Search PubMed⌕ Search

Biomedical subjects

E Hassall

Publications and source records attributed to E Hassall.

At least 55 records · Page 3Linked to original sources
PubMed1993

Hypersensitivity reaction to single contrast barium meal studies in children.

We report two children who developed hypersensitivity reactions of varying severity following barium meal examination, the more severe of which was associated with documented severe food allergy. For children with this risk factor, contrast studies should be performed only where facilities and personnel are available for immediate resuscitation of all sizes of child. For children such as these, consideration should be given to the use of pure barium sulphate.

Barium Sulfate↗
PubMed1993

Treatment and long-term follow-up of Helicobacter pylori-associated duodenal ulcer disease in children.

In a 7-year period, 33 children had endoscopically documented duodenal ulcer disease. Of the 33 children, 29 had Helicobacter pylori antral gastritis. All children with H. pylori-associated duodenal ulcer disease were treated with antibiotics but no H2-receptor blocking agents. For the first 3 years of the study, initial treatment was with bismuth subsalicylate or amoxicillin for 6 weeks. For the latter 4 years, therapy with both bismuth subsalicylate and amoxicillin for 6 weeks was used initially; those in whom treatment failed received bismuth subsalicylate and amoxicillin for 6 weeks, and metronidazole for 4 weeks. Follow-up with endoscopic biopsies was performed immediately after each treatment course and at a mean of 6.5 months after clearance of H. pylori from antral biopsy specimens. Data for noncompliant patients and those receiving nonsteroidal antiinflammatory drugs were analyzed separately. For compliant patients, the rates of H. pylori clearance from antral biopsy specimens immediately after each treatment were as follows: bismuth subsalicylate, 6 of 12 children; amoxicillin, 1 of 5 children; double therapy, 9 of 9 children; and triple therapy, 3 of 3 children. At long-term follow-up, the number of children with no H. pylori in antral biopsy specimens were as follows: monotherapy, 1 of 5; double therapy, 4 of 4; and triple therapy, 3 of 3. Of the noncompliant patients, only 1 of 5 had H. pylori eradication with combination therapy and none had H. pylori eradication with monotherapy. Duodenal ulcer disease had healed in all children with H. pylori-negative antral biopsy specimens at follow-up; duodenal ulcers recurred in all children with persistent or recurrent H. pylori infection. We conclude that therapy with two drugs for 6 weeks is the treatment of choice for endoscopically proved duodenal ulcer and histologically proved H. pylori antral gastritis, and that poor patient compliance reduces the rate of success. Our data strongly support a causal relationship between H. pylori and duodenal ulcer disease.

Adolescent↗
PubMed1993

Barrett's esophagus in children with cystic fibrosis: not a coincidental association.

Barrett's esophagus (BE) is a premalignant condition, and a recognized complication of severe gastroesophageal (GE) reflux. Children with cystic fibrosis (CF) have a marked predilection to develop GE reflux, but Barrett's esophagus is one complication of GE reflux not previously described in CF. We describe in detail two adolescents with CF who were found to have Barrett's esophagus, and mention three other cases. The presence of Barrett's esophagus in CF patients may be missed because GE reflux is often relatively silent in CF, because patients may consider mild upper gastrointestinal (GI) symptoms as "part of CF," and because of the nature of Barrett's epithelium itself. Upper gastrointestinal (GI) endoscopy with documentation of landmarks and multiple targeted biopsies should be performed in children with CF with even mild symptoms of GE reflux or an abnormal 24 h intra-esophageal pH study. Any biopsies containing columnar epithelium should be stained with Alcian blue at pH 2.5 to look for goblet cell metaplasia, i.e., Barrett's esophagus. Children with CF may be a high-risk group for development of Barrett's esophagus and its complications, especially given the increased survival in CF.

Adolescent↗
PubMed1993

Barrett's esophagus: new definitions and approaches in children.

BE is a disorder that occurs in children likely as a consequence of prolonged GE reflux of gastroduodenal contents. It usually presents with complications of GE reflux, but it also may be relatively silent in childhood and then present with adenocarcinoma in childhood or present in adulthood. Although seldom recognized in children until relatively recently, it is being diagnosed with greater frequency but not always accurately. The diagnosis of BE can be made with certainty only if landmarks are carefully documented, and a detailed histologic map is made from multiple, large biopsies taken under direct vision at endoscopy; the diagnosis should be reserved for those patients where Barrett's specialized epithelium i.e., goblet cell metaplasia, is present. BE is a diagnosis that should be made with thorough documentation because of the implications for regression, cancer, and the need for follow-up and endoscopic biopsy surveillance. For treatment of complications and because there may be a chance for regression of a young (i.e., childhood) lesion, antireflux surgery or indefinite aggressive acid suppressing medical therapy is required. Because bile reflux may have a pathogenic role in BE, and because of the proven benefits of surgery in producing partial regression and prevention of dysphagia and cancer in some patients, the author's preference at present is for surgery. For children who are poor candidates for surgery, long-term omeprazole should be used (159). Adenocarcinoma does occur in childhood as a complication of BE. Because it can be recognized early, regular surveillance of children with bona fide BE is advisable.

