Atypical celiac disease with IgA deficiency presenting as Plummer–Vinson syndrome: a case report

A 40-year-old man presented with insidious onset dysphagia for both solids and liquids for 4 years with recurrent oral ulcerations. On examination he was anemic, and barium swallow demonstrated a web in the postcricoid region. As part of the workup for unexplained iron deficiency anemia, a duodenal biopsy was taken that revealed moderate flattening of villi with increased intraepithelial lymphocytes consistent with the diagnosis of celiac disease. However, the serological tests for celiac disease (IgA antiendomysial antibody, IgA antitissue transglutaminase antibody, and IgA antigliadin antibody) were all negative. Serum level of IgA was markedly low. A diagnosis of atypical celiac disease with severe selective IgA deficiency was made. After the institution of a gluten-free diet (GFD), his general condition as well as anemia improved. Histological recovery was documented on repeat duodenal biopsy 6 months after GFD.     

Gluten-free diet induces regression of T-Cell activation in the rectal mucosa of patients with celiac disease

Objective: An increase in the number of intraepithelial lymphocytes (IEL) in the rectal epithelium of patients with active celiac disease has been described. No data are available about how they vary during a gluten-free diet. The aim of the study was to assess the effect of a gluten-free diet on T-cell activation in the rectal mucosa of adult patients with celiac disease.
Methods: Frozen duodenal and rectal biopsies were available in four celiac patients (one male, three female, mean age 39 yr) both before and after 7 to 24 months on a gluten-free diet. Biopsy samples were stained using monoclonal antibodies directed against CD3, βF1, TcRδ1, CD25, and HLADR. Numbers of IEL were estimated by counting the peroxidase-stained cells per 100 epithelial cells. Four patients without histological abnormalities were used as control subjects.
Results: In the four patients with active celiac disease but in none of the controls, CD25 was expressed by both duodenal and rectal lamina propria cells and HLADR was expressed by duodenal (4/4) and rectal (2/4) epithelial cells. In addition, two patients with active celiac disease had features of lymphocytic colitis, i.e. , >20 IEL per 100 epithelial cells. After a gluten-free diet, the mean number of rectal CD3⁺βF1⁺ IEL decreased (9% vs 21%) and the expression of CD25 and HLADR was no longer present. These changes mirrored those found in the small intestinal biopsies.
Conclusion: These results suggest that in celiac disease, gluten-driven T-cell activation is not restricted to the proximal part of the intestine but is present on the whole intestinal length. Assessment of the effectiveness of a gluten-free diet through rectal biopsies warrants investigation, as it could lessen discomfort for patients and prove more cost-effective.     

Cervical esophageal web and celiac disease

Background and Aim:  There is paucity of prospective data on association between cervical esophageal webs and celiac disease. It is not clear whether all patients with cervical esophageal web need screening for celiac disease. Hence, the present study was carried out to determine the association of cervical esophageal web with celiac disease.
Methods:  This prospective study included consecutive patients with symptomatic cervical esophageal web diagnosed over a period of 4.5 years. Tissue transglutaminase antibody was measured in serum of each patient. Patients with elevated tissue transglutaminase antibody titer were subjected to esophagogastroduodenoscopy and biopsies were obtained from the descending duodenum to look for histological changes of celiac disease. Esophageal web was treated with bougie dilatation. Celiac disease was diagnosed on the basis of elevated tissue transglutaminase antibody and suggestive duodenal histology.
Results:  Twenty one patients were diagnosed to have cervical esophageal web. Eighteen (85.7%) had evidence of iron deficiency. Five (23.8%) patients with cervical esophageal web fulfilled criteria for diagnosis of celiac disease. All five had evidence of iron deficiency. None of these patients gave a history of chronic diarrhea. All patients were treated with bougie dilatation. Patients with celiac disease were advised of a gluten-free diet. All five celiac disease patients are free of dysphagia without recurrence after a mean follow up of 10 months (range: 3 to 16 months).
Conclusions:  There is association between cervical esophageal web and celiac disease. All adult patients with cervical esophageal web and iron deficiency need screening for celiac disease even in the absence of chronic diarrhea.     

