Food Intolerance Panel™
Gluten Intolerance
Gluten intolerance is more prevalent than was previously understood. Historically the diagnosis relied
on biopsy of the small intestine. Patients with less severe or vague symptoms were in most cases excluded
as candidates for biopsy. In addition, a normal biopsy does not exclude the disease; inflammation may be
patchy, or tissue may show some degree of response that falls short of villous atrophy and other diagnostic
criteria. With the advent of biochemical markers for gluten intolerance, several studies have proven the
presence of specific antibody-verified, gluten-free diet-validated gluten intolerance in a large sector of
the society (12–18 % depending on ethnicity). A step forward in redefining the incidence of the disease was
the introduction of broader definitions of the disease entity. Newly added subtypes allow inclusion of variants
previously not included among gluten- intolerance patients.
Silent gluten intolerance: A completely asymptomatic form usually associated with gross damage to small
intestinal mucosa and positive biochemical markers (anti-gliadin and other antibodies).
Latent gluten intolerance: May be vaguely or mildly symptomatic and is associated with grossly normal intestinal
lining that shows signs of low-grade intestinal inflammation. It is associated with increased intra-epithelial
lymphocyte counts, and biochemical markers are usually positive.
Milk intolerance (sometimes termed cow milk sensitive enteropathy): Cow’s milk-induced small intestinal mucosal
damage that is reversed by a cow’s milk-free diet and recurs on challenge. It is an abnormal physiologic response
to casein in genetically predisposed individuals. The reaction includes metabolic, toxic and immunopathologic
(inflammatory) responses to casein.
Milk intolerance is caused by casein and other milk antigens or proteins. Casein triggers a toxic reaction on
contact with intestinal cells. This contact triggers an inflammatory cascade resulting in damage to the mucosal
barrier. The inflammatory cells produce mediators that signal local lymphocytes to produce antibodies against casein.
The first and main antibody response on the gut mucosal lining is secretory IgA.
Damage to small intestinal lining and clinical symptoms vary widely. In severe cases, the problem is apparent in
early age (< 3 years of age). In milder cases, the patient may be completely asymptomatic, yet suffering an ongoing
inflammatory insult to the small intestine. The mucosal barrier damage is in the form of mild to moderate villous
atrophy (villous shortening) in a patchy manner.
Lactose Intolerance
Lactose intolerance is a common condition caused by deficiency in the intestinal brush-border enzyme lactase. Its
effects are largely dose-dependent. In many cases, a transitional or reversible lactose intolerance is observed. This
is commonly experienced in patients with food intolerances where the sloughing of the mucosa leads to a decreased
availability of the lactase enzyme. The sloughing results in loss of the disaccharidase-containing mature enterocytes,
leading to a reduction in lactase small intestinal activity. Usually when patients implement a strict avoidance program
of the offending food, their lactose intolerance vanishes.
Egg Intolerance
It is defined as egg white-induced, small intestinal mucosa damage that is reversed by an egg-free diet and recurs on
challenge. It is an abnormal physiologic response to ovalbumin in genetically predisposed individuals. The reaction
includes metabolic, toxic and immunopathologic (inflammatory) responses to ovalbumin. Egg intolerance caused by ovalbumin
occurs with hen and most other bird eggs. Ovalbumin triggers a toxic reaction on contact with intestinal cells. This
contact triggers an inflammatory cascade resulting in damage to the mucosal barrier. The inflammatory cells produce
mediators that signal local lymphocytes to produce antibodies against casein. The initial and major antibody subclass
to increase in the gut mucosal lining is secretory IgA.
Soy Intolerance (termed soy protein-sensitive enteropathy)
It is defined as soy protein-induced small intestinal mucosa damage that is reversed by a soy-free diet and recurs
on challenge. It is an abnormal response to soy proteins in genetically predisposed individuals. The reaction includes
metabolic, toxic and immunopathologic (inflammatory) responses to soy. Damage to small intestinal lining and clinical
symptoms vary widely. In severe cases, the problem is apparent in early age (< 3 years of age). In milder cases the
patient may be completely asymptomatic, yet suffering an ongoing inflammatory insult to the small intestine as shown
by secretory IgA release.
For more information about tests in this panel, please refer to the links at the left.