Etiology
Gluten sensitivity can develop at any point in life, and symptomatic disease may appear years after disease develops. When enteropathy develops in early childhood symptomatic disease is more rapidly evident. A survey of geriatrics with celiac disease in Finland revealed that the incidence of disease was much higher than the general population. Allergic disease may rise or fall with age; however, certain evidence points to the increased or daily use of non-steroidal anti-inflammatory factors (aspirin, ibuprofen) as an increased risk factor for urticaria or anaphylaxis, and the sensitizing dose may include low-dose aspirin therapy used in the treatment of heart disease. Idiopathic disease appears largely late onset.
Gluten-sensitive enteropathy develops as a consequence of genetic and environmental factors. Other than the involvement of certain HLA-DQ isoforms (antigen presenting proteins in humans) and certain wheat proteins, there is no clarity in the involvement of other genes or other environmental factors (see risk modifiers). Strong genetic factors such as seen in GSE have not been seen in gluten allergy, and with idiopathic gluten-sensitivity the HLA-DQ associations are weaker than with GSE.
Researchers reported extreme fatigue and pain in patients without celiac disease, with gliadin antibodies. They called this a "non-celiac gluten intolerance" for which there is no explanation as to the mechanisms involved.
Read more about this topic: Gluten Sensitivity