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PubMed2006

Long-term outcome of patients with enterocolitis complicating Hirschsprung's disease.

Enterocolitis remains the most serious complication of Hirschsprung's disease (HD). The purpose of this study was to evaluate the risk factors in the development of enterocolitis and the long-term outcome in these patients. The hospital records of 259 consecutive patients with HD during 1975-2003 were examined. The data was analysed for age at presentation, associated anomalies, level of aganglionosis, clinical features, number of episodes of enterocolitis, type of pullthrough, necessity for post-pullthrough sphincterectomy. Follow up was carried out by personal interviews and interviews over the telephone with patients/parents. Enterocolitis was diagnosed on the basis of clinical features of diarrhoea, pyrexia, abdominal distention and vomiting. Of the 259 patients with HD, 74 patients (28.5%) were found to have enterocolitis. Out of 39 patients with Down's syndrome and HD, 19 (48%) had enterocolitis. Fifteen (20%) patients had other associated anomalies. Fifty-six patients (75.6%) were male and 18 (24.3%) were female. In 30 patients enterocolitis was the presenting feature in the neonatal period, 22 of which presented in the first 2 weeks of life. Fifty-six patients (75.6%) had rectosigmoid disease and 18 (24.3%) had long segment disease or total colonic aganglionosis. Eighteen (24.3%) had only preoperative enterocolitis and 31(41.8%) had only postoperative enterocolitis. Twenty-five (33.7%) had both pre- and post-operative enterocolitis. Twenty (27%) patients had more than 2 episodes of enterocolitis. Various pullthrough procedures were performed. Twenty-six patients (35.1%) required internal sphinctermyectomy to treat the enterocolitis. At the time of follow-up, 16 patients were lost to follow-up. Of the remaining 58 patients, 3 patients died, 2 due to enterocolitis and 1 due to sepsis. Six patients remained with a stoma. Twenty-two patients were continent and were stooling normally, but 14 of these were on laxatives for several years after pullthrough procedure. The mean age at achieving full continence was 4.95 years in the 22 patients with normal bowel function. Nineteen patients are still on laxatives and 8 patients are soiling. Eight patients continue to have multiple recurrent episodes of enterocolitis at follow-up. Down's syndrome is an important risk factor in the development of enterocolitis. The majority of patients with enterocolitis complicating HD continue to have disturbances of bowel function many years after surgery for HD.

Cathartics↗
PubMed1997

Necrotizing enterocolitis: diagnosis with CT examination of urine after enteral administration of iodinated water-soluble contrast material.

PURPOSE: To develop a new method for diagnosing necrotizing enterocolitis with use of computed tomography (CT). MATERIALS AND METHODS: Urine specimens from 22 neonates were obtained 8-12 hours after iohexol was administered enterally. Twelve neonates had suspected (n = 5) or definite (n = 7) necrotizing enterocolitis, and 10 neonates without necrotizing enterocolitis underwent routine upper gastrointestinal study. Urine from another 13 neonates without necrotizing enterocolitis who did not receive iohexol was collected. The attenuation coefficient of each urine specimen was determined with CT. RESULTS: The mean CT attenuation coefficient of urine from neonates who did not receive iohexol was 5.6 HU +/- 3.9, and that from neonates without necrotizing enterocolitis who underwent upper gastrointestinal study was 6.7 HU +/- 3.2. The mean CT attenuation coefficient of urine from patients with suspected necrotizing enterocolitis was 26.0 HU +/- 3.4, and that in patients with definite necrotizing enterocolitis was 71.0 HU +/- 18.8. The mean CT attenuation coefficients in neonates with necrotizing enterocolitis were significantly different from that in patients without necrotizing enterocolitis who underwent upper gastrointestinal study. CONCLUSION: Urine from neonates with necrotizing enterocolitis show significantly higher CT attenuation coefficients than those from patients without necrotizing enterocolitis. CT examination of urine may allow early detection of necrotizing enterocolitis.

Administration, Oral↗
PubMed2000

Indomethacin tocolysis and risk of necrotizing enterocolitis.

