Congenital diseases of the gastrointestinal tract.

With the rapid increase in knowledge on the genetic origin of diseases within the gastrointestinal tract the number of congenital diseases, which already manifest during childhood have drastically increased. Due to the large application of molecular genetics the number is steadily increasing. To make the access to these rare diseases fast and efficient the data base of the National Library of Medicine (Online Mendelian Inheritance of Man - OMIN) is a very helpful online tool, with which all these disease entities can be found easily (http://www.ncbi.nlm.nih.gov/omim). Detailed tables are given to find most of the congenitally inherited disease, which affect the gastrointestinal tract. A variety of congenital diarrheas with disturbances of digestion, hydrolysis, absorption and secretion is described in detail: lactose intolerance, sucrose intolerance, glucose-galactose malabsorption, fructose malabsorption, trehalase and enterokinase deficiency, congenital chloride and sodium diarrhea, congenital hypomagnesaemia, primary bile acid malabsorption, acrodermatitis enteropathica and Menke's syndrome. Also described in detail are diseases with structural anomalies of the intestine like microvillous inclusion disease, congenital tufting enteropathy and IPEX syndrome. The diagnosis in the disturbances of carbohydrate hydrolysis or absorption can be established by H2-breath tests after appropriate sugar challenge. Treatment consists of elimination of the responsible sugar from the diet. The diagnosis of the congenital secretory diarrheas is established by investigation of electrolytes in blood and stool. Substitution of high doses of the responsible mineral can improve the clinical outcome. In acrodermatitis enteropathica low serum zinc level together with the typical skin lesions guide to the diagnosis. High doses of oral zinc aspartate can cure the symptoms of the disease. The diagnosis of structural congenital lesions of the intestine can be established by histology and/or electron microscopy and molecular identification of the responsible mutations. The treatment of these diseases is difficult and therefore the prognosis remains poor. Immunosupressive therapy, total parenteral nutrition and even intestinal or bone marrow transplantation are the only choice for treatment.

Transforming growth factor ß1 genotypes in relation to TGFß1, interleukin-8, and tumor necrosis factor alpha in induced sputum and blood in cystic fibrosis.

BACKGROUND: High-producer TGFß1 genotypes are associated with severe lung disease in cystic fibrosis (CF), but studies combining IL-8, TNFα-, and TGFß1(+genotype) levels and their impact on CF lung disease are scarce. AIM: Assessing the relationship between TGF ß 1, IL-8, and TNF- α and lung disease in CF in an exacerbation-free interval. METHODS: Twenty four patients delta F508 homozygous (median age 20.5 y, Shwachman score 75, FEV1(%) 83) and 8 controls (median age 27.5 y) were examined. TGF ß 1 was assessed in serum and induced sputum (IS) by ELISA, for IL-8 and TNF- α by chemiluminescence in IS and whole blood. Genotyping was performed for TGF ß 1 C-509T and T+869C utilizing RFLP. RESULTS: TGF ß 1 in IS (CF/controls median 76.5/59.1 pg/mL, P < 0.074) was higher in CF. There was a negative correlation between TGF ß 1 in serum and lung function (LF) (FEV1 (r = -0.488, P = 0.025), MEF 25 (r = -0.425, P = 0.055), and VC (r = -0.572, P = 0.007)). Genotypes had no impact on TGF ß 1 in IS, serum, and LF. In IS TGF ß 1 correlated with IL-8 (r = 0.593, P < 0.007) and TNF- α (r = 0.536, P < 0.018) in patients colonized by bacteria with flagellin. CONCLUSION: TGF ß 1 in serum not in IS correlates with LF. In patients colonized by bacteria with flagellin, TGF ß 1 correlates with IL-8 and TNF- α in IS.

[Transient splenial lesion in influenza A H1N1 2009 infection]. / Transiente Spleniumläsion bei Influenza-A-H1N1-09-Infektion.

