Gluten-sensitive enteropathy–associated conditions
[33] Recent studies describe the co-occurrence between coeliac disease, in which IBD is common in venous thrombosis.
[34][35] A study of patients with dermatitis herpetiformis or coeliac disease revealed significantly more gluten in the blood than controls.
[38] Coeliac disease is associated with a number of epidermal conditions including psoriasis[39][40] Prurigo nodularis.
Rothmund–Thomson syndrome, or poikiloderma congenitale, is a rare disorder, generally attributed to mutations of the RECQL4 helicase gene on 8q24 with features that include photosensitivity and poikilodermatous skin changes, etc., and has been reported in one coeliac patient.
[43] GSE has been found to be associated with alopecia areata (patchy baldness),[44] however hair regrowth did not necessarily occur after taking up a gluten free diet.
The incidence of juvenile Type 1 Diabetes (T1D) is about 1:500 in the U.S. population, and is the result of autoimmune damage to the Islets of Langerhans cells in the pancreas.
Childhood (male) Type 1 diabetes increases the risk for GSE and vice versa[48] and it now appears that GSE precedes T1D in many cases[49] and an active search for coeliac disease in early juvenile diabetes patients revealed that GF diet resulted in some improvements.
From an evolutionary point of view it is difficult to explain the high association of T1D and DQ2.5 given negatively selective nature of the disease in NW European population given the number of studies suggesting that the "Super B8" haplotypes has been under positive selection, and appears to be the most characteristic HLA type in NW Europeans indicating an advanced natural history of the haplotype.
Some of this may be due to persistent undetected food allergies, increased sensitivity of the damaged gut, or problems masked by GSE itself.
In diarrhea dominant IB - a common symptom of GSE - increased coeliac disease-associated serum IgG was found in treated and untreated CD patients.
IB may not resolve on GF diet, even becoming more severe in rare cases, as it may not have initially been directly linked to gluten consumption.
The more powerful acid blockers (omeprazole, esomeprezole) can interfere with calcium adsorption and can aggravate preexisting hypocalcaemia and hypomagnesemia, which are more common GSE[65] One study of 17 children in Italy who were diagnosed with eosinophilic oesophagitis found 6 of them also had coeliac disease.
[66] However a systematic review of several similar studies suggested a publication bias and that any association was uncertain.
[73] A recent study looking for changes in the physiology of the brain found regional cerebral hypoperfusion in 73% of untreated CD.
[74] The calcification of channels at the surface of the brain appears to be a leading phenomenon associated with migraine, visual, auditory, schizophrenia, epilepsy, dementia.
Gulliane-Barre syndrome is associated with peripheral neuropathies, and it has been found that anti-ganglioside autoantibodies take part in the binding to axons and schwann cells.
[81][82] There is a growing body of evidence suggesting that subclinical cases in older adults will typically progress toward dementia,[83] a large number of studies in Italy and Spain have documented earlier onset cases, though the autoimmune condition is not known, folic acid malabsorption may be the cause.
According to recent studies, calcifications of channels seen in dementia can also occur in specific brain areas such as the visual complex in the occipital lobe.
Ten (of 75) young patients had neurologic findings such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development, but magnetic resonance imaging detected unilateral and bilateral T2-hyperintensive white-matter lesions in 15 patients (20%)[86] Depression in GSE has several causes; in the more severe CD, depression can be the result of lower vitamin adsorption[10] and essential fatty acid adsorption.
[88] Fibromyalgia was found in 9% of adult patients relative to 0.03% in the general population with a link common to IBD.
Small intestinal bacterial overgrowth is associated is common with a transient response to antimicrobial therapy.
[90] Chronic fatigue associated with GSE is a systemic disorder, however there are neurological components that are especially manifest in blood deficiencies like avitaminosis, amineralosis and anemia.
Reduced iron and the lack of vitamins folate, B6, B12 and malabsorption of essential fatty acids can cause depression and chronic fatigue.
[91] Anti-gliadin antibodies correlate with higher risk for chronic-fatique when no clinical finding of CD is present.
[95] In addition, cross-reactive anti-beef-collagen antibodies (IgG) may explain some rheumatoid arthritis (RA) incidences.
[98] Still's disease (AOSD) is a rheumatic disorder of unknown etiology characterized by a triad of fever, polyarthritis and evanescent rash.
This condition is known as refractory coeliac disease (RCD), defined as malabsorption due to gluten-related enteropathy (villous atrophy or elevated intraepitheal lymphocytes) after initial or subsequent failure of a strict gluten-free diet (usually 1 year) and after exclusion of any disorder mimicking coeliac disease.
[115] For non-EATL cancers it is thought the mineralemias such as zinc and selenium may play a role in increasing risk.
Other studies implicate the malabsorption of vitamin A and zinc as a result of multi-vitamin and mineral deficiencies seen in coeliac disease.
