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 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors undertook a retrospective study of the modes of prescription, the tolerance and efficacy of prostaglandin E1 in 62 consecutive neonates with congenital heart disease (average Age 1.6 days: 35 boys: weight: 3.1 +/- 0.6 Kg) admitted to the paediatric intensive care unit of Nancy University Hospital between 1998 and 2002. The infusion time and cumulative dosage were 134 +/- 112 (6-480) hours and 111 +/- 94 (4-396) microg/Kg respectively. The side effects that were observed were: Apnoea (19%), abdominal distension (16%), bradycardia (13%), enterocolitis (6.5%), hypotension (6.5%), vomiting (5%), fever (1.6%) and skin rash (1.6%). Gastrointestinal disturbances are associated with a low body weight (p<0.04), to prolonged treatment (p<0.02) with no influence of initial or cumulative dosages (P=NS), with respiratory assistance (p<0.03) and longer hospital stay (p<0.01). Hypotension was commoner in cases of poor neonatal adaptation. Mortality was correlated with severe initial acidosis (p<0.02), a low Apgar score, the initial prolonged use of high doses of prostaglandin (p<0.04), and the presence of severe valvular aortic stenosis or hypoplasia of the left heart (p<0.002). The authors conclude that treatment with prostaglandin is effective in the majority of cases despite the use of low maintenance doses (0.01 microg/Kg/min). Gastrointestinal disturbances favourised by the perinatal context, the cardiac disease, and prolonged treatment are significant factors for morbidity and mortality. The beneficial role of early neonatal enteral feeding was not demonstrated in this high risk population.
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PMID:[Complications of prostaglandin E1 treatment of congenital heart disease in paediatric medical intensive care]. 1596 3

We experienced two cases with disseminated HP and IND occurring with normal bowel in between (disseminated mixed intestinal dysmotility--DMID) and postulate whether it could be classified as a new intestinal motility disorder. Our cases, both boys, died at 3 and 7 months, respectively. Both had irregular stool passage, and abdominal distention with bilious vomiting since birth. On barium enema, both had rigid distal ileum and colon with narrow lumens, with dilated and atonic proximal ileum and jejunum. An ileostomy was created on days 3 and 2 of life, respectively, however, they did not function and jejunostomies were created, which also did not function well. Both boys died after repeated episodes of severe enterocolitis. In each case, three 10 cm specimens were obtained randomly from the jejunum and ileum, and two 5 cm specimens were obtained randomly from each of the ascending colon, transverse colon, descending colon, and rectum and treated with hematoxylin and eosin (H & E) staining, acetylcholine esterase (AchE) histochemistry, and protein gene product 9.5 (PGP9.5) and neural cell adhesion molecule (NCAM) immunohistochemistry for histopathologic assessment. All specimens showed a mixture of disseminated IND and HP, with normal intestine in between. There was abnormal expression of NCAM activity in the intestinal smooth muscle layers in small and large intestine. This is the first report about disseminated IND and HP occurring with normal bowel in between (DMID) and we suggest it should be classified as a new intestinal motility disorder. The present findings demonstrate that patients with DMID have a complicated abnormality of NMJ that may directly influence bowel motility and prognosis according to the severity of the abnormality.
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PMID:Disseminated mixed intestinal dysmotility (DMID): a new intestinal ganglion cell disorder? 1613 13

Gastrointestinal Schistosomiasis and Amebiasis are uncommon in the western world, while such infections are frequent in the African community. In addition to the problems associated with the clinical symptoms of these parasitic infections, it is important to stress the increase in cancer of the Gastro-Intestinal (GI) tract. In this study we evaluate the prevalence of cancer in patients affected by chronic inflammatory diseases caused by the above named parasites. In three years, from January 2000 to December 2003, we observed a total of 1199 subject. Of these, 950 presented with complaints of diarrhoea, vomiting, abdominal pain, melena, hematemesis, rectal discharges and alteration of bowel habits. A total of 818 patients were evaluated in Uganda (Mulago and Arua hospitals) and 381 at Luisa Guidotti Hospital in Zimbabwe. An exhaustive clinical history was collected for each patient and then physical and laboratory examinations were performed. The clinical files of all patients previously admitted to the respective hospitals were obtained and the information taken from these files was then integrated with our clinical findings. Subjects who were found free of gastro-intestinal disease after examinations and did not have a clinical history of infective GI disease but presented with other pathologies, were regarded as control group. The control group was composed of 249 subjects. The subjects who were positive on examination underwent further investigations. The number of patients affected by schistosomiasis and amebiasis were 221 and 224 respectively. The number of patients who suffered from aspecific enterocolitis was 454, intestinal tuberculosis was present in 21 patients and we found 30 patients with esophageal candidiasis. Patients who had the above mentioned GI diseases were then divided into 3 groups. First group was composed of patients who had a clinical history of infective GI diseases and were re-admitted for similar symptoms, and on examination were positive for the presence of the same infective GI diseases. Such patients were placed in the Chronic group. The second group was formed of patients who had previously undergone treatment for infective GI diseases but on readmission were found free of infective GI disease, and this group was described as the Cured group. They had symptoms associated with other pathologies. A third group, which we described as the Acute group was composed of patients who did not have any previous case of GI infection and were admitted for the first time. Such patients were found positive on examination for infective GI diseases. In the 950 patients, we found a total of 45 tumors. The tumors were prevalent (42 tumors) in the chronic group. In 34 patients the tumor was in the colo-rectal region, in 3 patients in the stomach, in 4 patients in the esophagus and 1 patient had cancer in the small bowel. Our results show a strong association between the chronic infection of the GI tract and the likelihood to develop tumors. However, it is not clear which biological mechanisms are implicated in such transformations. They may depend on the chronic inflammation of the GI mucous which permits the entrance of carcinogenic materials or on the effects of mutagenic products produced by the parasites or both.
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PMID:Risk of cancer onset in sub-Saharan Africans affected with chronic gastrointestinal parasitic diseases. 1656 65