Severe neurologic complications have been rarely reported during novel pandemic influenza A(H1N1) virus infections. We describe the case of an 10-year-old boy with new onset seizures and proven influenza A(H1N1) 2009 infection showing a reversible hyperintense lesion in the splenium of the corpus callosum on T2-weighted and FLAIR magnetic resonance images without contrast enhancement. Transient splenial lesions have been described in the context of virus encephalopathy and do not require specific treatment.

Immunocytochemical demonstration of ecto-galactosyltransferase in absorptive intestinal cells.

Galactosyltransferase immunoreactive sites were localized in human duodenal enterocytes by the protein A-gold technique on thin sections from low temperature Lowicryl K4M embedded biopsy specimens. Antigenic sites detected with affinity-purified, monospecific antibodies were found at the plasma membrane of absorptive enterocytes with the most intense labeling appearing along the brush border membrane. The lateral plasma membrane exhibited a lower degree of labeling at the level of the junctional complexes but the membrane interdigitations were intensely labeled. The labeling intensity decreased progressively towards the basal part of the enterocytes and reached the lowest degree along the basal plasma membrane. Quantitative evaluation of the distribution of gold-particle label proved its preferential orientation to the outer surface of the plasma membrane. In addition to this membrane-associated labeling, the glycocalyx extending from the microvillus tips was heavily labeled. Occasionally, cells without plasma membrane labeling were found adjacent to positive cells. The demonstration of ecto-galactosyltransferase on membranes other than Golgi membranes precludes its general use as a marker for Golgi membrane fractions. The possible function of galactosyltransferase on a luminal plasma membrane is unclear at present, but a role in adhesion appears possible on the basolateral plasma membrane.

Sucrase-isomaltase deficiency in humans. Different mutations disrupt intracellular transport, processing, and function of an intestinal brush border enzyme.

Eight cases of congenital sucrase-isomaltase deficiency were studied at the subcellular and protein level with monoclonal antibodies against sucrase-isomaltase. At least three phenotypes were revealed: one in which sucrase-isomaltase protein accumulated intracellularly probably in the endoplasmic reticulum, as a membrane-associated high-mannose precursor, one in which the intracellular transport of the enzyme was apparently blocked in the Golgi apparatus, and one in which catalytically altered enzyme was transported to the cell surface. All patients expressed electrophoretically normal or near normal high-mannose sucrase-isomaltase. The results suggest that different, probably small, mutations in the sucrase-isomaltase gene lead to the synthesis of transport-incompetent or functionally altered enzyme which results in congenital sucrose intolerance.

Biogenesis of intestinal lactase-phlorizin hydrolase in adults with lactose intolerance. Evidence for reduced biosynthesis and slowed-down maturation in enterocytes.

Enzymatic activity, biosynthesis, and maturation of lactasephlorizin hydrolase (LPH) were investigated in adult volunteers with suspected lactose intolerance. Mean LPH activity in jejunal biopsy homogenates of these individuals was 31% compared to LPH-persistent individuals, and was accompanied by a reduced level of LPH-protein. Mean sucrase activity in individuals with low LPH was increased to 162% and was accompanied by an increase in sucrase-isomaltase (SI)-protein. Biosynthesis of LPH, SI, and aminopeptidase N (APN) was studied in organ culture of small intestinal biopsy specimens. In individuals with LPH restriction, the rate of synthesis of LPH was drastically decreased, reaching just 6% of the LPH-persistent group after 20 h of culture, while the rate of synthesis of SI appeared to be increased. In addition, maturation of pro-LPH to mature LPH occurred at a slower rate in LPH-restricted tissue. Immunoelectron microscopy revealed an accumulation of immunoreactive LPH in the Golgi region of enterocytes from LPH-restricted individuals and reduced labeling of microvillus membranes. Therefore, lactose intolerance in adults is mainly due to a decreased biosynthesis of LPH, either at the transcriptional or translational level. In addition, intracellular transport and maturation is retarded in some of the LPH-restricted individuals, and this leads to an accumulation of newly synthesized LPH in the Golgi and a failure of LPH to reach the microvillus membrane.

