That can occur in genetically predisposed people where the ingestion of gluten leads to damage in the small intestine. It is estimated to affect 1 in 100 people worldwide. Two and one-half million Americans are undiagnosed and are at risk for long-term health complications (http://celiac.org). Other complications include the development of other autoimmune disorders like Type I diabetes, multiple sclerosis, neurological conditions like epilepsy, and intestinal cancers. Celiac disease can develop at any age after people start eating foods or medicines that contain gluten.
When people with celiac disease eat gluten which is a protein found in wheat, rye and barley, their body mounts an immune response that attacks the small intestine. These attacks lead to damage on the villi, small fingerlike projections that line the small intestine, that promote nutrient absorption. When the villi get damaged, nutrients cannot be absorbed properly into the body (http://celiac.org). Celiac disease is an hereditary disease, meaning that it runs in families. Currently, the only treatment for celiac disease is lifelong adherence to a strict gluten-free diet.
Gluten is a general name for the proteins found in wheat, rye, barley and triticale, which is a cross between wheat and rye. Gluten helps foods maintain their shape, acting as a glue that holds food together. Its name comes from the Latin word for “glue,” as it gives flour a sticky consistency when mixed with water. Gluten can be found in many types of foods, even ones that would not be expected. Anyone can survive without ingesting gluten because gluten itself it not a dietary need. Other foods are available that one can get their carbohydrate intake without consuming foods that include gluten.
As previously discussed the main source of gluten to stay away from includes wheat, barley, and rye. Other foods someone with celiac disease should also stay away from is, all wheat-based bread, all wheat-based pasta, cereals unless labeled gluten-free, baked goods including cakes, cookies, muffins, and pastries, snack foods including roasted nuts, flavored chips and popcorn, pretzels, beverages such as beer, and flavored alcoholic beverages. Foods that are naturally gluten free and are safe to eat when maintaining a gluten free diet include all meats and fish, all types of eggs are naturally gluten-free, plain dairy products, such as plain milk, plain yogurt and cheeses, fruits and vegetables, grains which includes quinoa and rice, starches and flours, potatoes, all nuts and seeds, and all herbs and spices. Genes that predispose people to gluten intolerance are very widespread in the population and, as a result, they are only a minor part of the explanation for the way in which gluten intolerance is inherited. However, the knowledge of the genes behind gluten intolerance is valuable in itself, as it helps researchers explore the reasons behind gluten intolerance, which in turn builds potential for developing new treatments and preventive methods.
This is essential, because the condition is often relatively symptom-free, yet it can have serious complications unless treated (www.news-medical.net). The most common ways to test for Celiac disease consists of a blood test and biopsy of from your small intestine. A blood test will look for antibodies that incorrectly interact with the gluten protein. The most common test is a tTG-IgA test.
Biopsy from your small intestine. People with a positive blood test will likely need to have a biopsy. This is a process in which a small tissue sample is taken from your intestine and checked for damage. The following two cases document how gluten intolerance affects not only Celiac disease but also Cystic fibrosis.
Other conditions can be triggered by gluten intolerance other than celiac disease. Cystic Fibrosis which is a progressive, genetic disease that causes persistent lung infections and limits the ability to breathe over time. Cystic fibrosis is one of the most common autosomal recessive disorders among populations, affecting approximately one in 3000 live births. The symptoms of celiac disease may be difficult to distinguish from those related to Cystic fibrosis, particularly in patients with malabsorption from pancreatic insufficiency. The combination of these two conditions may result in a significant insult to skeletal health. We report two cases of young adults who presented to our CF Center Endocrine Clinic in the past year with CF-related bone disease and upon further evaluation were subsequently diagnosed with concurrent celiac disease.
