Gut microflora associated characteristics in first-degree relatives of children with celiac disease

OBJECTIVE: In celiac disease (CD), enteropathy of the small bowel results from a T-cell-mediated reaction to gluten in the diet. In addition to gluten, other environmental and genetic factors participate in the disease pathogenesis. We have recently reported the finding of a significantly different short-chain fatty acid (SCFA) profile in fecal samples from children with CD compared to healthy controls reflecting an aberrant gut microflora. The aim of the present study was to make a functional evaluation of the gut microflora status in non-celiac 1st degree relatives of children with CD. MATERIAL AND METHODS: Fecal samples from 76 symptom-free, non-celiac, 1st degree CD relatives and from 91 aged-matched healthy controls were analyzed for fecal tryptic activity (FTA) and a number of SCFAs. RESULTS: There was a significantly lower level of acetic acid and total SCFAs as well as a significantly increased level of i-butyric acid and FTA in relatives compared to healthy controls. CONCLUSIONS: The FTA and the SCFA profiles in fecal samples from 1st degree relatives of children with CD are different from those of healthy individuals. The implication of this observation provides insight into the pathogenesis of CD and opens up the possibility of future new diagnostic, therapeutic and prophylactic strategies.     

Short-chain fatty acids in the normal human feces

The short-chain fatty acids ( SCFAs ) have been studied in the feces of 20 healthy subjects--10 methane excretors and 10 non-methane excretors. The analytical procedure included homogenization of fecal samples followed by vacuum distillation and subsequent gas chromatography. This method for analysis of fecal SCFAs showed recoveries of the individual acids from 90% to 109% and coefficients of variation for the inter-assay reproducibility from 6.0% to 19.7%, highest for those acids present in the smallest concentrations. There was no difference in the concentrations or relative compositions of SCFAs between methane-excreting subjects and non-methane-excreting subjects. The concentrations of SCFAs , given as mmol/kg feces (wet weight), were (median and range): total, 76.8 (27.9-187.7); acetic acid, 37.4 (12.8-103.4); propionic acid, 12.5 (4.5-27.8); i-butyric acid, 2.2 (0.7-3.8); n-butyric acid, 12.4 (4.0-53.0); i-valeric acid, 3.2 (0.8-5.9); n-valeric acid, 2.4 (0.6-3.8) and n-caproic acid, 0.5 (0.0-3.6). The study shows that the SCFAs are quantitatively the most important anions in the feces of healthy subjects. The pronounced individual variations in the concentrations of SCFAs are real biological variations and cannot be explained by methodological variations.     

Serum ghrelin levels in children with celiac disease

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.     

Serum leptin levels in childhood celiac disease

OBJECTIVE: Leptin has effects on growth and is also involved in immune regulation. We thought that with its intestinal histopathologic alterations due to immune mechanisms, and subsequent malnutrition and/or growth failure, celiac disease (CD) deserves interest regarding leptin status. METHOD: Serum leptin levels of 19 children with CD on admission and 1 year after gluten-free diet (GFD) and of 16 healthy children were determined. RESULTS: Mean age was 9.7+/-3.3 years. Mean serum leptin level of children with CD on admission and of healthy children were 1.60+/-0.63 ng/mL, and 3.98+/-1.49 ng/mL, respectively (P: 0.0001). Mean serum leptin level under GFD was 4.55+/-1.97 ng/mL. There was a statistical significant difference between serum levels determined before and 1 year after GFD (P: 0.001) and between those of under GFD and healthy children (P: 0.001). Of 19 patients with CD, 10 (52.6%) showed Marsh IIIc, other 9 (47.4%) showed Marsh IIIa histologic lesions. Mean serum leptin level of children with Marsh IIIc and Marsh IIIa were not different (1.70+/-0.73 ng/mL vs. 1.45+/-0.59 ng/mL). Leptin was correlated with body mass index in healthy children, and in CD both before and after GFD (P<0.001). Mean lumbar z score of the patients on admission and after GFD were 2.7+/-1.3 and 1.9+/-0.8, respectively (P: 0.048). Serum leptin level was not correlated with lumbar z score either before or after GFD. CONCLUSIONS: Serum leptin level is affected in childhood CD, it is not directly related to histopathologic findings, and is responsive to GFD. Further studies investigating its level in different clinical and histopathologic presentations might give clear clues about the role of leptin in CD.     

