Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GLUTEN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1998

Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia.

BACKGROUND: Ataxia is the commonest neurological manifestation of coeliac disease. Some individuals with genetic susceptibility to the disease have serological evidence of gluten sensitivity without overt gastrointestinal symptoms or evidence of small-bowel inflammation. The sole manifestation of disease in such patients may be ataxia. We describe the clinical, radiological, and neurophysiological features of this disorder. METHODS: Patients with ataxia attending the neurology outpatient clinics at the Royal Hallamshire Hospital, Sheffield, UK, were screened for gluten sensitivity as shown by the titre of antibody to gliadin. Those with other causes of ataxia were excluded. We carried out clinical, neurophysiological, neuroradiological, and, in two cases, neuropathological examinations. FINDINGS: 28 patients with gluten ataxia were identified. All had gait ataxia and most had limb ataxia. Those with more severe gait ataxia had longer disease duration. No patient had tremor or other extrapyramidal features. 19 patients showed some form of peripheral neuropathy on neurophysiological examination. 16 patients had no gastrointestinal symptoms. Distal duodenal biopsy showed lymphocytic infiltration in two patients, and changes compatible with coeliac disease in 11. Six patients had evidence of cerebellar atrophy on magnetic-resonance imaging. Necropsy was done on two patients who died; there was lymphocytic infiltration of the cerebellum, damage to the posterior columns of the spinal cord, and sparse infiltration of the peripheral nerves. INTERPRETATION: Gluten sensitivity is an important cause of apparently idiopathic ataxia and may be progressive. The ataxia is a result of immunological damage to the cerebellum, to the posterior columns of the spinal cord, and to peripheral nerves. We propose the term gluten ataxia to describe this disorder.

Adult↗
PubMed2001

Tyrosine cross-links: molecular basis of gluten structure and function.

The formation of the large protein structure known as "gluten" during dough-mixing and bread-making processes is extremely complex. It has been established that a specific subset of the proteins comprising gluten, the glutenin subunits, directly affects dough formation and breadmaking quality. Glutenin subunits have no definitive structural differences that can be directly correlated to their ability to form gluten and affect dough formation or breadmaking quality. Many protein structural studies, as well as mixing and baking studies, have postulated that disulfide bonds are present in the gluten structure and contribute to the process of dough formation through the process of disulfide-sulfhydryl exchange. Evidence presented here indicates that tyrosine bonds form in wheat doughs during the processes of mixing and baking, contributing to the structure of the gluten network. The relative contributions of tyrosine bonds and disulfide--sulfhydryl interchange are discussed.

Amino Acids↗
PubMed2001

Protein-enriched spaghetti fortified with corn gluten meal.

Spaghetti was prepared by replacing either 5 or 10% semolina or farina with corn gluten meal, a high-protein fraction from the wet milling of corn, to increase the protein content of pasta. Spaghetti fortified with corn gluten meal had a similar cooked weight and cooking loss but was less firm compared with the control. The overall flavor quality score of the spaghetti decreased with the increasing additions of either water-washed, water/ethanol-washed or regular corn gluten meal because of the higher intensity of the fermented flavor. Spaghetti with acceptable quality can be prepared with 5% water/ethanol-washed corn gluten meal, thereby improving its nutritional value while providing an additional market for corn gluten meal.

Cooking↗
PubMed1997

Gluten-free diet normalizes mouth-to-cecum transit of a caloric meal in adult patients with celiac disease.

