Abstracts
Adults & Celiac disease
The dietary presence of gliadin, an alcohol-soluble subfraction of gluten, in immunologically susceptible hosts will lead to small intestinal mucosal inflammation and subsequent mucosal villous atrophy which results in nutrient and vitamin malabsorption. Symptoms of coeliac disease are related to this malabsorption process which can be reversed in the vast majority of patients with a gluten-free diet.
Pham-TH & Barr-GD: Coeliac disease in adults. Presentation and management. Aust-Fam-Physician. 1996 Jan; 25(1): 62-5
Blood flow & Celiac disease
Successful treatment reduced the mesenteric blood flow in celiac disease to normal values. Our study demonstrates that pathophysiological changes in the small bowel mucosa during the active clinical phase of celiac disease induce an abnormal splanchnic circulation.
Alvarez-D. Et al: Superior mesenteric artery blood flow in celiac disease. Dig-Dis-Sci. 1993 Jul; 38(7): 1175-82.
Bone Mass & Celiac disease
Osteopenia is a common complication of celiac disease.
Evaluated whether treatment produces bone remineralization and whether calcium and vitamin D supplementation are necessary to reduce osteopenia.
All newly diagnosed celiac patients were treated with a gluten-free diet and randomized to receive diet only (n = 7) or diet plus calcium (1.0 g/day) and vitamin D (32,000 IU/wk) supplementation (n = 7).
At diagnosis, 11 patients had evidence of osteopenia (> 1 SD below normality) in the spine and total skeleton. After 12 months of gluten restriction, overall bone mass had increased 5.0% in the lumbar spine and 5.0% in the total skeleton.
11 patients who strictly followed gluten restriction, bone density increased 8% in the lumbar spine and in the total skeleton. Remineralization occurred throughout the skeleton but was more pronounced in the axial than in the peripheral skeleton. The increase in bone mass was independent of age or menopause.
Remineralization in patients treated with diet only was similar to that of patients treated with diet and supplements. Basal biochemical parameters showed a high bone turnover with secondary hyperparathyroidism. Treatment induced a decrease in bone turnover activity. However, a complete restoration of biochemical parameters was not achieved.
Strict gluten avoidance promoted a significant increase in bone mineral density. However, values still remain markedly low after 1 year in several patients. Although calcium and vitamin D supplementation did not provide additional benefit to that obtained by diet alone in the doses administered, this does not preclude a possible effect of vitamin D at higher dose.
Mautalen C et al., Effect of treatment on bone mass, mineral metabolism, and body composition in untreated celiac disease patients. Am J Gastroenterol, 1997 Feb, 92:2, 313-8.
Children & Celiac disease
Children (1)
A diagnosis of Coeliac Disease (CD) indicates a lifelong compliance to a gluten-free diet (GFD), which implies a change in deeply ingrained dietary habits and may cause dietary imbalances.
Coeliac children on a GFD have low caloric and carbohydrate intakes and a high fat intake. An unbalance towards simple sugar and saturated fat ingestion was detected. A lifelong protraction of these dietary habits may favour the onset of metabolic diseases in mature age.
Dell'Olio-D. Et al: [What do celiac children eat? Dietary analysis of a group of children with celiac disease on a diet]. Minerva-Gastroenterol-Dietol. 1995 Dec; 41(4): 269-73.
Children (2)
Surprisingly only 24 CD patients were found among the Danish children, compared with 155 in the Swedish group, despite the close ethnic, geographical, and cultural background of the two populations.
The estimated content of gliadin in the officially recommended diets of the two countries in 1987 differed substantially, the Swedish diet containing more than 40 times more gliadin than the Danish (4,400 vs. 100 mg) at the age of 8 months, and 4 times more (3,600 vs. 900 mg) at the age of 12 months. The Danish infant diet differed significantly from the Swedish in containing a larger amount of the lower gluten-containing rye flour. The earlier introduction of food items with a high gluten content in the Swedish compared with the Danish diet seems to be an obvious explanation for the great difference in incidence and symptomatology of CD between the two populations.
Weile-B. et al: Striking differences in the incidence of childhood celiac disease between Denmark and Sweden: a plausible explanation. J-Pediatr-Gastroenterol-Nutr. 1995 Jul; 21(1): 64-8.
Children (3)
Coeliac disease usually presents in infancy or early childhood with diarrhoea, vomiting and interference with weight gain and growth. Withdrawal of dietary gluten is followed by resolution of the symptoms and signs and restoration of normal weight gain and growth; the characteristic subtotal villous atrophy of the jejunal mucosa also recovers.
Littlewood-JM. : Coeliac disease in childhood. Baillieres-Clin-Gastroenterol. 1995 Jun; 9(2): 295-327.
Elderly & Celiac disease
Clinicians should be alert to the possibility of coeliac disease in the elderly particularly in patients with non-specific complaints in the presence of unexplained anaemia.
Hankey-GL & Holmes-GK: Coeliac disease in the elderly. Gut. 1994 Jan; 35(1): 65-7.
