Gluten-free Diet In Patients Research Articles

Is a life-long gluten-free diet for patients with celiac disease successful?

The ubiquity of gluten in foodstuffs, patient compliance, and variable patient susceptibility to gluten are all limiting factors of the gluten-free diet—the treatment of choice for celiac disease. New therapeutic strategies are emerging as a result of improved understanding of the molecular events underlying celiac disease; this Viewpoint considers whether a gluten-free diet is still adequate.

Neurologic presentation of celiac disease

Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results. Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity.

Factors relating to compliance with a gluten-free diet in patients with coeliac disease: comparison of white Caucasian and South Asian patients

Background & aims: To identify factors relating to compliance with a gluten-free diet amongst white Caucasian and South Asians with coeliac disease. Methods: Cross-sectional survey, with case note review of 130 adult patients with coeliac disease (90 white Caucasian and 40 South Asians). Results: 87 (66.9%) of the 130 questionnaires were returned; whites: 73.3%, South Asians: 52.5% ( P=0.02). White Caucasians’ assessment of their own strictness to the gluten-free diet correlated with small bowel histological recovery (OR 10.00, 95% CI 3.2–33.06) and negative endomysial antibodies (OR 34.94, CI 6.58–185.40). This was not seen in the South Asian patients. Amongst the white coeliacs, factors correlating with compliance with a gluten-free diet were: Coeliac Society membership, understanding food labelling, obtaining sufficient gluten-free products, explanation by a physician, and regular dietetic follow-up. These factors were not identified amongst the South Asians, who were less likely to attend dietetic clinics, join the Coeliac Society and be satisfied with information provided by doctors and dieticians. Conclusions: In contrast to the South Asians, factors were identified which related to compliance with a gluten-free diet amongst white Caucasian coeliac patients. This study has shown that the treatment approach to ethnic minorities with coeliac disease must be improved.

The symptomatic and histologic response to a gluten-free diet in patients with borderline enteropathy.

A clinical problem is posed by patients with symptoms suggestive of gluten sensitivity (diarrhea, weight loss, unresponsive iron-deficiency anemia, etc.); however, small intestinal biopsies reveal only minor abnormalities, such as lymphocytosis with or without crypt hyperplasia (Marsh I-II). Our aim was to assess the benefit of a gluten-free diet (GFD) in patients with these small bowel mucosal abnormalities. We studied 35 patients (11 men, 24 women; mean age, 28 years; range, 22-51 years) referred to us for gastrointestinal symptoms or unexplained or unresponsive diseases. Because celiac disease was suspected to be the underlying pathology, small intestinal biopsies were taken. These revealed only minor abnormalities: 11 patients showed Marsh I type lesions, whereas 24 patients demonstrated Marsh II type lesions. Although the histologic lesions were inconsistent for celiac disease and a suspicion of a borderline celiac disease persisted, all patients were motivated to adhere to GFD. RESULTS Only 23 patients adhered to our advice and followed a GFD; follow-up biopsies were taken after 8 to 12 months. In the Marsh I lesion group (seven patients), five patients showed mucosal normalization to Marsh 0 and two showed persistence of Marsh I lesions. In the Marsh II lesion group (16 patients), 9 patients revealed mucosal normalization, 5 improved to a Marsh I lesion, and 3 revealed persistence of Marsh II lesions. A dramatic clinical improvement in symptoms was noted in all patients who were on a GFD, with symptoms virtually disappearing in all patients. Seven patients who refused GFD were reevaluated 8 to 12 months later. Symptoms and histologic lesions were unchanged in six, all of whom refused again to adhere to a GFD. One of the seven with Marsh I lesions had a worsening of symptoms and of histologic lesions (from Marsh I to Marsh IIIa); so, this last patient adhered to a GFD. Symptoms disappeared after GFD in patients suspected to have celiac disease but with slight histologic lesions. Although Marsh I-II lesions cannot be classified as celiac lesions (ESPGAN criteria), the patients' symptoms at presentation and the clear improvement of symptoms when on GFD, with or without improvement of histologic lesions, supports the assumption that these patients are sensitive to gluten and may justify treatment with a GFD.

