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PubMed1997

Citrobacter freundii and fatal neutropenic enterocolitis following adjuvant chemotherapy for breast cancer.

Neutropenic enterocolitis is increasingly being recognized as a life-threatening complication of chemotherapy, mainly for haematological and lymphoproliferative malignancies. It is under-recognized clinically, with the diagnosis often being made on post-mortem examination. Although active medical management is generally preferred, surgical intervention may be indicated. We report a case of fatal neutropenic enterocolitis, secondary to Citrobacter freundii, following adjuvant chemotherapy for breast cancer. We also review the literature, examining the aetiology, diagnosis and management of this often fatal entity.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Pseudomembranous enterocolitis after gynecologic endoscopy.

A 21-year-old nulligravida underwent diagnostic hysteroscopy and laparoscopic potassium-titanyl-phosphate laser ablation of pelvic peritoneal endometriosis (revised American Fertility score of 10) for dysmenorrhea, dyspareunia, and dyschezia. Preoperatively the patient had an electrolyte bowel preparation but no antibiotic prophylaxis. Six days postoperatively she developed symptoms of nausea, vomiting, and diarrhea, which were not affected by diet and over-the-counter bowel medications. Examination of stool samples for culture, ova, parasites, and Clostridium difficile toxin led to the diagnosis of C. difficile pseudomembranous enterocolitis. The patient was referred to a gastroenterologist. She required 4 months of metronidazole therapy, including two hospitalizations, before her symptoms resolved. The stool assay became negative for C. difficile toxin 6 months after surgery. Pseudomembranous enterocolitis may occur rarely in patients without the usual risk factors of antibiotic therapy. The role of electrolyte bowel preparation is uncertain, but it may have permitted overgrowth of C. difficile.

Adult↗
PubMed2000

Low endogenous prostaglandin E2 predisposes to relapsing inflammation in experimental rat enterocolitis.

Intramural injection of peptidoglycan-polysaccharide (PG-PS) induces acute enterocolitis that spontaneously relapses in Lewis but not Fischer rats. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) induce prostaglandin E2 (PGE2) secretion, which inhibits secretion of these cytokines by macrophages, suggesting an inhibitory feedback mechanism. We postulate that Lewis rat susceptibility to relapse is due to an imbalance between protective prostaglandins and cytokines. Female Fischer and Lewis rats were injected with PG-PS (37.5 microg/g) or human serum albumin intramurally. Tissue IL-1alpha and PGE2 immunoreactivities and myeloperoxidase (MPO) activity were determined. Relapsing rats had lower PGE2 and PGE2/IL-1alpha ratios than nonrelapsing rats (P < 0.05). In Fischer rats, 2 mg/kg/day of indomethacin potentiated cecal MPO and IL-1alpha concentrations above PG-PS alone (P < 0.05). Misoprostol treatment blocked PG-PS induced IL-1alpha and MPO and inhibited the potentiating effect of indomethacin on MPO and IL-1alpha (P < 0.05). In conclusion, increased endogenous PG may be protective against relapsing inflammation in PG-PS induced enterocolitis, at least partially via inhibition of proinflammatory cytokines. Imbalance between protective prostaglandins and proinflammatory cytokines may be involved in the pathogenesis of chronic relapsing inflammation in genetically susceptible hosts.

Animals↗
PubMed1999

Low endogenous prostaglandin E2 predisposes to relapsing inflammation in experimental rat enterocolitis.

Intramural injection of peptidoglycan-polysaccharide (PG-PS) induces acute enterocolitis that spontaneously relapses in Lewis but not Fischer rats. Interleukin-1 (IL-1) and tumor-necrosis factor-alpha (TNF-alpha) induce prostaglandin E2 (PGE2) secretion, which inhibits secretion of these cytokines by macrophages, suggesting an inhibitory feedback mechanism. We postulate that Lewis rat susceptibility to relapse is due to an imbalance between protective prostaglandins and cytokines. Female Fischer and Lewis rats were injected with PG-PS (37.5 microg/g) or human serum albumin intramurally. Tissue IL-1alpha and PGE2 immunoreactivities and myeloperoxidase (MPO) activity were determined. Relapsing rats had lower PGE2 and PGE2:IL-1alpha ratios than nonrelapsing rats (P < 0.05). In Fischer rats, 2 mg/kg/day indomethacin potentiated cecal MPO and IL-1alpha concentrations above PG-PS alone (P < 0.05). Misoprostol treatment blocked PG-PS-induced IL-1alpha and MPO and inhibited the potentiating effect of indomethacin on MPO and IL-1alpha (P < 0.05). In conclusion, increased endogenous PG may be protective against relapsing inflammation in PG-PS induced enterocolitis, at least partially via inhibition of proinflammatory cytokines. An imbalance between protective prostaglandins and proinflammatory cytokines may be involved in the pathogenesis of chronic relapsing inflammation in genetically susceptible hosts.

