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PubMed2001

Normal parathyroid function with decreased bone mineral density in treated celiac disease.

Decreased bone mineral density (BMD) has been reported in patients with celiac disease in association with secondary hyperparathyroidism. The present study investigated whether basal parathyroid hormone (PTH) remained elevated and whether abnormalities of parathyroid function were still present in celiac disease patients treated with a gluten-free diet. Basal seric measurements of calcium and phosphate homeostasis and BMD were obtained in 17 biopsy-proven patients under treatment for a mean period of 5.7+/-3.7 years (range 1.1 to 15.9). In addition, parathyroid function was studied with calcium chloride and sodium citrate infusions in seven patients. Basal measurements of patients were compared with those of 26 normal individuals, while parathyroid function results were compared with those of seven sex- and age-matched controls. Basal results were similar in patients and controls except for intact PTH (I-PTH) (3.77+/-0.88 pmol/L versus 2.28+/-0.63 pmol/L, P<0.001), which was higher in the former group but still within normal limits. Mean 25-hydroxy vitamin D and 1,25-dihydroxy vitamin D values were normal in patients. Parathyroid function results were also found to be similar in both groups. Compared with a reference population of the same age (Z score), patients had significantly lower BMDs of the hip (-0.60+/-0.96 SDs, P<0.05) and lumbar spine (-0.76+/-1.15 SDs, P<0.05). T scores were also decreased for the hip (-1.3+/-0.9 SDs, P<0.0001) and lumbar spine (-1.4+/-1.35 SDs, P<0.0001), with two to three patients being osteoporotic (T score less than -2.5 SDs) and seven to eight osteopenic (T score less than -1 SDs but greater than or equal to -2.5 SDs) in at least one site. Height and weight were the only important determinants of BMD values by multivariate or logistical regression analysis in these patients. The results show higher basal I-PTH values with normal parathyroid function in treated celiac disease. Height and weight values are, but I-PTH values are not, an important determinant of the actual bone mass of patients. Normal parathyroid function in treated patients suggests a lack of previous severe secondary hyperparathyroidism and/or complete adaptation to prior changes in parathyroid function.

Absorptiometry, Photon↗
PubMed2004

Multiple sclerosis and celiac disease: is there an increased risk?

Multiple sclerosis and celiac disease are both considered immune-mediated diseases. Recently, improved serological screening methods provided a higher prevalence of celiac disease (CD) in the general population worldwide and also demonstrated gastrointestinal symptoms may be lacking. The aim of this study was to determine the prevalence of (CD) in an unselected group of 95 adults with multiple sclerosis using transglutaminase antibodies. No patients showed pathological values. Different immune and genetic basis between the two diseases may represent crucial insights to explain our results.

Adult↗
PubMed1982

Degeneration of the central nervous system associated with celiac disease.

The following report describes a 57-year-old man with celiac disease who developed a progressive and fatal neurologic disorder despite intensive medical and nutritional care. The clinical and pathological CNS findings in this patient are compared with those of 9 previously reported patients with well documented celiac disease in whom a progressive CNS disorder was carefully studied both pre-and postmortem. An entity of CNS degeneration associated with celiac disease appears to emerge from the study of these 10 cases. This disorder affects predominantly the cerebellum, deep gray masses, certain brain stem nuclei, and spinal cord; its cause and pathogenesis are unknown.

Brain↗
PubMed2000

Prevalence of celiac disease in Down syndrome in the United States.

BACKGROUND: Numerous studies in Europe have documented a high prevalence of celiac disease in Down syndrome. This study was undertaken to estimate the prevalence of celiac disease in Down syndrome in the southeastern United States. METHODS: Seventy-five patients with Down syndrome were screened using immunoglobulin (Ig)A-anti antiendomysium antibodies, IgA-antigliadin antibodies, and total IgA level. When either antiendomysium or antigliadin antibodies produced positive findings, patients were referred to a pediatric gastroenterologist for consideration of a duodenal biopsy. RESULTS: Thirteen percent (10/75) were positive for antiendomysium antibodies. Half of these patients were also positive for antigliadin antibodies. Six of 10 patients positive for antiendomysium antibodies underwent intestinal biopsy. Changes consistent with celiac disease were documented in five. Histologic findings ranged from focal to total villous atrophy. None had IgA deficiency. CONCLUSIONS: There was a high prevalence of positivity to antiendomysium antibody in Down syndrome. Antiendomysium antibody was a more sensitive screening test than antigliadin antibody. The prevalence of celiac disease in Down syndrome in the southeastern United States was 1 in 14 cases. Screening with antiendomysium antibody and IgA for all children with Down syndrome is recommended, even if there are no gastrointestinal symptoms.