A 28-year-old white male with a history of CF (homozygous for the F508del mutation), CF-related diabetes (CFRD), and pancreatic insufficiency presented for evaluation of low bone density. Dual energy X-ray absorptiometry (DXA) scan showed low bone density with a significant decline in BMD compared to a previous scan obtained four years prior, as follows:?Femoral neck: -score ?2.6, decline in BMD by 13.3% over the preceding four years?Total hip: -score ?2.3, decline in BMD by 11.2%?PA spine: -score ?1.8, decline in BMD by 11.1%. The patient reported no significant oral or inhaled glucocorticoid use, delayed puberty, tobacco or alcohol use, or other risk factors for low bone density. He was compliant with pancreatic enzymes.
He endorsed excellent dietary calcium intake, and his 25-hydroxyvitamin D (25OHD) level was at goal 57?ng/mL on cholecalciferol 3000?IU daily. His BMI at the time of evaluation was 22.1?kg/m2, which had improved after starting insulin for treatment of CFRD several months before. He reported a possible rib fracture occurring earlier in the year, though this was not confirmed on X-ray. Pertinent family history included an aunt with celiac disease.
Laboratory evaluation showed normal parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase, renal function, and morning testosterone level. Screening tests for celiac disease showed a total immunoglobulin A (IgA) of 375?ng/dL (reference range 69–309?mg/dL) and an elevated anti-tissue transglutaminase (TTG) IgA level of 195.09?U/mL (reference range 0–15?U/mL). He was also found to have significant iron deficiency with a low ferritin level of 6?ug/L (reference range 20–300?ug/L) and a low transferrin saturation of 5%. He underwent endoscopy with duodenal biopsies, and pathology revealed villous blunting with intraepithelial lymphocytosis consistent with celiac disease.
A gluten-free diet was recommended for treatment. Follow-up DXA scans after initiation of treatment are not yet available given that the diagnosis of celiac disease was made within the past year. A 28-year-old white male with a history of CF (homozygous for the F508del mutation), pancreatic insufficiency, and progressive pulmonary decline over the preceding 6 months presented for evaluation of bone health prior to lung transplantation. Pretransplant screening DXA scan showed low bone mineral density (BMD) with femoral neck -score ?2.6, total hip -score ?2.3, and PA spine -score ?2.2. As with the first case, the patient reported no prior significant oral or inhaled glucocorticoid use, delayed puberty, or significant tobacco or alcohol use. He endorsed reduced physical activity over the year prior to his evaluation related to his advanced lung disease.
He had never suffered any fractures. He reported robust dairy intake every day, but he had persistent vitamin D deficiency (25OHD level 26?ng/mL) despite being compliant with ergocalciferol 50,000?IU twice weekly. His BMI was low at 18.8?kg/m2, and he reported longstanding difficulty with weight gain despite taking pancreatic enzymes with all meals and snacks. He denied any family history of celiac disease or other autoimmune or gastrointestinal disorders. Laboratory evaluation showed normal PTH, calcium, phosphorus, alkaline phosphatase, renal function, and morning testosterone level. Total IgA was 729?mg/dL and TTG IgA level was elevated at 82.60?U/mL.
The patient was evaluated by gastroenterology but was deemed too ill to undergo confirmatory testing with endoscopy and duodenal biopsy. He was empirically started on a gluten-free diet. Shortly thereafter, he underwent lung transplantation and was treated with intravenous zoledronic acid to prevent bone loss and fractures in the posttransplant period. To our knowledge, these are the first reported cases of celiac disease diagnosed in patients presenting with CF-related bone disease. In both cases, celiac disease was discovered in young adults with CF who had significantly low BMD -scores by DXA, and one patient had a marked decline in BMD despite few other risk factors for progressive bone loss. CF and celiac disease are each associated with low bone density and increased fracture risk, and the combination of these two conditions may lead to even further compromise in bone health.
Ethnicity may predispose patients to both of these conditions, since celiac disease and CF tend to occur in Caucasian populations. Moreover, recent studies suggest that celiac disease may occur more frequently in CF patients than in the general population. Future studies will be needed to determine the effect of a gluten-free diet on bone health in patients with CF and celiac disease (https://www.hindawi.com).