Dysphagia due to triple A syndrome: successful treatment of achalasia by balloon dilatation.

UNLABELLED: Triple A syndrome is a rare autosomal recessive inherited disorder which is characterized by alacrima, adrenal insufficiency, and achalasia. We report on a 14-year old girl with dysphagia, regurgitation, and vomiting since 5 years. At the age of five years an Addison crisis was diagnosed and cortisone substitution was initiated. In addition, the patient had episodes of conjunctivitis. Severe esophagitis and candida infection were diagnosed by esophago-gastro-duodenoscopy and treated with omeprazole and fluconazole. The esophageal barium swallow was typical for achalasia. Medical treatment of achalasia with oral nifedipine resulted only in a partial and temporal improvement. But after seven balloon dilatations dysphagia and nocturnal coughing improved clearly and a remarkable gain of weight could be seen. Direct sequencing showed a homozygous nonsense mutation in exon 11 of the AAAS gene leading to truncation at position 342 of the 546 amino acid protein. CONCLUSION: Triple A syndrome has to be considered in patients with dysphagia. In our patient, the absence of tears since birth followed by adrenal insufficiency were early signs of the triple A syndrome. Balloon dilatation of the esophago-gastric junction is an effective treatment, which can avoid surgical interventions.

Metabolism of glycosyl ureides by human intestinal brush border enzymes.

13C-labeled glycosyl ureides were recently proposed as a new marker of the orocecal transit time: after passing the small bowel the sugar-urea bond is split by bacterial allantoicase. Further degradation results in 13CO2 which can be measured in the exhaled breath. The aim of this study was to detect an eventual allantoicase-like activity in the human gut and to elucidate the metabolism of glycosyl ureides by human intestinal brush border enzymes. Biopsies of 15 duodenal specimen and 6 colon specimen were homogenised and incubated with several disaccharides and their corresponding disaccharide ureides under various experimental conditions. Hydrolysis of the sugar-urea bond could not be observed neither in the small bowel nor in the colon. However, the conjugation between the two sugars was split. In a modified Dahlqvist assay lactase showed the same kinetics with lactose and lactose ureide as substrates whereas maltose showed a significantly 2.6-fold higher affinity to maltase than maltose ureide (P < 0.001). No major difference between these two substrates could be detected when total maltase activity was inhibited by acarbose. In summary, the human gut tissue possesses no allantoicase-like activity. Therefore, glycosyl ureides seem to be appropriate substances to test the orocecal transit time.

Molecular and cellular aspects of hydrolysis and absorption.

Digestion and hydrolysis of macronutrients by the gastrointestinal tract are required to provide substrates for absorption and subsequent utilization. Carbohydrates are hydrolyzed by brush border enzymes of the small intestine, leading to monosaccharides that are then absorbed across the microvillus membrane by specific transport proteins. During development, the activities of disaccharidases and glucose transporters evolve in a similar time sequence, which is subject to individual regulation. Biosynthesis of disaccharidases involves initial synthesis of enzyme precursor molecules, followed by post-translational modification and intracellular trafficking. Various patterns of genetic defects of disaccharidases have been described, involving defects in enzyme synthesis, alterations in intracellular transport, and catalytically altered apoenzyme. The absorption of specific monosaccharides is facilitated by different transport proteins, with glucose using the sodium-dependent glucose transporter. A steady supply of monosaccharides, derived from varying nutritional sources, is assured by the interplay between sugar hydrolases and transport proteins within the microvillar membrane of the enterocyte in association with amino acid transport proteins.

Whole-body cesium 137 activity up to 4 years after the Chernobyl reactor accident in premature newborns, newborns, infants, and children.

