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This brief paper presents findings of 17 (3.4 per cent) of the patients involved in the ARMS research programme which is investigating the role of nutrition and physiotherapy in the management of MS. These 17 were following gluten-free diets. Our findings support the view that there is no conclusive evidence that GF diets are universally beneficial in the management of MS.
The two-month feeding of male August rats with the wheat gluten-containing diet led to an increase in the blood level of low density lipoproteins (LP), free and esterified cholesterol, free fatty acids and acylglycerides. Meanwhile the content of very low density LP and high density LP declined. Cholesterol esters showed a rise in the content of cholesterol linolenate, cholesterol oleate and cholesterol palmitate. Liver microsomes demonstrated an increase in the amount of arachidonic and eucosotrienic acids. The shifts cited were largely determined by the changes in cholate formation and bile excretion, which were marked by the reduced levels of tauro- and glycocholic acids, increased amount of phospholipids and free fatty acids in the bile, and decreased content of cytochromes P-450 and b5 in hepatocyte microsomes.
The rhythm of nutritional recovery in 11 children with celiac disease after the introduction of a gluten-free diet was studied. The mean age of the patients at the moment of the diagnosis was 2.8 +/- 1.2 years and they were followed up for a period of 3.4 +/- 1.9 years. The nutritional status was evaluated by the utilization of the following parameters: the weight-for-age, height-for-age and weight-for-height. It was verified that none child was well nourished at the moment of the diagnosis and during the evolution 9 of them reached a complete recovery of their nutritional status for the weight in a mean period of time of 5.8 +/- 2.7 months; 5 of these children remained well nourished during the follow-up, 3 for 33 months and 1 for just a month. The other 2 children were initially classified as PCM II and turned to PCM I. The height-for-age index revealed that only 6 children had recovered from malnutrition and only 4 remained like this during all the follow-up. The other 2 children suffered nutritional aggravation and turned to be PCM I, but after a mean time of 18.4 months both resumed the rhythm of growth. Nutritional dwarfsism in 45.45% and chronic evoluted malnutrition in 54.55% were the patterns of malnutrition observed in this group of patients.
We examined the genetic control of the murine humoral immune response to purified A-gliadin, a protein derived from wheat gluten, which is known to cause small intestinal disease in susceptible individuals. Studies with congenic and noncongenic inbred strains of mice revealed that the T-dependent humoral immune response to A-gliadin is under the control of genes mapping to the mouse major histocompatibility complex (MHC). These findings in mice establish a clear linkage between the MHC and the regulation of the immune response to a protein capable of causing human disease.
OBJECTIVE: Evaluation of the clinical reaction of 10 children with food allergy, including allergy to cow's milk protein, to the introduction of a new biscuit, free of cow's milk protein, chicken egg protein, lactose and gluten. DESIGN: Descriptive prospective study. SETTING: Outpatient clinic, Beatrix Children's Hospital, University Hospital Groningen. METHOD: In 10 patients (mean age 28 months, range 13-78 months) with a proven cow's milk protein allergy the new biscuit (25 biscuits of 15.5 g each in 2 weeks) was introduced without otherwise changing the diet. The clinical symptoms, total serum IgE, the IgE radio-allergosorbent test (RAST), the skin test, the intestinal permeability (measured with the sugar absorption test), and energy and nutrient intake were determined before and after the introduction of the biscuits. Results were evaluated by the Wilcoxon test. RESULTS: Laboratory results were not significantly different between the groups. A recurrent clinical reaction was seen in one patient after consumption of a biscuit (probably due to a potato component). During the period of biscuit consumption energy and nutrient intake were increased in all children when a maximum of 1.5 biscuit per day was consumed. CONCLUSION: No problems were seen in 9/10 children following introduction of the new biscuit. Energy and nutrient intake were improved. An allergic reaction was seen in 1/10 children, probably due to the potato component.
Among 228 relatives of 101 gluten-sensitive patients, 13 anti-endomysium antibody (EmA) positive persons (7 children and 6 adults) were identified. In 12/13 cases jejunal biopsy confirmed severe villous atrophy consistent with celiac disease. In the single EmA positive sibling without villous atrophy the histology is thought to be influenced by a steroid treatment because of pulmonary disease. By routine EmA-testing 12 unexpected EmA positive patients were found out of 756 children with complaints and laboratory results otherwise not justifying jejunal biopsy at the first evaluation. Their initial diagnoses were: proteinuria, colitis, Crohn's disease, rickets, recurrent vomiting, resolved postinfectious lactase deficiency, "previously excluded" celiac disease. Severe villous atrophy could be demonstrated in all EmA positive patients subsequently. In further 204 EmA negative children the biopsy showed no atrophy. EmA positivity may reveal clinically not apparent severe villous atrophy emphasizing the role of a new non invasive and highly specific serological screening method for celiac disease.