Adolescent↗
PubMed2006

Prevalence of celiac disease in an urban area of Brazil with predominantly European ancestry.

AIM: To determine the prevalence of celiac disease in a group of volunteer blood donors at a blood bank in the city of Curitiba, Brazil through detection of the serum marker immunoglobulin A (IgA) antitransglutaminase antibody. METHODS: Blood samples collected from 2086 healthy subjects at the Paraná State Center for Hematology and Hemotherapy in Curitiba were submitted to ELISA testing for the IgA antitransglutaminase antibody. Positive samples received IgA antiendomysium antibody test through indirect immunofluorescence using human umbilical cord as substrate. Subsequently, patients who were positive on both tests underwent small bowel (distal duodenum) biopsy. RESULTS: Six subjects, four males and two females, tested positive for the two serum markers. Five of the six were submitted to intestinal biopsy (one declined the procedure). Biopsy results revealed changes in the distal duodenum mucosa (three classified as Marsh IIIb lesions and two as Marsh II lesions). Most donors diagnosed having celiac disease presented multiple symptoms (gastrointestinal tract complaints). One donor reported having a family history of celiac disease (in a niece). CONCLUSION: Among apparently healthy blood donors, the prevalence of biopsy-confirmed celiac disease was approximately 1:417, similar to that seen in European countries.

Adult↗
PubMed2005

Celiac disease presenting as a paraneoplastic syndrome in a patient with synchronous endometrial and ovarian cancers.

OBJECTIVE: Celiac disease is characterized by gluten intolerance and commonly manifests with unexplained diarrhea, abdominal distention and weight loss. Infrequently, patients present with vague, non-specific symptoms which often delay diagnosis and treatment. CASE: A 52-year-old female with a history of synchronous endometrial and ovarian cancers, previously treated with surgical resection, staging and pelvic irradiation, presented with progressive paresthesias in her extremities. Extent of disease work-up was unremarkable. Neurologic evaluation suggested celiac disease which was later proven by duodenal biopsy. CONCLUSION: The development of new or worsening neurologic symptoms in the cancer patient requires a thorough evaluation especially to exclude metastatic disease and/or paraneoplastic syndromes. Once neoplastic processes are excluded, celiac disease should be considered in the differential diagnosis of patients with unexplained neurologic dysfunction.

Celiac Disease↗
PubMed2000

All that scallops is not celiac disease.

BACKGROUND: Scalloping of duodenal folds as well as a mosaic mucosal pattern, decreased folds, and increased vascularity are markers of duodenal mucosal injury, the most common cause being celiac disease. We have recognized scalloping in patients with a variety of conditions other than celiac disease. METHODS: Clinical, endoscopic and histologic data were reviewed from selected patients with endoscopically visualized scalloped folds along with testing for endomysial antibodies. Biopsy specimens were examined histologically for villous:crypt ratio, intraepithelial lymphocytes, and inflammation. RESULTS: Thirteen patients with scalloped folds underwent endoscopy for the following reasons: family history of celiac disease and osteoporosis, gastrointestinal bleeding, dyspepsia (2), B(12)/ folate deficiency (4), and diarrhea (8). Histologic examination was abnormal in all but 1 patient. Villous atrophy or flattening as evidenced by reduced villous:crypt ratio was seen in 11 of 13 patients. Other abnormalities were edematous or broadened villi (10), intraepithelial lymphocytosis (7), and infiltration of lamina propria (6). An infectious organism was identified in 6 patients (46%). Celiac disease was excluded by the lack of specific biopsy findings combined with endomysial antibody testing. Final diagnoses were normal (1), eosinophilic enteritis (1), giardiasis (1), tropical sprue (4), human immunodeficiency virus-related diseases (6) including human immunodeficiency virus enteropathy (1). CONCLUSION: We conclude that scalloping is not specific for celiac disease but rather a predictor of mucosal disease as evidenced by villous atrophy, widening, and edema.

Biopsy↗
PubMed1994

Lymphocytic gastritis: a positive relationship with celiac disease.

