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It has recently been recognized that many pharmaceutical products contain gluten. Patients with celiac disease are at risk of acute illness if they are treated with such products. This paper lists the products available in Canada, according to the "Compendium of Pharmaceuticals and Specialties, 1985", that contain gluten and the Canadian manufacturers who stated that they do not use gluten as an excipient.
Sixty-three-year-old woman requested medical attention for osteoporosis. Bone densitometry revealed: T(spine (L1-L4))= -3.5 SD [Bone mineral density (BMD): 0.766 g/cm(2)]. T(femoral neck) = -2.4 SD (BMD: 0.716 g/cm(2)). She has been in calcium and vitamin D supplementation for 2 years. She informed a 5-year-history of hypothyroidism in levothyroxine replacement. Alendronate sodium 70 mg/week was initiated with significant increase in BMD in the first year (6.1% equally in spine and femoral neck). After a 5-year follow-up, the patient presented with weight loss, anemia and decrease in BMD (12.6% in spine and 20.9% in femoral neck). Clinical history revealed intermittent diarrhea episodes for 2 years and the hypothesis of celiac disease was suspected. Anti-gliadin and anti-endomysium antibodies were positive: 25.3 U/mL (< 20) e 1/5 U/mL (RV: negative), respectively. Bone biochemical parameters revealed normal levels of calcium and phosphate, increased parathyroid hormone: 283 pg/mL (10-65) and increased levels of bone reabsortion markers, consistent with secondary hyperparathyroidism in response to malabsorptive syndrome. One year after gluten-free diet, patient improved of malabsorptive symptoms and gained BMD (47.3% in spine and 31.6% in femoral neck), confirming the hypothesis of celiac disease as aggravating factor of osteoporosis in this patient.
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Inflammation is characterized by increased nitric oxide production. Nitrotyrosine has recently been suggested to be useful as a marker for NO-mediated tissue damage. In context of the development of an ELISA for detection of nitrotyrosine in plasma, monoclonal anti-nitrotyrosine antibodies were developed by injecting mice with nitrated keyhole limpet hemocyanin. The specificity of the antibodies was determined by binding to nitrated BSA, lack of binding to unmodified BSA, tyrosine, 3-chlorotyrosine or phenylalanine and inhibition of binding by nitrotyrosine. The antibodies developed are useful for Western blot analysis and immunohistochemical staining. Using these antibodies a nitrotyrosine sandwich ELISA was developed with a lower detection limit of approximately 0.2 nM. The intra- and interassay variance were 2.4% and 11.9%, respectively. Using this newly developed ELISA, 1.27 +/- 1.03 microM nitrotyrosine was detected in plasma samples of celiac disease patients whereas nitrotyrosine was undetectable in control samples. Elevated nitrotyrosine levels were paralleled by an increase in plasma concentrations of NO-oxidation products (NOx), nitrite and nitrate from 15.1 +/- 6.1 microM in controls to 61.0 +/- 28.2 microM in celiac disease patients. Both nitrotyrosine and NOx levels declined when the patients were on a gluten-free diet, suggesting a relation between intestinal inflammation and plasma nitrotyrosine and NOx levels.
Jejunal mucosal specimens from twenty children with celiac disease were studied by light microscopy (LM), scanning electron microscopy (SEM), and transmission electron microscopy (TEM) after one year of dietary treatment. An ultrastructural morphometric study was performed in five patients who had an intestinal permeability (IP) test. Seventeen patients were tested for serum antigliadin antibodies (AGA). In ten children, in whom LM showed partial villous atrophy, SEM and TEM examination confirmed the lesion. In the second group (10 children) with normal morphology at routine LM, SEM showed lesions of variable degree in 70% of cases. The morphological ultrastructural investigation showed good correlation with the immunological and functional data (IP test): ultrastructural damage of the jejunal mucosa after one year of a gluten-free diet was found in patients with positive serum AGA and an abnormal IP test. Furthermore, the morphometric study of the ultrastructural alterations allowed a quantitative, closer correlation between morphological and functional data. Our results suggest: 1) SEM and TEM investigations offer additional and more complete information on celiac patients, over LM alone. 2) The morphometric evaluation of the ultrastructural alterations highlights quantitative and reproducible correlations between morphological and clinical data, not strengthened by the subjective, qualitative study.