Animals↗
PubMed2004

IL-12 p40 prevents the development of chronic enterocolitis in IL-10-deficient mice.

T-helper-1 (Th1) cytokines play an important role in Crohn's disease, and interleukin-12 (IL-12), which is composed of two subunits, p40 and p35, drives Th1 differentiation. In previous reports, IL-12 p40 was shown to prevent IL-12 from binding to the receptor. We demonstrate here the effect of IL-12 p40 overexpression in intestinal epithelia on enterocolitis mediated by Th1 cells in IL-10-deficient (IL-10(-/-)) mice on a C57BL/6J background. IL-10 deficient (IL-10(-/-))/T3b-IL-12 p40+ (IL-12 p40+) mice and IL-10(-/-)/T3b-IL-12 p40- (IL-12 p40-) mice were generated by crossing T3b-IL-12 p40 transgenic mice and IL-10(-/-) mice. At 8 weeks of age, IL-12 p40+ mice did not show any clinical manifestations of colitis. The colon length of IL-12 p40- mice became shorter than that of IL-12 p40+ mice. The histological score of IL-12 p40+ mice was lower. Interferon-gamma (IFN-gamma) production was suppressed in both the mesenteric lymph node cell culture and colon tissue culture of IL-12 p40+ mice. There was no significant difference in IL-4 production and tumor necrosis factor-alpha (TNF-alpha) production between the two groups. These results show that overexpression of IL-12 p40 in intestinal epithelia prevents enterocolitis in IL-10(-/-) mice by suppressing IFN-gamma production, and suggest a potential clinical application of IL-12 p40 for Crohn's disease. Furthermore, these results also suggest that local gene transduction in the intestinal epithelium may be a potent therapeutic approach for Crohn's disease.

Animals↗
PubMed2003

Necrotizing enterocolitis among neonates in the United States.

BACKGROUND: Prior studies have identified individual risk factors that are associated with necrotizing enterocolitis (NEC); however, the small sample sizes of these previous studies have not allowed the analysis of potential interaction between multiple variables and NEC. Our purpose was to describe the incidence and risk factors for NEC in premature neonates admitted for intensive care. METHODS: We identified neonates as having NEC if they met accepted diagnostic criterion for necrotizing enterocolitis. Using a national database, we assessed the association between NEC and a battery of risk factors previously reported in peer-reviewed literature. RESULTS: There were 15,072 neonates that met inclusion criteria; 14,682 did not have NEC, while 390 (2.6%) met criterion for NEC. Multivariate analysis showed that low birth weight was the most important risk factor for NEC. Other factors that were associated with an increased risk of NEC were exposure to antenatal glucocorticoids, vaginal delivery, need for mechanical ventilator support, exposure to both glucocorticoids and indomethacin during the first week of life, absence of an umbilical arterial catheter, and low Apgar score at 5 minutes. Length of hospital stay and mortality were higher in neonates with NEC than in neonates without NEC. CONCLUSIONS: NEC remains an important cause of morbidity and mortality in prematurely born neonates. In contrast to previous studies, we found that exposure to antenatal glucocorticoids was associated with an increased risk for NEC independent of birth weight.

Birth Weight↗
PubMed2005

Platelet transfusions in infants with necrotizing enterocolitis do not lower mortality but may increase morbidity.