Cesium 137 activity was measured after the Chernobyl incident in a whole-body radiation counter (4-pi-scintillation counter) in 85 premature and mature newborns (group 1), 174 infants and young children up to 2 11/12 years (group 2), and 48 children between 3 and 8 years (group 3) from Bonn (Germany) and surroundings. In 1987 the mean level of radioactivity in group 2, at 3.7 Bq/kg body weight corresponding to a mean radiation exposure of 11 muSv/y, was lower than that of group 1 (5.8 Bq/kg, 17 muSv/y) and 3 (9.4 Bq/kg, 28 muSv/y). Up to 1990 the values of all groups revealed a continuous decrease. The latest measurements showed mean values of 0.5 Bq/kg (1.5 muSv/y) in group 1, 0.6 Bq/kg (1.8 muSv/y) in group 2, and 0.8 Bq/kg (2.4 muSv/y) in group 3. A comparison with present cesium 137 values and determinations of the end of the 1950s and beginning of 1960s, both in adults, showed good agreement. The effective dose-equivalent rates amounted to less than 1% of that from natural radiation exposure. These levels should present no teratogenic risks to the population studied and, while there are theoretical mutagenic risks, the dose is so low that no increase in measurable mutagenic effects should be observed.

Cisapride reduces postoperative gastrocaecal transit time after cardiac surgery in children.

OBJECTIVE: To investigate the influence of the prokinetic drug cisapride on gastrocaecal transit time (GCTT) in children after open heart surgery. DESIGN: Prospective, randomized and controlled study. SETTING: Interdisciplinary paediatric intensive care unit in a tertiary-care children's hospital. PATIENT: Twenty-one children with a median age of 6.2 years on day 1 after uncomplicated open heart surgery for isolated septal defects, acquired mitral or aortic valve disease or tetralogy of Fallot. Control group consisting of 10 healthy children with a median age of 8.1 years. INTERVENTIONS: Ten children were randomized to receive cisapride 0.2 mg/kg body weight, 30 min prior to measurement of GCTT. MEASUREMENTS AND RESULTS: GCTT was measured using hydrogen breath testing with a test solution containing lactulose and mannitol (0.4 g/kg and 0.1 g/kg body weight respectively). GCTT was markedly delayed in all patients compared to the control group. Within 8 h 8/10 patients in the treatment group versus 4/11 patients in the non-cisapride group achieved gastrocaecal transit. No adverse side-effects were observed. CONCLUSIONS: Cisapride accelerates gastrocaecal transit after open heart surgery in children. In intensive care patients on inotropic support or opioid medication, it may facilitate the earlier reintroduction of enteral feeding.

Association analysis between a regulatory-promoter polymorphism of the human monoamine oxidase A gene and idiopathic generalized epilepsy.

Monoaminergic neurotransmission plays an important role in the regulation of neuronal network excitability and seizure activity. Therapeutic inhibition of the mitochondrial enzyme monoamine oxidase A (MAO-A), which is involved in the degradation and inactivation of monoaminergic neurotransmitters, has been shown to confer a potent anticonvulsant effect. These and other findings suggest a possible role of the X-linked MAO-A gene in epileptogenesis. Therefore, our study was designed to test for an association between a novel MAO-A gene promoter polymorphism and common subtypes of idiopathic generalized epilepsy (IGE). The length of a 30-bp repetitive sequence approximately 1.2 kb upstream of the ATG initiation codon was assessed in 126 patients with juvenile myoclonic epilepsy (JME), 122 patients with idiopathic absence epilepsy (IAE), and 248 healthy controls of German descent. Both sexes were analyzed separately. Although we observed a trend towards a lower number of heterozygotes carrying the 3 and 4 copy alleles in female IAE patients (chi2 = 3.813, df = 1, P = 0.053), allele frequencies did not deviate significantly between patients and controls. Thus, our results do not provide evidence for a contribution of the functional MAO-A gene promoter polymorphism to the pathogenesis of common IGE subtypes.

The beta2-microglobulin/cystatin C ratio--a potential marker of post-transplant lymphoproliferative disease.