Iron deficiency anemia in celiac disease

Iron is an important micronutrient that may be depleted in celiac disease. Iron deficiency and anemia may complicate well-established celiac disease, but may also be the presenting clinical feature in the absence of diarrhea or weight loss. If iron deficiency anemia occurs, it should be thoroughly evaluated, even if celiac disease has been defined since other superimposed causes of iron deficiency anemia may be present. Most often, impaired duodenal mucosal uptake of iron is evident since surface absorptive area in the duodenum is reduced, in large part, because celiac disease is an immune-mediated disorder largely focused in the proximal small intestinal mucosa. Some studies have also suggested that blood loss may occur in celiac disease, sometimes from superimposed small intestinal disorders, including ulceration or neoplastic diseases, particularly lymphoma. In addition, other associated gastric or colonic disorders may be responsible for blood loss. Rarely, an immune-mediated hemolytic disorder with increased urine iron loss may occur that may respond to a gluten-free diet. Reduced expression of different regulatory proteins critical in iron uptake has also been defined in the presence and absence of anemia. Finally, other rare causes of microcytic anemia may occur in celiac disease, including a sideroblastic form of anemia reported to have responded to a gluten-free diet.     

Are Complicated Forms of Celiac Disease Cryptic T-Cell Lymphomas?

We assessed the clonality of duodenal mucosal T cells in patientswith celiac disease and controls. Fifteen adult patients were studied.Four patients had a complicated celiac disease, 3 did not respond to agluten-free diet, and 2 had an ulcerative jejunitis (including 1 patient with nonresponsive celiac disease). Seven patients had anuntreated celiac disease responsive to a gluten-free diet. Histologicalexamination of duodenal biopsies of these 11 patients showedbenign-appearing celiac disease without evidence of lymphoma. Fourpatients with nonulcer dyspepsia and normal duodenal biopsies served ascontrols. TCR gene rearrangements were analyzed by multiplexpolymerase chain reaction on DNA extracted from duodenal biopsies.Major clonal rearrangements of the T-cell receptor were found in 4 cases, all with complicated celiac disease. Monoclonality was confirmedby DNA sequencing of the junctional region in 3 cases and byhybridization with clone-specific oligoprobes. Patients with celiacdisease responsive to gluten-free diet had mainly a polyclonal pattern,with 1 of them having an oligoclonal rearrangement. An oligoclonalpattern was also observed in 2 control patients. Three patients withcomplicated celiac disease evolved to T-cell lymphoma with liver (n = 2) or bone marrow (n = 1) invasion. Identical clones were found inthe enteropathic duodenojejunum and peripheral blood in the patientwith large-cell lymphoma with bone marrow invasion. This study suggeststhat complicated celiac disease is a cryptic T-cell lymphoma.     

Dermatomyositis associated with celiac disease: response to a gluten-free diet.

The association between dermatomyositis and celiac disease in children has been well documented. In the adult population, however, the association has not been clearly established. A rare case of concomitant dermatomyositis and celiac disease in a 40-year-old woman is presented. After having been diagnosed with dermatomyositis and iron deficiency anemia, this patient was referred to the gastroenterology clinic to exclude a gastrointestinal malignancy. Blood tests revealed various vitamin deficiencies consistent with malabsorption. The results of gastroscopy with duodenal biopsy were consistent with celiac disease. After she was put on a strict gluten-free diet, both nutritional deficiencies and the dermatomyositis resolved. The patient's human leukocyte antigen haplotype study was positive for DR3 and DQ2, which have been shown to be associated with both juvenile dermatomyositis and celiac disease. It is suggested that patients with newly diagnosed dermatomyositis be investigated for concomitant celiac disease even in the absence of gastrointestinal symptoms.     

Prevalence of celiac disease in nutritional anemia at a tertiary care center

Background

While anemia occurs in 80 % to 90 % of patients with celiac disease (CD), it may be the sole manifestation of CD. The prevalence of CD in Indian patients with nutritional anemia is not known.

Patients and Methods

Adolescent and adult patients presenting with nutritional anemia were prospectively screened for CD using IgA anti-tissue transglutaminase antibody (anti-tTG Ab) followed, if positive, by upper gastrointestinal endoscopy and duodenal biopsy.