Celiac disease (CD) is a common condition that occurs in genetically predisposed individuals when they ingest products containing wheat, barley, or rye. It produces an autoimmune-mediated enteropathy with characteristic histologic features on small intestinal mucosal biopsy. The clinical manifestations of CD are highly variable and initially may be unrelated to the gastrointestinal system. The condition is also strongly associated with other autoimmune and nonautoimmune conditions. Physicians caring for children and adolescents are challenged with identifying those who might have CD and require referral for definitive testing, recognizing the potential pitfalls in the diagnostic work-up of the pediatric patient, and providing ongoing care for those with a positive diagnosis. Confirmation of the diagnosis mandates that the individual be placed on a strict gluten-free diet (GFD) for life, as this is the only treatment currently available for CD. This article will discuss the immunopathogenesis, epidemiology, and clinical manifestations of CD and will outline a strategy of active case-finding using serological tests to identify those who require an intestinal biopsy for definitive diagnosis. The need for lifelong treatment by means of a GFD and for continued follow-up of children and adolescents after diagnosis is emphasized.
There continues to be much research interest in celiac disease, with well over 200 papers published in the year under review, covering a multitude of areas from population screening to the molecular immunology of disease pathogenesis. The high prevalence of "silent" disease again has been demonstrated, and there is continued emphasis on the increasingly wide recognized range of associated conditions and extraintestinal manifestations. The case for the safety of oats is further strengthened by a study involving patients with dermatitis hepetiformis. One of the most significant scientific advances has been the discovery of a potential role for tissue transglutaminase, recently found to be the autoantigen of antiendomysial antibodies, in disease pathogenesis, by enhancing gliadin peptide class II binding and consequent T-cell activation. However, the very central role of T cells has been thrown into doubt with an elegant study that assessed the effect of blocking costimulation in T-cell activation.
OBJECTIVES: Ghrelin, a gastrointestinal hormone, has effects on nutrient intake and growth. Because celiac disease (CD) has intestinal histopathologic alterations and subsequent malnutrition and/or growth failure, we hypothesized that there would be alterations in serum ghrelin levels of those patients. In this study, we aimed to determine serum ghrelin levels in childhood CD, to observe probable alterations under gluten-free diet (GFD), and to see whether there is a relationship between ghrelin levels and the presentation of the disease and/or diet compliance. METHODS: Thirty-six children with CD and 10 healthy children were included. Serum fasting ghrelin level was measured using radioimmunoassay method. After 6 months under GFD, sera of 19 patients were retested for ghrelin level. RESULTS: Mean serum ghrelin levels in children with CD and in controls were 478.2+/-154.6 and 108.3+/-49.1 pg/mL, respectively (P<0.001). Serum ghrelin level was not different in different clinical presentations. Ghrelin was negatively correlated with body mass index, both in healthy children and in children with CD on admission (P<0.01). Ghrelin level was lower after 6 months under GFDcompared with the level detected on admission (P<0.001), but was still higher compared with that of healthy children (P<0.001). Strict diet compliance lowered ghrelin level, although not statistically. CONCLUSIONS: Ghrelin is increased in childhood CD and is responsive to GFD. Further studies are needed to clarify the mechanism underlying its action in CD.
Follow-up studies on 36 children, in whom celiac disease (gluten-sensitive enteropathy) was established by gluten challenge, were carried out after management on gluten-free diets for a mean of six years. Evaluations included measurement of height and weight, which for the group approximated normal distributions, and histologic examination of the duodenal or jejunal mucosa. Mucosal morphology was regarded as normal in 16, and there were minimal changes in 20. Epithelial cell height was within the normal range in all the children. Interepithelial lymphocytes were within normal range in the majority and lymphoid cells in the lamina propria were not different from those in control subjects. Mucosal lactase was significantly lower in patients than in control subjects in the duodenum and the jejunum, whereas sucrase and alkaline phosphatase values were significantly lower in the jejunum but not in the duodenum. Low content of mucosal lactase and increased numbers of interepithelial lymphocytes may be sensitive indicators of persisting ingestion of gluten in mucosa that is otherwise normal or approximately so in appearance.