The mechanisms responsible for bowel disturbances in celiac disease are still relatively unknown. Recent reports suggested that small bowel motor abnormalities may be involved in this pathological condition; however, there are no studies addressing small bowel transit in celiac disease before and after a gluten-free diet. We studied the mouth-to-cecum transit time of a caloric liquid meal in a homogeneous group of celiac patients presenting with clinical and biochemical evidence of malabsorption and complaining of diarrhea. Sixteen patients were recruited and investigated by means of hydrogen breath test through ingestion of 20 g lactulose together with an enteral gluten-free diet formula. A urinary D-xylose test was also done in each patient. Both breath tests and D-xylose tests were carried out basally and after a period of gluten-free diet. Twenty healthy volunteers were recruited as a control group and underwent the same breath testing. At the time of the diagnosis, mouth-to-cecum transit time was significantly prolonged in celiacs with respect to controls (243 +/- 10 vs 117 +/- 6 min, P = 0.0001). The D-xylose test was also abnormal (average urinary concentration 2.8 +/- 0.25 g, normal values >4.5). No correlation was found in patients between mouth-to-cecum transit time and urinary D-xylose output (r = 0.22). After the gluten-free diet period, mouth-to-cecum transit time in celiacs was significantly reduced compared to prediet transit (134 +/- 8 vs 243 +/- 10 min, P = 0.0001) and did not show statistical difference when compared to that found in controls (P = 0.1). The D-xylose test reverted to normal in all but two subjects, who were found to be noncompliant with the diet. Mouth-to-cecum transit time is significantly prolonged in patients affected by untreated celiac disease when compared to healthy controls. This alteration might not be correlated to intestinal malabsorption, and the prolonged orocecal transit could be due to impaired small bowel function (deranged motility?). Since intestinal transit returned to normal values after an adequate gluten-free period, a link with severe active mucosal lesions is suggestive.

Adult↗
PubMed1997

Long-term effect of gluten restriction on bone mineral density of patients with coeliac disease.

AIM: To assess the long-term effect of a gluten-free diet on bone mineral density of adults with untreated coeliac disease. METHODS: Bone mineral density was assessed at baseline and after a mean duration of 37 months of treatment in 25 unselected newly diagnosed coeliac patients. RESULTS: At baseline, osteopenia (> -1 s.d. below normal) was evident in the lumbar spine and total skeleton in 18 (72%) and 21 (84%) patients, respectively. At the end of the study, bone density had increased (mean bone mass Z-score increase: Z-score +1.0 for the lumbar spine and +1.1 for total skeleton) in 22 and 23 patients, respectively. Patients who adhered to strict gluten restriction (n = 15) demonstrated a similar bone remineralization in the spine than those patients with partial compliance (n = 10) (mean Z-score increase: +1.0, in both areas). A greater mean annual change in Z-score in the total skeleton was noted in patients who followed strict gluten restriction (0.4 +/- 0.1) respect to those with partial compliance (0.3 +/- 0.1); however, this difference was not statistically significant. Pre-menopausal women had significantly greater remineralization that post-menopausals (P > 0.05). Remineralization showed an inverse correlation with the degree of basal osteopenia (r = -0.525; P < 0.002). CONCLUSIONS: Long-term treatment with gluten-free diet produces a significant improvement in bone density in coeliac patients. Remineralization was more pronounced in patients who better comply with gluten-free diet, in pre-menopausal women and in patients with the lowest baseline bone mineral density.

Adult↗
PubMed1996

Gluten activation of peripheral blood T cells induces a Th0-like cytokine pattern in both coeliac patients and controls.

Coeliac disease is apparently a T cell-mediated disease, precipitated in the proximal small intestine of susceptible individuals by gluten. Preferential presentation of gluten peptides most probably takes place in coeliac mucosa by the disease-associated HLA-DQ2 and -DQ8 molecules. In peripheral blood, however, both HLA-DR, -DQ and -DP-restricted T cell responses to gluten have been observed. We examined gluten-specific T cell clones (TCC) derived from peripheral blood for cytokine production to see if their profiles were related to the HLA restriction or the disease state of the donors. As previously found for mucosal TCC, the main product was interferon-gamma (IFN-gamma), often with additional IL-4, IL-5, IL-6, IL-10, tumour necrosis factor, and transforming growth factor-beta. Regardless of restriction element or disease state, gluten-reactive TCC from peripheral blood therefore seem to secrete cytokines compatible with a Th0 profile.

Clone Cells↗
PubMed2003

The HLA-DQ2 gene dose effect in celiac disease is directly related to the magnitude and breadth of gluten-specific T cell responses.