BACKGROUND: As a consequence of more intensified immunosuppression, post-transplant lymphoproliferative disease (PTLD) is increasingly observed in patients after solid-organ transplantation. Beta2-microglobulin, a low-molecular weight protein (MW 11.8 kDa), is produced by all nucleated cells as part of the HLA complex. Its serum concentration is directly correlated with prognosis in patients with lymphatic neoplasms. Like other low-molecular weight proteins, beta2-microglobulin is eliminated by glomerular filtration. This complicates its use as a tumor marker in renal insufficiency. Cystatin C, a low-molecular weight protein of 13.3 kDa, is a new marker of kidney function largely unaffected by extrarenal disease. We, therefore, sought to assess the potential of the beta2-microglobulin/cystatin C ratio (beta2M/Cys) as a marker of lymphoproliferation. PATIENTS AND METHODS: Beta2M/Cys was determined by particle-enhanced immunonephelometry in sera from 132 children with different degrees of renal insufficiency, 5 of whom had lymphoproliferative disease. Renal function was assessed using the Schwartz formula. RESULTS: Beta2M/Cys was constant between 1.2 and 2.4 mg/mg for Schwartz GFR > or = 40 ml/min x 1.73 m2. With lower GFR, beta2M/Cys rose progressively, maximum values being found in the hemodialysis patients (4.85-11.73). Healthy renal transplant recipients had beta2M/Cys comparable to controls. With acute lymphoproliferative disease, all but one patient had significantly elevated beta2M/Cys between 2.68 and 3.68 mg/mg, which returned to normal in remission (1.67-2.35 mg/mg). The sensitivity of a beta2M/Cys ratio > 2.4 mg/mg for the detection of PTLD was 80%, the specificity 100%, positive predictive value 100%, negative predictive value 90%. CONCLUSION: The beta2-microglobulin/cystatin C ratio is a promising parameter of lymphoproliferation in patients with normal or mildly impaired renal function.

Transient abnormal neurologic signs (TANS) in a longitudinal study of very low birth weight preterm infants.

OBJECTIVE AND METHODS: In the Bonn Longitudinal Study (BLS), the course of neurologic development was analysed with regard to transient abnormal neurologic signs (TANS). Abnormal neurologic signs (ANS) are defined when present in at least one developmental area at one examination. From birth to adulthood (mean 23 years) 108 preterm infants, 81% of very low birth weight (VLBW) were examined with regard to their psychological, neurologic and physical development: 62 appropriate for gestational age (AGA), 46 small for gestational age (SGA), 27 with postnatal catch-up growth of head circumference (group A) and 19 without catch-up (group B); 73 full terms served as controls. The dropout rate was 7.6%. RESULTS: ANS showed a great inter- and intraindividual variability. Episodes of neurologic abnormalities changed with those of normality. ANS reappeared when new abilities developed. ANS were observed mainly during the first year. The incidence was higher in preterms (AGA 49%, SGA A 63%, SGA B 61%) than in full terms (15%). Transient ANS (TANS) were diagnosed in 42% of AGA, 63% of SGA A, 33% of SGA B preterms and 12% of full terms. The recovery rate, i.e., the TANS to ANS percentage, was higher in AGA (86%), SGA A (100%) and full terms (82%) than in SGA B (55%) preterms. CONCLUSION: It is impossible to predict early on whether ANS will be transient, i.e. TANS. Longitudinal analyses are needed. The outcome depends on recovery from or persistence in ANS.

Secretion of 13C-labelled oligosaccharides into human milk and infant's urine after an oral [13C]galactose load.

