Celiac disease--a worldwide problem.

Celiac disease and dermatitis herpetiformis are caused by the alcohol soluble fractions of wheat, barley, and rye. Reliable serological tests are available for both mass and risk group screening and recent epidemiological studies on celiac disease suggest that the prevalence varies between 1:100-300 in different continents. The clinical manifestations of the disease has changed in the West and the classical symptomatic cases represent only approximately 1/7th of all diagnosed cases. Symptoms such as, anemia, short stature, dental enamel defect or osteoporosis can be the only manifestations of the atypical disease. There is an increased prevalence of celiac disease in patients with autoimmune diseases. Recent data suggest that there is a correlation between the prevalence of autoimmune diseases and the number of years that an individual consumes gluten-containing foods. Genetic studies revealed a high prevalence of certain HLA antigens in celiac patients, however, there is likelihood that non-HIA genes are also important in the pathomechanism. An interesting new development is the recognition of tissue transglutaminase (tTG), an enzyme that probably forms an autoantigen with gluten. It is generally accepted that antibodies to tTG are identical to the previously described antiendomysium antibodies. Whether or not tTG is responsible for the initiation of an immunoreaction against prolamines or just exacerbates the immune response is a subject of further investigations.

Isolated pancreatic amylase deficiency: probable error in maturation.

A boy with failure to thrive and isolated pancreatic amylase deficiency is described. Immunoprecipitation confirmed only salivary isoamylase in duodenal fluid at ages 20 and 33 months. Because normal pancreatic amylase messenger RNA was detected by reverse-transcriptase polymerase chain reaction in the fluid, failure of the normal maturation of pancreatic amylase secretion may explain the deficiency.

Increased susceptibility to Helicobacter pylori infection in pregnancy.

OBJECTIVE: Helicobacter pylori plays a major role in abdominal symptoms and gastroduodenal pathology, including gastric cancer. Pregnancy has been associated with changes in both humoral and cell-mediated immunity. These changes include alterations in the various classes of antibodies during different gestational periods. It has been previously suggested that these alterations may expose pregnant women to an increased risk of infection with this microorganism. METHODS: To further investigate this hypothesis, we assayed sera from 229 asymptomatic pregnant women for the presence of H.-pylori-specific immunoglobulin G (IgG) and immunoglobulin M (IgM) antibodies by means of a commercially available serum ELISA test (Malakit, Biolab, Belgium). Both tests were previously validated in large series of H.-pylori-positive and -negative subjects. While the presence of H.-pylori-specific IgG antibodies is only a marker for a "chronic" infection with this bacterium and therefore no indicator of the time of acquisition of the infection, specific IgM antibodies are a more specific marker for a recently acquired infection with H. pylori. Results were compared with those previously obtained in asymptomatic, healthy, nonpregnant individuals. RESULTS: One hundred twenty of 229 women (52.4%) and 55/118 nonpregnant subjects (46.6%) were seropositive for H.-pylori-specific IgG antibodies (P > 0.3). Out of these 120 IgG-antibody-positive women, 36 (30%) were positive for H.-pylori-specific IgM antibodies, as were 25/109 (22.9%) in the IgG-antibody-negative group (P > 0.3). Overall, 61/229 (26.6%) of the pregnant women had recently been infected with H. pylori, compared with 11% of the healthy, nonpregnant population (P > 0.01). CONCLUSIONS: Our observations confirm the possibility of an increased susceptibility to H. pylori infection in pregnancy. Additional studies are necessary to further understand the immune response to H. pylori in pregnancy.

Acute and chronic pancreatitis in childhood.

The incidence of acute and chronic pancreatitis in childhood is unknown. Both are associated with significant morbidity and mortality. The role of clinical suspicion is vital as these disorders can be misdiagnosed easily. Molecular basis of several disorders are being elicited and promising new diagnostic tests are being developed, including tests to assess fat malabsorption by non-invasive methods. Etiological spectrum of acute pancreatitis ranges from congenital, structural or inherited disorders to trauma, infections, drug toxicity and interventions such as endoscopic retrograde cholangiopancreatography and organ transplantation. Chronic tropical calculus pancreatitis is a progressive disorder that presents in childhood with recurrent abdominal pain, progressing to diabetes by puberty. Idiopathic recurrent pancreatitis has recently been associated with higher frequency of cystic fibrosis gene mutations. Therapeutic use of lexipafant opens the field to new powerful therapies designed to reduce the systemic inflammatory response syndrome and thus reduce the morbidity and mortality significantly.

Pediatric gastritis and peptic ulcer disease.

Inflammation of the gastric and duodenal mucosa is the end result of an imbalance between mucosal defensive and aggressive factors. The degree of inflammation and imbalance between defensive and aggressive factors can then result in varying degrees of gastritis and/or mucosal ulceration. Gastritis and ulcers of the duodenum or stomach can be classified as primary or secondary. The majority of children with chronic gastritis and ulcers in the stomach or duodenum have secondary inflammation or mucosal ulceration. These secondary ulcers generally occur due to a systemic condition like head trauma or overwhelming sepsis, or as sequelae to drug ingestion (i.e. non-steroidal anti-inflammatory agents), but secondary gastroduodenal ulcers can also occur in specific disease conditions such as Zollinger-Ellison syndrome or Crohn's disease. In almost all children with primary duodenal or gastric ulcers mucosal inflammation and, less frequently, ulceration is caused by a spiral shaped, gram-negative, microaerobic rod Helicobacter pylori. Recent epidemiological evidence has linked chronic H. pylori infection with the development of gastric carcinomas.