In patients with celiac disease, inflammatory T cell responses to HLA-DQ2-bound gluten peptides are thought to cause disease. Two types of HLA-DQ2 molecules exist, termed HLA-DQ2.5 and HLA-DQ2.2. Whereas HLA-DQ2.5 predisposes to celiac disease, HLA-DQ2.2 does not. We now provide evidence that the disease-associated HLA-DQ2.5 molecule presents a large repertoire of gluten peptides, whereas the non-disease-associated HLA-DQ2.2 molecule can present only a subset of these. Moreover, gluten presentation by HLA-DQ2 homozygous antigen-presenting cells was superior to presentation by HLA-DQ2/non-DQ2 heterozygous antigen-presenting cells in terms of T cell proliferation and cytokine secretion. Gluten presentation by HLA-DQ2.5/2.2 heterozygous antigen-presenting cells induced intermediate T cell stimulation. These results correlated with peptide binding to the antigen-presenting cells. Finally, we demonstrate that HLA-DQ trans dimers formed in HLA-DQ2.5/2.2 heterozygous individuals have properties identical with HLA-DQ2.5 dimers. Our findings explain the strongly increased risk of disease development for HLA-DQ2.5 homozygous and HLA-DQ2.2/2.5 heterozygous individuals, and they are indicative of a quantitative model for disease development, where HLA-DQ expression and the available number of T cell-stimulatory gluten peptides are critical limiting factors. This model may have important implications for disease prevention.

Antigen-Presenting Cells↗
PubMed2002

Circular dichroism and nuclear magnetic resonance spectroscopic analysis of immunogenic gluten peptides and their analogs.

Celiac Sprue, or gluten-sensitive enteropathy, is an inheritable human disease of the small intestine that is triggered by the dietary intake of gluten. Recently, several Pro- and Gln-rich peptide sequences (most notably PQPQLPY and analogs) have been identified from gluten with potent immunogenic activity toward CD4(+) T cells from small intestinal biopsies of Celiac Sprue patients. These peptides have three unusual properties. First, they are relatively stable toward further proteolysis by gastric, pancreatic, and intestinal enzymes. Second, they are recognized and deamidated by human tissue transglutaminase (tTGase) with high selectivity. Third, tTGase-catalyzed deamidation enhances their affinity for HLA-DQ2, the disease-specific class II major histocompatibility complex heterodimer. In an attempt to seek a mechanistic explanation for these properties, we undertook secondary structural studies on PQPQLPY and its analogs. Circular dichroism studies on a series of monomeric and dimeric analogs revealed a strong polyproline II helical propensity in a subset of them. Two-dimensional nuclear magnetic resonance spectroscopic analysis confirmed a polyproline II conformation of PQPQLPY, and was also used to elucidate the secondary structure of the most helical variant, (D-P)QPQLPY. Remarkably, a strong correlation was observed between polyproline II content of naturally occurring gluten peptides and the specificity of human tTGase toward these substrates. Analogs with up to two D-amino acid residues retained both polyproline II helical content and transglutaminase affinity. Since the Michaelis constant (K(m)) is the principal determinant of tTGase specificity for naturally occurring gluten peptides and their analogs, our results suggest that the tTGase binding site may have a preference for polyproline II helical substrates. If so, these insights could be exploited for the design of selective small molecule inhibitors of this pharmacologically important enzyme.

Amino Acid Sequence↗
PubMed2000

Gastrointestinal symptoms rating scale in coeliac disease patients on wheat starch-based gluten-free diets.

BACKGROUND: A wheat starch-based gluten-free diet is widely adopted in the treatment of coeliac disease, even though the products contain trace amounts of gluten. The aim here was to establish whether such a diet sustains abdominal symptoms. METHODS: The Gastrointestinal Symptom Rating Scale (GSRS) was applied to 58 coeliac disease patients on gluten-free diets and 110 non-coeliac controls. An estimate was made of daily dietary fibre and wheat starch-derived gluten. Psychological well-being was evaluated by a structured interview. Twenty-three coeliac patients consented to small-bowel biopsy. RESULTS: The mean GSRS score in coeliac disease patients did not differ from that in control subjects. Poorer psychological well-being was associated with abdominal symptoms in coeliac patients, whereas the daily amount of wheat starch had no effect on GSRS score. Overall dietary compliance was good, and villous atrophy was found in only 2 out of 23 patients. The average fibre consumption, 13 g per day, was lower than recommended. CONCLUSIONS: Wheat starch-based gluten-free products are well-tolerated in coeliac disease patients, provided that their diets are otherwise strict.

Adult↗
PubMed2001

Increased rectal nitric oxide in coeliac disease after local challenge with gluten.