Cardiovascular disease risk factor profiles in children with celiac disease on gluten-free diets

AIM:To describe the cardiovascular disease(CVD)risk factors in a population of children with celiac disease(CD)on a gluten-free diet(GFD).METHODS:This cross-sectional multicenter study was performed at Schneider Children’s Medical Center of Israel(Petach Tiqva,Israel),and San Paolo Hospital(Milan,Italy).We enrolled 114 CD children in serologic remission,who were on a GFD for at least one year.At enrollment,anthropometric measurements,blood lipids and glucose were assessed,and compared to values at diagnosis.The homeostasis model assessment-estimated insulin resistance was calculated as a measure of insulin resistance.RESULTS:Three or more concomitant CVD risk factors[body mass index,waist circumference,low density lipoprotein(LDL)cholesterol,triglycerides,blood pressure and insulin resistance]were identified in 14%of CD subjects on a GFD.The most common CVD risk factors were high fasting triglycerides(34.8%),elevated blood pressure(29.4%),and high concentrations of calculated LDL cholesterol(24.1%).On a GFD,four children(3.5%)had insulin resistance.Fasting insulin and HOMA-IR were significantly higher in the Italian cohort compared to the Israeli cohort(P<0.001).Children on a GFD had an increased prevalence of borderline LDL cholesterol(24%)when compared to values(10%)at diagnosis(P=0.090).Trends towards increases in overweight(from 8.8%to 11.5%)and obesity(from 5.3%to 8.8%)were seen on a GFD.CONCLUSION:This report of insulin resistance and CVD risk factors in celiac children highlights the importance of CVD screening,and the need for dietary counseling targeting CVD prevention.     

What is the role of celiac disease in enteropathy-type intestinal lymphoma? A retrospective study of nine cases

BACKGROUND AND AIMS: It is generally accepted that enteropathy-type intestinal lymphoma (EATL) arises against a background of gluten enteropathy. We investigate whether patients with this diagnosis had celiac disease or pre-existing celiac disease, based on gliadin and endomysium antibodies, as well as duodenal biopsies, HLA typing and response to gluten-free diet. METHODS AND RESULTS: Retrospective study of patients with the diagnosis of peripheral T cell lymphoma of the intestine between January 1990 and January 2002 at the university hospital Gasthuisberg Leuven (n = 14). Patients in whom serologic testing was performed or patients known with pre-existing celiac disease (CD) were included (n = 9). Six of these nine patients were tested for endomysium antibodies (AEM), none of them were positive. Of the six patients with biopsies of mucosa uninvolved by lymphoma, all of them had villous atrophy; five had increased intraepithelial lymphocytes (IEL). In the four patients were HLA typing was performed, the results were compatible with CD. The three patients with initially diagnosed celiac disease all improved on gluten free diet (control biopsies improved as well, but failed to normalise). Of the six other patients, one patient never started GFD, two didn't get better, one initially went better after GFD, and one went better with the concomitantly started chemotherapy. CONCLUSION: There are two possible explanations: Either these patients with EATL have indeed gluten intolerance but the sensitivity of AEM is overestimated in this patient population; or these patients don't have gluten intolerance and EATL itself can mimic CD or other factors mimicking CD are at risk for developing EATL.     

Cell Density Counts of the Intestinal Intraepithelial Lymphocytes in the Celiac Patients

Background: Increased number of intestinal intraepithelial lymphocytes (IELs) is a key histological finding in the diagnosis of celiac disease (CD); however, the number of IELs in celiac patients and healthy subjects may vary from one region to another. Additionally, there are some seronegative celiac patients with a borderline histology. Objective: To determine the number of the CD3+ and CD8+ IELs T-cells in the celiac patients and healthy subjects (controls) in Isfahan. Methods: The duodenal biopsies were obtained from the celiac patients (n=15) and the controls (n=19). The total number of IELs/100 epithelial cells (ECs) were counted using the hematoxylin-eosin (H&E) staining method, and that of CD3+ and CD8+ IELs/100 ECs were counted using the immunohistochemistry (IHC) staining method. Results: This study defined the upper normal limit for each variable as mean + 2SD. Accordingly, the upper normal limits of the total IELs, CD3+ IELs, and CD8+  IELs/100 ECs were calculated as 37 (95% confidence intervals, CI: 33–41), 22 (95% CI: 19–25) and 12 (95% CI: 10–14), respectively. In 3 clinically CD diagnoses, the total IELs counts/100 ECs were below the upper normal limit, and the histopathological and serologic assays were negative. Nevertheless, the CD8+ IELs T-cells counts/100 ECs showed borderline values. Interestingly, these patients responded to a gluten-free diet (GFD). Conclusions: The study findings suggest that in the clinically diagnosed celiac disease, IELs count/100 ECs below the upper normal limit as well as negative histopathological and serologic assays and the cell density counts of the CD8+ IELs T-cells/100 ECs could be a useful parameter for CD diagnosis and make a decision to put them on a GFD.     