Lymphocytic gastritis is characterized by lymphocytic infiltration of the surface and pit epithelium. Its cause has not been established, but an association with Helicobacter pylori infection or celiac disease has been suggested. We evaluated the histologic features of both gastric and duodenal biopsy specimens from 245 consecutive children and adolescents, and found chronic gastritis in 60 children and celiac disease in 25. Chronic gastritis was associated with H. pylori infection in 36 children and with celiac disease in 15. Lymphocytic gastritis was found in nine children with celiac disease. Children with lymphocytic gastritis had a mean of 40.64 lymphocytes per 100 epithelial cells, compared with a mean of 3.92 lymphocytes per 100 epithelial cells in children with H. pylori-associated gastritis and 5.15 lymphocytes in normal control subjects. Immunohistochemical studies showed that the intraepithelial lymphocytes in lymphocytic gastritis were T cells. No child with lymphocytic gastritis had serologic evidence of past H. pylori infection. We conclude that lymphocytic gastritis in children is associated with celiac disease. Dyspeptic symptoms are frequent; the endoscopic appearance is not characteristic.

Adolescent↗
PubMed2005

Can tissue transglutaminase antibody titers replace small-bowel biopsy to diagnose celiac disease in select pediatric populations?

OBJECTIVES: The use of screening tests for celiac disease has increased the number of patients referred for evaluation. We proposed that the subgroup of patients with very high tissue transglutaminase antibody (TTG) titers is positive for celiac disease and a small-bowel biopsy is not necessary to make the diagnosis. A gluten-free diet should be attempted and, if the patient's symptoms do not improve, then a biopsy should be performed to confirm the diagnosis. METHODS: A chart review of data for 103 patients who underwent both TTG testing and a small-bowel biopsy was performed. We examined the impact of using TTG values of >100 U and <20 U as cutoff values and suggested performing biopsies for patients with TTG values of 20 to 100 U, as is current practice. RESULTS: Fifty-eight of 103 patients demonstrated positive biopsy results. Forty-nine of 103 patients had TTG levels of >100 U, with 48 of 49 exhibiting positive biopsy results. Only 7 of 16 patients with TTG values of 20 to 100 U exhibited positive biopsy results. Three patients with TTG levels of <20 U had positive biopsies; 2 were IgA negative and 1 had a duodenal ulcer. With the cutoff values of >100 U and <20 U with known IgA status, the sensitivity was 0.980 (48 of 49 cases) and the specificity was 0.972 (35 of 36 cases). An incremental cost analysis found that this proposal could potentially decrease the costs of investigation and diagnosis by almost 30%. CONCLUSIONS: When the cutoff values were changed to >100 and <20 U and IgA levels were verified, the sensitivity and specificity were very high. Patients with mid-range TTG values (20-100 U) or values of <20 U with negative IgA status should continue to undergo biopsies for diagnosis of celiac disease.

Autoantibodies↗
PubMed2002

A longitudinal study of the effects of a gluten-free diet on glycemic control and weight gain in subjects with type 1 diabetes and celiac disease.

OBJECTIVE: To describe the longitudinal growth characteristics and glycemic control in type 1 diabetic children diagnosed with celiac disease and started on a gluten-free diet (GFD). RESEARCH DESIGN AND METHODS: Data on growth and glycemic control for 11 case subjects diagnosed with celiac disease (cd(+) group) and started on a GFD were collected prospectively, and two control subjects without celiac disease matched for age, sex, and duration of diabetes (cd(-) group) were selected for comparison. RESULTS: In the period between diagnosis of type 1 diabetes and start of a GFD in the cd(+) compared with the cd(-) group, BMI standard deviation score (SDS) was lower (-0.2 vs. 0.7, P = 0.015), as was HbA(1c) (8.9 vs. 9.8%, P = 0.002). In a regression model the cd(+) group had lower BMI SDS (P < 0.001) and lower HbA(1c) (P = 0.04), independent of other variables. On a GFD, BMI SDS increased by 12 months in the cd(+) group and then was no different than the cd(-) group (1.1 vs. 1.0, P = 0.11), whereas HbA(1c) improved further within case subjects compared with pre-GFD (8.9 vs. 8.3%, P = 0.002). On a GFD, case subjects in contrast to control subjects showed no deterioration in HbA(1c) during the years of puberty (8.3 vs. 10.0%, P = 0.022) CONCLUSIONS: In children with type 1 diabetes, untreated celiac disease resulted in lower BMI SDS and lower HbA(1c). Recovery of BMI SDS with a GFD was associated with further improvement in HbA(1c) as compared with pre-GFD, with no expected deterioration in glycemic control during puberty. These apparent clinical benefits need confirming by larger studies.

Adolescent↗
PubMed1990

Serological markers and celiac disease: a new diagnostic approach?