Bone mineral density and importance of a gluten-free diet in patients with celiac disease in childhood.

Celiac disease (CD), a common cause of malabsorption, is known to be associated with disorders of the skeleton, but there are conflicting data about the effect of diet on bone metabolism. The aims of this study were to investigate the prevalence of osteopenia; to identify the relationship between bone mineral density (BMD), serum calcium, and parathyroid hormone levels; and to determine the effect of gluten-free diet on BMD in children with celiac disease. The study included 32 patients with CD (group 1) and 82 healthy controls (group 2). The patients with CD were evaluated under 2 subgroups, ie, 16 patients with recent diagnosis (group 1a) and 16 patients who follow their diet strictly (group 1b). BMD values and concentrations of calcium, phosphorus, alkaline phosphatase, and intact parathyroid hormone were determined on entry to the study and at 12 months in celiac patients. These values were compared with those of healthy control participants. BMD and bone mineral content values in patients with recent diagnosis were found to be significantly lower than the control group. The BMD values in patients with recent diagnosis were significantly increased after a gluten-free diet for 1 year. Osteopenia was found more commonly in patients with recent diagnosis than patients in whom a gluten-free diet had been instituted. At 1-year follow-up, osteopenia was not resolved with the gluten-free diet, and this was especially true in patients without gastrointestinal manifestation. In patients with recent diagnosis (group 1a), the mean calcium level was found to be lower than the patients who follow their diet strictly (group 1b). There was a positive correlation between calcium level and BMD and bone mineral content. BMD is almost invariably low in newly diagnosed celiac patients in childhood. We therefore recommend that BMD should be evaluated in patients with CD. Strict gluten avoidance promoted a significant increase in BMD. However, values still remained markedly low after 1 year of follow-up in some patients. These patients should be followed for longer periods of time with yearly BMD evaluation, as 1 year of diet therapy was found to be insufficient for osteopenia to be resolved.

Duodenal Disaccharidase Activities in the Follow-up of Villous Atrophy in Coeliac Disease

Background: In active coeliac disease, mucosal atrophy is associated with a marked decrease in intestinal disaccharidase enzyme activities. We investigated the value of duodenal mucosal disaccharidases to predict the severity of mucosal villous atrophy and its recovery in 50 patients with coeliac disease. Methods: Duodenal mucosal histology and disaccharidase activities were studied at least twice with a mean interval of 9 months. Histology of specimens from all patients was examined by the same pathologist blinded to the data on disaccharidase activities. Mucosal damage was scored into four groups as follows: Grade 0 = normal mucosa; grade 1 = slight villous atrophy, that is, cryptic component 30%- 50%; grade 2 = moderate villous atrophy, that is, cryptic component 50%-90%; grade 3 = severe villous atrophy, that is, cryptic component >90%. The enzyme activities of the disaccharidases were determined as U/g protein. Results: Duodenal mucosal disaccharidase activities were good predictors of the grade of mucosal villous atrophy. Positive predictive values for moderate or severe villous atrophy were 90% for maltase (maltase activity <150 U/g protein), 86% for sucrase (<40 U/g protein) and 71% for lactase (<20 U/g protein). Accordingly, negative predictive values, that is, none or only minimal villous atrophy (grades 0 or 1) with normal disaccharidase activities, were 71% for maltase, 70% for sucrase and 63% for lactase. Conclusions: The increase in duodenal disaccharidase activities correlated with recovery of the mucosa based on histology. Besides the histological examination, measurement of disaccharidase activities offers an additional tool to evaluate response to a gluten-free diet in patients with coeliac disease.