OBJECTIVE: Necrotizing enterocolitis (NEC), a serious multisystemic inflammatory disease most commonly seen in premature neonates, is often associated with thrombocytopenia. Infants with severe forms of NEC commonly have platelet counts of less than 50,000/mm(3), occasionally less than 10,000/mm(3). Despite an absence of data to support the practice, platelet transfusions are commonly used to maintain a certain arbitrary platelet count in an effort to prevent bleeding. As platelet transfusions contain a variety of bioactive factors including pro-inflammatory cytokines, we hypothesized that a higher number and volume of platelet transfusions would not be associated with an improvement in mortality or morbidity. STUDY DESIGN: A retrospective cohort analysis was conducted of the medical records of all infants between 1997 and 2001 with Bell's Stage 2 or 3 NEC associated with platelet counts of <100,000/mm(3). The medical records were evaluated for the following variables: platelet counts, number and volume of platelet transfusions, symptoms of bleeding, and hospital course. Mortality and development of short bowel syndrome and/or cholestasis were correlated to the total number and volume (total ml and ml/kg) of platelet transfusions. Differences between the outcome groups were compared using the independent t-test, Fisher's exact test and Mann-Whitney tests. RESULTS: A total of 46 infants met the study criteria (gestational age 28+/-4 weeks and birth weight 1166+/-756 g, mean+/-SD). There were a total of 406 platelet transfusions administered to the study population. Of these, 151 (37.2%) were given in the presence of active bleeding, with 62% of these resulting in the cessation of bleeding within 24 hours. Other listed indications for platelet transfusions were hypovolemia and severe thrombocytopenia. On analysis of the entire cohort, there was no statistical improvement in either mortality or morbidity (short bowel syndrome and cholestasis) with greater number and/or volume of platelet transfusions. Furthermore, we found that infants who developed short bowel syndrome and/or cholestasis had been given a significantly higher number and volume of platelet transfusions when compared to those who did not have these adverse outcomes [median (minimum - maximum) - number of transfusions : 9 (0 to 33) vs 1.5 (0 to 20), p=0.010; volume of transfusions (ml/kg): 121.5 (0 to 476.6) vs 33.2 (0 to 224.3), p=0.013]. CONCLUSION: This retrospective analysis suggests that greater number and volume of platelet transfusions in infants with necrotizing enterocolitis are associated with greater morbidity in the form of short bowel syndrome and/or cholestasis without the benefit of lower mortality.

Cholestasis↗
PubMed2002

A patient with paroxysmal nocturnal haemoglobinuria in whom granulocyte colony-stimulating factor administration resulted in improvement of recurrent enterocolitis and its associated haemolytic attacks.

We report an elderly patient with paroxysmal nocturnal haemoglobinuria (PNH), having recurrent enterocolitis and haemolytic attacks associated with cellular immunodeficiency. On admission, the patient had normal neutrophil count and function but a decreased T-cell count, decreased mitogenic reactions, and a negative tuberculin test. Granulocyte colony-stimulating factor (G-CSF) was administered, resulting in an increased T-cell count, normalization of T-cell function, increased blood levels of helper T cell (Th)1 and Th2 cytokines and improvement in the enterocolitis and haemolytic attacks. This suggests that G-CSF may be useful in the treatment of elderly PNH patients with cellular immunodeficiency.

Aged↗
PubMed1996

Nongranulomatous chronic idiopathic enterocolitis: clinicopathologic profile and response to corticosteroids.

BACKGROUND & AIMS: Nongranulomatous ulcerative enterocolitis has been reported in association with celiac sprue, lymphoma, and hypogammaglobulinemia. The objective of this study is to present evidence that this disorder exists as a primary entity. METHODS: The medical records and histological material of 9 patients (mean age, 45.7 +/- 5.9 years) who presented with severe chronic diarrhea without specific diagnosis after extensive investigations were reviewed. RESULTS: Endoscopically, the duodenum and proximal jejunum were inflamed in 6 of 7 patients, with superficial ulcerations in 5 patients. On histology, the lamina propria was infiltrated by polymorphonuclear and chronic inflammatory cells, with varying degrees of villous atrophy. There were no significant cellular abnormalities of the epithelial enterocytes. A similar inflammatory infiltrate was present in the colon in 4 or 5 patients. Eight of 9 patients responded to corticosteroids with clinical and variable histological improvement. Four patients developed bleeding from ulcerations in the small or large intestine. Three patients died: 1 patient who did not respond to treatment with corticosteroids and 2 patients with systemic infection. Four of the 6 surviving patients required maintenance low-dose corticosteroid therapy. No underlying disease was discovered during prolonged follow-up. CONCLUSIONS: Idiopathic nongranulomatous enterocolitis may present as a primary, frequently fatal disease. Corticosteroid therapy provides immediate benefit and may be required indefinitely.