Effects of a gluten-free diet on gut microbiota and immune function in healthy adult humans

Diet is a major environmental factor influencing gut microbiota diversity and functionality, which might be relevant to subjects following dietary therapies. Celiac disease (CD) is an enteropathy caused by an aberrant immune response to cereal gluten proteins and the only therapy is the adherence to a gluten-free diet (GFD). In this context, a preliminary study was conducted to establish whether the GFD in itself could modify the composition and immune properties of the gut microbiota. The trial included 10 healthy subjects (30.3 years old), which were submitted to a GFD over 1 month. Analysis of fecal microbiota and dietary intake indicated that numbers of healthy gut bacteria decreased, while numbers of unhealthy bacteria increased parallel to reductions in the intake of polysaccharides after following the GFD. Fecal samples of subjects under a GFD, which represent an altered microbiota, also exerted lower immune stimulatory effects on peripheral blood mononuclear cells than those of subjects on a regular gluten-containing diet. This addendum presents further discussion on the rationale behind these findings, limitations of the study and possible consequences of dietary counseling in the care process of celiac disease patients.     

Effects of a gluten-free diet on gut microbiota and immune function in healthy adult humans

Diet is a major environmental factor influencing gut microbiota diversity and functionality, which might be relevant to subjects following dietary therapies. Celiac disease (CD) is an enteropathy caused by an aberrant immune response to cereal gluten proteins and the only therapy is the adherence to a gluten-free diet (GFD). In this context, a preliminary study was conducted to establish whether the GFD in itself could modify the composition and immune properties of the gut microbiota. The trial included 10 healthy subjects (30.3 years-old), which were submitted to a GFD over one month. Analysis of fecal microbiota and dietary intake indicated that numbers of healthy gut bacteria decreased, while numbers of unhealthy bacteria increased parallel to reductions in the intake of polysaccharides after following the GFD. Fecal samples of subjects under a GFD, which represent an altered microbiota, also exerted lower immune stimulatory effects on peripheral blood mononuclear cells than those of subjects on a regular gluten-containing diet. This addendum presents further discussion on the rationale behind these findings, limitations of the study and possible consequences of dietary counselling in the care process of celiac disease patients.     

Intestinal Diffuse Large B-Cell Lymphoma Associated with Celiac Disease: A Japanese Case

Intestinal non-Hodgkin's lymphoma (NHL), especially the T-cell type, is well known to be associated with celiac disease (CD), an enteropathic disorder with a propensity for certain racial and genetic backgrounds. CD is typically characterized by gastrointestinal (GI) symptoms, anti-transglutaminase antibodies in the sera, and microscopical findings of the intestinal mucosa, which resolve with a gluten-free diet (GFD). In Asian populations, including the Japanese, CD and the associated NHL have been supposed to be quite rare, and studies concerning the frequency of CD or its relationship with NHL are scarce. We describe a Japanese middle-aged man with intestinal diffuse large B-cell lymphoma associated with CD. Following multi-combined chemotherapy, the patient's lymphoma has been in a state of complete response, and his GI symptoms have improved with a GFD. This case suggests that the possibility of CD and its association with intestinal NHL should be kept in mind, even in Asian populations.     

Angiotensin-converting enzyme activity in stools of healthy subjects and patients with celiac disease

Angiotensin-converting enzyme (ACE) is a dipeptidylcarboxypeptidase that occurs in three types of cells: endothelial, epithelial, and neuroepithelial. ACE activity is present in plasma, urine, and vascular endothelium. High levels of ACE are found in the brush border of human small bowel. The aim of this study was to evaluate ACE activity in human stools and to find a correlation with the intestinal loss of epithelial cells. Fifteen healthy subjects (HS) (8 males, 7 females; age range 6–56 years), 20 patients with celiac disease (CD) (11 males, 9 females; age range 15–53 years), and 18 patients with CD in remission after a gluten-free diet (CD-GFD) (8 males, 10 females; age range 14–54 years) were enrolled in the study. The fecal ACE activity was measured in all groups. Fecal samples were kept at –20°C for a subsequent test. In HS, fecal ACE activity was 21.03±16.17 nmol/min/100 g (mean ±sd). In patients with CD with subtotal mucosa atrophy, ACE activity was significantly higher (113 ± 88.94) than in HS and CD on GFD (36.65±23.9). We have demonstrated ACE activity in human stools. ACE activity in stools seems to derive from the microvilli of the intestinal mucosa, thus suggesting the potential usefulness of ACE determination as an index of enterocyte damage.     