A retrospective study of 487 patients with dermatitis herpetiformis showed that lymphoma developed in eight patients, the expected incidence being 0.21 (standardized registration ratio 3810). All lymphomas occurred in patients whose dermatitis herpetiformis had been controlled without a gluten-free diet (GFD) or in those who had been treated with a GFD for less than 5 years. The results are suggestive of a protective role for a GFD against lymphoma in dermatitis herpetiformis and give further support for advising patients to adhere to a strict GFD for life.
Two cases of prurigo nodularis are described. Each is considered to have a gluten sensitive enteropathy. This association may be one facet of prurigo nodularis.
Familial occurrence of coeliac disease (gluten-sensitive enteropathy, GSE) is well known, but the mode of inheritance remains unclear. Pena et al proposed that the genetic basis for GSE was due to disease-predisposing alleles at two loci: DRw3 at the HLA-D locus and a GSE-associated B-cell alloantigen at another, unlinked locus. They concluded that clinical disease required one DRw3 (dominant inheritance) and two B-cell alloantigen alleles (recessive inheritance), but the observed gene frequencies were not consistent with the observed disease prevalence. Here we examine the gene frequencies allowed, assuming a 2-locus model, under the constraints of known disease prevalence limits and the segregation ratio calculated from 42 published families. The gene frequencies found by Pena et al predict the segregation ratio observed in the published pedigrees and the best estimates of disease prevalence of GSE, provided 1) a 2-locus model is assumed and 2) both loci exhibit recessive inheritance. The segregation ratio appears incompatible with a 2-locus dominant-recessive model without assuming reduced penetrance.
Expression of endothelial adhesion molecules is a key factor in localizing inflammatory processes. We have evaluated the time-course expression of E-selectin, ICAM-1, and VCAM-1 in rectal mucosae from coeliac patients (CD) with T-lymphocyte sensitization to wheat (gliadin) protein. Ten treated, eight untreated CD patients and five disease controls underwent a dynamic 4 h rectal gluten challenge. Seven treated CD patients had a 24 h challenge to evaluate the time-course changes. Coeliac tissue significantly increased VCAM-1 expression [p < 0.001 (untreated and treated CD)] and E-selectin [p = 0.01 (untreated CD only)]-expression compared to controls but not ICAM-1. VCAM-1 continued to increase up to 24 h, while E-selectin decreased after 4 h. These findings relate to a 8 h rise in CD3 (+) lymphocytes [p < 0.05 (treated)] and a 4 h rise in neutrophils (p < 0.005). This approach permits a novel study of the inflammatory response to a known immunogen in human patients.
This is a 21-month-old boy with pseudohypoaldosteronism (PHA) in coincidence with celiac disease. The diagnosis of PHA was made on the basis of hyponatremia, hyperkalemia and large urinary salt losses, as well as high renin activity and aldosterone levels and increased urinary plasma aldosterone. Whereas mineralocorticoid therapy was ineffective, salt therapy has proven successful. The patient's HLA type was found to be characteristic of gluten-enteropathy (A1, B8, DR3). The combination of PHA and celiac disease has not yet been described and is probably a coincidence. However, it is suggested that other PHA patients be typed in order to investigate the segregation between HLA type, PHA and celiac disease.
Southern-blot hybridization with a probe specific for genes encoding for low M(r) glutenin subunits showed that the high quality bread wheat cv Salmone contains two DNA fragments designated as SF720 and SF750. These fragments were found to occur on the chromosome-1B satellite, and to be associated with the presence of two strongly staining low M(r) glutenin subunits in the two-dimensional A-PAGE x SDS-PAGE pattern of cv Salmone. Comparison of 65 F(6) random lines derived from the cross between cv Salmone and the medium quality line FAP74809 revealed that the presence of fragments SF720 and SF750 had significant positive effects on several quality related parameters such as SDS sedimentation volume, Farinograph stability and Alveograph strength (W), tenacity (P) and elasticity (L). Additive effects of high M(r) glutenin subunits 1 and 7+9 on gluten quality were found as well. Fragments SF720 and SF750 were suggested to occur at a locus other than Glu-B3, as indicated by their relatively high frequency of recombination with the Gli-B1 locus.
Thirty-two consecutive adult celiac disease (CD) patients (pts), complaining of peripheral neuropathy (12 pts), autonomic dysfunction (17 pts), or both (3 pts), were evaluated to assess the presence of neurological damage (by clinical neurological evaluation and electrophysiological study) and antineuronal antibodies and to assess the effect of a gluten-free diet (GFD) on the course of the neurological symptoms and on antineuronal antibodies. At entry, 12 of 32 (38%) pts showed signs and symptoms of neurological damage: 7 of 12 (58%), peripheral neurological damage; 3 of 12 (25%), autonomic dysfunction; and 2 (17%), both peripheral neurological damage and autonomic dysfunction. The overall TNS score was 105 at entry. Anti-GM1 antibodies were present in 5 of 12 (42%) pts: 3 showed peripheral neurological damage and 2 showed both peripheral neurological damage and autonomic dysfunction. One year after the GFD was started, histological lesions were still present in only 10 of 12 (83%) pts. TNS score was 99, 98, 98, and 101 at the 3rd, 6th, 9th, and 12th month after the GFD was started, so it did not improve throughout the follow-up. None of the pts showed disappearance of antineuronal antibodies throughout the follow-up. We conclude that adult CD patients may show neurological damage and presence of antineuronal antibodies. Unfortunately, these findings do not disappear with a GFD.