Adrenal Cortex Hormones↗
PubMed2004

Enterocolitis complicating Hirschsprung's disease.

Enterocolitis remains a relatively common complication of Hirschsprung's disease with significant morbidity and mortality. The etiology of Hirschsprung's enterocolitis (HEC) is multifactorial and remains poorly understood. Preventative measures and better treatment modalities will evolve out of a better understanding of the underlying pathophysiology. Prompt recognition of HEC allows early intervention and a potential reduction in disease severity and mortality. This review of HEC describes the epidemiology, clinical and pathological features and current best practice in management. Some of the areas of research into etiology and treatment are discussed.

Biopsy, Needle↗
PubMed2000

Rectosigmoid pHi monitoring during experimental necrotizing enterocolitis.

BACKGROUND/PURPOSE: Gastric or rectosigmoid intramural pH (pHi) is considered a reliable indicator of splanchnic perfusion. The aim of this study was to evaluate whether rectosigmoid pHi reflects the severity of bowel damage in experimental necrotizing enterocolitis (NEC). METHODS: A total of 36 neonatal piglets, (median age, 3; range, 1 to 11 days; median weight, 2.5; range, 1.2 to 3.8 kg), were anesthetized, ventilated mechanically, and had invasive monitoring of hemodynamics. A sigmoid tonometer was inserted into the rectosigmoid colon. Enterocolitis was induced in 27 piglets by intraluminal injection of casein-d-gluconate (16.0 mL/kg) into terminal 100 cm of the ileum. Nine control piglets received an equal amount of intraluminal saline. NEC was graded macroscopically as follows: 0, no changes; 1, mild; 2, moderate; and 3, severe. Histology was evaluated according to Chiu scale from 0 to 5. RESULTS: The macroscopical bowel injury in caseine-injected piglets was as follows: grade 3 (n = 6), grade 2 (n = 9), grade 1 (n = 12). All control piglets showed macroscopically normal bowel (grade 0). All affected bowels showed histologic changes (Chiu's scale 2 to 4). All study animals had an initial drop of pHi after injection of casein or saline. In control piglets and those with mild NEC (grade 1) pHi tended to return to preinjection level. In animals with moderate or severe NEC (grade 2 to 3) the initial drop was deeper and the pHi continued to decrease significantly throughout the experiment (P < .05). In the arterial pH and mean blood pressure there were no statistically significant differences between piglets with no NEC and mild NEC, and these with moderate or severe NEC. CONCLUSION: Drop in rectosigmoid pHi was the most sensitive and earliest sign of severe mucosal necrosis of ileum in this experimental NEC model.

Animals↗
PubMed2002

Protective effects of recombinant human interleukin-10 on intestines of hypoxia-induced necrotizing enterocolitis in immature rats.

BACKGROUND/PURPOSE: The role of cytokines in the pathogenesis of hemodynamic instability or tissue destruction in patients with necrotizing enterocolitis (NEC) remains undefined. The aim of this study was to determine the effects of recombinant human interleukin-102 (rhIL-10) on intestines of hypoxia-induced necrotizing enterocolitis in immature rats. METHODS: The study was performed on 1-day-old Sprague Dawley rat pups. Group 1 (n = 8) served as nonhypoxic controls. Group 2 (untreated, n = 11) rats were subjected to hypoxia-reoxygenation (H/O) and then were returned to their mothers. Group 3 (rhIL-10 treated, n = 10) rats were subjected to H/O, were returned to their mothers, and were treated with rhIL-10 (75 microgram/kg subcutaneously) for the next 3 days. All animals were killed on day 4, and intestine specimens were obtained to determine the tissue level of malondialdehyde (MDA) and histologic changes. RESULTS: The microscopic lesions in the untreated rats were virtually the same as those seen in neonatal NEC, with destruction of villi and crypts, and in some cases extension to the muscularis. In contrast, in the rats treated with rhIL-10, lesions were limited essentially to the very tips of the villi. Intestinal injury score was significantly less in the rhIL-10-treated rats than in the untreated rats (P <.05). In the rhIL-10-treated group, Malondialdehyde (MDA) levels were not significant in comparison to the control group. In the untreated group, MDA levels were significantly increased when compared with the control and the rhIL-10-treated groups (P <.001 and P <.05, respectively). CONCLUSION: RhIL-10 has a protective effect on intestinal injury in NEC in an experimental model.