OBJECTIVE: To investigate the possible association of indomethacin tocolysis with neonatal necrotizing enterocolitis. METHODS: A case-control study was performed for the period November 1, 1997, through May 1, 1999. All cases of proven necrotizing enterocolitis were ascertained, and four controls for each case were randomly identified from all Special Care Nursery admissions before 37 weeks' gestation without necrotizing enterocolitis during that same period. RESULTS: During the 18-month period there were 24 cases of necrotizing enterocolitis out of 10,200 deliveries. Infants with necrotizing enterocolitis were more preterm (29.7 +/- 3.9 compared with 32.7 +/- 6.0 weeks; P =.03) and had lower birth weights (1453 +/- 777 compared with 1820 +/- 678 g; P =.02) compared with controls (n = 96). Respiratory distress syndrome (RDS) and sepsis were both significantly associated with an increased risk of necrotizing enterocolitis: 16 of 24 cases compared with 40 of 96 controls had RDS (odds ratio [OR] 2.8, 95% confidence interval [CI] 1.0, 8.3) and 14 of 24 cases compared with 11 of 96 controls were septic (OR 10.8, 3.4, 95% CI 34.2). Indomethacin as a single agent was not associated with necrotizing enterocolitis (OR 1.0, 95% CI 0.2, 4.8). Using a logistic regression model, necrotizing enterocolitis was strongly associated with sepsis (adjusted OR 8.5, 95% CI 2.2, 32.5). When sepsis was removed from the model, double-agent tocolytic therapy was significantly associated with necrotizing enterocolitis (adjusted OR 6.9, 95% CI 1.1, 43.6). CONCLUSION: Tocolysis with indomethacin as a single agent was not associated with necrotizing enterocolitis in this case-control study. Combination tocolytic therapy may be a marker for subclinical infection and not causally related to necrotizing enterocolitis.

Adult↗
PubMed1992

Mucosal immune defence mechanisms in enterocolitis complicating Hirschsprung's disease.

Enterocolitis remains an important cause of morbidity and mortality in Hirschsprung's disease. The aetiology of enterocolitis is uncertain-ischaemic and bacterial causes and recently, rotavirus infections, have been suggested. Bowel tissue from 12 patients with Hirschsprung's disease who underwent Swenson's operation (five of whom had clinical evidence of enterocolitis) and colon from six controls subjects were examined to investigate possible immunopathological mechanisms associated with the disease. IgA, IgM, and J chain (but not IgG) containing plasma cells were significantly increased in the lamina propria along the entire length of resected bowel in enterocolitis patients, compared with non-enterocolitis patients and controls (p less than 0.01). Luminal secretory component staining of the anganglionic segment of colon from enterocolitis patients was considerably reduced. Lamina propria CD68 positive monocyte/macrophages and CD45RO positive leukocytes were increased in enterocolitis patients compared with non-enterocolitis patients (p less than 0.01). CD57 positive natural killer (NK) cells showed a unique distribution pattern compared with other cell types. Patients with enterocolitis showed a significant increase in CD57 positive NK cells in the lamina propria of ganglionic bowel only (p less than 0.05). NK cell values in ganglionic bowel of non-enterocolitis patients and in aganglionic bowel in all patients were similar to controls. The diversity of altered local immune response seen in this study may reflect a multifactorial microbial aetiology in enterocolitis associated with Hirschsprung's disease.

Antigens, CD↗
PubMed1998

Changing presentation and management of neutropenic enterocolitis.