Results

Ninety-six patients [mean?±?SD age 32.1?±?13.1 years and median duration of anemia 11 months (range 1 to 144 months)] were screened. Of these patients, 80 had iron deficiency anemia, 11 had megaloblastic anemia, and 5 had dimorphic anemia. Seventy-three patients were on hematinics and 36.4 % had received blood transfusions. Nineteen had a history of chronic diarrhea and the mean?±?SD duration of diarrhea in them was 9.7?±?35.8 months. IgA anti-tTG Ab was positive in 13 patients, of whom 12 agreed to undergo duodenal biopsy. Ten patients had villous atrophy (Marsh grade 3a in three, 3b in one, and 3c in six) and two did not. Thus, 10 patients with nutritional anemia (iron deficiency 9, vitamin B₁₂ deficiency 1) were diagnosed to have CD. On multivariate logistic regression, age, duration of symptoms, and presence of diarrhea were found to be the predictors of CD. All the patients with CD were put on gluten-free diet and with iron and vitamin supplementations and showed a significant improvement in hemoglobin concentration.

Conclusions

CD screening should be included in the work up of otherwise unexplained nutritional anemia.     

Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms.

BACKGROUND: The standard evaluation of a patient with iron deficiency anemia includes a complete evaluation of the gastrointestinal tract to identify a source of bleeding. However, even after a careful examination, many patients remain without a diagnosis. Because iron deficiency anemia results from iron loss or defective absorption, we sought to determine the prevalence of potential gastrointestinal sources for iron deficiency anemia in patients without gastrointestinal symptoms. METHODS: Over a 10-month period, 668 outpatients were referred to the University Hematology Department with iron deficiency anemia, defined by a hemoglobin concentration less than 14 g/dL (less than 12 g/dL in women), mean corpuscular volume less than 80 fL, and ferritin level less than 30 microg/L. After excluding patients with obvious causes of blood loss, inadequate diet, chronic diseases, or malignancies, there were 81 eligible patients, 10 of whom refused investigation. The remaining 71 patients (51 women, median age 59 years) underwent colonoscopy, as well as gastroscopy with gastric (antrum and body) and duodenal biopsies. RESULTS: A likely cause of iron deficiency anemia was detected in 60 patients (85%). Diseases associated with bleeding were found in 26 patients (37%), including colon cancer (10 patients), gastric cancer (2), peptic ulcer (7), hiatal hernia with linear erosions (5), colonic vascular ectasia (3), colonic polyps (2), and Crohn's disease (1). Causes not associated with bleeding were found in 36 patients (51%), including 19 with atrophic gastritis, 4 with celiac disease, and 13 with Helicobacter pylori gastritis. Six (8%) patients had coincident gastrointestinal findings, and 11 (15%) had no cause identified. Patients with an identified nonbleeding-associated cause were younger than those with a bleeding-associated cause (median, 56 vs 70 years; P = 0.001) and included 59% of women (n = 30) versus 30% of men (n = 6) (P = 0.04). Hemoglobin level was not related to the site and severity of disease. CONCLUSION: Gastrointestinal diseases that do not usually cause bleeding are frequently associated with iron deficiency anemia in patients without gastrointestinal symptom or other potential causes of gastrointestinal bleeding.     

Clinical, biochemical and histological abnormalities in adult celiac patients on gluten-free diet

Twenty-six adult patients with histologically confirmed celiac disease on gluten-free diet after apparent disease remission were reexamined at 4-6 months intervals for a mean period of 55.4 months (range 13-137). Eight patients remained clinically well with normal blood tests. Eighteen patients had clinical or biological abnormalities. Eleven patients reported repeated episodes of meteorism and abdominal pain and/or diarrhea which disappeared in 2 after lactose withdrawal. Iron deficiency and macrocytic anemia were sometimes observed in 5 and 4 patients respectively. Altered plasma calcium, phosphorus and alkaline phosphatase and/or bone densitometry findings were detected in 7 patients. Seventeen patients (12 presenting some of the above findings) agreed to a repeat biopsy: 13 of these showed grade II and 4 grade III abnormalities. Although adult celiac patients may show marked improvement during gluten-free diet, minor clinical disturbances and biochemical abnormalities may still be present.     