Animals↗
PubMed2002

Surgical decision making in necrotizing enterocolitis and focal intestinal perforation: predictive value of radiologic findings.

BACKGROUND/PURPOSE: Given the current controversy over the appropriate surgical management (peritoneal drainage versus exploratory laparotomy) of advanced necrotizing enterocolitis and focal intestinal perforation, the authors examined the predictive value of radiologic findings. METHODS: The medical records of 80 infants undergoing exploratory laparotomy for presumed advanced necrotizing enterocolitis (NEC) or focal intestinal perforation (FIP) were reviewed. Radiologic criteria were evaluated as predictors of NEC (pneumatosis intestinalis, portal venous gas) or perforation (free air, gasless abdomen). The standard epidemiologic measures were calculated for each criterion. RESULTS: For pneumatosis intestinalis, the sensitivity was 44% (n = 27) and specificity, 100% (n = 19). For portal venous gas, the sensitivity was 13% (n = 8) and specificity, 100% (n = 19). The sensitivity and specificity calculated for free air was 52% (n = 23) and 92% (n = 33), respectively. The sensitivity and specificity calculated for a gasless abdomen was 32% (n = 14) and 92% (n = 33), respectively. CONCLUSIONS: While demonstrating high specificity, the radiologic signs traditionally associated with NEC and FIP have unexpectedly low sensitivities. Although positive radiologic findings are of great predictive value, negative radiologic findings acquired while determining the need for and specific type of surgical intervention in suspected NEC or FIP must be interpreted with extreme caution.

Enterocolitis, Necrotizing↗
PubMed2003

MUC-2 mucin production in Hirschsprung's disease: possible association with enterocolitis development.

BACKGROUND/PURPOSE: The etiology of Hirschsprung's-associated enterocolitis (HAEC) is unknown. Previous investigations have suggested that abnormal production of mucins may have an etiologic role. Recently, a series of mucin genes have been identified. MUC-2 is the predominant mucin expressed in humans. The authors have shown previously in vitro that use of MUC-2 can prevent bacterial translocation. Based on this, it was hypothesized that those patients with Hirschsprung's disease (HD) would have an abnormal production of MUC-2 compared with normal patients. METHODS: Fresh stool specimens were collected from children with a diagnosis of HD (with or without HAEC) and from age-matched control patients. Protein was extracted, and MUC-2 was detected with Western blot analysis. MUC-2 protein expression was quantified by densitometry measurements. Results are expressed as mean density +/- SD. Statistical comparison was done with unpaired t tests, with P less than.05 being considered significant. RESULTS: MUC-2 expression was detected in all control patients (mean density, 121 +/- 47). MUC-2 level was lowest in one child with a viral-induced diarrhea (density = 71). In those patients with HD, levels of MUC-2 protein expression were significantly lower (P <.05) than controls (12 +/- 15 for all HD patients). Levels of MUC-2 were lowest (nondetectable) in 2 HD patients who had clinical evidence of HAEC. CONCLUSIONS: MUC-2 production is markedly depressed in patients with Hirschsprung's disease and is absent with enterocolitis. This decline in protein expression may result in a decrease in epithelial barrier function and be a predisposing factor in the development of HAEC.

Bacterial Translocation↗
PubMed2003

Peri-operative blood lactate concentrations in pre-term babies with necrotising enterocolitis.