OBJECTIVE: To characterize the current clinical presentation and management of neutropenic enterocolitis. DESIGN: Retrospective review of records of oncology unit patients requiring general surgical consultation for abdominal complaints in a 1-year period. SETTING: Oncology unit of a tertiary care, university teaching hospital. PATIENTS AND INTERVENTIONS: Fourteen patients diagnosed as having neutropenic enterocolitis were managed conservatively with operation reserved for failure of conservative therapy. MAIN OUTCOME MEASURES: Clinical data from patients at the time of presentation and during treatment for neutropenic enterocolitis. RESULTS: All 14 patients diagnosed as having neutropenic enterocolitis were receiving chemotherapy for solid tumors or leukemias. Seven patients were undergoing stem cell or autologous bone marrow transplantation. Presenting symptoms and physical examination findings were nonspecific. All patients except one had neutropenia at the time of diagnosis. Computed tomographic scans of the abdomen were the most useful confirmatory study for the diagnosis of neutropenic enterocolitis. All patients except one had resolution of neutropenic enterocolitis with conservative therapy. One patient whose course of conservative management failed had protracted neutropenia and required operation for resection of bowel with full-thickness necrosis. CONCLUSIONS: Neutropenic enterocolitis has evolved from a complication of patients with leukemia to a disease of patients receiving high-dose chemotherapy for many malignancies, solid as well as hematologic. Diagnosis of neutropenic enterocolitis continues to be a challenge, as patients typically present with nonspecific gastrointestinal tract symptoms. Neutropenia and computed tomographic scan findings are useful adjuncts in diagnosing neutropenic enterocolitis. Timely conservative treatment frequently allows resolution of neutropenic enterocolitis without operation.

Adult↗
PubMed1994

Tocolysis with indomethacin increases the incidence of necrotizing enterocolitis in the low-birth-weight neonate.

OBJECTIVE: The null hypothesis states that prolonged antenatal indomethacin exposure within 24 hours of delivery does not increase the incidence of necrotizing enterocolitis in the low-birth-weight neonate. STUDY DESIGN: The neonates of patients receiving indomethacin tocolysis admitted in preterm labor (N = 56) were compared with the neonates of preterm labor patients who received no indomethacin tocolysis (N = 703). These neonatal groups were then compared with regard to gestational age at delivery, birth weight, mode of delivery, antenatal magnesium and steroid exposure, incidence of respiratory distress syndrome, perinatal depression, sepsis, umbilical catheterization, and feeding rates and volumes. The overall incidence of necrotizing enterocolitis, mortality secondary to necrotizing enterocolitis, and the intervals from delivery and feeding to necrotizing enterocolitis diagnosis were also compared. The association between necrotizing enterocolitis and the duration of indomethacin exposure and the interval from exposure to delivery for both the indomethacin and control groups was determined. RESULTS: The incidence of necrotizing enterocolitis in neonates who were delivered within 24 hours of maternal indomethacin therapy was 20% compared with 9% in the control group (p = 0.005). The incidence of necrotizing enterocolitis in neonates with > 48 hours of antenatal indomethacin exposure was 26.4% compared with 4.1% in those with < 48 hours exposure (p = 0.042). The interval from first feeding to necrotizing enterocolitis development was significantly shorter in the indomethacin group versus the control group (2.1 +/- 3.0 vs 6.8 +/- 6.3 days) (p = 0.001), as was the mean interval from delivery to development of necrotizing enterocolitis (10.2 +/- 3.7 vs 15.2 +/- 3.8 days) (p = 0.019). CONCLUSIONS: Antenatal indomethacin exposure occurring within < or = 24 hours of delivery and of at least 48 hours' duration is associated with a significant increase in the incidence of necrotizing enterocolitis in the low-birth-weight neonate.

Birth Weight↗
PubMed1989

Severity of necrotizing enterocolitis: influence on outcome at 2 years of age.

The long-term outcome of very low birth weight (VLBW) infants with necrotizing enterocolitis has been reported to be similar to that of other VLBW infants. To examine the influence of disease severity on outcome, the growth and neurodevelopment of survivors of necrotizing enterocolitis were evaluated when the babies were 20 months' corrected age. Between 1975 and 1983, 1506 VLBW infants were admitted to the hospital, and necrotizing enterocolitis developed in 84 (5.6%). Forty infants (48%) survived to be 20 months' corrected age, and complete follow-up data were available for 36. Survivors were classified by modified Bell's criteria into four groups by increasing severity of disease; 13 had mild necrotizing enterocolitis (stage IIA, IIB), and 23 had severe necrotizing enterocolitis (stage IIIA, IIIB). The 36 survivors were compared with 766 surviving VLBW infants without necrotizing enterocolitis. There were no perinatal or socioeconomic differences between groups. Compared with infants with stage II necrotizing enterocolitis at 20 months, infants with stage III necrotizing enterocolitis had a higher rate of subnormal body weight (39% vs 15%) and subnormal head circumference (30% vs 0%). Thirty-three percent of necrotizing enterocolitis survivors had significant neurodevelopmental impairment; the majority of impaired infants (10 of 12) were survivors of stage III necrotizing enterocolitis. These findings highlight the importance of continued evaluations for medical and neurodevelopmental sequelae.