Anemia in celiac disease is multifactorial in etiology

Anemia in celiac disease (CD) has been attributed to nutritional deficiencies; however, the clinical manifestations of CD have changed with nongastrointestinal presentations predominating. We collected hematologic parameters from a cohort of patients seen at a tertiary care center for CD to assess the characteristics of anemia in this population. Hematological parameters measured 1995 was analyzed. Ferritin levels were compared with population controls (NHANES III). Iron deficiency was common, occurring in 33% of men and 19% of women (P < 0.001). Folate deficiency was seen in approximately 12% of the total sample and B12 deficiency in approximately 5%. Anemia was present in approximately 20% of the cohort. Among the anemic patients, ferritin was less than the 10th percentile in 45%, between the 10th and 50th percentile in 39% and greater than the 50th percentile in 13%. Ferritin > 50th percentile was more common in anemic men (24%) than in anemic women (9%; P > 0.20). Macrocytic anemia with concurrent B12 or folate deficiency was rare (3%). Elevated ESR was observed in patients with ferritin < 10th percentile and >50th. A gluten-free diet resulted in increased serum ferritin in iron-deficient patients, and decreased ferritin levels in those with high ferritin (r(2) = 0.46, P < 0.001). Although anemia is still a common presentation of celiac disease, nutritional deficiencies alone do not explain this phenomenon in all cases; inflammation appears to contribute as evidenced by the presence of anemia of chronic disease in some individuals.     

Disappearance of endomysial antibodies in treated celiac disease does not indicate histological recovery

OBJECTIVE: Although serum IgA-class endomysial antibody (EmA) has high sensitivity for villous atrophy (VA) in patients with untreated celiac disease, few studies have attempted to correlate EmA seroconversion with histological recovery after starting a gluten-free diet. We prospectively studied changes in EmA status and in duodenal histology of seropositive patients after dietary treatment. METHODS: Patients with VA and EmA had repeat EmA testing at 3, 6, and 12 months after starting gluten-free diet, plus assessment of dietary compliance by dietitians and follow-up duodenal biopsy at 12 months. VA before and after treatment was classified as partial (P), subtotal (ST), and total (T). RESULTS: Of 77 patients with newly diagnosed VA and without IgA deficiency, 62 (81%) had EmA: 46 of 57 (81%) with T or STVA and 16 of 20 (80%) with PVA. Of 53 initially EmA-positive patients who completed study criteria, EmA was undetectable in 31 patients (58%) after 3 months' diet, in 40 (75%) after 6 months, and in 46 (87%) after 12 months. However, only 21 patients (40%), all seronegative by 12 months, had complete villous recovery. Only three (33%) of 10 patients with persisting ST or TVA and two (9%) of 22 with PVA remained EmA positive. Four of the five patients with persisting EmA had poor dietary compliance. CONCLUSIONS: EmA is a poor predictor of persisting VA after patients have started gluten-free diet, although it may be of value in monitoring dietary compliance. Although there are no clear guidelines regarding the need for follow-up biopsy, EmA seroconversion cannot substitute. The apparent association between dietary compliance and seroconversion suggests that gluten intake may determine whether untreated celiac patients are EmA positive or negative for a given degree of small bowel damage.     

Methotrexate induced sprue-like syndrome

A 52 year-old male patient diagnosed of ankylosing spondylitis presented with an iron deficiency anemia after a ten-month treatment of methotrexate. He did not respond to treatment with oral iron not a proton pump inhibitor and an upper endoscopy was performed. The histological study of the duodenal biopsies showed villus atrophy. After removing the methotrexate, administrating intramuscular iron and undertaking a gluten-free diet, the histological and analytical alterations progressively resolved.     

Celiac disease-associated autoimmune cholangitis

There is an association between celiac disease (CD) and primary biliary cirrhosis, but there is little information regarding the association between CD and autoimmune cholangitis (antimitochondrial antibody-negative primary biliary cirrhosis). We describe a case of a 60-yr-old woman with chronic serum liver biochemistry elevations, recent onset of pruritus, and unexplained iron deficiency anemia. Liver biopsy was suggestive of stage 1 primary biliary cirrhosis, but serum antimitochondrial antibody testing was negative. Subsequent evaluation revealed CD based on markedly elevated antiendomysial antibody titers and characteristic histological features on mucosal biopsies. Initiation of a gluten-free diet led to resolution of iron deficiency anemia, pruritus, and elevated serum liver biochemistries. This suggests that CD may play a direct role in the development of autoimmune cholangitis. Additionally, normalization of hepatic biochemistries may be achieved without the use of immunosuppressive agents in some patients. CD should be considered in all patients diagnosed with autoimmune cholangitis as a gluten-free diet may avoid the need for immunosuppressive therapy in affected patients.     

