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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori (H. pylori) colonizes the human stomach, especially during childhood. H. pylori gastritis, in the absence of duodenal ulcer, does not appear to be associated with specific symptoms. After eradication of H. pylori infection, abdominal pain is improved only in children with duodenal ulcer. Children with H. pylori gastritis cannot be distinguished from uninfected children on the basis of initial symptoms. However, although not demonstrated, a relationship between H. pylori and recurrent abdominal pain might exist since some studies showed that H. pylori-infected children present more frequent pain related to meals or ulcer-like symptoms. These discrepancies could be explained by the fact that H. pylori is probably not a frequent cause of recurrent abdominal pain. The use of refined clinical characteristics of abdominal pain could be of help identifying a subgroup of patients with abdominal pain in whom H. pylori infection needs to be sought and treated. Recent pediatric consensus conferences recommend testing for H. pylori infection by endoscopy only those patients presenting symptoms suggestive of an organic origin.
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PMID:[The role of Helicobacter pylori in abdominal pain in children]. 1070 Oct 66

Consensus was achieved on the following issues: in children H. pylori infection causes chronic gastritis, but rarely gastric and duodenal ulcer disease. Eradication of H. pylori leads to healing of these conditions. To-date, there is no evidence demonstrating a link between H. pylori gastritis and abdominal pain except in those children where a gastric or duodenal ulcer is present. Children should be investigated for H. pylori infection only if their symptoms are suggestive of organic disease rather than functional abdominal pain. Endoscopy with biopsies is the optimal method to investigate a child with upper gastrointestinal symptoms suggestive of organic disease but this should only be carried out when a diagnostic work up using non-invasive methods has excluded other causes such as lactose maldigestion, constipation, coeliac disease, liver or biliary tact disease. If H. pylori is identified through investigations carried out during endoscopy the infection should be treated. Treatment should be monitored with a reliable non-invasive test and the 13C-urea breath test is the preferred method. H. pylori eradication in such children will cure gastritis but there is no data to support a relationship between a cure of H. pylori gastritis and symptom relief except in patients with ulcer disease. Further studies are needed to establish whether there are any specific symptoms associated with H. pylori gastritis alone and whether infected children without ulcer disease benefit from anti-H. pylori therapy regarding their symptoms. This consensus meeting did not deal with the optimal therapy for H. pylori infection as there are insufficient studies concerned the best treatment in children.
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PMID:[Helicobacter infection in children]. 1080 28

Annular Pancreas (AP) is a rare congenital anomaly that usually presents in childhood with symptoms referable to duodenal obstruction; nonetheless, this condition can manifest in adulthood with abdominal pain, pancreatitis, duodenal ulcer, pancreatic head mass. The Authors hereby discuss a case of AP observed in a 63 year-old patient in which EUS played a decisive role in achieving a certain diagnosis.
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PMID:[Annular pancreas in adults: diagnostic considerations on a case]. 1086 61

Abdominal pain is a common presenting symptom in adults with sickle cell disease (SCD). One case of Helicobacter pylori gastritis has been reported in a child with sickle cell anemia. H. pylori-induced peptic ulcer disease (PUD) has not previously been reported in adults with SCD. We report eight cases of H. pylori infection in adult sickle cell patients presenting with acute or recurrent abdominal pain and/or gastrointestinal bleeding. In all cases, H. pylori serology (IgG) was positive, and three patients had gastric or duodenal ulcer by endoscopic examination. All patients responded to H. pylori treatment with complete resolution of symptoms by 4 weeks. The prevalence of H. pylori infection in SCD is unknown, but patients may be at increased risk for H. pylori-induced PUD and complications due to pre-existing anemia, increased nonsteroidal anti-inflammatory drug use, and alloimmunization which may delay necessary transfusion. It is important that the differential diagnosis of abdominal pain in adults with SCD include nonsickle cell-related disorders such as PUD. When confirmed, a definitive etiology of PUD must be determined so that appropriate treatment strategies can be initiated promptly and excess morbidity avoided.
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PMID:Helicobacter pylori infection in sickle cell disease. 1094 32

We studied cholelithiasis that occurred after gastrectomy in 52 patients (35 males and 17 females) encountered at our department between January, 1978 and December, 1998. Gastrectomy had been performed for gastric or duodenal ulcer in 35, gastric cancer in 14, gastroptosis in 2, and gastric trauma in 1 of these patients. Reconstruction after gastrectomy was performed by the Billroth II method (B-II method) in 31 patients, Billroth I method (B-I method) in 17, Roux-en-Y method (Roux-Y method) in 3, and esophagogastrostomy in 1. The period between gastrectomy and discovery of gallstones was 1-5 years in 9, 5-10 years in 10, and 10 years or longer in 33, or more than 60% of the patients. Gallstones were present in the gallbladder alone in 33, bile duct alone in 9, gallbladder and bile duct in 10; the percentage of bile duct stones was high. The type of stones was bilirubin-calcium stones in 21, black stones in 12, pure cholesterol stones in 1, combined stones in 4, mixed stones in 12, and others in 2; pigment stones accounted for 63.5%. Gallstones were symptomatic in 78.8% of the patients, and abdominal pain was the most frequent symptom. Bile was positive on bacterial culture in 68.4%, and Gram-negative bacilli were the most frequently isolated. Lymph node dissection, vagotomy, cholestasis, and biliary tract infection are considered to be related to cholelithiasis after gastrectomy.
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PMID:Study of cholelithiasis after gastrectomy. 1094 47