Child Development↗
PubMed1991

Necrotizing enterocolitis in very low birth weight infants: biodemographic and clinical correlates. National Institute of Child Health and Human Development Neonatal Research Network.

We studied the occurrence of necrotizing enterocolitis in 2681 very low birth weight infants during an 18-month period to characterize the biodemographic and clinical correlates. Proven necrotizing enterocolitis (Bell stage II and beyond) occurred in 10.1% of study infants; necrotizing enterocolitis was suspected in 17.2% of study infants. Positivity of blood cultures was related to necrotizing enterocolitis staging. The mortality rate increased only for stage III necrotizing enterocolitis (54% died). Logistic regression identified medical center of birth, race, gender, birth weight, maternal hemorrhage, duration of ruptured membranes, and cesarean section as significant risk factors. For one center the odds ratio was 3.7, whereas for another center it was only 0.3. For black boys, the odds ratio was 2.3 relative to nonblack boys; for girls, race did not affect prevalence of necrotizing enterocolitis. Age at onset was related to birth weight and gestational age. Intercenter differences in necrotizing enterocolitis prevalence were related to time required to regain birth weight and other indicators of fluid management. Gram-positive organisms predominated in positive blood cultures for stage I and II necrotizing enterocolitis; enteric bacteria were isolated more frequently in infants with stage III disease. We conclude that necrotizing enterocolitis prevalence varies greatly among centers; this may be related to early clinical practices of neonatal care.

Birth Weight↗
PubMed2001

Sodium cromoglycate in the management of chronic or recurrent enterocolitis in patients with Hirschsprung's disease.

BACKGROUND/PURPOSE: Chronic or recurring enterocolitis is a rare but perplexing complication of Hirschsprung's disease affecting especially patients with altered immune defense such as those with Down's syndrome. Sodium cromoglycate (SCG) is a nonabsorbable mast cell stabilizing agent that has been documented to be effective in the treatment of inflammatory bowel disease. The authors studied the effect of SCG in Hirschsprung patients with refractory chronic or recurrent enterocolitis. METHODS: Eight patients (4 with Down's syndrome, 2 with other chromosomal aberrations, 2 otherwise healthy; age range from 4 to 22 years) with chronic (5 patients) or recurrent (>6 episodes/year, 3 patients) enterocolitis received 100 to 200 mg of SCG 4 times a day depending on the age of the patient. The chronic diarrhea or recurrent bouts of enterocolitis in the patients were refractory to dietary management and enteral antibiotics. Before the treatment all patients had ileocolonoscopy, the results of which showed macroscopic and histological chronic inflammation in all cases. No neuronal abnormalities were detected in biopsy results. None of the patients had colonic dilatation or increased anorectal resting pressures suggesting outlet obstruction. RESULTS: The follow-up of the patients ranges from 8 months to 26 months. Three of the 5 patients with chronic enterocolitis responded favorably. In these 3 patients the median number of daily bowel movements decreased from 6 to 3, and none experienced bouts of abdominal distension. Diarrhea-related soiling decreased also significantly. Two of the 3 patients with recurrent enterocolitis have remained asymptomatic, and none has required antibiotics after the onset of SCG treatment; one patient had an episode of enterocolitis after 12 months treatment. Two patients with chronic enterocolitis did not respond to SCG. No side effects of SCG were encountered. CONCLUSIONS: This preliminary and nonrandomized study suggests that SCG is an effective treatment modality for chronic or recurrent enterocolitis in patients with Hirschsprung's disease. Because SCG is not absorbed From the intestinal tract there are no systemic side effects.