Vitamin B12 deficiency in untreated celiac disease

OBJECTIVES: Iron and folate malabsorption are common in untreated celiac disease as the proximal small intestine is predominantly affected. Vitamin B12 deficiency is thought to be uncommon, as the terminal ileum is relatively spared. This study aims to investigate the prevalence of vitamin B12, deficiency in patients with untreated celiac disease. METHODS: Prospective study of 39 consecutive biopsy-proven celiac disease patients (32 women, seven men; median age 48 yr, range 22-77 yr) between September 1997 and February 1999. The full blood count, serum vitamin B12, red blood cell folate, and celiac autoantibodies (IgA antigliadin and IgA antiendomysium antibodies) were measured before and after a median of 4 months (range 2-13 months) of treatment with a gluten-free diet. In vitamin B12-deficient patients, intrinsic factor antibodies and a Schilling test, part 1, were performed. RESULTS: A total of 16 (41%) patients were vitamin B12 deficient (<220 ng/L) and 16 (41%) patients (11 women and live men) were anemic. Concomitant folate deficiency was present in only 5/16 (31%) of the vitamin B12 patients. The Schilling test, performed in 10 of the vitamin B12-deficient patients, showed five low and five normal results. Although only five patients received parenteral vitamin B12, at follow-up the vitamin B12 results had normalized in all patients. Acral paraesthesia at presentation in three vitamin B12-deficient patients resolved after vitamin B12 replacement. CONCLUSIONS: Vitamin B12 deficiency is common in untreated celiac disease, and concentrations should be measured routinely before hematinic replacement. Vitamin B12 concentrations normalize on a gluten-free diet alone, but symptomatic patients may require supplementation.     

Duodenal histology in patients with celiac disease after treatment with a gluten-free diet

BACKGROUND: The diagnosis of celiac disease requires characteristic histopathologic changes in an intestinal biopsy with clinical improvement in response to a gluten-free diet. Endoscopy with procurement of biopsy specimens is often performed to document response to the diet, but there are little data on the appearance of treated celiac disease. This study examined the endoscopic and histopathologic appearance of the duodenum of patients with celiac disease whose diet was gluten-free. METHODS: A cohort of 39 adult patients (mean age 52 years, range 20-74 years) with biopsy-proven celiac disease was retrospectively reviewed. All had responded clinically to a gluten-free diet that they had maintained for a mean of 8.5 years (range 1-45 years). The endoscopic and histopathologic appearances of the duodenal mucosa were reviewed. Blinded review of the diagnostic (initial) and post-treatment biopsy specimens was also performed to assess response of individual patients to the diet. RESULTS: The endoscopic appearance was normal in 23%, reduced duodenal folds were present in 46%, scalloping of folds in 33%, mucosal fissures in 44%, and nodularity in 33%. There was more than 1 abnormality present in 46%. Histology was normal in only 21%. The remainder had villous atrophy (69% partial, 10% total). Paired (diagnostic and follow-up) biopsy specimens were reviewed blindly for 12 patients. The mean (SD) intraepithelial lymphocyte count fell from 61 (22) to 38 (17) (normal <30 per 100 epithelial cells) and the crypt-to-villous ratio improved although it did not normalize. CONCLUSIONS: Despite a good clinical response, abnormal endoscopic and histopathologic appearances persist in the majority of patients with celiac disease treated with a gluten-free diet.     

Celiac disease and recurrent pancreatitis

BACKGROUND: Celiac disease is associated with pancreatico-biliary disease. Postulated mechanisms include reduced gallbladder emptying due to impaired cholecystokinin release and pancreatitis due to malnutrition. We hypothesize that celiac disease may also be associated with pancreatico-biliary abnormalities due to duodenal inflammation and papillary stenosis. METHODS: Over a 48-month period, 169 patients referred for possible sphincter of Oddi dysfunction who underwent pancreatico-biliary manometry were tested for gliadin and endomysial antibodies. Duodenal and papillary biopsies were preformed in those patients who were positive. RESULTS: Celiac disease was diagnosed in 12 (7.1%; 3 men, 9 women). The mean age was 61 years as compared with 37 years for those patients without celiac disease. All of the celiac patients had been referred for recurrent abdominal pain and/or idiopathic pancreatitis. Ten had idiopathic recurrent pancreatitis with elevated amylase and lipase levels. Two of these patients also had mildly elevated liver function tests associated with the abdominal pain. Only 3 of 12 patients had a prior diagnosis of celiac disease. These 12 patients had manometric evidence of stenosis and histologic evidence of periampullary inflammation as well as histologic changes consistent with celiac disease. In 10 of 12 patients sphincterotomy or extension of a prior papillotomy was performed. Two patients were treated with a gluten-free diet alone. CONCLUSIONS: We describe 12 patients with papillary stenosis and celiac disease. In 9 cases the celiac disease was a new diagnosis. Celiac disease should be considered in the etiology of papillary stenosis or idiopathic recurrent pancreatitis.     

