Medication and Supplement Use in Celiac Disease

Ashley N. Johnson, PharmD, BCPS; Angela N. Skaff, BS, PharmD Candidate; Lauren Senesac, PharmD Candidate


US Pharmacist. 2014;39(12):44-48. 

In This Article

Clinical Presentation and Diagnosis

CD pathogenesis involves both environmental and genetic factors, including several genes that predispose an individual to the disease.[7] Depending upon the trigger, symptoms may appear in early childhood or later in life. Typically, patients present with symptoms that are secondary to malabsorption of nutrients; however, some present with nonspecific GI discomfort or extraintestinal symptoms, either alone or in addition to manifestations of malabsorption (Table 2). For this reason, there is often a delay in diagnosing CD, particularly because patients are commonly misdiagnosed with other disorders prior to confirmation of CD. Misdiagnoses include irritable bowel syndrome, inflammatory bowel disease, gastroesophageal reflux disease, ulcers, viral gastroenteritis, chronic fatigue syndrome, allergies, parasitic infection, gallbladder disease, colitis, cystic fibrosis, psychological dysfunction, and lactose intolerance.[5]

Lactose intolerance is a common misdiagnosis in CD patients because the mucosal injury renders them unable to digest lactose-containing products. Malabsorption secondary to mucosal injury also explains nutritional deficiencies of the fat-soluble vitamins A, D, E, and K, as well as the B vitamins, thereby diminishing the absorption of iron, calcium, and folic acid.[1] As a result, patients may develop iron-deficiency anemia refractory to oral iron supplementation, and potentially osteoporosis and osteopenia due to bone loss secondary to decreased calcium and vitamin D absorption.[1] Reproductive abnormalities, such as delayed puberty, secondary amenorrhea, infertility, or subfertility, may be explained by the combination of nutritional deficiencies and the damaging effects of systemwide chronic inflammation.[11] Other common manifestations, such as dermatitis herpetiformis (DH; a papulovesicular rash), result from the immunologic responses to gluten ingestion.[1]

While all persons with CD are intolerant to gluten, not all individuals who are intolerant to gluten have CD. Recent studies have confirmed the existence of nonceliac gluten sensitivity (NCGS), a hypersensitivity or form of gluten intolerance wherein individuals experience a complex of symptoms similar to that of CD. Unlike CD, NCGS is not hereditary and is not associated with malabsorption, nutritional deficiency, or an increased risk of autoimmune disorders or intestinal malignancies.[3,7] Furthermore, immunologic mechanisms or serologic markers for NCGS have not yet been identified.[3] Diagnosis of NCGS is made by excluding both CD and an IgE-mediated allergy to wheat, and is otherwise based on the manifestation of symptoms associated with gluten consumption.

According to the American College of Gastroenterology's (ACG) clinical guideline on diagnosis and management of celiac disease, CD should be tested for if the patient has signs and symptoms of malabsorption (e.g., chronic diarrhea with weight loss, steatorrhea, postprandial abdominal pain, bloating) or laboratory evidence of malabsorption, particularly in the case of a first-degree family member with a confirmed diagnosis of CD, a personal history of an autoimmune disease, or an IgA deficiency.[7] CD should also be suspected in patients with biopsy-proven DH, iron-deficiency anemia refractory to oral supplementation, or hypertransaminasemia with no other etiology.[7]

In all cases, the adoption of a lifelong GFD has been shown to relieve symptoms, and in CD patients it has been shown to normalize serologic markers of CD and restore intestinal villi otherwise degenerated by inflammatory reactions.[3] Nonadherence to the GFD can result in serious complications associated with malabsorption, including fractures secondary to low bone mineral density, and in some cases intestinal malignancies such as intestinal T-cell lymphomas, small-bowel adenocarcinoma, esophageal cancer, and B- and T-cell non-Hodgkin lymphomas.[7]