The diagnosis of celiac disease (CD) was uniformly established between 1960 and 1983 in 314 infants and children according to the following criteria: a flat proximal small bowel mucosa in untreated patients and an unequivocal response and remission on a gluten-free diet (GFD). In 91 patients, one or more interruptions of the GFD (challenges) were documented by repeated intestinal biopsies. Sixty-eight percent of the challenges were initiated by the patients themselves. Seventy-one patients (Group A, 81.4%) had a flat mucosa after 0.25-14.67 years off diet. In 11 (Group B, 12%), a successive deterioration of the mucosa occurred during 0.5-6.67 years after interruption of GFD without becoming flat. Six patients (Group C, 6.6%) had a normal intestinal mucosa after 2.24-6.92 years off diet. Three patients are still under study, being off diet for less than 2 years. Median age at diagnosis was similar in all three groups (1.16, 1.16, and 1.12 years). Median duration of GFD prior to challenge was 4.54 years in Group A, 12.16 years in Group B (p less than 0.001), and 6.38 years in Group C. A mucosal relapse within 2 years after the beginning of challenge was observed in 21 of 24 patients (87.5%) studied longitudinally during planned challenges. It is concluded that only a minority (6.6%) of CD patients, when diagnosed as above, will not relapse after an interruption of GFD and that another small group (12%) will deteriorate very slowly. Routine gluten challenges in all CD patients, interrupting established life and dietary habits and including repeated biopsies in the majority of patients who deteriorate and relapse, seem therefore not justifiable.
Gluten-free diet (GFD) plays a key role in the treatment of celiac disease (CD), but it is difficult to evaluate the effect of GFD on the improvement of villous architecture using sensitive, non-invasive tests. Aim of this study is to evaluate anti-transglutaminase (tTG) antibodies in the follow-up of CD to detect histologic recovery. We studied 42 consecutive patients with CD. In all the patients anti-tTG antibodies (evaluated by the enzyme linked immunosorbent assay method) and EGDscopy with multiple bioptic samples before GFD and then 6, 12, and 18 months after GFD were evaluated. For comparison, a sorbitol H2-breath test (H2-BT) and anti-endomysium (EMA) antibodies test were carried out concomitantly. Anti-tTG results were positive in 36 of 42 patients before GFD (80.95%), while they were positive in 11 of 34 (32.35%), 1 of 17 (5.88%), and 0 of 6 (0%) of patients with a persistence in histologic lesions 6, 12, and 18 months of GFD respectively, without any correlation with persistence of histologic lesions (P = NS). Also EMA failed to show correlation with improvement of histologic lesions. They were positive in 31 of 42 patients before GFD (73.80%), while they were positive in 18 of 34 (52.94%), 3 of 17 (17.64%), and 0 of 6 (0%) cases 6, 12, and 18 months of GFD respectively (P = NS). Regarding sorbitol H2-BT, it was positive in 40 of 42 (95.24%) patients before GFD, while it was positive in 31 of 34 (91.17%), 13 of 17 (76.47%), and 4 of 6 (50%) of patients with a persistence in histologic lesions 6, 12, and then 18 months after GFD starting (see Fig. 2, infra). So, anti-tTG and EMA were ineffective in assessing the histologic recovery at each follow-up visit (P = NS), while sorbitol H2-BT seems more effective than anti-tTG and EMA in this field (P < 0.0001 sorbitol H2-BT versus anti-tTG and versus EMA at 18 months after gluten withdrawal). Thirty-eight of 42 (90.47%) patients adhered to a strict GFD. Four patients were found to have occasional dietary transgression, and in all we noted a progressive decreasing of anti-tTG after 6 months of GFD and negative anti-tTG after 12 months of GFD, but sorbitol H2-BT persisted being positive during the entire follow-up. Intestinal damage persisted during the follow-up, despite anti-tTG and EMA negativity, and worsened in the presence of dietary lapses. Anti-tTG does not seem effective to assess histologic recovery in the follow-up of celiac patients after they have started GFD due to its poor correlation with histologic damage.