The majority of Helicobacter pylori (H. pylori) infections appear to be acquired during childhood. Despite this fact, the natural history of H. pylori infection in children, such as the mode of acquisition, the clinical symptoms and signs of infection and the appropriate treatment, is poorly understood. There is no consensus regarding which children with H. pylori infection deserve treatment nor is there agreement on the appropriate treatment regimen. This stems from the lack of controlled studies into H. pylori infection during childhood. For example, there have been no controlled studies to determine effective treatment of H. pylori infection in children. Although published guidelines for the treatment of childhood H. pylori infection do not currently exist, there is reasonable evidence to support treatment in children with gastric or duodenal ulcer, gastric MALT (mucosa-associated lymphoid tissue) lymphoma and atrophic gastritis. There is no strong evidence to recommend treatment of children with H. pylori infection and recurrent abdominal pain, asymptomatic infection, children in chronic care facilities and children who have a family member with H. pylori infection. Current evidence suggests that single and dual therapy regimens for H. pylori infection in children are not effective. Triple therapy , generally the combination of 2 antibiotics and a proton pump inhibitor, given two times daily for 2 weeks appears to offer the best current treatment.
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PMID:Treatment of Helicobacter pylori infection in children. 1097 49

A potential virulence determinant of Helicobacter pylori is the cagA gene product. To determine the relevance of the expression of CagA to the clinical picture and outcome of H. pylori infection in children, we examined 104 consecutive children diagnosed with H. pylori infection. Serum samples were collected to test for the presence of immunoglobulin G (IgG) anti-CagA antibodies. Forty-five patients (43%) had antibodies to the CagA protein (group I), and 59 did not (group II). Seropositive patients had a longer prediagnostic history of abdominal pain (P = 0.02), more severe abdominal pain (defined as ulcer pain) (P = 0.05), a higher prevalence of duodenal ulcer (38 versus 7%; P<0.01), more active chronic gastritis (82 versus 32%; P<0.001), and a higher titer of serum IgG anti-H. pylori antibodies (P<0.001). Ninety percent of the patients were monitored for 27+/-18 months. On multivariate analysis, CagA-negative patients had a 3.8-fold-higher chance of achieving a disease-free state than CagA-positive patients (95% confidence interval, 1.5- to 9.5-fold). We conclude that infection with CagA-producing strains of H. pylori is a risk factor for severe clinical disease and ongoing infection.
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PMID:Relevance of CagA positivity to clinical course of Helicobacter pylori infection in children. 1101 59

There are no reports, to our knowledge, on the expression of Lewis (Le) antigens in Helicobacter pylori isolates from children. The aim of this study was to compare the expression of Le antigens by H. pylori isolates from children and from adults. Totals of 278 clones from 22 children with recurrent abdominal pain and 293 clones from 22 adults with (n=10) or without (n=12) duodenal ulcer were studied. Expression of Le(x) and Le(y) antigens was determined by ELISA, using monoclonal anti-Le antibodies. The Le phenotype of the patients was determined in gastric juice with a hemagglutination assay. Clones expressing Le(x) were more common in children than in adults (55.4% vs. 33.4%, respectively; P<.001), and Le(y) was more common in adults than in children (81.6% vs. 66%, respectively; P<.01). A trend analysis showed a significant decline in frequency of clones expressing Le(x) with age (P=.021). In this community, expression of Le antigens differs in H. pylori isolates obtained from children versus adults.
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PMID:A comparison of Lewis x and Lewis y expression in Helicobacter pylori obtained from children and adults. 1123 46

Anisakis simplex is a nematode which can parasitize many different kinds of fish or cephalopods (codfish, salmon, tuna, mackerel, hake, etc). Anisakis simplex can cause different diseases in humans. The human being acquires the larvae by eating raw or undercooked seafood. Acute anisakiasis is probably caused by an inflammatory and/or allergic response in the digestive tract mucosa with abdominal pain. It can also induce IgE-mediated reactions with several clinical manifestations ranging from urticaria/angioedema to anaphylaxis. Chronic anisakiasis results from abscesses or eosinophilic granulomas caused by parasite invasion. This later form can mimic appendicitis, duodenal ulcer, inflammatory bowel diseases and intestinal obstruction. An early gastroduodenoscopy can confirm the diagnosis and prevent the complications. Serodiagnosis of anisakiasis is difficult since many Anisakis antigens show cross-reativity complications. In fact many people have high IgE titles in the absence of obvious allergic reactions to seafoods. As preventive measures heating for 10 min over 65 degrees C or freezing (minus 20 degrees for 24 h) destroys the infectivity of the larval stage but not always prevent allergic reactions.
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PMID:[Anisakiasis: a borderline disorder]. 1138 51

This report describes a case of spontaneous esophageal perforation that was considered to be etiologically related to a duodenal ulcer with pyloric stenosis. The patient was a 54-year-old Japanese man who presented following the sudden onset of severe abdominal pain and dyspnea after an episode of vomiting. He had a history of duodenal ulcer. Computed tomography revealed an extremely dilated stomach containing abundant food residue, intraabdominal effusion, bilateral pleural effusion, and mediastinal emphysema, findings that strongly suggested esophageal perforation. Esophagoscopy confirmed perforation of the lower esophagus. Laparotomy revealed marked contamination, including food residue in the abdominal cavity, and a severely dilated stomach attributed to pyloric stenosis caused by a duodenal ulcer. A 2-cm longitudinal perforation was found on the right side of the lower esophagus. Because the patient's general condition was too poor to tolerate a one-stage operation (primary closure of the perforation, gastrectomy, and reconstruction), we initially performed decompression gastrostomy and control of the esophageal leakage with T-tube placement. Following the T-tube was removed 1 month later, distal gastrectomy and reconstruction of the gastrojejunostomy (Billroth II method) could be safely performed.
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PMID:Spontaneous esophageal perforation related to a duodenal ulcer with pyloric stenosis: report of a case. 1182 88


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