BACKGROUND: Coeliac disease is an inflammatory disorder characterized by reversible atrophy of small intestinal villi following the ingestion of gluten. Earlier studies indicate that the inflammatory response to gluten may occur also very distally in the gastrointestinal tract. The aim of this study was to evaluate whether rectal challenge with gluten would trigger an increased local production of the gas nitric oxide (NO), a novel marker of intestinal inflammation. METHODS: Rectal challenge with partially digested gluten was performed in 20 patients with treated coeliac disease and in 13 healthy controls. Luminal levels of NO were measured in the rectum at 0, 8 and 24 h using a chemiluminescence technique. RESULTS: In patients with coeliac disease mean rectal NO increased from 235+/-90 parts per billion (ppb) at 0 h to 4965+/-1653 ppb at 24 h (P < 0.005). In the control group there was no significant increase. One control subject responded with high NO levels at 24 h and the same individual tested positive for anti-endomysium IgA antibodies. Subsequent duodenal biopsing showed substantial villusatrophy. CONCLUSIONS: Rectal challenge with gluten results in increased luminal levels of NO in a group of patients with treated coeliac disease. Further studies are needed to evaluate the role of NO in coeliac disease and the potential usefulness of rectal NO measurements in aiding diagnosis of this intestinal disorder.

Adult↗
PubMed2001

Gastric emptying of realistic meals with and without gluten in patients with coeliac disease. Effect of jejunal mucosal recovery.

BACKGROUND: Few data are available on disturbed gastric emptying in patients with coeliac disease. The aims of the study were to investigate (a) the presence of delayed gastric emptying: (b) the acute effect on gastric emptying of gliadin; and (c) the effect of jejunal recovery on gastric emptying of meals with or without gluten in such patients. METHODS: We measured gastric emptying of two meals in 16 patients with coeliac disease; one meal contained gliadin. Results were compared with those obtained in 24 controls. In 12 patients, both measurements were repeated after mucosal recovery. Statistical analysis was performed using the analysis of variance for repeated measurements and Student's t test. Mean +/- 1 s(mean) (standard error of the mean) are shown. RESULTS: No difference was found in fasting and in maximal antral sections after the two meals. On entry, gastric emptying was significantly (P < 0.001) delayed compared to controls both after the meal containing gluten (326.9 +/- 12.4 min versus controls 213.5 +/- 11.5) and after the gluten-free meal (315.3 +/- 16.7 min). After jejunal recovery, emptying of the meal containing gluten remained unchanged (337 +/- 18.9 min), whereas emptying of the gluten-free meal was significantly shortened (280.6 +/- 10.5 min; P < 0.001). CONCLUSIONS: In coeliac disease there is an impairment of gastric emptying which is at least partially reversible. This suggests either an immunological disorder or that unabsorbed meal constituents are responsible for an ileal-brake effect.

Adolescent↗
PubMed2005

Coeliac disease, autoimmune diseases and gluten exposure.

OBJECTIVE: Gluten-free diet treatment has been proposed to prevent the development of autoimmune diseases in coeliac subjects. The aim here was to investigate the occurrence of autoimmune disorders in relation to gluten intake in coeliac patients in a well-defined area. MATERIAL AND METHODS: The frequency of autoimmune disorders was evaluated in 703 adults and children with coeliac disease and in 299 controls with normal duodenal histology. Incidence figures were given per 10,000 person-years. In logistic regression analysis, where the prevalence of autoimmune disorders was a dependent variable, the effect of age at end of follow-up, age at diagnosis of coeliac disease, actual gluten exposure time, gender and diagnostic delay were assessed. RESULTS: The prevalence of autoimmune diseases was significantly higher in coeliac subjects than in controls. In logistic regression analysis, age at end of follow-up, age at diagnosis of coeliac disease and female gender increased the risk of autoimmune disorders, whereas actual gluten exposure time reduced the risk; diagnostic delay had no effect. A similar, though not statistically significant, trend was seen in childhood coeliac disease to that in the whole study group. CONCLUSIONS: Despite that fact that patients with coeliac disease are at increased risk of various autoimmune conditions, the duration of gluten exposure seems not to be of crucial importance in the development of autoimmune diseases.

Adolescent↗
PubMed2005

Kinetics of mucosal granulocyte activation after gluten challenge in coeliac disease.