A controlled,prospective screening study of celiac disease presenting as iron deficiency anemia

BACKGROUND: anemia is the most frequent presenting feature of celiac disease in adults using endomysial antibody (EmA) screening. Endomysial antibody screening of anemia may allow detection of celiac disease at an earlier stage of investigation and after a shorter duration of symptoms. The characteristics of celiac patients identified by screening require further study. GOALS: a goal of this study was to evaluate the prevalence of celiac disease in adult patients with iron deficiency anemia compared with a nonanemic control population using immunoglobulin A (IgA) EmA screening. We also studied the positive predictive value (PPV) of the EmA assay and correlated the severity of histologic abnormalities in distal duodenal biopsy samples with EmA and tissue transglutaminase (tTG) antibody titer. STUDY: four hundred eighty-four patients with microcytic, hypochromic anemia underwent IgA EmA assay. Four hundred ninety-eight nonanemic age- and sex-matched patients from the same source comprised the control group. Patients with positive serology results were invited for endoscopic duodenal biopsies. RESULTS: one in 44 anemic patients was diagnosed with histologically confirmed celiac disease compared with one in 498 nonanemic patients ( < 0.01). Fifty percent of women were premenopausal, and 25% of patients were older than 65 years. The PPV for EmA assay varied between 73% and 93% for anemic patients and improved at higher antibody titer, with all false-positive results occurring at the lowest titers. CONCLUSIONS: screening for celiac disease using IgA EmA assay is effective in anemic patients, including premenopausal women and patients older than 65 years, and it can be recommended in clinical practice.     

Celiac Disease in African-Americans

Celiac disease is generally under diagnosed in the United States and it is unclear whether the disease is encountered in ethnic minorities. Our purpose is to describe a case series of African-American patients with celiac disease. Nine (1.3%) African-American patients with celiac disease were identified from a prospectively generated database of 700 patients with biopsy proven celiac disease and seen between 1981 and 2004. Females predominated, with seven, compared to two males. Diarrhea was the presentation in only two patients, while three presented with iron deficiency anemia. One third had at least one autoimmune disease. Compliance with a gluten-free diet, the only medical therapy of this disease, was poor. Only four patients adhered strictly to the diet. Celiac disease occurs in African-Americans and may well be underdiagnosed. Special attention needs to be given to methods that encourage adherence to the diet in minority groups.     

Helicobacter pylori infection in patients with celiac disease

BACKGROUND AND AIMS: Patients with Helicobacter pylori gastritis are more likely to have increased duodenal intraepithelial lymphocytes (IEL); this can be reversed by H. pylori eradication. We hypothesized that: (1) H. pylori-infected celiac disease (CD) patients could have different clinicopathological features from noninfected subjects; and (2) the histopathological responses to a gluten-free diet could be different in H. pylori-infected and noninfected patients. METHODS: Duodenal and gastric biopsies obtained from 80 adults with histologically and serologically confirmed CD before and after 12-18 months of a gluten-free diet were retrospectively evaluated. Gastritis was classified and scored according to the Updated Sydney System; duodenal biopsies were classified using both the Marsh-Oberhuber and a simplified classification proposed by our group. RESULTS: At baseline, 30 patients had H. pylori infection and 50 did not; at follow-up five new infections were detected. Fifteen patients (3 H. pylori-positive and 12 negative) had lymphocytic gastritis. At baseline, a greater proportion of H. pylori-negative patients had severe villous atrophy (p < 0.01), but milder forms were more prevalent in H. pylori-positive patients (p < 0.01). After a gluten-free diet, significant improvement occurred in all duodenal features (p < 0.001), irrespective of H. pylori status; gastric variables did not change, except for lymphocytic, which resolved in 2 infected and 10 noninfected patients. CONCLUSIONS: The clinical features of CD patients are unrelated to H. pylori gastritis, and a gluten-free diet is equally effective in infected as in uninfected patients. The higher prevalence of milder duodenal lesions in CD patients with H. pylori infection suggests that lymphocytosis induced by H. pylori gastric infection becomes less obvious as profound inflammatory and structural changes alter the mucosal architecture. This study also provides further support for a pathogenetic relationship between CD and lymphocytic gastritis.