Effect of a gluten-free diet on growth and small-bowel histology in children with celiac disease in India

BACKGROUND AND AIM: Follow-up studies on growth and histological recovery of children with celiac disease (CD) while on a gluten-free diet (GFD) are lacking from Asia. We therefore assessed the effects of this diet. METHODS: Forty-two children with CD were enrolled. Weight and height were expressed as weight for height (WfH) and height standard deviation scores (HSDS), respectively. Twenty-five children had repeated duodenal biopsies after 1-2 years and 14 had a third biopsy after 3-7 years of GFD. Compliance was checked by regular interview and IgA antiendomysial antibody estimation (EMA). RESULTS: At diagnosis (n = 25), mean HSDS was -3.3 +/- 1.6 with 76% having a HSDS of <-2; 60% were undernourished (WfH mean 81.6 +/- 5.7). Over a mean follow up of 3.7 years, HSDS improved to -1.3 +/- 1.7 and 84% cases achieved normal nutrition. Mean height velocity was 13.9 cm during first year and 5.6 cm in subsequent years. Small-bowel biopsies at diagnosis showed subtotal villous atrophy (Marsh IIIb) in 18 (72%) and partial villous atrophy (Marsh IIIa) in seven (28%) patients. Repeat biopsy at 1-2 years showed shift from subtotal to partial villous atrophy in 94% (n = 17/18) and normalization in one patient. In patients with Marsh IIIa improvement of partial villous atrophy was observed in all. Immunoglobulin A endomysial antibody was negative in 81%. Repeat biopsies at 5 years of GFD showed improvement to Marsh I-II, but none normalized. CONCLUSION: The majority of children with CD show normalization of nutrition and growth after GFD. Small-bowel histology improves markedly but does not normalize even after 5 years of GFD.     

Non-diarrheal celiac disease: a report of 31 cases from northern India.

BACKGROUND AND AIMS: Non-diarrheal presentation of celiac disease (CD) is being increasingly recognized. Data on this form of CD from India are limited. METHODS: Consecutive patients with CD presenting to a tertiary referral center in northern India over a 3-year period were studied, with special emphasis on non-diarrheal celiac disease (NDCD). Diagnosis was based on the presence of autoantibodies typical of CD (IgA anti-tissue transglutaminase antibodies and/ or IgA endomysial antibodies), abnormal duodenal biopsy and response to gluten-free diet (GFD). Clinical, hematological and histological responses were assessed over a one-year period after instituting GFD. RESULTS: Of 86 patients with CD, 31 (16 children, 15 adult) had NDCD. Mean (SD) age of these children (12 boys) and adults (4 male) was 10.2 (4.2) y and 35.3 (12.0) y, respectively. Failure to thrive was the most common (11/16) presentation in children, as was refractory anemia in adults (10/15). Malabsorption was found in 8 adults (54%) and 10 children (64%) with NCCD. The duration from onset of symptoms to diagnosis was 2.9 (1.5) y in children and 3.3 (0.3) y in adults. There was significant improvement in body weight (children--baseline 18.9 [5.8] Kg, follow up 27.4 [12.4] Kg; adults--baseline 47.6 [18.2] Kg, follow up 54.9 [5.1] Kg) and hemoglobin (children--8.1 [2.0] g/dL to 11.2 [1.4] g/dL; adults--7.3 [2.3] g/dL to 9.7 [1.7] g/dL) in both groups after one year of GFD; duodenal biopsy also improved, with a majority of patients attaining normal to IIIa Marsh grading. Five adults and all children had evidence of metabolic bone disease at presentation, which did not revert completely with GFD. Eight adults and nine children showed dietary transgression 6 weeks after starting GFD. CONCLUSION: NDCD ac-counted for nearly one-third of all cases with CD at our center, with 'failure to thrive' and refractory anemia being the most common presentations in children and adults, respectively.     