Genetic epidemiology clearly has shown that there is a genetic predisposition to gluten-sensitive enteropathy (GSE), or celiac disease. The strong genetic component, as determined by the lambda sib (lambda s), has been calculated to lie in the range of 7.5 to 30, based on a 5% to 10% recurrence risk for siblings. Ninety-five percent of northern European patients with GSE carry a particular HLA-DQ alpha beta heterodimer. Studies support the concept that the HLA-DQ gene acts as a dominant gene, and they also found that, in addition to HLA-DQ, a second locus within the major histocompatibility complex (MHC) is involved in the predisposition to GSE in the Dutch population. Genome scans conducted so far suggest that MHC and non-MHC loci collectively contribute to disease susceptibility. Since one, and probably even two, gene(s) from the MHC region itself determine at least 40% to 50% of the genetic predisposition to GSE, it is expected that the other loci each contribute only a little to the total genetic variation. The exact role of these additional genes (i.e., whether they are involved in the initiation or the progression of the disease) remains to be determined.
In the present work, for the first time, a method for the quantification of the alimentary opioid peptide Gluten Exorphin A5 (GE-A5; Gly-Tyr-Tyr-Pro-Thr) in cerebrospinal fluid (CSF) was developed. Aliquots (5 microL) of CSF were injected into a liquid chromatography-mass spectrometry (LC-MS) instrument equipped with a reversed-phase C18 column at a flow-rate of 0.4 mL/min. The mobile phase consisted of Eluent A water with 0.6% acetic acid as an ion-pairing reagent and Eluent B acetonitrile/methanol (75:25, v/v). The LC-MS system was programmed to divert column flow to waste for 4 min after injection, after which time flow was directed into the mass spectrometer that operated in positive ion mode. No significant interfering peaks were detected at the retention times of GE-A5 in CSF blanks. The lower limit of detection and the lower limit of quantitation values for GE-A5 in CSF were established at 0.60 and 1.50 ng/mL, respectively. The intra- and inter-day precision values were <5% relative standard deviation. The intra- and inter-day accuracy were 99.6-102.8% and 100.0-101.9%, respectively. The reported assay employs extremely small volumes of CSF, thus allowing the analysis of GE-A5 from both small and large animal models.
Effects of dietary supplementation of orotic acid to a diet containing the casein protein were compared with diets containing egg protein, soy protein, or wheat gluten on lipid levels in the liver and serum and activities of ornithine carbamoyltransferase (OCT) and alanine aminotransferase in the serum of rats. We found that supplementation of orotic acid to each diet increased the contents of the liver total lipids, triacylglycerol, and phospholipids compared with those not supplemented. The contents of liver total lipids, triacylglycerol, cholesterol, and phospholipids in rats fed the casein diet were significantly higher than those of rats fed the other three diets when orotic acid was supplemented. The levels of triacylglycerol, cholesterol, and phospholipids in the serum of rats fed the casein diet were markedly decreased by addition of orotic acid. The supplementation of orotic acid significantly increased the activities of both serum OCT and alanine aminotransferase in rats fed the casein diet, but not in rats fed the other diets. In conclusion, liver lipid accumulation induced by dietary orotic acid depends on the type of dietary protein. The enhancement of serum OCT activity may result from liver lipid accumulation in rats fed the casein diet supplemented with orotic acid, demonstrating hepatic damage.
A procedure for the formulation of biocontrol fungi involving the immobilization of wet biomass within gluten was developed. The release of active fungi from formulated preparations to soil was governed by the soil pH, the moisture content in soil, and the entrapped biomass content. After incorporation to loamy soils having initial moisture content of 5-20%, all formulated agents could generate 10(6)-10(7) colony forming units g(-1) soil in the second week. The use of formulated preparations reduced the amount of biomass required, compared with non-formulated fungi as biocontrol agents.
Adult coeliac patients taking a gluten-free diet for one year showed an increase of 33% in the concentrations in CSF of major monoamine metabolites (5-HIAA, HVA and MOPEG). Tryptophan in CSF rose by 10%. There was concomitant morphological improvement in the jejunal mucosa, and the results would seem to indicate that the reduced central monoamine metabolism in untreated adult coeliacs is not primarily genetically determined but is probably related to the poor intestinal absorption.