circular muscle and overall scores for cyclooxygenase-2 expression in manipulated tissues. Manipulated tissues had significantly less HIF-1α expression at 4 hours than did control tissues. Mucosa from manipulated and control segments obtained at 4 hours had lower TER and greater mannitol flux than did control tissues at 0 hours. Lidocaine did not significantly decrease calprotectin expression. Severity of neutrophil infiltration was similar in control, ischemic, and manipulated tissues at 4 hours. CONCLUSIONS AND CLINICAL RELEVANCE Manipulated jejunum did not have a significantly greater increase in neutrophil infiltration, compared with 4-hour control (nonmanipulated) jejunum remote to sites of manipulation, ischemia, and reperfusion. Lidocaine did not consistently reduce neutrophil infiltration in jejunum.