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  1. D.I. Kufeji,
  2. A. Anggiansah,
  3. E.H. Dykes,
  4. W.J. Owen
  1. University Hospital Lewisham & Guys and St Thomas' Hospitals, London, UK
  1. N. Thapar,
  2. N.M. Croft,
  3. N. Meadows,
  4. D. Evans
  1. Dept of Adult and Paediatric Gastroenterology, Medical and Dental School of St Bartholomew's, Queen Mary, University of London, London EC1A 7BE, UK

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Background/aim: The vast majority of West African adults are colonised withH. pylori and most children acquire the infection in early life. There is an inverse relationship between the prevalence of H. pylori and socioeconomic development throughout the world. In Greater Glasgow 50% of postcodes belong to Deprivation Categories 5–7 (poorest socioeconomic status). Our aim was to study intrafamilial patterns of H. pylori infection in Glasgow and to identify possible modes of spread.

Methods: The families of 32 children, who presented at the RHSC Glasgow with suspected H. pylori-related disease, were studied. H. pylori status was determined by faecal antigen testing, a method that we have validated against the urea breath test in children.

Results: The families consisted of 57 parents, 47 siblings and 32 index children. Of these 136 subjects 93% provided stool samples. The prevalence of H. pylori in this sample was 35% (41% of parents and 30% of children). Those index children who were of Dep Cats 5–7 were 7 times more likely to be infected with H. pylorithan those of Dep Cats 1–4 (p=0.03 Fisher's exact test). Index children whose siblings were H. pylori +ve were 9 times more likely to be H. pylori +ve themselves (p=0.06). Both the H. pyloristatus of parents (p=0.3, OR=2) and family size (p=0.6, OR=1) were not significantly related to the H. pyloristatus of the index child.

Conclusions: Poor socioeconomic status and having an H. pylori infected sibling are significant risk factors for H. pylori in children, suggesting that infection may be transmitted horizontally within families. We plan to extract DNA from the stool for genotyping in order to investigate these findings further.


Introduction: Children with gastro-oesophageal reflux related respiratory symptoms (GORRS) are often referred for evaluation by 24-hour pH study using dual pH sensors (in the lower and upper oesophagus). The aim was to determine the usefulness of dual sensor pH monitoring in this group of patients.

Patients and methods: Eighty children (48 males) with suspected GORRS (apnoiec attacks 38, recurrent chest infection 31, chronic cough and wheezing 11) aged 1 month-15years (median 5.5months) were studied. 24-hour ambulatory pH study was performed using dual channel antimony electrode (Synectics Medical, Sweden). The lower sensor position was located according to the child's length with the upper sensor 5cm proximal. Position confirmed by X-ray. Study was positive if the reflux index (RI = % time pH <4) was >10% in lower sensor.1-1 Positive proximal reflux = RI > 3% in upper sensor. Total number of reflux episodes (TRE), longest reflux episode (LRE), number of episodes >5min(NLRE) in the lower oesophagus were compared for positive proximal reflux.

Results: Thirty-two children (40%) had a positive pH study result (21 children < 1 year of age). 24/80 children (30%) had positive proximal reflux, only 1 had no significant lower reflux. Children with proximal reflux were more likely than those with no proximal reflux to have had pathological reflux distally (n=23 (95.8%) versus 1 (4.2%)) (χ2 =44.53, df=1, p=0.000). Patients with positive proximal oesophageal reflux had significantly greater LRE(p=0.001), NLRE(p=0.007) and RI(p=0.000) in the lower oesophagus.

Conclusion: Presence of acid in the upper oesophagus is determined by events in the lower oesophagus. Children presenting with possible GORRS can be adequately investigated with a single channel pH sensor.


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Background: Achalasia in children is a rare disorder of oesophageal motility characterised by abnormal relaxation of the Lower Oesophageal Sphincter (LOS) and peristalsis. Among all ages the incidence is estimated to be between 0.03 -1.1 per 100 000 population / year. In this review we report 6 children who presented within a period of 18 months.

Methods: Retrospective case review.

Results: 6 children presented with achalasia over an 18/12 period (5 over 1 year), comprising 3 males and 3 females with ages ranging from 7/12 to 14 yrs (median 10 yrs). Prior to diagnosis there was a median 2 month duration of symptoms (range 2—12/12) including dysphagia, vomiting, feeding problems, pain and weight loss. On presentation a diagnosis of achalasia was made on barium swallow, and oesophageal perfusion manometry performed on all cases. Mean LOS pressure ranged from 37.5—70 mmHg (mean 50) with typical loss of LOS relaxation and absent peristalsis. Nifedipine was used as the first line agent with symptomatic improvement in 2 of the 6 for 2—4 weeks. Botulinum Toxin (BTX) was used as second line (endoscopic injection into LOS; <2 years-50 units / quadrant, >2 years-100 units /quadrant). All 6 had good clinical response within one week, lasting up to 3 months (median 8 weeks). 4 had repeat BTX injection (2 awaiting) with similar response. Of these 3 had repeat oesophageal manometry showing a mean reduction in LOS pressure of 40mmHg (35–50) from diagnosis but no improvement in peristalsis. One has had successful surgery and the other two referred.

Discussion: This yearly incidence of achalasia is considerably higher than the 1 - 2 expected from the centre's referral population. This may be partly explained by underdiagnosis, and we suggest barium studies as a first line investigation for recurrent or acquired vomiting, dysphagia or feeding difficulties. If available, oesophageal manometry is a valuable tool for diagnosis and monitoring treatment response. Nifedipine has no benefit. To our knowledge this is the first report of the use of Botulinum Toxin in children with achalasia in the UK, and the biggest single centre use. The short lived effects warrant repeat dosage at shorter intervals or combination with other therapy e.g. balloon dilatation. Surgery remains the definitive treatment.


Background: The13C-mixed triacylglycerol (13C-MTG) breath test is a measure of intraluminal fat digestion. In normal digestion 20–40% of the 13C label is recovered in breath. The fate of the remaining 60–80% is unknown. It may be excreted in stool, or remain in slow-turnover carbon pools within the body. In this study, we aimed to identify the proportions of the ingested label that were excreted in stool and breath following ingestion of 13C-MTG by children with cystic fibrosis (CF).

Methods: 8 children with CF and 2 healthy controls ingested 20 mg/kg (CF) or 10 mg/kg (control)13C-MTG with a standard breakfast, and their normal enzyme replacement therapy. Breath samples were collected at baseline, then half-hourly for 6 hours and hourly for a further 4 hours. All stools were collected from baseline to day 5. CO2 production rate was measured hourly using an indirect calorimeter. 13C enrichment of breath samples was measured by isotope ratio mass spectrometry (IRMS) and the cumulative percent dose recovered (cPDR) in 10 hours was calculated. Total 13C of the Jeejeebhoy faecal fat extract from each stool was measured by combustion-IRMS, and the13C enrichment and concentration of the TBDMS derivative of octanoic acid was measured by GC/MS after hydrolysis of the fat extracts.3-1 Stool 5 day cPDR was calculated.

Results: Mean (SD) cPDR in breath was 33 (13)% for children with CF and 45% for controls. Mean (SD) cPDR in stool by combustion-IRMS and GC/MS, respectively, was 0.66 (0.61)% and 0.26 (0.20)% for children with CF and 1.41 and 4.18% for controls.

Conclusions: Ingestion of13C-MTG by children with CF is followed by almost complete intestinal absorption of the digested substrate. The label not identified in breath must remain in the body, and the variation of cPDR in breath is therefore largely due to factors other than the variation in efficiency of lipolysis.


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