Human milk oligosaccharides seem to play an important role in the infant's defense against bacterial and viral infections of the gastrointestinal and the urogenital tract. In this study, we investigated the influence of dietary carbohydrates on the biosynthesis of lactose and oligosaccharides in the human mammary gland and their renal excretion by the human milk-fed infant. For this purpose, a lactating woman was given 27 g galactose (Gal) containing 2 g [13C] Gal (1-13C/99%) immediately after breakfast. In the following 36 h, milk (5-10 ml) was collected before each nursing. Infant's urine was collected over a period of 24 h. 13C-enrichment was measured in total milk, milk fat and protein, in the carbohydrate fraction as well as in urine by isotope ratio mass spectrometry (IRMS). Milk carbohydrates and deproteinized urine samples were fractionated by Sephadex G25 gel filtration and further analyzed by IRMS, high performance thin layer chromatography and and high pH anion exchange chromatography with pulsed amperometric detection (HPAEC-PAD). IRMS revealed that in milk a maximal delta 13CPDB was reached within 8 h after Gal intake which then rapidly declined in the following 8 h. The cumulative 13C-elimination over this first peak was 6.9% of the oral 13C-dose. The highest 13C-enrichment was detectable in the carbohydrate fraction, mainly in lactose and neutral oligosaccharides. Compared to the enrichment of human milk, the delta 13CPDB of infant's urine was delayed. In urine, the highest amount of 13C was found in the Sephadex G25 fractions which mainly contained lactose, fucosyl-lactose, lacto-N-tetraose (LNT), fucosyl-LNT and difucosyl-LNT. For further characterization, individual components were separated by HPAEC-PAD and subsequently analyzed by fast atom bombardment mass spectrometry and IRMS. The data show, that orally applied Gal is incorporated in milk, especially in lactose and neutral oligosaccharides. Obviously, some of these components were absorbed by the infant and then excreted with urine. There, oligosaccharides may serve as analogous receptors for bacterial or viral adhesion molecules, and, hence, may prevent urogenital infections in breastfed infants.

[Food allergies]. / Nahrungsmittelallergien.

Food allergy in childhood presents with different clinical manifestations depending on the age of the affected child. Whereas toddlers and children with food allergy or pseudo-allergy present with similar symptoms as adults, two different forms have been identified in the newborn and infant period. One can occur as allergic colitis in breast or bottle fed infants. In breast fed infants the bloody mucoid stools are produced because of an allergic reaction of the colonic mucosa to foreign proteins which are delivered to the baby via breast milk. In bottle fed infants the given foreign protein itself can trigger the allergic reaction. The clinical, endoscopical and histological appearance is similar to that of ulcerative colitis. Elimination of foreign proteins from the diet of the mother or in bottle fed infants from the child is the therapy of choice. The second manifestation of food allergy in this age group is the cow's milk protein intolerance with predominantly gastrointestinal symptoms such as vomiting, diarrhea and failure to thrive. The diagnosis is based on the clinical picture alone. The usual laboratory tests don't discriminate enough and can therefore not confirm the diagnosis. Elimination of the affecting protein and replacement by a semi-elementary diet are recommended for therapy. The prevention of allergies by dietetic means has become of great importance since it was possible to identify newborns at risk for allergies. The prolonged breast feeding and the late introduction of solids later than the sixth month of life is the preventive measure. "Hypoallergenic" formulae are not recommended because not enough solid data are available to confirm their preventive effect.

Influence of 16,16-dimethyl prostaglandin E2 on morphology and brush border enzymes of small-bowel mucosa. Differences in reactivity between adult and suckling rats.

High doses of 16,16-dimethyl prostaglandin E2 (dmPGE) are trophic to the small bowel of adult and suckling rats. In suckling rats this effect is paralleled by an increase in brush border enzyme activities, possibly indicating accelerated mucosal maturation. To investigate the possible physiological significance of this phenomenon, we examined whether this induction of intestinal enzyme activities can be reproduced in adult rats and whether cell growth and enzyme activity might be suppressed by indomethacin. Treatment twice daily for 2 weeks with 100 micrograms/kg dmPGE by intragastric instillation increased villus length in the proximal and distal small bowel by 36% and 40%, respectively, while 2 mg/kg indomethacin by subcutaneous injection had no effect. Maltase, trehalase, lactase, and sucrase activities were unchanged after dmPGE or indomethacin. [3H]-thymidine incorporation into DNA was not significantly influenced for up to 24 h after a single dose of both 100 micrograms/kg PGE intragastrically or 10 mg/kg indomethacin subcutaneously. These studies confirm that in adult rats large doses of 16,16-dm PGE2 increase the volume of the small-bowel mucosa. In contrast to the situation in suckling rats, the activity of hydrolytic brush border enzymes is not increased. There is thus no evidence that endogenous prostaglandins are trophic or influence brush border enzymes in the adult rat.

