Andre sykdommer koblet til gluten- og melkeproteinintoleranse
Scand J Gastroenterol. 2007 Aug;42(8):962-7.Links
Gluten sensitivity in patients with primary Sjögren's syndrome.
Lidén M, Kristjánsson G, Valtýsdóttir S, Hällgren R.
Department of Medical Sciences Rheumatology, University Hospital. Uppsala. Sweden.
Objective. To evaluate the rectal mucosal response to gluten as an indication of gluten sensitivity in patients with primary Sjögren's syndrome (pSS). Material and methods. Rectal challenges with wheat gluten were performed in 20 patients with pSS and 18 healthy control subjects. Fifteen hours after challenge the mucosal production of nitric oxide (NO) was measured. Results. Five patients with pSS had a significant increase in the luminal release of NO after the rectal gluten challenge, indicating gluten sensitivity. All were HLA-DQ2 and/or -DQ8-positive. Two of the patients with increased NO had antibodies against transglutaminase and a duodenal biopsy showed an absolutely flat mucosa consistent with coeliac disease in one of the patients. Before gluten challenge, 15 of the Sjögren's syndrome (SS) patients reported gastrointestinal symptoms, and 8 reported intolerance to various food products. No correlation was found between gluten sensitivity and self-reported food intolerance or gastrointestinal symptoms. Conclusions. Rectal mucosal inflammatory response after gluten challenge is often seen in patients with pSS, signifying gluten sensitivity. However, this reactivity is not necessarily linked to coeliac disease.
PMID: 17613926 [PubMed - in process]
Eur J Dermatol. 2006 Jan-Feb;16(1):4-11.Links
Gluten intolerance and skin diseases.
Humbert P, Pelletier F, Dreno B, Puzenat E, Aubin F.
Department of Dermatology, University of Franche-Comté, CHU Saint Jacques, 25030 Besançon, France. Denne e-postadressen er beskyttet mot programmer som samler e-postadresser. Du må aktivere javaskript for å kunne se den.
Gluten sensitivity with or without coeliac disease (CD) symptoms and intestinal pathology has been suggested as a potentially treatable cause of various diseases. CD is a chronic disease which improves on withdrawal of wheat gliadins and barley, rye and oat prolamins from the diet. There have been numerous reports linking CD with several skin conditions. A body of evidence shows that dermatitis herpetiformis is actually a cutaneous manifestation of CD. Autoimmune diseases, allergic diseases, psoriasis and miscellaneous diseases have also been described with gluten intolerance. Dermatologists should be familiar with the appraisal of gluten sensitive enteropathy and should be able to search for an underlying gluten intolerance (GI). Serological screening by means of antigliadin, antiendomysial and transglutaminase antibodies should be performed. HLA typing is often useful in association with serologic tests. Intestinal biopsy is usually needed to establish the diagnosis of CD or GI. Thus, gluten intolerance gives rise to a variety of dermatological manifestations which may benefit from a gluten-free diet.
PMID: 16436335 [PubMed - indexed for MEDLINE]
Ann Rheum Dis. 2004 Nov;63(11):1501-3.Links
Gluten sensitivity masquerading as systemic lupus erythematosus.
Hadjivassiliou M, Sanders DS, Grünewald RA, Akil M.
Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK. Denne e-postadressen er beskyttet mot programmer som samler e-postadresser. Du må aktivere javaskript for å kunne se den.
CASE REPORTS: Three patients are described whose original presentation and immunological profile led to the erroneous diagnosis of systemic lupus erythematosus. The correct diagnosis of gluten sensitivity was made after years of treatment with steroids and other immunosuppressive drugs. CONCLUSIONS: The immunological profile of IgA deficiency and/or raised double stranded DNA in the absence of antinuclear factor together with raised inflammatory markers and symptoms suggestive of an immune diathesis should alert the physician to the possibility of gluten sensitivity. The presence of an enteropathy is no longer a prerequisite for the diagnosis of gluten sensitivity, which can solely present with extraintestinal symptoms and signs. Knowledge of the diverse manifestations of gluten sensitivity is essential in avoiding such misdiagnosis.
PMID: 15479903 [PubMed - indexed for MEDLINE]
1: J Clin Gastroenterol. 2003 Jan;36(1):13-7.Links
J Clin Gastroenterol. 2003 Jan;36(1):6-7.
The symptomatic and histologic response to a gluten-free diet in patients with borderline enteropathy.
Tursi A, Brandimarte G.
Department of Emergency, L. Bonomo Hospital, Andria (BA), Italy. Denne e-postadressen er beskyttet mot programmer som samler e-postadresser. Du må aktivere javaskript for å kunne se den.
GOALS: A clinical problem is posed by patients with symptoms suggestive of gluten sensitivity (diarrhea, weight loss, unresponsive iron-deficiency anemia, etc.); however, small intestinal biopsies reveal only minor abnormalities, such as lymphocytosis with or without crypt hyperplasia (Marsh I-II). Our aim was to assess the benefit of a gluten-free diet (GFD) in patients with these small bowel mucosal abnormalities. STUDY: We studied 35 patients (11 men, 24 women; mean age, 28 years; range, 22-51 years) referred to us for gastrointestinal symptoms or unexplained or unresponsive diseases. Because celiac disease was suspected to be the underlying pathology, small intestinal biopsies were taken. These revealed only minor abnormalities: 11 patients showed Marsh I type lesions, whereas 24 patients demonstrated Marsh II type lesions. Although the histologic lesions were inconsistent for celiac disease and a suspicion of a borderline celiac disease persisted, all patients were motivated to adhere to GFD.RESULTS Only 23 patients adhered to our advice and followed a GFD; follow-up biopsies were taken after 8 to 12 months. In the Marsh I lesion group (seven patients), five patients showed mucosal normalization to Marsh 0 and two showed persistence of Marsh I lesions. In the Marsh II lesion group (16 patients), 9 patients revealed mucosal normalization, 5 improved to a Marsh I lesion, and 3 revealed persistence of Marsh II lesions. A dramatic clinical improvement in symptoms was noted in all patients who were on a GFD, with symptoms virtually disappearing in all patients. Seven patients who refused GFD were reevaluated 8 to 12 months later. Symptoms and histologic lesions were unchanged in six, all of whom refused again to adhere to a GFD. One of the seven with Marsh I lesions had a worsening of symptoms and of histologic lesions (from Marsh I to Marsh IIIa); so, this last patient adhered to a GFD. CONCLUSIONS: Symptoms disappeared after GFD in patients suspected to have celiac disease but with slight histologic lesions. Although Marsh I-II lesions cannot be classified as celiac lesions (ESPGAN criteria), the patients' symptoms at presentation and the clear improvement of symptoms when on GFD, with or without improvement of histologic lesions, supports the assumption that these patients are sensitive to gluten and may justify treatment with a GFD.
PMID: 12488700 [PubMed - indexed for MEDLINE]