Effects of Saccharomyces boulardii on fecal short-chain fatty acids and microflora in patients on long-term total enteral nutrition

AIM: To assess the effects of Sb on fecal flora and short-chain fatty acids (SCFA) in patients on long-term TEN. METHODS: Ten patients (3 females, 7 males, 59±5.5 years), on TEN for a median of 13 mo (1-125), and 15 healthy volunteers (4 females, 11 males, 32±2.0 years) received Sb (0.5 g bid PO) for 6 d. Two stool samples were taken before, on the last 2 d and 9-10 d after treatment, for SCFA measurement and for culture and bacterial identification. Values (mean±SE) were compared using sign tests and ANOVA. RESULTS: Fecal butyrate levels were lower in patients (10.1±2.9 mmol/kg) than in controls (19.2±3.9, P= 0.02). Treatment with Sb increased total fecal SCFA levels in patients (150.2±27.2 vs 107.5±18.2 mmol/kg, P= 0.02) but not in controls (129.0±28.6 vs 113.0±15.2 mmol/kg, NS). At the end of treatment with Sb, patients had higher fecal butyrate (16.0±4.4 vs 10.1 [2.9] mmol/kg, P= 0.004). Total SCFAs remained high 9 d after treatment was discontinued. Before the treatment, the anaerobe to aerobe ratio was lower in patients compared to controls (2.4±2.3 vs 69.8±1.8, P= 0.003). There were no significant changes in the fecal flora of TEN patients. CONCLUSION: Sb-induced increase of fecal SCFA concentrations (especially butyrate) may explain the preventive effects of this yeast on TEN-induced diarrhea.     

Cirrhosis in children with celiac disease

BACKGROUND: Liver involvement represents an extra-intestinal feature of celiac disease (CD) and shows a clinical spectrum varying from nonspecific reactive hepatitis to cirrhosis. Here we report the association of cirrhosis with CD in 5 children. PATIENTS AND METHODS: The mean age of the patients was 9.4 +/- 2.8 years. Viral, metabolic, and autoimmune etiology of liver disease was ruled out. Intestinal and liver biopsies were performed to confirm the histologic diagnosis in all subjects. RESULTS: Three of the patients had chronic diarrhea and hepatosplenomegaly in whom diagnoses of CD and cirrhosis were established at presentation simultaneously. In the other 2 patients, CD was diagnosed following an initial diagnosis of cirrhosis. At diagnosis, alanine aminotransferase (range, 64-271 IU/L) and aspartate aminotransferase (range, 90-225 IU/L) values were elevated. After 1 to 5 years of a gluten-free diet (GFD), normalization of serum aminotransferase levels and clinical improvement were observed in 3 patients with strict GFD. The other 2 patients without improvement of the liver disease had poor dietary compliance. CONCLUSION: CD may be associated with severe hepatic damage in children and strict GFD may have beneficial effect on the course of liver disease. Serologic screening of CD should be included in differential diagnosis of chronic liver disease of unknown origin.     

Assessment of sexual maturity in a cohort of adolescents with celiac disease on gluten-free diet

Delayed sexual maturation is a known complication of celiac disease (CD). There is paucity of data regarding the effect of gluten-free diet (GFD) on sexual maturity in patients with CD in India. We did a cross-sectional observational study to assess the sexual maturity in 30 adolescents with CD on GFD for at least 1 year, and evaluated factors which affect their sexual maturity. Sexual maturation was assessed using Tanner's stages of sexual development. All adolescents had completed 2 years of GFD and 53 % had completed 4 years of GFD. Sexual maturation was delayed in 30 %. Age at initiation of GFD was associated with attaining appropriate sexual maturity (p?=?0.048). We conclude that delayed sexual maturation is not uncommon in adolescents with CD and may be corrected by early diagnosis and initiation of GFD.     

High prevalence of small intestinal bacterial overgrowth in celiac patients with persistence of gastrointestinal symptoms after gluten withdrawal