Adolescent↗
PubMed2005

Patent ductus arteriosus, indomethacin and necrotizing enterocolitis in very low birth weight infants: a population-based study.

BACKGROUND: Patent ductus arteriosus is a risk factor for the development of necrotizing enterocolitis. The use of indomethacin to treat patent ductus arteriosus in preterm infants may either decrease the incidence of necrotizing enterocolitis by stabilizing or closing the ductus arteriosus or increase its incidence by a direct constricting effect on mesenteric blood vessels. The authors sought to evaluate the interrelationship between patent ductus arteriosus, treatment with indomethacin and the risk of necrotizing enterocolitis in very low birth weight infants. METHOD: The Israel National database includes prospectively collected data on 99% of all very low birth weight infants in Israel. The study population comprised 6146 infants of 24-34 weeks' gestation born between 1995 and 2000. The effect of patent ductus arteriosus on necrotizing enterocolitis was assessed using multiple regression analysis. RESULTS: Necrotizing enterocolitis occurred in 5.5% (n = 343) of all infants, in 9.4% of infants with patent ductus arteriosus and in 8.9% of infants who received indomethacin. The occurrence of necrotizing enterocolitis was independently associated with the presence of patent ductus arteriosus among infants not treated with indomethacin (odds ratio, 1.85) and those who received indomethacin therapy (odds ratio, 1.53). Indomethacin therapy in absence of patent ductus arteriosus was not associated with an increased risk of necrotizing enterocolitis (odds ratio, 0.72). CONCLUSIONS: Patent ductus arteriosus is an independent risk factor for the development of necrotizing enterocolitis in very low birth weight infants. Therapy with indomethacin did not have a significant effect on the risk for necrotizing enterocolitis.

Cardiovascular Agents↗
PubMed2003

Toll-like receptor-dependent production of IL-12p40 causes chronic enterocolitis in myeloid cell-specific Stat3-deficient mice.

Stat3 plays an essential role in IL-10 signaling pathways. A myeloid cell-specific deletion of Stat3 resulted in inflammatory cytokine production and development of chronic enterocolitis with enhanced Th1 responses in mice. In this study, we analyzed the mechanism by which a Stat3 deficiency in myeloid cells led to the induction of chronic enterocolitis in vivo. Even in the absence of Stat1, which is essential for IFN-gamma signaling pathways, Stat3 mutant mice developed chronic enterocolitis. TNF-alpha/Stat3 double-mutant mice developed severe chronic enterocolitis with enhanced Th1 cell development. IL-12p40/Stat3 double-mutant mice, however, showed normal Th1 responses and no inflammatory change in the colon. RAG2/Stat3 double-mutant mice did not develop enterocolitis, either. These findings indicate that overproduction of IL-12p40, which induces potent Th1 responses, is essential for the development of chronic enterocolitis in Stat3 mutant mice. Furthermore, enterocolitis was significantly improved and IFN-gamma production by T cells was reduced in TLR4/Stat3 double-mutant mice, indicating that TLR4-mediated recognition of microbial components triggers aberrant IL-12p40 production by myeloid cells, leading to the development of enterocolitis. Thus, this study clearly established a sequential innate and acquired immune mechanism for the development of Th1-dependent enterocolitis.

Animals↗
PubMed2006

Necrotizing enterocolitis: a practical guide to its prevention and management.