OBJECTIVE: To elucidate the dynamics of the rectal inflammatory response to rectal gluten challenge in coeliac disease by measuring inflammatory mediators released by activated neutrophils, eosinophils and mast cells/basophils. MATERIAL AND METHODS: The release of myeloperoxidase (MPO), eosinophilic cationic protein (ECP) and histamine was measured continuously during the early challenge period (3-6 h after gluten challenge) in coeliac patients (n = 9) and healthy controls (n = 5). A segmental perfusion technique was used to carry out this part of the study. Another method, the mucosal patch technique, was used to enable studies of the late challenge period (5-48 h after gluten challenge) in coeliac patients (n = 10) and healthy controls (n = 15). RESULTS: During the early challenge period the MPO levels began to increase as early as 3 h after challenge and increased progressively (p < 0.001) during the next 3 h. A decline in MPO levels was seen 15 h after challenge and another phase of increasing levels at 24 h. The MPO values declined 48 h after challenge but still remained significantly increased (p < 0.05). The ECP levels started to increase 4 h after challenge and increased progressively during the next 2 h (p < 0.05). The ECP kinetics during the late challenge period was similar as for MPO but the relative increase in ECP was more modest. No increase in histamine was found except in one patient who had a transient, early increase of histamine (3-5 h after challenge). No signs of inflammatory reaction to gluten were seen in the controls. CONCLUSIONS: There is a pronounced neutrophil activation in coeliac patients after rectal gluten challenge. This activation is apparent 4 h after challenge and remains for at least 48 h. A more modest eosinophil activation defined by ECP levels starts 1-2 h later and also remains for at least 48 h. The biphasic pattern of MPO and ECP after challenge suggests a biphasic inflammatory reaction.

Adult↗
PubMed2000

Gastric emptying of solids is delayed in celiac disease and normalizes after gluten withdrawal.

UNLABELLED: Several gastrointestinal motor abnormalities have been detected in patients with celiac disease, but it is unclear whether they are able to influence the gastric emptying rate. The aim of this work was to evaluate the gastric emptying rate of solids in children with celiac disease before and after a gluten-free diet. Nine children with celiac disease and nine healthy controls (age range 4-16 y) underwent a 13C-octanoic acid breath test to measure gastric emptying. Half emptying time (t1/2) and lag phase (t(lag)) were calculated. After 6 mo of a gluten-free diet, all celiac children underwent a repeat 13C-octanoic acid breath test. The gastric motility parameters, t1/2 and t(lag), were significantly longer in patients than in controls. No significant correlation between abnormal gastric emptying and specific symptom patterns or severity of histological damage was found. On a gluten-free diet, the gastric emptying rate normalized in all celiac patients. This finding supports the hypothesis that gluten-driven mucosal inflammation might determine motor abnormalities by affecting smooth muscle contractility or impairing the release of neurotransmitters. Alternatively, nutrient malabsorption might determine significant changes in intraluminal milieu, which, in turn, may affect intestinal motor functions. CONCLUSION: patients affected by celiac disease have a markedly delayed gastric emptying of solids, which returns to normal after gluten withdrawal.

Adolescent↗
PubMed2001

Sporadic cerebellar ataxia associated with gluten sensitivity.

A total of 104 patients with sporadic cerebellar ataxia were tested for antigliadin and antiendomysium antibodies. Twelve individuals (11.5%) with gluten sensitivity underwent duodenal biopsy and extensive clinical, electrophysiological, neuropsychological, radiological and laboratory investigations including human leucocyte antigen (HLA) typing. Two patients showed typical changes of gluten-sensitive enteropathy with crypt hyperplasia and mucosal flattening. In five patients, the intraepithelial lymphocyte count was elevated. Sporadic ataxia with gluten sensitivity was found to be tightly linked to the HLA DQB1*0201 haplotype (70%). Neurological symptoms were not related to hypovitaminosis or inflammatory CSF changes. The clinical syndrome was dominated by progressive cerebellar ataxia with ataxia of stance and gait (100%), dysarthria (100%) and limb ataxia (97%). Oculomotor abnormalities were gaze-evoked nystagmus (66.7%), spontaneous nystagmus (33.3%), saccade slowing (25%) and upward gaze palsy (16.7%). Extracerebellar features also included deep sensory loss (58.3%), bladder dysfunction (33.3%) and reduced ankle reflexes (33.3%). In accordance with clinical findings, electrophysiological investigations revealed prominent axonal neuropathy with reduced amplitudes (50%) and abnormal evoked potentials (58.3%). On neuropsychological testing, patients presented with moderate verbal memory and executive dysfunction. All patients had evidence of cerebellar atrophy on MRI. We conclude that sporadic ataxia may be associated with positive antibodies against gliadin. Nevertheless, mucosal pathology does not represent an obligatory condition of ataxia with gluten sensitivity. The fact that the disease is strongly associated with the same HLA haplotypes found in coeliac disease not only demonstrates coeliac disease and ataxia with gluten sensitivity to be part of the same disease entity but supports the hypothesis of an immunological pathogenesis of cerebellar degeneration.