Idiopathic chronic urticaria (ICU) is a chronic relapsing cutaneous disease. Some case reports or studies on small series of celiac disease (CD) patients have suggested a possible association between CD and ICU. The aim of this study was to assess the prevalence of CD in a population of adults ICU patients with respect to healthy controls. We consecutively enrolled 80 patients affected by ICU and 264 blood donors as the control population without a history of ICU. Serum anti-transglutaminase IgG and anti-endomysium IgA antibodies were evaluated in all subjects. In the case of positivity to serology, diagnosis was confirmed by duodenal biopsy. One of 80 (1.25%) ICU patients were positive to both anti-transglutaminase and anti-endomysium antibodies. Duodenal biopsy showed partial villous atrophy. One control of 264 (0.38%) had CD. No statistical difference was found in the prevalence of CD between the two groups. ICU patients do not seem to bear a greater risk for CD compared to the general population.
HLA class II beta-chain polymorphism was investigated in the haplotype HLA-DR3 to determine if patients with HLA-DR3-associated diseases express normal or variant class II polymorphisms. Analysis was carried out by two-dimensional gel electrophoresis of immunoprecipitated HLA class II molecules, DNA hybridization with DR beta and DQ beta gene probes on Taq 1, Bam H1, or Rsa 1 digests, and mixed lymphocyte culture. Two subtypes of HLA-DR3 were identified in normal homozygous DR3 individuals on the basis of polymorphism in one of two DR beta chains detected, corresponding to differences in DR beta restriction fragment patterns. These polymorphisms exhibited significant linkage disequilibrium with the A1,B8,DR3 and B18,DR3 haplotypes, respectively. In proliferative experiments, cells with the B18,DR3-associated polymorphism strongly stimulated cells from donors with the B8,DR3-related polymorphism, suggesting that a T-cell epitope recognized by B8,DR3 cells lies on the B18,DR3-associated DR beta chain. In seven HLA-DR3 homozygous patients with celiac disease and three HLA-DR3-homozygous patients with idiopathic membranous nephropathy, only the normal patterns of HLA class II molecules were displayed, the B8,DR3 type occurring in all patients and the B18,DR3 type in one patient. These data suggest that celiac disease and idiopathic membranous nephropathy are not related to disease-specific HLA-DR beta or -DQ beta gene variants within the DR3 population that are revealed by these methods.
Celiac disease (CD) is an inflammatory condition of the gut with a known autoimmune pathogenesis. Many similarities exist between the pathogenesis of CD and systemic lupus erythematosus (SLE); it is still unknown whether there is an association. There are 13 case reports in the literature of both diseases occurring simultaneously. We report another patient who was diagnosed with SLE and 8 years later, developed CD. A review of the literature is also presented.
A new statistical approach to the analysis of laboratory data has been introduced to optimize the use of absorption tests and gliadin antibody measurement for the diagnosis of childhood celiac disease. Serum antigliadin antibodies, as well as blood xylose, iron, and tryglycerides after oral load, were evaluated in 40 celiac children and 43 age-matched patients affected by other gastrointestinal diseases. Each test evaluated individually gave a considerable rate of false-positive and false-negative results. Discriminant coefficients produced for each test were used to compute a score that allowed correct classification of 99% of patients; 2.3% of false-positive and no false-negative results were recorded. This approach improves significantly the overall sensitivity and specificity for celiac disease of these laboratory tests and we propose its use for screening patients to be submitted to jejunal biopsy.
We report on a 17-year-old young woman with a speech impediment, developmental delay, short stature, and facial anomalies consistent with the Floating-Harbor syndrome (FHS). In addition, she has clinical and histological evidence of celiac disease, which was observed in 1 of the 6 previously reported cases of FHS, suggesting a possible association between the 2 conditions or pleiotropism of a presumed autosomal recessive disorder.
The authors report six patients with multifocal axonal polyneuropathy and the subsequent diagnosis of celiac disease (CD). Five patients did not improve or had only modest improvement following dietary intervention or immune therapies; one patient with marked weakness and mild electrodiagnostic findings had complete resolution of the neuropathy following immunomodulatory therapy. CD may be a cause of multifocal axonal polyneuropathy.