Adenocarcinoma↗
PubMed1993

Adenocarcinoma in childhood Barrett's esophagus: case documentation and the need for surveillance in children.

A 17-yr-old boy underwent esophagectomy for multifocal high-grade dysplasia and adenocarcinoma complicating Barrett's esophagus (BE). He is believed to be the first child or young adult to have prolonged healthy survival following resection of esophageal adenocarcinoma. Dysplasia in a short retained segment of his Barrett's mucosa appears to have regressed with acid-suppressing therapy. Of nine other reported cases of adenocarcinoma in young people 11-25 yr of age, all died. All had progressive dysphagia and an esophageal mass at presentation, unlike our patient who had only histologic evidence of cancer at presentation. This was found only after repeated and extensive biopsy of the esophagus. We conclude that adenocarcinoma does occur under age 25 yr as a complication of BE arising in childhood, and it may be curable if diagnosed early. Endoscopic surveillance with multiple stepwise biopsies, beginning at age 10 yr, is suggested in those few children who have BE with specialized mucosa and goblet cells.

Adenocarcinoma↗
PubMed1993

Barrett's esophagus: congenital or acquired?

Barrett's esophagus (BE) is a premalignant condition in which metaplastic specialized columnar epithelium with goblet cells is present in the tubular esophagus. BE is much more prevalent in adults than in children, but largely because of its occurrence in children, a congenital etiology for BE has been proposed by some. However, there is extensive, compelling evidence to indicate that Barrett's specialized metaplasia is an acquired disorder in children and adults, resulting from both a severe mucosal injury and an abnormal intraesophageal milieu during mucosal repair. Acid reflux has been emphasized as being the usual inciting and ongoing injurious factor, but more recently the additional importance of refluxed duodenal contents has been recognized. Despite recent advances in our understanding, it remains unclear why pathologic gastroesophageal reflux results in squamous esophagitis in some persons and Barrett's specialized metaplasia in others. Although the evidence cited for a purely congenital cause of BE can be readily refuted, a congenital component in combination with severe mucosal injury cannot be ruled out.

Adult↗
PubMed1992

Giardiasis mimicking inflammatory bowel disease.

An adolescent had marked systemic features suggestive of inflammatory bowel disease. Giardia lamblia trophozoites were present in endoscopic biopsy specimens from the terminal ileum and from the duodenum. His illness rapidly and completely resolved after metronidazole therapy. Giardiasis must be included in the differential diagnosis of inflammatory bowel disease in children.

Adolescent↗
PubMed1992

Familial inflammatory bowel disease in a paediatric population.

Familial aspects of inflammatory bowel disease (IBD) were assessed as part of an age and sex matched case control study of 91 children with IBD and 131 controls. The prevalence of IBD in family members of the children was studied, the affected side (mother's side or father's side) of the family was documented and the type of inflammatory bowel disease was traced among relatives. Data were collected from children in out-patient clinics at a large urban tertiary-care facility. All family data were verified with the affected relatives and/or their physicians. The children with IBD (the cases) had significantly (P = 0.0000385) more IBD in their families than the controls. Among all children with IBD in their family, IBD was found significantly (P = 0.0073) more often on the mother's side of the family than on the father's side. Patterns of disease varied within families. A mixture of ulcerative colitis and Crohn's disease was found within families. The implications of the findings are discussed. Directions for prevention, screening, early intervention and further study are given.

Adolescent↗
PubMed1992

Partial regression of childhood Barrett's esophagus after fundoplication.

A 12-yr-old boy presented with Barrett's esophagus, the nature and extent of which were thoroughly documented with multiple endoscopic biopsies. He had an excellent symptomatic response to antireflux surgery. Radiologic studies, esophageal manometry, and intraesophageal pH studies were performed before surgery and at intervals thereafter, and documented the success of antireflux surgery. Within 2 yr of surgery, there was endoscopic and histologic evidence of squamous regression of columnar mucosa, and this process of regression to squamous epithelium continued over a further 3 yr. This case suggests that partial squamous regression of Barrett's esophagus may occur in children. Studies dealing with regression are reviewed and proposals are made for a standardized approach to its documentation.