Adult↗
PubMed1990

Influence of cow's milk proteins and gluten on human duodenal mucosa in organ culture.

Forty-five duodenal biopsies from 33 children and 3 adult patients were maintained in organ culture for 24 h and exposed to various cow's milk proteins and gluten. In 10 of 11 celiac patients with a flat duodenal mucosa, and in 2 of 4 patients with partial villous atrophy, a significant reduction in the mean enterocyte height was found after in vitro gluten exposure, compared to culture in basic culture medium. Three patients had coexisting celiac disease and cow's milk protein intolerance. alpha-Lactalbumin and beta-lactoglobulin exhibited toxic effects on flat biopsies from two of these patients, and casein was toxic in one. In 10 patients with cow's milk protein intolerance, a significant reduction in enterocyte height was noted in one case with gluten, and in three patients with casein and lactoglobulin, whereas lactalbumin did not affect the tissues. In seven control patients having a normal duodenal mucosa, no in vitro influences were noted, whereas in four patients with partial villous atrophy, a toxic reaction to gluten was seen in one and a reduced enterocyte height was seen after lactoglobulin exposure in another. In vitro toxicity induced by gluten corresponded well with the diagnosis of celiac disease, whereas toxic reactions to cow's milk proteins during organ culture were inconsistent in cow's milk intolerance, except for cases in which a marked enteropathy was documented.

Adolescent↗
PubMed1991

Transient gluten hypersensitivity.

We report a case of transient gluten hypersensitivity, demonstrated by jejunal histology at diagnosis, normalization after gluten-free diet, and acute clinical and histological relapse after a challenge with gluten powder at the age of 1 year, resembling that observed in cow's milk protein intolerance. Subsequent provocation tests did not show any alteration. Cases of supposed transient gluten hypersensitivity are rarely reported; our patient is characterized by the acute reaction to gluten challenge associated with a damaged histological picture and depressed levels of complement.

Duodenum↗
PubMed1991

The role of the exocrine pancreas in early-onset vitamin B12 malabsorption in gluten-challenged celiac children.

The fractional absorption of vitamin B12 (FAB12) was measured by a double-isotope technique specially adapted for children. In six celiac children on a strict gluten-free diet and with a normal small intestinal biopsy, the FAB12 performed in the fasting patient averaged 30% (23-40%). After gluten challenge for a mean of 2 months (range 1-4), when mucosal damage was demonstrated by biopsy, the average fasting FAB12 in these patients decreased to 10% (0-17%) (p less than 0.05). However, when the FAB12 test was repeated by means of stimulation by a B12-free meal 1-3 weeks later, while the patients were still on a diet containing gluten, a significant increase was observed (mean 21%, range 14-27%) (p less than 0.05). In four of the six patients the B12 absorption was further evaluated by repeating the FAB12 test by means of intravenous cholecystokinin (CCK) stimulation (n = 3) or by administration of exocrine pancreas enzyme supplementation (EPES) (n = 2) or cobinamide (n = 1). These tests all showed FAB12 values within the range of the meal-stimulated FAB12. Moreover, in eight gluten-free celiac children with normal biopsies, no difference was found between fasting and meal-stimulated FAB12 values. Therefore, it is likely that the early-onset B12 malabsorption observed in the gluten-challenged celiac child with upper-small-intestinal mucosal damage is in part due to an insufficient stimulation of the exocrine pancreas when using the standard fasting B12 absorption test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