CLINICAL PRESENTATION OF GS
Although CD is a disorder associated with the GI system, the “classic” GI symptoms of bloating, flatulence, diarrhea, and/or constipation are often absent (silent CD), especially in older individuals. It is for this reason that the diagnosis of CD is easily missed.
Delaying diagnosis can have serious health consequences, as CD is associated with significant morbidities, such as malnutrition (worse in children), iron-deficiency anemia, neuropsychiatric aberrations (depression, anxiety, attention-deficit, and cerebral ataxia), osteoporosis, lymphoma, and death (see Table 1).4,13 CD may also present with dermatitis herpetiformis, a chronic vesicular rash, seen most often in adult males.
The role of gluten in the development of autism spectrum disorders or schizophrenia, though not proven, remains hotly debated, especially as close biochemical links are now recognized between the gut and the brain. It is clear, however, that gluten intake in severely gluten-sensitive individuals can directly affect mood and brain function. Most CD-associated morbidities will resolve after one year of complete gluten avoidance.1,13
Prominent symptoms of NCGS occur soon after gluten ingestion and disappear within days to weeks of gluten avoidance. The classic NCGS presentation combines IBS-like symptoms, such as abdominal cramps, bloating, diarrhea, and constipation, with systemic manifestations that include “brain fog,” fatigue, headache, joint and muscle pain, peripheral numbness, skin rash, aphthous stomatitis, anemia, and depression or anxiety. As with CD, GI symptoms usually predominate in children and abate with gluten avoidance.14,15
Allergic reactions to wheat will present within minutes to two hours of wheat exposure and may manifest with pruritic rash, hives, swelling of the lips or tongue, rhinitis, abdominal cramps, vomiting, diarrhea, constipation, and/or anaphylaxis. Subtle reactions may make diagnosis difficult.12
DIAGNOSTIC STUDIES FOR GS
The effectiveness of diagnostic testing for CD has been well established. Testing for antitissue transglutaminase antibodies (tTG-IgA) is the preferred laboratory test for CD, with a sensitivity of 93%, specificity of 98%, and few false-negative results. The endomysial antibody (EMA-IgA) test, though highly specific for CD, lacks the sensitivity of tTG-IgA. Newer antibody tests, such as deamidated gliadin peptide IgA and IgG, have not proven superior in detecting CD. Genetic testing for HLA-DQ2 and HLA-DQ8 may also be performed, but many people carry the gene without ever developing CD.13
To improve the reliability of CD antibody tests, the patient should have consumed gluten regularly for at least one month prior to testing. If the patient has been on a gluten-free diet for several weeks, then a gluten challenge should be done: The patient would be instructed to consume at least 3 g/d of gluten (two slices of bread) for a minimum of two weeks (versus eight weeks in previous protocols), after which the celiac antibody tests would be repeated.16
If these antibody test results are negative but the suspicion for CD remains high, an endoscopy with a duodenal biopsy should be performed. The appearance of villous atrophy would confirm the diagnosis of CD.1,13,16
Unlike CD, there are currently no reliable diagnostic tests for NCGS, although some researchers suggest testing for IgG antigliadin antibodies (AGA); NCGS is currently a diagnosis of exclusion.7 In NCGS, celiac antibodies will be negative and the duodenal biopsy will demonstrate only mild inflammation without the mucosal atrophy of CD. As with CD, patients affected by NCGS will also test negative for the wheat allergy IgE response.
Another option is a gluten challenge. The patient is instructed to follow a gluten-free diet for six weeks and monitor for NCGS symptoms. If symptoms abate, a gluten-containing diet is then reintroduced and the patient is evaluated for the reemergence of NCGS symptoms. If symptoms are not reduced with a gluten-free diet, NCGS may be excluded. Newer GS laboratory tests will emerge that can assay more forms of gliadin antibodies, possibly aiding in NCGS diagnosis.4,14
To make a diagnosis of WA, skin prick tests and allergen-specific IgE testing are used, along with a medical history, clinical presentation, and possibly a food challenge.
Continue for management of GS >>