Folate & Celiac disease
Folate deficiency
In a patient with celiac disease, folate and iron deficiency, and epilepsy, CT over a 4-month period showed parietoocipital calcifications in the corticomedullary junctions. The calcification was progressive, but it and the seizures stabilized after institution of a gluten-free diet and iron and folic acid supplements.
Lea-ME. Et al: Bilateral occipital calcification associated with celiac disease, folate deficiency, and epilepsy. AJNR-Am-J-Neuroradiol. 1995 Aug; 16(7): 1498-500.
Gluten & Celiac disease
Gluten-free diet [GFD] (1)
This study suggests that a gluten-free diet increases bone mineral density in celiac patients, thereby leading to a complete recovery of bone mineralization. In evaluating 44 celiac patients between 2.58-20.42 years at diagnosis and comparing them to a subset of 25 patients 1.4 years after a gluten-free diet compared to 177 healthy controls between 1.52-20.99 years, the lumbar spine and whole-body bone mineral density values of celiac disease patients were significantly lower than in the control subjects.
Mora, Stefano, et al: Reversal of Low Bone Density With a Gluten-Free Diet in Children and Adolescents With Celiac Disease, American Journal of Clinical Nutrition, 1998;67:477-481.
Gluten-free diet [GFD] (2)
Celiac disease is a well-known entity in which intolerance to wheat gluten and related proteins from barley, rye, and oats (collectively known as prolamins) damage intestinal mucosa.
The ubiquitous presence of prolamins in the Western diet make treatment challenging.
Frick-TJ & Olsen-WA.: Celiac disease and the spectrum of gluten sensitivity. Gastroenterologist. 1994 Dec; 2(4): 285-92.
Gluten-free diet [GFD] 3)
Gluten-free diet (GFD) as the standard treatment for coeliac disease (CD) was discovered by Dicke.
Mulder-CJ et al., Coeliac disease. Diagnostic and therapeutic pitfalls. Scand-J-Gastroenterol-Suppl. 1993; 200: 42-7.
Gluten-free diet [GFD] (4)
Celiac Sprue is a malabsorption disease (not to be confused with a food allergy or hypersensitivity to food products) that can occur at any age. This disease is characterized by changes in the mucosal lining of the small intestine.
The mucosal lining is damaged by protein fragments of gliadin, which is found in gluten (wheat, rye, barley, oats), and the small intestine is unable to carry out its main functions of digestion and absorption.
Treatment is to discontinue gluten from the diet permanently, allowing the small intestine to heal itself. As the healing process continues, digestion and absorption resume. Celiac Sprue is an opportunistic disease which never goes away, so a gluten-free diet must be maintained for the rest of one's life.
Murphy-D: Celiac sprue. Gastroenterol-Nurs. 1995 Jul-Aug; 18(4): 133-7.
Infants & Celiac disease
Infant feeding
Studied the impact of infant feeding habits and actual gluten intake on gluten induced enteropathy.
85 siblings, carrying the genes DQA1*0501-DQB1*02 conferring susceptibility for the disease, were investigated by interview, food recording, and taking a small intestinal biopsy sample. 8 cases of silent celiac disease were found and these were compared with the 73 siblings in whom the diagnosis was excluded.
No statistically significant differences were found between cases and referents in terms of: duration of breast feeding, age at introduction of cows' milk products, frequency of breast feeding after gluten introduction, and gluten consumption.
The study’s factors may be of less importance for the development of gluten induced enteropathy.
Ascher H et al., Influence of infant feeding and gluten intake on coeliac disease. Arch Dis Child, 1997 Feb, 76:2, 113-7.
Nutrition & Celiac disease
Nutrients and nutritional status
Concentrations of serum ferritin, vitamin B12, and erythrocyte folate were lower in patients with untreated coeliac disease than in those in remission.
nutritional status was quite normal in both groups of coeliac patients.
Kemppainen-T. Et al: Intakes of nutrients and nutritional status in coeliac patients. Scand-J-Gastroenterol. 1995 Jun; 30(6): 575-9.
Celiac disease in the USA
Celiac disease is relatively rare in the United States and many of the facets of this complex disorder are not completely understood. In the gluten-sensitive individual, celiac disease is activated by ingestion of cereal glutens. An abnormal immune system response to dietary gluten causes damage to the small bowel mucosa, which results in nutrient malabsorption. When gluten is removed from the diet, malabsorption resolves.
Saunderlin-G: Celiac disease: a review. Gastr. Nurs. 1994, 17(3): 100-5.
Wheat intolerance
Evaluated the tolerance of prolonged consumption of small amounts of gliadin contained in products containing wheat starch in patients with celiac disease.
A quantifiable amount of immunoreactive gliadin (0.75 mg/100 g) was found in the wheat starch. The majority of the patients with celiac disease (11 of 17) who had never consumed wheat starch previously developed symptoms, which resolved within weeks of discontinuing the product. Relapse of skin lesions was seen in 2 of 3 patients with coexisting dermatitis herpetiformis.
The innocuousness of the long-term ingestion of "gluten-free" products containing wheat starch is still unproven, and prolonged use of such products by patients with celiac disease cannot be recommended.
Chartrand LJ et al., Wheat starch intolerance in patients with celiac disease. J Am Diet Assoc, 1997 Jun, 97:6, 612-8.
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