Chronic diarrhea in infancy and childhood.

Important inroads are being made into understanding the pathophysiology of acute diarrhea. Clear understanding of key mechanisms should suggest new approaches to combat disease. Exciting developments are occurring in terms of super-ORS solutions, particularly with the promise of short-chained glucose polymers and glutamine. Perhaps the most important development is the prospect of a good rotavirus vaccine being available before the end of the decade. Chronic diarrhea seems to be on the increase globally, probably because of the success of ORS. The mechanisms that lead to mucosal injury are elusive and therapy is still largely supportive and empiric. Celiac disease continues to be a puzzle, not least because of the uncomfortable feeling that a majority of cases may be being missed because of atypical presentations. The successful use of long-term parenteral nutrition has allowed survival and better characterization of cases that otherwise would have perished as "lethal protracted diarrhea". Microvillus inclusion disease may be the most common congenital secretory diarrhea. The role of the recently reported high prevalence of glucoamylase deficiency may be important. Lastly attention to micronutrients, particularly low vitamin A and probably zinc, may prove to be important in prevention and amelioration of diarrhea and growth failure.

Escherichia coli and the hemolytic-uremic syndrome.

BACKGROUND: The hemolytic-uremic syndrome (HUS) comprises hemolytic anemia, acute renal failure, and thrombocytopenia. It is the most frequent cause of acute renal failure in children. METHODS: This review is based on an extensive overview of the literature dealing with the HUS in children. RESULTS: HUS is the most common cause of acute renal failure in infants and young children and follows a diarrheal prodrome approximately 90% of the time. Nearly all postdiarrheal cases are caused by enterohemorrhagic E coli infections, in particular serotype O157:H7. Mortality is around 5%, and approximately 50% of survivors manifest some types of sequelae. CONCLUSION: Surveillance and contact investigation are important to control outbreaks, as well as early and aggressive treatment of symptomatic subjects to prevent mortality and severe complications, such as chronic renal disease.

Modified food starches in baby foods.

Modified food starches were developed as a stabilizer, providing desirable consistency, texture, and storage ability. They are used primarily in strained and junior foods and, to a minor extent, in infant formulas. However, despite the fact that there is an increasing tendency to introduce solid foods to infants at a very early age, there is few long-term studies to delineate the effect of starch feeding on the growth of young infants. Modified food starches used by the food industry for infants and young children are of concern and there is an urgent need for additional data regarding their bioavailability, effect on nutrient absorption, intestinal changes, and toxic, mutagenic, and carcinogenic effects. Therefore, the inclusion of modified food starches should be used prudently and sparingly.

Epidermal growth factor up-regulates sodium-glucose cotransport in enterocyte models in the presence of cholera toxin.

BACKGROUND: Sodium-glucose cotransport by enterocytes is key to the successful implementation of oral rehydration in diarrhea. Confluent, differentiated Caco-2 cells have enterocyte-like characteristics. We have previously shown that short-term incubation of isolated rat jejunal enterocytes with epidermal growth factor (EGF) results in the up-regulation of sodium-glucose cotransport. The aim of this study was to examine the effect of EGF on Caco-2 cells in the presence of cholera toxin. METHODS: Caco-2 cells grown on tissue culture dishes were used for glucose and sodium uptake studies and cells were grown on polycarbonate membranes for transport examinations. Effects of EGF on the kinetic parameters of sodium-glucose contransporter, thymidine transport, and on the activity of Na+/K(+)-ATPase were examined. The efficacy of basolateral vs apical EGF on sodium and glucose transport was compared after incubation of the monolayers with 10 nmol/L of cholera toxin. RESULTS: EGF increased both glucose and sodium uptake and transport, and we observed a simultaneous increase in the activity of Na+/K(+)-adenosine triphosphatase (ATPase). Kinetic studies performed on brush-border membrane vesicles prepared from EGF-incubated confluent monolayers and on intact cells showed an increase in the maximum velocity but not the Michaelis constant, suggesting increased availability of transporters rather than conformational change. This effect was seen within minutes in both of the two putative transporters, high-affinity, low-capacity and low-affinity, high-capacity. There was no acute effect on thymidine uptake. Studies in the presence of cholera toxin demonstrated a significant up-regulation in sodium-glucose cotransport when EGF was applied from the basolateral side; the increase was smaller but significant with apical application. CONCLUSIONS: Differentiated Caco-2 cells have two kinetically distinct sodium-glucose cotransporters. Short-term incubation of Caco-2 cells with EGF resulted in an up-regulation of sodium-glucose cotransport and subsequent increase in Na+/K(+)-ATPase activity. The effect of basolaterally applied EGF was more significant with or without incubation with cholera toxin. The early effect of EGF on glucose and sodium cotransport may have important therapeutic implications in diarrhea and dehydration states. The in vitro model described here uses a homogeneous cell population and provides a versatile system for uptake and transport studies.