Foods that account for 90% of allergic reactions in children are cow's milk protein, eggs, peanut, soy, tree nuts, fish, and wheat. Food allergy can manifest as urticaria/angioedema, anaphylaxis, atopic dermatitis, respiratory symptoms, or a gastrointestinal (GI) disorder. GI allergic manifestations can be classified as immunoglobulin E (IgE) mediated (immediate GI hypersensitivity and oral allergy syndrome); "mixed" GI allergy syndromes (involving some IgE components and some non-IgE or T-cell-mediated components) include eosinophilic esophagitis and eosinophilic gastroenteritis. Non-IgE-mediated or T-cell-mediated allergic GI disorders include dietary protein enteropathy, protein-induced enterocolitis, and proctitis. All these conditions share a common denominator: the response of the immune system to a specific protein leading to pathologic inflammatory changes in the GI tract. This immunological response can elicit symptoms such as diarrhea, vomiting, dysphagia, constipation, or GI blood loss, symptoms consistent with a GI disorder. The detection of food allergies can be accomplished by the use of radioallergosorbent (RAST) testing and skin prick tests in helping to assess the IgE-mediated disorders. Patch tests may help evaluate delayed hypersensitivity reactions. Treatment of GI allergic disorders ranges from strict dietary elimination of offending food(s), use of protein hydrolysates, and use of L-amino acid-based formula when protein hydrolysates fail. Treatment with topical (for eosinophilic esophagitis) or systemic steroids is used if all dietary measures are unsuccessful. Maternal breast feeding or the use from birth of hydrolysate formulas (extensive or partial hydrolysates) may be efficacious in the prevention of atopic disease in "high-risk" families (with at least 1 parent or sibling with a history of atopic disease).
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PMID:Gastrointestinal manifestations of food allergies in pediatric patients. 1620 93

While 6% of children under three years of age suffer from a food allergy, the figure for adults varies between 1.5 and 3%. Leading allergens in foodstuffs are glycoproteins having a molecular weight of between 10,000 and 60,000. The symptoms of an immediate type nutrient allergy mediated by IgE usually manifest within a matter of a few minutes to two hours after ingestion of the offending nutrient and take the form, for example, of tingling and itching, tissue swelling in the mouth, hoarseness, asthma, gastrointestinal complaints or acute urticaria; in severe cases anaphylactic shock may even occur. In contrast, no IgE antibodies are to be found in nutrient-induced enterocolitis, which is associated with diarrhea and vomiting occurring after a delay of one to six hours. Differential diagnostic considerations must include intolerance for certain foodstuffs, such as lactose intolerance, or pseudoallergic reactions.
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PMID:[Food allergies are often an unrecognized cause of clinical complaints]. 1630 89

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.
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PMID:Long-term outcome of patients with enterocolitis complicating Hirschsprung's disease. 1646 33

Two neonatal cases of cow's milk allergy showing bilous vomiting and massive bloody stool are presented. In both cases, laboratory data on admission showed no eosinophilia. The immediate upper gastrointestinal series of both cases demonstrated no evidence of intestinal malrotation, but revealed a narrowing of the duodenum and upper jejunal loops and marked stasis of barium in one case, suggesting an edema with inflammation. Rectal mucosal punch biopsy of the other case showed eosinophilic infiltration in the lamina propria. These findings suggested an allergic origin, useful information for avoiding confusion with some diseases requiring emergency surgery. In both cases, bleeding resolved soon after elimination of cow's milk from the diet. Thereafter both cases showed a moderate to marked increase in peripheral eosinophilia, while serum radioallergosorbent tests for cow's milk protein were negative. Definitive diagnosis of allergic enterocolitis is difficult because there is neither specific laboratory data nor tests. Allergic enterocolitis can occur in the early neonatal period and should be considered in differential diagnosis of any newborn developing gastrointestinal bleeding.
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PMID:Massive bloody stools in two neonates caused by cow's milk allergy. 1693 13

