Elevated serum aminotransferase activity as an early manifestation of gluten-sensitive enteropathy

Vajro, Pietro; Fontanella, Angiola; Mayer, M; Vincenzo, Anna De; Terracciano, Luigi; D’Armiento, Maria; Vecchione, Raffaella

doi:10.1016/s0022-3476(05)83430-4

Cited by 78 publications

(53 citation statements)

References 9 publications

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“…The problem of liver damage in association with CD has been outlined since 1977, and serological screening for antigliadin has long been recommended in patients with cryptogenic hepatitis. [31][32][33] Nevertheless, complete analysis of the major autoantibodies that characterise the various forms of chronic hepatitis (that is, ANA, SMA, AAA, LKM, AMA, SLA, LC-1, and ANCA) 18 has never been carried out in CD. 33 In our study most coeliac patients with associated liver involvement had positive AAA of either the IgG or the IgA type or both, while analysis of other autoantibodies associated with chronic hepatitis proved negative.…”

Section: Discussionmentioning

confidence: 99%

Immune Reaction Against Cytoskeleton in Coeliac Disease

Clemente

Frau

Brusco

et al. 1999

Journal of Pediatric Gastroenterology & Nutrition

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Background-The cytoskeleton actin network of intestinal microvilli has been found to be rapidly impaired after gluten challenge in coeliac disease (CD). The aim of this study was to investigate the presence of an immune reaction towards cytoskeleton structures such as actin filaments in CD. Methods-Eighty three antiendomysial antibody positive CD patients (52 children and 31 adults) were studied at our outpatient clinics from 1996 to 1998 using indirect immunofluorescence, ELISA, and western blotting for antiactin (AAA) and antitissue transglutaminase (TGA) antibodies before and after a gluten free diet (GFD). Sixteen patients with smooth muscle antibody positive autoimmune hepatitis, 21 with inflammatory bowel diseases, seven with small bowel bacterial overgrowth, and 60 healthy subjects were studied as controls. Results-Fifty nine of 83 CD patients (28/31 adults (90.3%); 31/52 children (59.6%)) were positive for IgA and/or IgG AAA. Seventy seven (92.7%) were positive for IgA TGA. IgA AAA were strongly correlated with more severe degrees of intestinal villous atrophy (p<0.0001; relative risk 86.17). After a GFD, AAA became undetectable within five months. Conclusions-Apart from the immune reaction against the extracellular matrix, we have described an immune reaction against the cytoskeleton in both children and adults with CD. As AAA are strongly associated with more severe degrees of villous atrophy, they may represent a useful serological marker of severe intestinal atrophy in CD. (Gut 2000;47:520-526)

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Section: Discussionmentioning

confidence: 99%

Immune Reaction Against Cytoskeleton in Coeliac Disease

Clemente

Frau

Brusco

et al. 1999

Journal of Pediatric Gastroenterology & Nutrition

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“…An altered growth hormone (GH)/IGF-I axis may be induced by malnutrition and can theoretically also be the result of direct interference of the GH-signalling pathway or of impaired liver function with low synthesis of IGF-I. Several studies have shown the liver to be involved in coeliac disease, with increase of serum levels of alanine and aspartate aminotransferases (ALAT and ASAT), even in the absence of malabsorption (10,11).…”

Section: Introductionmentioning

confidence: 99%

The decrease of IGF-I, IGF-binding protein-3 and bone alkaline phosphatase isoforms during gluten challenge correlates with small intestinal inflammation in children with coeliac disease

Jansson

Kristiansson²,

Magnusson

et al. 2001

European Journal of Endocrinology

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Objective: In children with coeliac disease, the ingestion of gluten causes small intestinal inflammation and a clinical picture of malabsorption, weight reduction and short stature. Decreased alkaline phosphatase (ALP) during gluten challenge was found in a previous study. ALP is a marker of bone formation and ALP activities are correlated with growth velocity. The aim of this study was to characterise the previously observed decrease of total ALP by investigating three specific bone ALP isoforms (bone/intestinal, B1 and B2) and three specific liver ALP isoforms (L1, L2 and L3) and, moreover, to correlate these ALP isoforms with other growth factors and growth markers. In addition, we also studied the association with possible weight changes, small intestinal mucosa inflammation, sex, age and gluten dose during gluten challenge. Materials and methods: Bone and liver ALP isoforms, IGF-I, IGF-binding protein (IGFBP)-3 and serum cross-linked carboxy-terminal telopeptide of type I collagen (ICTP) were measured together with change in weight and small intestinal mucosa histopathology in 54 children with earlier enteropathy who participated in a 4-week gluten challenge. Results: We observed a decreased total ALP activity after 4 weeks of gluten challenge, 7X8^1X8 to 6X5^1X7 mkatal means^S.D.), which was mainly due to a reduction of the bone ALP isoforms. The sum of all three bone ALP isoforms decreased from 6X3^1X7 to 5X1^1X6 mkatalX The decreased activities of the bone ALP isoforms correlated with the observed reductions of IGF-I r 0X74Y P , 0X001Y IGFBP-3 r 0X51Y P , 0X001 and ICTP r 0X57Y P , 0X001X The decrease of the growth factors and growth markers correlated with weight reduction, but when influences from the change in weight were adjusted for, the partial correlation of the small intestinal mucosa inflammation was significant for IGF-I r 20X56Y P , 0X001 and IGFBP-3 r 20X55Y P , 0X001X Conclusion: The decrease of total ALP was due to a reduction of bone ALP. The decrease of IGF-I and IGFBP-3 was independently correlated with weight change and small intestinal inflammation.

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“…Z kolei wg obserwacji różnych autorów ok. 4-9% pacjentów diagnozowanych z powodu izolowanej przewlekłej hiperaminotransaminazemii może wykazywać serologiczne i histopatologiczne cechy atypowej postaci celiakii [15,36,37]. W piśmiennictwie notuje się również pojedyncze opisy pacjentów z przewlekłą hiperaminotransaminazemią o nieustalonej przyczynie, którą ostatecznie identyfikowano jako początkową manifestację celiakii zarówno u dzieci [38,39], jak i u osób dorosłych [40].…”

Section: Hiperaminotransaminazemia Jako Jedyna Manifestacja Choroby Tunclassified

“…[39] zmiany sugerujące uszkodzenie miąższu wątroby w postaci długo utrzy mującej się hiperaminotransaminazemii u pacjentów pediatrycznych, przy braku innych klinicznych cech celiakii, mogą wskazywać na atypową postać choroby trzewnej. Powyższe wnioski autorzy włoscy sformuło -wali na podstawie obserwacji 6 pacjentów pediatrycznych, u których wyłączenie glutenu z diety spowodowało poprawę w zakresie stwierdzanych poprzednio nieprawidłowych serologicznych i histopatologicznych markerów celiakii.…”

Section: Hiperaminotransaminazemia Jako Jedyna Manifestacja Choroby Tunclassified

Hyperaminotransaminasaemia and coeliac disease

Nowak-Oczkowska¹,

Szaflarska-Popławska²

2010

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Elevated serum aminotransferase activity as an early manifestation of gluten-sensitive enteropathy

Cited by 78 publications

References 9 publications

Immune Reaction Against Cytoskeleton in Coeliac Disease

Immune Reaction Against Cytoskeleton in Coeliac Disease

The decrease of IGF-I, IGF-binding protein-3 and bone alkaline phosphatase isoforms during gluten challenge correlates with small intestinal inflammation in children with coeliac disease

Hyperaminotransaminasaemia and coeliac disease

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