Barrett Esophagus↗
PubMed1992

Primary hemochromatosis in children: report of three newly diagnosed cases and review of the pediatric literature.

Hereditary hemochromatosis was diagnosed in three asymptomatic siblings following the unexpected finding of elevated serum iron concentrations. This diagnosis was confirmed by hepatic biopsy. Repeated phlebotomies resulted in a significant decline of serum iron and ferritin concentrations and a decrease of hepatic iron content. This report and a review of the literature indicate that the diagnosis of hereditary hemochromatosis must be considered more frequently in childhood. Organ dysfunction from iron overload may be minimized in children by the early commencement of regular phlebotomy.

Child↗
PubMed1991

Unique features of Helicobacter pylori disease in children.

In a six-year period, 41 children had endoscopically documented duodenal ulcer disease or primary H. pylori antral gastritis without duodenal ulcer. Of 37 children with H. pylori gastritis, group 1 comprised 23 patients with duodenal ulcer disease and group 2 had 14 patients without ulcers (primary H. pylori gastritis). Group 3 comprised four children with duodenal ulcer disease and H. pylori-negative antral biopsies. During the study period, all primary chronic ulcer disease was duodenal; no primary chronic gastric ulcer was present. Two distinct types of duodenal ulcer disease were identified; the majority (85%) was always associated with significant active H. pylori antral gastritis (group 1). The minority (15%) had virtually absent gastritis and no H. pylori (group 3). Native Indian children were represented in group 1 quite out of proportion to the referral population and had the most severe disease. While it is established that a higher prevalence of asymptomatic H. pylori infection exists in non-Caucasians, this appears to be the first demonstration of a higher prevalence of symptomatic ulcer disease in non-Caucasian children or adults. Caucasian children tended to have primary H. pylori gastritis (group 2) or duodenal ulcer without H. pylori (group 3). Antral nodularity was found to be an important specific endoscopic sign, unique to those children with H. pylori disease. It has not been described in adult H. pylori disease. Non-Caucasian children, especially Native Indians, in British Columbia have more prevalent and more severe H. pylori disease than Caucasians. Endoscopy with gastric antral biopsies is necessary to distinguish different types of duodenal ulcer disease and to diagnose primary H. pylori gastritis.

Adolescent↗
PubMed1990

Halothane hepatitis in children.

Halothane hepatitis is now a well-recognized distinct entity in adults, but there prevails an often-taught "axiom" that halothane hepatitis "does not occur" in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane-specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained high fevers for 10 days following a single halothane exposure. Gradually increasing cholestasis ensued in the absence of other causes of liver disease. Halothane antibodies were negative. These cases illustrate different clinical presentations of halothane hepatitis, such as delayed onset of jaundice or fever following halothane exposure. The difficulties in making a definitive diagnosis and the need to exclude other causes of liver disease are detailed. Risk factors and other presentations are discussed. While halothane hepatitis appears to be an uncommon entity in children, it does occur, and may present with manifestations less than fulminant hepatic failure. A high index of suspicion and a detailed history of the time sequence of events are necessary as the diagnosis is primarily clinical. Halothane-specific antibodies are helpful if positive. In any child developing unexplained jaundice or high fevers following halothane anesthesia, further exposures should be avoided and halothane-specific antibodies obtained.

Chemical and Drug Induced Liver Injury↗
PubMed1989

Sclerotherapy for extrahepatic portal hypertension in childhood.

Ten children with extrahepatic portal hypertension who had major bleeding from esophageal varices were treated with sclerotherapy of esophageal varices by means of flexible fiberoptic endoscopy and intravenous sedation. Four had had no previous therapy, five had had previous surgery for variceal bleeding, and five had received propranolol orally. During therapy and follow-up monitoring of 1.4 to 7.1 years (mean 4.7 years), only two patients bled again from esophageal varices, one before complete obliteration of varices and one who temporarily defaulted on follow-up. The few complications were easily managed, and only three required any specific therapy. No child bled from gastric varices. Frequency of sclerotherapy sessions and quantity of sclerosant could be decreased with time, usually after 3 years of sclerotherapy, suggesting that the natural history of decreased bleeding with time in extrahepatic portal hypertension may be accelerated by sclerotherapy. Esophageal varices in children with extrahepatic portal hypertension may be treated safely with sclerotherapy, which is effective in preventing chronic and recurrent gastrointestinal bleeding.

Adolescent↗