Duodenal Disaccharidase Activities in the Follow-up of Villous Atrophy in Coeliac Disease

Background: In active coeliac disease, mucosal atrophy is associated with a marked decrease in intestinal disaccharidase enzyme activities. We investigated the value of duodenal mucosal disaccharidases to predict the severity of mucosal villous atrophy and its recovery in 50 patients with coeliac disease. Methods: Duodenal mucosal histology and disaccharidase activities were studied at least twice with a mean interval of 9 months. Histology of specimens from all patients was examined by the same pathologist blinded to the data on disaccharidase activities. Mucosal damage was scored into four groups as follows: Grade 0 = normal mucosa; grade 1 = slight villous atrophy, that is, cryptic component 30%- 50%; grade 2 = moderate villous atrophy, that is, cryptic component 50%-90%; grade 3 = severe villous atrophy, that is, cryptic component >90%. The enzyme activities of the disaccharidases were determined as U/g protein. Results: Duodenal mucosal disaccharidase activities were good predictors of the grade of mucosal villous atrophy. Positive predictive values for moderate or severe villous atrophy were 90% for maltase (maltase activity <150 U/g protein), 86% for sucrase (<40 U/g protein) and 71% for lactase (<20 U/g protein). Accordingly, negative predictive values, that is, none or only minimal villous atrophy (grades 0 or 1) with normal disaccharidase activities, were 71% for maltase, 70% for sucrase and 63% for lactase. Conclusions: The increase in duodenal disaccharidase activities correlated with recovery of the mucosa based on histology. Besides the histological examination, measurement of disaccharidase activities offers an additional tool to evaluate response to a gluten-free diet in patients with coeliac disease.

Adherence to Gluten-Free Diet and Serum Antigliadin Antibodies in Celiac Disease

In 134 patients with celiac disease the compliance with a gluten-free diet (GFD) and the presence of antigliadin antibodies (AGA) were evaluated. Compliance with the GFD was good in 71%, moderate in 11% and poor in 18%. High levels of AGA (IgA and IgG) were found in 24.2% of patients with good GFD, in 40% of those with moderate GFD and in 75% of those with poor GFD compliance. Our data suggest that the presence of AGA is correlated with the degree of adherence to the GFD, and that AGA measurement may be of some value in the monitoring of GFD in patients with celiac disease.

Dietary Management of Dermatitis Herpetiformis

Dermatitis herpetiformis (DH) is an extremely itchy, papulovesicular skin disease characterized in part by the presence of IgA at the dermal-epidermal junction. Eighty-five percent to 90% of DH patients have granular deposits of IgA at the dermal-epidermal junction, and essentially all of these patients have an associated, for the most part asymptomatic, gluten-sensitive enteropathy (GSE). The association of GSE and DH suggested that the cutaneous manifestations of DH could be controlled by the use of a gluten-free diet. Institution of a gluten-free diet in patients with DH and granular IgA deposits has been shown to be effective in controlling the cutaneous eruption of DH. Seventy percent to 100% of patients who begin a strict gluten-free diet have been shown to be able to decrease the dosage of medication needed to control their DH after a mean of eight to 18 months on the diet. Furthermore, 40% to 70% of patients with DH can control their skin disease completely, without any medication, after longer periods of time on the gluten-free diet (two years and longer). Although the gluten-free diet has been shown to be of great benefit in the control of the skin manifestations of DH, at the present time there is no evidence to suggest that the gluten-free diet is in any way protective against the risk of intestinal lymphoma that has been documented in GSE. Evaluation of the cutaneous IgA deposits in DH skin after long periods of time on a gluten-free diet suggests that there may be a slight decrease in the intensity of the IgA deposits, but the true pathogenetic relationship between the cutaneous IgA deposits, the cutaneous manifestations of DH, and the associated GSE remains unknown.

Gluten-free diet in patients with dermatitis herpetiformis. Effect on the occurrence of antibodies to reticulin and gluten

Gluten-free diet in patients with dermatitis herpetiformis. Effect on the occurrence of antibodies to reticulin and gluten