Neonatal necrotizing enterocolitis is the second most common cause of morbidity in premature infants and requires intensive care over an extended period. Despite advances in medical and surgical techniques, the mortality and long-term morbidity due to necrotizing enterocolitis remain very high. Recent advances have shifted the attention of researchers from the classic triad (ischemia, bacteria, and the introduction of a metabolic substrate into the intestine) of necrotizing enterocolitis, to gut maturation, feeding practices, and inflammation. The focus on inflammation includes proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-6, IL-18, and platelet-activating factor. Research related to the etiology of necrotizing enterocolitis has moved quickly from clostridial toxin to bacterial and other infectious agents. More recently, the pattern of bacterial colonization has been given emphasis rather than the particular species or strain of bacteria or their virulence. Gram-negative bacteria that form part of the normal flora are now speculated as important factors in triggering the injury process in a setting where there is a severe paucity of bacterial species and possible lack of protective Gram-positive organisms. Although the incidence of necrotizing enterocolitis has increased because of the survival of low birthweight infants, clinicians are more vigilant in their detection of the early gastrointestinal symptoms of necrotizing enterocolitis; however, radiographic demonstration of pneumatosis intestinalis remains the hallmark of necrotizing enterocolitis. With prompt diagnosis, a large proportion of infants with necrotizing enterocolitis are now able to be managed medically with intravenous fluid and nutrition, nasogastric suction, antibacterials, and close monitoring of physiologic parameters. In the advanced cases that require surgery, clinicians tend to opt for either simple peritoneal drainage (for very small and sick infants) or laparotomy and resection of the affected part. Intestinal transplantation later in life is available as a viable option for those who undergo resection of large segments of the intestine. It is becoming more evident that treatment of this devastating disease is expensive and comes with the toll of significant long-term sequelae. This has resulted in renewed interest in designing alternative strategies to prevent this serious gastrointestinal disease. Simple trophic feeding and the use of L-glutamine and arginine are novel avenues that have been examined. The use of probiotics ('friendly' bacterial flora) has been introduced as a promising tool for establishing healthy bacterial flora in the newborn gut to block the injury process that may ultimately lead to necrotizing enterocolitis.

Enterocolitis, Necrotizing↗
PubMed2005

Prevalence of ischemic enterocolitis in patients with acute pancreatitis.

BACKGROUND: A considerable number of acute pancreatitis cases have been reported to be complicated by nonocclusive mesenteric ischemia. However, no reports have ever referred to the incidence of ischemic enterocolitis in patients with acute pancreatitis, using a series of autopsy cases. Here, we report our review of autopsy cases of patients with acute pancreatitis to examine the incidence of associated ischemic enterocolitis. METHODS: The intestinal and pancreatic slides of 48 autopsy cases of patients with acute pancreatitis were reviewed and the incidence of ischemic enterocolitis was determined. Clinical case records were also reviewed. RESULTS: Thirteen (27%) of 48 autopsy cases of patients with acute pancreatitis were complicated by ischemic enterocolitis. The frequency of shock was significantly higher in patients with ischemic enterocolitis than in those without ischemic enterocolitis. The intestinal lesion was diffuse in many cases and gangrene was not an unusual finding. CONCLUSIONS: The incidence of ischemic enterocolitis in patients with acute pancreatitis was much higher than that in the previous reports. Clinicians who treat patients with acute pancreatitis should consider ischemic enterocolitis as one of the frequent and severe complications of this condition.

Acute Disease↗
PubMed1989

A prospective survey of necrotising enterocolitis in very low birthweight infants.

Necrotising enterocolitis is the most common gastrointestinal complication of pre-term infants. In order to determine the strength of the association of hypoxia/ischaemia and infection as causative factors in necrotising enterocolitis, we evaluated all liveborn pre-term infants with a birthweight less than 1500 g and/or gestational age less than 32 weeks in The Netherlands in 1983. The factors related to hypoxia/ischaemia included: asphyxia, respiratory distress syndrome, ventilatory assistance, persistent fetal circulation, persistent ductus arteriosus, apnoea, bradycardia, exchange transfusion and peri/intraventricular haemorrhage; those related to infection were: congenital infections, pneumonia, sepsis and meningitis. Of the 1338 infants enrolled, 1187 survived for more than 24 hours and had complete data. Mean (+/- s.d.) birthweight was 1278 (+/- 297) g and mean (+/- s.d.) gestational age 30.7 (+/- 2.6) weeks. Seventy-three (6.1%) infants developed necrotising enterocolitis: 46 (63.0%) stage I disease (clinically very suspect), 11 (15.1%) stage II (pneumatosis intestinalis) and 16 (21.9%) stage III (intestinal perforation). Mean +/- s.d. birthweight of the infants with necrotising enterocolitis (1197 +/- 284 g) was lower (P less than 0.02) than in those without necrotising enterocolitis (1283 +/- 297 g). Gestational ages were comparable. Mortality in the group with necrotising enterocolitis was 21.9% versus 15.8% in the non-necrotising enterocolitis group (NS). Stepwise logistic regression analysis indicated that among those factors studied, only sepsis and birthweight were truly associated with the occurrence of necrotising enterocolitis.