Cow's milk protein allergy is the most common food allergy in infants and young children. It is estimated that up to 50% of pediatric cow's milk allergy is non-IgE-mediated. Allergic proctocolitis is a benign disorder manifesting with blood-streaked stools in otherwise healthy-appearing infants who are breast- or formula-fed. Symptoms resolve within 48-72 h following elimination of dietary cow's milk protein. Most infants tolerate cow's milk by their first birthday. Food protein-induced enterocolitis syndrome presents in young formula-fed infants with chronic emesis, diarrhea, and failure to thrive. Reintroduction of cow's milk protein following a period of avoidance results in profuse, repetitive emesis within 2-3 h following ingestion; 20% of acute exposures may be associated with hypovolemic shock. Treatment of acute reactions is with vigorous hydration. Most children become tolerant with age; attempts of re-introduction of milk must be done under physician supervision and with secure i.v. access. Allergic eosinophilic gastroenteritis affects infants as well as older children and adolescents. Abdominal pain, emesis, diarrhea, failure to thrive, or weight loss are the most common symptoms. A subset of patients may develop protein-losing enteropathy. Fifty percent of affected children are atopic and have evidence of food-specific IgE antibody but skin prick tests and serum food-IgE levels correlate with response to elimination diet poorly. Elemental diet based on the amino-acid formula leads to resolutions of gastrointestinal eosinophilic inflammation typically within 6 wk.
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PMID:Educational clinical case series for pediatric allergy and immunology: allergic proctocolitis, food protein-induced enterocolitis syndrome and allergic eosinophilic gastroenteritis with protein-losing gastroenteropathy as manifestations of non-IgE-mediated cow's milk allergy. 1758 15

Primary volvulus means idiopathic volvulus without predisposing factor and is rare in children. The etiology is unknown. The incidence is relatively higher in neonates. The most common symptoms are abdominal distension and bilious vomiting. Our patient was a preterm baby at age of 89 days. Acute onset of abdominal distension and sepsis-like symptoms were noted. After operation, no anatomical anomaly was noted. Probable primary midgut volvulus was diagnosed. Early diagnosis of primary volvulus of the small intestine is difficult. Operation should be performed as soon as possible in a neonate with quick progression toward unstable hemodynamics and acidosis with ileus. Postoperative short bowel syndrome was noted. There are often sepsis, enterocolitis, and poor body weight gain noted among short bowel patients. With breast milk feeding and probiotics usage, there were few complications of short bowel syndrome noted in our patient. The duration for establishing intestinal adaptation was shorter than for other patients. The patient's body weight, body length and development caught up gradually within 18 months.
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PMID:Possible effect of probiotics and breast milk in short bowel syndrome: report of one case. 1762 9

This study was performed to identify clinical factors that facilitate the diagnosis of typical cow's milk protein-induced enterocolitis (CMPIE). Data from 142 consecutive patients (aged 15 to 45 days, cow's milk formula- or cow's milk and breast milk mixed-fed) admitted due to vomiting and/or diarrhea were retrospectively analyzed. These 142 subjects were divided into three groups: the CMPIE, infection, and non-infection group. Each group was composed of 16 (11.3%), 102 (71.8%), and 24 (16.9%) patients, respectively. On admission, poor weight gain (p=0.003), hypoalbuminemia (p=0.035), peripheral leukocytosis (p=0.012), and metabolic acidosis (p=0.015) were found to be more significant in the CMPIE group than those in other two groups. In CMPIE, serum albumin levels decreased from 3.3+/-0.9 g/dL on admission to 2.6+/-0.3 g/dL during admission (p<0.05), and methemoglobinemia was observed in 3 patients (18.8%) (p=0.012). Multiple logistic regression analysis showed that the independent predictors of CMPIE versus the infection group were failure to gain weight (OR, 10.75 [95% CI, 1.53-66.12]) (p= 0.014) and hypoalbuminemia (OR, 9.53 [95% CI, 1.62-49.01]) (p=0.010). The early recognition of indexes of suspicion for CMPIE may be of help in the diagnosis and treatment of this disorder.
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PMID:Indexes of suspicion of typical cow's milk protein-induced enterocolitis. 1816 12


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