AIM: Hyperlactaemia has been shown to predict mortality in preterm babies undergoing intensive care. The value of such measurement has not been evaluated in babies undergoing laparotomy for necrotising enterocolitis (NEC). The aim of this study was to determine whether peri-operative blood lactate measurements (L) can be used to predict outcome in preterm babies with necrotising enterocolitis. METHODS: Clinical and laboratory data in 24 babies who underwent laparotomy for NEC over 3 years were collected. The data were analysed to correlate blood lactate level with the clinical outcome. RESULTS: There were no statistically significant differences between babies who died and those who survived in terms of gestation, birth weight, condition at birth, etc. There was no difference in pre-operative acid-base status parameters between the groups. Median (range) of pre- and post-operative blood lactate measurements (L) are shown: Pre-op Lactate: 0.9 (0.3 to 2.4) n = 15 (Survivors); 2.7 (0.5 to 10.9) n = 5, p = 0.05 (Non-survivors). Post-op Lactate: 1.2 (0.5 to 6) n = 19 (Survivors); 4.7 (0.2 to 19.5) n = 5, p = 0.06 (Non-survivors). Babies with pre-operative hyperlactaemia ([L] > 1.6 mmol/L) were more likely to die. (Odd's Ratio 22, Confidence Interval 1.54 to 314.3, p = 0.04). Pre-operative L was not higher in babies who subsequently had bowel resection compared to those who had no bowel resection ([L] = 0.88 mmol/L [0.3 to 10.9] vs. 1.6 mmol/L [0.6 to 2.7], [p = 0.2]). Post-operative L was generally higher than pre-operative L but was a less useful predictor of death. CONCLUSION: This study suggests that elevation of L in the pre-operative period carries a poor prognosis in babies with NEC. As L was not significantly different between babies who had necrotic bowel and those who had a healthy bowel, we postulate that it reflects inadequate global tissue oxygen delivery rather than local disease process. Pre-operative optimisation of oxygen delivery has been shown to reduce mortality in high-risk adult surgical patients. Babies with NEC may also benefit from further peri-operative resuscitation.

Enterocolitis, Necrotizing↗
PubMedDate not supplied

[Linezolid in two premature babies with necrotizing enterocolitis and infection with vancomycin-resistant enterococcus].

The use of the antibiotic Linezolid in two premature babies with necrotizing enterocolitis and infection with vancomycin-resistant enterococcus is described. Therapy with Linezolid in cause of necrotizing enterocolitis is an exception. Actually there are no proven recommendations for the use in this age group. Despite the successfully results more investigations for the use of linezolid in newborns and prematures are necessary.

Acetamides↗
PubMed2005

Entero-enteric fistula following mild necrotizing enterocolitis.

We report a 26-week gestational age newborn who developed an entero-enteric fistula associated with a small bowel stricture following a mild episode of necrotizing enterocolitis. The fistula led to a delay in the diagnosis and surgical treatment of the stricture, and should therefore be considered in the setting of partial or intermittent obstruction in the newborn who has had necrotizing enterocolitis.

Constriction, Pathologic↗
PubMed2005

Outcome of primary peritoneal drainage for perforated necrotizing enterocolitis: comparison between laparotomy and drainage.

Perforation of the gastrointestinal tract in neonates is still associated with high mortality rates. Laparotomy is usually required to treat gastrointestinal perforation, however peritoneal drainage under local anesthesia has been also described as an alternative mode of treatment. In our institute, laparotomy was the first choice for the management of gastrointestinal perforation in neonates until 1999. Because of the high mortality rates in this group of patients, our policy has since changed to the use of primary peritoneal drainage instead. The aim of this study is to compare the effectiveness of primary peritoneal drainage (PPD) and primary laparotomy (PL) procedures in the management of gastrointestinal perforation due to necrotizing enterocolitis in neonates. Between 1994 - 1998, ten babies with intestinal perforation underwent PL, whereas fifteen newborns with similar findings were treated with PPD between 1999 and 2003. Eight (80 %) of the patients died in the PL group prior to 1999. In the PPD group 8 (53.3 %) of babies required no further treatment and were discharged without any complications. Four (26.7 %) patients in this group needed laparotomy later, and three (75 %) of them survived. In conclusion, we believe that PPD is more effective than PL for the management of perforated necrotizing enterocolitis in neonates. Laparotomy can be used in particularly unresponsive cases after primary peritoneal drainage.

Drainage↗