The role of modified food starches in baby food.

Modified food starches were developed as a stabilizer, suspending the food particles and providing a desirable consistency, texture, and storage ability. They are used primarily in strained and junior foods and to a minor extent in infant formulas. This review discusses modified food starches because of four principal concerns. The first relates to the bioavailability of the starch itself. The second is the potential that indigestible starch may have for producing diarrheal symptoms, malabsorption, and changes in gastrointestinal flora. The third is the possibility that modified food starches might be implicated in gastrointestinal disease like Crohn's ileocolitis. The fourth is the toxicological effect of the chemicals used to modify the starch and their possible mutagenic and carcinogenic properties.

Diagnosis of Helicobacter pylori.

In view of its potential risk for the development of gastrointestinal disease or even gastric cancer at a later age, the study of Helicobacter pylori infection in childhood is gaining increasing importance and H. pylori infection is being considered a major issue of public health. H. pylori infection can be detected by a variety of methods. Because of its easy use, affordability, and overall availability, serology is the preferred diagnostic test, especially for large epidemiological studies. Based on our results, one might consider treating a child with recurrent abdominal pain and positive serology for H. pylori without further work-up, and only perform additional investigations when an anti-H. pylori therapy fails to resolve the complaints. According to this proposition, endoscopy of the upper gastrointestinal tract remains indicated in children if the noninvasive tests for Helicobacter pylori are negative in the absence of a diagnosis, or if symptomatology persists despite treatment.

Chronic diarrhea: causes, presentation, and management.

Important inroads are being made into understanding the pathophysiology of diarrhea. Clear understanding of key mechanisms should suggest new approaches to combat disease. Exciting developments are occurring in terms of super-ORS solutions, particularly with the promise of short chained glucose polymers and glutamine. Perhaps the most important development is the prospect of a good rotavirus vaccine being available before the end of the decade. Chronic diarrhea seems to be on the increase globally, probably because of the success of ORS. The mechanisms that lead to mucosal injury are elusive, and therapy still largely supportive and empiric. Celiac disease continues to be a puzzle, because of the uncomfortable feeling that a majority of cases may be missed because of atypical presentations. The successful use of long term parenteral nutrition has allowed survival and better characterization of cases that otherwise would have perished as 'lethal protracted diarrhea'. Microvillus inclusion disease may be the commonest congenital secretory diarrhea. The role of the recently reported high prevalence of glucoamlase deficiency may be important. Lastly, attention to micronutrients, particularly low vitamin A and probably zinc may prove to be important in prevention and amelioration of diarrhea and growth failure.

Presentation and management of Helicobacter pylori infection in childhood.

Helicobacter pylori is responsible for one of the most frequently encountered infectious diseases worldwide. Helicobacter pylori infection can lead to the development of gastritis and peptic ulcer disease. The presence of Helicobacter pylori in the human stomach also represents an increased risk of gastric cancer and gastric lymphoma. Epidemiological data obtained in adults suggest that the actual colonization with Helicobacter pylori is in fact determined by childhood factors. Therefore, the pediatric age group represents the ideal target population for studies concerning the pathogenesis and epidemiology of Helicobacter pylori infection. The present work reflects our experience with regard to the diagnosis, epidemiology and pathogenesis of Helicobacter pylori infection in childhood.

Serology as a valid screening test for Helicobacter pylori infection in asymptomatic subjects.

Serologic testing is generally accepted as a valid noninvasive screening method for the detection of a Helicobacter pylori infection. To validate serology as an appropriate screening test for H pylori infection in symptom-free subjects, a recent-generation enzyme-linked immunosorbent assay for the detection of H pylori-specific IgG was performed in a large series of asymptomatic women. Blood samples for H pylori serology were taken from 542 apparently healthy women (aged 20 to 40 years) during prenatal screening. In this group, 120 (22.1%) had a positive titer for H pylori. We observed a significantly higher overall prevalence of H pylori seropositivity in nonwhites (62.3%) when compared with Belgian-born whites (17.8%). In both groups there was a significant increase in seropositivity with increasing age. To investigate the correlation between a positive enzyme-linked immunosorbent assay and the actual presence of an active H pylori infection, carbon 13-labeled urea breath tests were performed in 85 seropositive and in 65 randomly selected seronegative subjects. These breath tests were positive in 82 (96.5%) of 85 seropositive and in none of the seronegative subjects, reflecting an actual presence of H pylori in the gastric mucosa of the seropositive women. We conclude that in our population of H pylori-seropositive subjects positive serologic findings correlates extremely well with an active infection with this bacterium. However, because all subjects who were investigated were actually symptom-free, it still should be determined whether these patients should undergo upper gastrointestinal endoscopy and/or be treated with an eradication therapy against H pylori. Further long-term follow-up studies will be required to answer this question.