OBJECTIVE: Celiac disease is a gluten-sensitive enteropathy with a broad spectrum of clinical manifestation, and most celiac patients respond to a gluten-free diet (GFD). However, in some rare cases celiacs continue to experience GI symptoms after GFD, despite optimal adherence to diet. The aim of our study was to evaluate the causes of persistence of GI symptoms in a series of consecutive celiac patients fully compliant to GFD. METHODS: We studied 15 celiac patients (five men, 10 women, mean age 36.5 yr, range 24-59 yr) who continued to experience GI symptoms after at least 6-8 months of GFD (even if of less severity). Antigliadin antibody (AGA) test, antiendomysial antibody (EMA) test, and sorbitol H2-breath test (H2-BT), as well as esophagogastroduodenoscopy (EGD) with histological evaluation, were performed before starting GFD. Bioptic samples were obtained from the second duodenal portion during EGD, and histopathology was expressed according to the Marsh classification. To investigate the causes of persistence of GI symptoms in these patients, we performed AGA and EMA tests, stool examination, EGD with histological examination of small bowel mucosa, and sorbitol-, lactose-, and lactulose H2-breath tests. RESULTS: Histology improved in all patients after 6-8 months of GFD; therefore, refractory celiac disease could be excluded. One patient with Marsh II lesions was fully compliant to his diet but had mistakenly taken an antibiotic containing gluten. Two patients showed lactose malabsorption, one patient showed Giardia lamblia and one patient Ascaris lumbricoides infestation, and 10 patients showed small intestinal bacterial overgrowth (SIBO) by lactulose H2-BT. We prescribed a diet without milk or fresh milk-derived foods to the patient with lactose malabsorption; we treated the patients with parasite infestation with mebendazole 500 mg/day for 3 days for 2 consecutive wk; and we treated the patients with SIBO with rifaximin 800 mg/day for 1 wk. The patients were re-evaluated 1 month after the end of drug treatment (or after starting lactose-free diet); at this visit all patients were symptom-free. CONCLUSIONS: This study showed that SIBO affects most celiacs with persistence of GI symptoms after gluten withdrawal.     

Population screening for celiac disease: follow up of patients identified by positive serology

BACKGROUND AND AIM: A previous study that evaluated the prevalence of celiac disease (CD) in a cohort of healthy blood donors, found that 3.8% of subjects had positive serology for CD. The aim of the present study was to examine how the screening results and the diagnosis of CD affected these patients' lifestyle and attitude toward CD. METHODS: All subjects with positive serology for CD (n = 59) found in the previous study of healthy blood donors (n = 1571) were contacted and interviewed. Data collected included current and previous symptoms compatible with CD, medical follow up since being informed of positive serology for CD and adherence to gluten-free diet (GFD). Information was obtained regarding attitude towards the screening for CD, the results of the screening, and the effect of screening on subjects' lifestyle. RESULTS: Of the 59 subjects, 51 were available for telephone interview, including all 10 subjects diagnosed with CD (positive serology and biopsy), 17/20 with positive serology and normal intestinal mucosa, and 24/29 with positive serology who refused to undergo intestinal biopsy. Of the 10 patients diagnosed with CD, four adhere to GFD. Only 1/17 subjects with normal intestinal mucosa repeated serology. Two of the 24 who initially refused a biopsy, underwent an intestinal biopsy, and one of them was currently diagnosed with CD. Only one patient diagnosed with CD had all his family members screened for CD. CONCLUSIONS: The data suggest that many of the patients identified in this screened population do not ultimately benefit from the purpose of the screening, which was early identification and treatment of a common disease with potential serious consequences.     

Partially responsive celiac disease resulting from small intestinal bacterial overgrowth and lactose intolerance

Background  

Celiac disease is a common cause of chronic diarrhea and malabsorption syndrome all over the world. Though it was considered uncommon in India in past, it is being described frequently recently. Some patients with celiac disease do not improve despite gluten free diet (GFD). A study described 15 cases of celiac disease unresponsive to GFD in whom small intestinal bacterial overgrowth (SIBO) or lactose intolerance was the cause for unresponsiveness.     

Macroamylasemia in patients with celiac disease

OBJECTIVE: Macroamylasemia is considered to be rarely associated with celiac disease (CD). We have evaluated patients in whom macroamylasemia or elevated total amylase (TA) led to the diagnosis of CD. These cases served as a catalyst for examining the prevalence of elevated TA and macroamylase (MA) in patients with active CD. METHOD: Total amylase and MA measurements were performed in the sera of 124 celiac patients with positive antiendomysium and tissue transglutaminase tests, in 100 patients on gluten-free diet (GFD) with negative serology test results, and in the sera of 89 healthy controls. Macroamylasemia was measured by using the PEG precipitation method. RESULTS: Twenty-three newly diagnosed celiac patients had elevated serum amylase levels (>2 SD above the controls). The average TA and MA levels were significantly elevated in both celiac groups. The nonprecipitated amylase levels (pancreatic and salivary amylase fractions) were not different from those of the controls. Three controls (3.4%), 21 newly diagnosed celiac (16.8%), and seven patients on GFD (7%) had significantly elevated MA activity in their sera. CONCLUSIONS: A significant percentage of the newly diagnosed patients with CD have macroamylasemia. Serum MA remained elevated in some patients on strict GFD. In addition, in the presence of an elevated amylase or MA the possibility of CD should be considered.