Enterocolitis, Pseudomembranous↗
PubMed2006

Invasive fungal infections in neutropenic enterocolitis: a systematic analysis of pathogens, incidence, treatment and mortality in adult patients.

BACKGROUND: Neutropenic enterocolitis is a life-threatening complication most frequently occurring after intensive chemotherapy in acute leukaemias. Gramnegative bacteria constitute the most important group of causative pathogens. Fungi have also been reported, but their practical relevance remains unclear. The guidelines do not address concrete treatment recommendations for fungal neutropenic enterocolitis. METHODS: Here, we conducted a metaanalysis to answer the questions: What are frequency and mortality of fungal neutropenic enterocolitis? Do frequencies and microbiological distribution of causative fungi support empirical antimycotic therapy? Do reported results of antimycotic therapy in documented fungal neutropenic enterocolitis help with the selection of appropriate drugs? Following a systematic search, we extracted and summarised all detail data from the complete literature. RESULTS: Among 186 articles describing patients with neutropenic enterocolitis, we found 29 reports describing 53 patients with causative fungal pathogens. We found no randomised controlled trial, no good quality cohort study and no good quality case control study on the role of antifungal treatment. The pooled frequency of fungal neutropenic enterocolitis was 6.2% calculated from all 860 reported patients and 3.4% calculated from selected representative studies only. In 94% of the patients, Candida spp. were involved. The pooled mortality rate was 81.8%. Most authors did not report or perform antifungal therapy. CONCLUSION: In patients with neutropenic enterocolitis, fungal pathogens play a relevant, but secondary role compared to bacteria. Evidence concerning therapy is very poor, but epidemiological data from this study may provide helpful clues to select empiric antifungal therapy in neutropenic enterocolitis.

Adult↗
PubMed2006

Enterocolitis in patients with cancer after antibody blockade of cytotoxic T-lymphocyte-associated antigen 4.

PURPOSE: Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) is an inhibitory receptor on T cells. Knocking out CTLA4 in mice causes lethal lymphoproliferation, and polymorphisms in human CTLA4 are associated with autoimmune disease. Trials of the anti-CTLA4 antibody ipilimumab (MDX-010) have resulted in durable cancer regression and immune-mediated toxicities. A report on the diagnosis, pathology, treatment, clinical outcome, and significance of the immune-mediated enterocolitis seen with ipilimumab is presented. PATIENTS AND METHODS: We treated 198 patients with metastatic melanoma (MM) or renal cell carcinoma (RCC) with ipilimumab. RESULTS: The overall objective tumor response rate was 14%. We observed several immune mediated toxicities including dermatitis, enterocolitis, hypophysitis, uveitis, hepatitis, and nephritis. Enterocolitis, defined by grade 3/4 clinical presentation and/or biopsy documentation, was the most common major toxicity (21% of patients). It presented with diarrhea, and biopsies showed both neutrophilic and lymphocytic inflammation. Most patients who developed enterocolitis responded to high-dose systemic corticosteroids. There was no evidence that steroid administration affected tumor responses. Five patients developed perforation or required colectomy. Four other patients with steroid-refractory enterocolitis appeared to respond promptly to tumor necrosis factor alpha blockade with infliximab. Objective tumor response rates in patients with enterocolitis were 36% for MM and 35% for RCC, compared with 11% and 2% in patients without enterocolitis, respectively (P = .0065 for MM and P = .0016 for RCC). CONCLUSION: CTLA4 seems to be a significant component of tolerance to tumor and in protection against immune mediated enterocolitis and these phenomena are significantly associated in cancer patients.