We analyze the diagnostic efficacy of two celiac disease serological markers: anti-gliadin (IgA and IgG class) and anti-endomysium IgA-class (EmA-IgA) antibodies applied to 336 serum samples from celiac patients on both gluten-challenge and gluten-free diets, and a control group. The anti-gliadin and anti-endomysium antibodies levels were significantly higher among the gluten-consuming celiac patients than in the other groups. The greatest efficacy in diagnosing celiac disease was achieved in the Ema-IgA class test. The IgA-class anti-gliadin antibodies proved to be more specific, with a higher positive test predictive value than the IgG-class anti-gliadin antibodies, whereas the latter proved to be more sensitive, with a higher negative test predictive value than those of the IgA-class anti-gliadin antibodies. Our results also demonstrate that the simultaneous assessment of anti-gliadin IgA- and IgG-class antibodies constitutes a valid test in selecting patients suspected of having celiac disease. In turn the EmA-IgA antibodies constitute a confirmative test for indication of an intestinal biopsy.

Adolescent↗
PubMed1988

An HLA-DQ alpha allele identified at DNA and protein level is strongly associated with celiac disease.

An HLA-DQ alpha cDNA probe showed upon hybridization a highly significant discrepancy between the RFLP of celiac disease patients and healthy controls. The 4.0-kb Bgl II restriction fragment was present in 97% of celiac disease patients (n = 30), compared to 56% in a healthy control population (n = 72) (RR = 14.9; p less than 0.0005). At the product level all celiac disease patients tested to date have one DQ alpha chain in common, designated HLA-DQ alpha 2.3, which is associated with the 4.0-kb Bgl II fragment. This HLA-DQ alpha allele identified at the DNA level and product level seems to be a better marker for genetic susceptibility to develop celiac disease than those available to date.

Alleles↗
PubMed1996

[Adult celiac disease presenting as tetany].

Tetany is a rare form of presentation of adult celiac disease. We present three patients with spontaneous episodes of tetania who were finally diagnosed of celiac disease. All were women. In two of them an unexplained chronic anemia was previously detected. The origin of tetania was severe hypocalcemia and hypomagnesemia. After intravenous restoration of calcium and posterior free gluten diet with supplements, clinical and biological remission was achieved. In the presence of isolated tetania or unexplained anemia resistant to treatment an adult celiac disease must be disclosed.

Adult↗
PubMed2005

Outcome of infants with celiac disease.

AIMS: Determine the proportion of infants whose celiac disease (CD) was confirmed in childhood and evaluate their prognosis in adulthood. PATIENTS AND METHODS: The diagnosis of CD was established between 1971 and 1982 in 84 infants based on intestinal biopsy data; a gluten-free diet was prescribed and the cohort followed prospectively. RESULTS: Thirty-six infants were followed less than 5 years. A second biopsy was performed in 25. Mucosa had healed in 13 and remained atrophic in 12. Three children developed partial villous atrophy between 6 and 12 years of age in spite of the gluten-free diet. Forty-five patients underwent a gluten challenge between 5 and 10 years of age: in 41 histological lesions relapsed, in two mucosa remained normal and clinical and immunological relapse developed in two. Among those 45 patients, 18 were examined after 18 years follow-up: the exclusion diet was resumed in four, overt clinical relapse developed in four and four experienced intermittent gastrointestinal disorders. All biopsies performed during a period of normal diet showed villous atrophy (except in one patient) without correlation with clinical symptoms. CONCLUSION: The diagnosis of celiac disease in infants was confirmed in nearly all cases in childhood. When they reached adulthood, these patients had few symptoms but their histological lesions persisted. These data are in favor of a lifelong exclusion diet.

Adolescent↗
PubMed1983

Short stature and celiac disease: a relationship to consider even in patients with no gastrointestinal tract symptoms.

To determine the incidence of celiac disease in a group of nonselected children with short stature, duodenal biopsy was performed in 60 unselected children with short stature (below third centile) and absence of gastrointestinal tract symptoms. Examination revealed probable celiac disease in five children (8.3%). Analysis of the results of other tests that might possibly be considered as alternatives to biopsy (e.g., xylose test, antireticulin antibodies, gastrointestinal tract symptoms in the first two years of life, bone age, serum iron, iron load, triglyceride load) led us to conclude that no test or clinical measurement could have allowed us 100% certainty in making the correct diagnosis. None of the children with celiac disease had growth hormone deficiency. We conclude that asymptomatic celiac disease represents a cause of short stature that cannot be ignored, and that only by intestinal biopsy can all such patients be identified.

Adolescent↗
PubMed1984

Serum IgG antibodies to gliadin in children with celiac disease as measured by an immunofluorescence method.