16,16-Dimethyl prostaglandin E2 stimulates growth and maturation of rat gastric and small-intestinal mucosa.

In adult rats topical application of 16,16-dm PGE2 (PGE) every 8 h for three weeks led to a dose-dependent increase of the height of the gastric and duodenal mucosa, especially pronounced in the antrum (+115% with the high dose). In the gastric corpus this resulted from an enlargement of the lamina propria and the epithelial cell mass, the latter mainly from a hyperplasia of the surface and foveolar mucous cells. In contrast, the number of parietal cells was not affected. These findings were corroborated by the observation that an increase of antral mucosal height was also induced by a similar parenteral PGE treatment regimen (dosage 25 micrograms/kg). Both longterm intragastric and intraperitoneal PGE treatment led to an increase in DNA synthesis within the mucosa of the gastric antrum and corpus by 19 to 74%. In a third study 25 or 100 micrograms/kg of PGE applied every 8 h intragastrically to 10 suckling rats from the 7th to 11th postnatal day resulted in a dose-dependent increase in the length of the villi and the disaccharidase activities (30-630%). These studies suggest that 16,16-dm PGE2 exhibits a trophic effect on both the stomach and the small bowel.

Both topical and systemic treatments with 16,16-dimethyl prostaglandin E2 are trophic to rat gastric mucosa.

As shown in a previous study, intragastric administration of 16,16-dimethyl prostaglandin E2 (PGE, 100 micrograms/kg t.i.d.) for three weeks induces growth of the gastric mucosa. The present experiments were designed to study the time course of histological changes after intragastric PGE and to test whether a similar effect could be observed after parenteral administration. Significant thickening of the corpus, but not the antral mucosa was observed after 3 days of intragastric treatment with PGE (100 micrograms/kg t.i.d.), whereas after three weeks the effect was more marked in the antrum than in the corpus. At a dose of 25 micrograms/kg t.i.d., intraperitoneal PGE increased the height of antral mucosa to a similar degree as seen after intragastric treatment. DNA synthesis as assessed by autoradiography after administration of 3H-thymidine at the end of the three week PGE treatment was increased both in the gastric corpus and antrum. Preliminary studies in suckling rats provide evidence that intragastric administration of PGE (100 micrograms/kg t.i.d.) from day 7 to 11 accelerates maturation of the gastric mucosa. It is concluded that thickening of gastric mucosa can be induced by both local and systemic administration of PGE and is due, at least in part, to increased proliferation of gastric mucosal cells.

[Vegetarian and outsider diets in childhood]. / Vegetarische Ernährung und Aussenseiterdiäten im Kindesalter.

Nutrition of children on vegetarian diet is considered to be adequate and well-balanced when the diet contains dairy products and eggs. A severe or strict vegetarian diet (i.e. vegan or macrobiotic diet) is not suitable for babies or infants. Serious deficiency-states have been described after such regimens i.e. rickets, osteoporosis, anemia and growth retardation. Under ovo-lacto-vegetarian diets growth- and weight-measurements at regular intervals are recommended over the first two years of life. Critical food-components in vegetarians are: energy, protein, calcium, vitamins D and B12 and iron. An ovo-lacto-vegetarian diet provides an adequate supply with these substances with the exception of iron. A benevolent information about eventual deficiency states by the physician aids in keeping children thriving well and assures parents that their children will not incur damages.