Adrenal Cortex Hormones↗
PubMed2001

An epidemiological study of neonatal necrotizing enterocolitis.

OBJECTIVE: To study epidemiology including various risk factors incorporated in neonatal necrotizing enterocolitis in Kashmir. METHODS: A retrospective hospital based study on 3235 neonates admitted in Neonatal Intensive Care Unit of Sheri-Kashmir Institute, were evaluated. Forty two were diagnosed as cases of Neonatal Necrotizing Enterocolitis on the basis of various clinical and radiological parameters and grouped in 3 stages as per modified Bell's classification. The case records of these 42 babies and 303 of the control group were reviewed for the purported risk factors and recorded on pretested proforma and finally statistically analyzed. RESULTS: Over a period of 10 years, we documented necrotizing enterocolitis in 42 neonates, with an incidence of 1% of all Neonatal Intensive Care Unit admissions and 1% of all live births. Eighty one percent were less than 2000 gms and 76% less than 36 weeks of gestation. Twenty four percent had stage I disease, 33% had stage II, and 43% babies had stage III disease. Multiple risk factors were present in these babies, with significant differences among Necrotizing Enterocolitis and the control group of patients, particularly hypothermia (P < 0.001), respiratory distress (P < 0.05), polycythemia (P < 0.001) acidosis (P < 0.01), sepsis (P < 0.001), enteral feeding and asphyxia (P < 0.001). Of the 59 babies (< 2000 gms) with hypothermia (< 35 degrees C), 39% developed Necrotizing Enterocolitis, compared to 4% babies (11/278), who did not have hypothermia, statistically a significant finding. Mean birth weight and gestational age were lower than in control group (P < 0.05). The age of presentation was 5.2 +/- 4.0 days and majority (81%) presented during first week of life, most severe cases presenting earlier than the mild cases. Severity of Necrotizing Enterocolitis as per modified Bell's classification and mortality was inversely related to birth weight and gestational age. One hundred percent mortality was noted in the babies, with birth weight less than 1000 gms and gestational age less than 28 weeks. The overall mortality was 45%, for stage I, 20%; for stage II, 36% and 67% for stage III. Necrotizing Enterocolitis cases accounted for maximum mortality in Neonatal Intensive Care Unit than in control group (P < 0.001). CONCLUSION: Recognition of factors such as prematurity, low birth weight, hypothermia, asphyxia and their timely prevention would help in reducing morbidity and mortality due to Necrotizing Enterocolitis.

Birth Weight↗
PubMed2004

Effects of mode of delivery and necrotising enterocolitis on the intestinal microflora in preterm infants.

To investigate the effects of mode of delivery and of necrotising enterocolitis on the faecal microflora, 140 infants born before 33 weeks of gestation were followed up for symptoms of necrotising enterocolitis. Stool samples for gas-liquid chromatography and culture were collected twice weekly, and, when necrotising enterocolitis was suspected, for 2 months. For each infant with necrotising enterocolitis (n=21), two control infants matched for birth weight and gestational age were selected from the remaining study population. In gas-liquid chromatography analysis, the faecal bacterial microflora of infants born via caesarean section differed significantly from the gut microflora of those born via the vaginal route. The intestinal microflora showed a significant alteration in the necrotising enterocolitis group at time of diagnosis. At the onset of necrotising enterocolitis, faecal colonisation with Enterococcus species and Candida albicans was significantly more frequent in symptomatic infants than in controls. In infants with positive blood cultures and positive intestinal biopsy cultures, concomitant stool samples revealed the same microbial pathogens. In conclusion, the intestinal microbial colonisation in preterm infants born by caesarean section differs from that in preterm infants born via the vaginal route. A significant change in faecal microbial colonisation seems to occur at the onset of necrotising enterocolitis. Pathogens detected in the stools at that time might have a causative role in the development of the disease.

Analysis of Variance↗