Antigliadin antibodies (AGAs) were studied in sera from 190 patients divided into five clinical groups. Group I included 28 sera from children with newly diagnosed celiac disease on a normal diet. Group II consisted of 43 sera from children with celiac disease who were fed a gluten-free diet (GFD). Group III included 25 sera from children with celiac disease who had been in remission but exposed to a gluten-containing diet (GCD). Group IV consisted of 46 sera from children with chronic diarrheal disorders other than celiac disease. Group V included 43 sera from healthy children. The observed p values proved that (a) mean titer levels of AGAs in Groups I and III were significantly higher than the mean values for all other groups (p less than 0.001), and (b) the mean titer level of AGAs in Group II was significantly higher than the mean values for Groups IV and V. A good correlation between the AGA titers and the morphology of the duodenal mucosa was found in children with celiac disease. The examination of IgG AGAs by the immunofluorescence technique used in our study appears to be a useful tool in the follow-up of individual patients to determine adherence to a GFD.

Animals↗
PubMed1997

Pancreatitis-associated protein in patients with celiac disease: serum levels and immunocytochemical localization in small intestine.

Since PAP is a stress protein expressed in human pancreas during pancreatitis but also constitutively synthesized in the small intestine, we looked whether its expression would be altered in patients with celiac disease. Serum PAP concentrations were determined consecutively in 54 patients with celiac disease on a free diet (group A), in 47 patients with celiac disease on a gluten-free diet (group B), in 22 patients with other intestinal pathologies but with normal intestinal mucosa (group C), in 14 patients with retarded growth, no gastrointestinal disease and normal intestinal mucosa (group D), and in 17 controls (group E). Serum PAP levels (ng/ml) were significantly higher in group A (127.3 +/- 56.8) than in the other groups (B: 47.2 +/- 20.5; C: 51.5 +/- 32.2; D: 47 +/- 22.8; E: 27.6 +/- 9.0), which were not different from each other. In group A, a positive correlation was observed between serum PAP values and antigluten antibody levels (vs. AGA IgG r = 0.58, p < 0.001; vs. AGA IgA r = 0.66, p < 0.001). Furthermore, 12 patients from group A were evaluated after 10-12 months of gluten-free diet and in all of them PAP serum concentration had decreased (mean +/- SE before the diet 122.5 +/- 36.4, after the diet 48.7 +/- 13.7, p < 0.0001). In addition, we performed an immunocytochemical study to localize PAP in the intestinal mucosa of patients from all groups except E. PAP was localized to the Paneth cells and to some globet cells, in patients with mucosal atrophy as well as in those with normal mucosa with no obvious quantitative difference. We concluded that in patients with celiac disease the active phase of the disease was accompanied by an increased serum concentration of PAP. Further studies are necessary to understand the mechanism leading to PAP elevation in the serum of patients with celiac disease.

Acute-Phase Proteins↗
PubMed2003

Alterations of the intestinal transport and processing of gliadin peptides in celiac disease.

BACKGROUND & AIMS: The hypothesis of a defect in the intestinal transport and processing of toxic (31-49) or immunostimulant (57-68 and the 33-mer 56-89) gliadin peptides was tested in patients with active celiac disease (ACD), patients with treated celiac disease (TCD), and controls. METHODS: Using duodenal biopsy specimens mounted in Ussing chambers, we measured electrical resistance, mucosal-to-serosal radiolabeled-peptide fluxes, and peptide processing during transport using radio-reverse-phase high-performance liquid chromatography. RESULTS: Peptide 31-49 fluxes (24.7 microg x 3 h(-1). cm(-2)) were increased in patients with ACD compared with controls and patients with TCD (12.7 and 12.3 microg x 3 h(-1). cm(-2); P < 0.01). In contrast, no increase was observed for peptide 57-68 or 56-89 (33-mer). Electrical resistance was decreased in patients with ACD versus controls (15.3 vs. 23.9 ohms. cm(2); P < 0.001). Peptide 57-68 was partially degraded by brush-border peptidases in controls but not in patients with celiac disease. However, it was totally degraded after intestinal transport both in controls and patients with celiac disease. Peptides 31-49 and 56-89 were resistant to brush-border peptidases in all groups of patients but were totally degraded during intestinal transport in controls and patients with TCD. In patients with ACD, however, 50% of peptide 31-49 was delivered intact into the serosal compartment and only partial degradation of the 33-mer was observed. These abnormalities were not related to a nonspecific paracellular leakage. CONCLUSIONS: Our data indicate that gliadin peptides, although poorly or not digested by intraluminal enzymes, can be fully digested by enterocytes in controls and patients with TCD. In patients with ACD, incomplete degradation of the 33-mer and protected transport of the peptide 31-49 might favor their respective immunostimulatory and toxic effects.

Adult↗