Long-term remission in patients with dermatitis herpetiformis on a normal diet

Bardella, Maria Teresa; Fredella, C.; Trovato, C.; Ermacora, E.; Cavalli, Ricardo Carvalho; Saladino, Valeria; Prampolini, L.

doi:10.1111/j.1365-2133.2003.05579.x

Cited by 41 publications

(29 citation statements)

References 14 publications

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“…Early CD diagnosis was also noted as one factor associated with the lack of relapse in patients with dermatitis herpetiformis that resumed a normal diet after prolonged gluten avoidance. 34 Studies showing that delayed introduction of gluten into infant diets reduces the incidence of childhood CD are in line with our results. 44 Yet, how early GFD in our patients may promote progressive silencing of the disease despite continuous antigen exposure remains intriguing.…”

Section: Discussionsupporting

confidence: 89%

“…9 More recently, Bartella et al observed that 7 out 38 patients with dermatitis herpetiformis did not relapse upon gluten reintroduction after several years on a GFD. 34 Schmitz et al were the first in 1984 to describe spontaneous histological recovery during normal diet in three female coeliac patients with CD diagnosed in childhood. 35 The same group subsequently showed in 1993 that among 34 asymptomatic CD children returned to a normal diet, four had recovered a fully normal and six a partially normal villous architecture 5-13 years later.…”

Section: Discussionmentioning

confidence: 99%

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Long-term follow-up of 61 coeliac patients diagnosed in childhood: evolution toward latency is possible on a normal diet

Matysiak‐Budnik

Malamut

Serre

et al. 2007

Gut

124

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Background/Aims: Whether a life-long gluten-free diet (GFD) is necessary in all children with diagnosed coeliac disease (CD) remains debated. To address this question, a retrospective analysis of the clinical and biological status of adult coeliac patients diagnosed in childhood, who remained on a normal diet after gluten challenge and were clinically silent, was carried out. Methods: Patients aged 18-65 years with CD diagnosed in childhood were included. Clinical status, gluten intake, biological parameters of malabsorption, bone mineral density, human leucocyte antigen (HLA) genotype, serological markers of CD, and histological and immunohistochemical parameters in duodenal biopsies were recorded. Results: Sixty-one patients had resumed a normal diet and were asymptomatic. Forty-eight showed different degrees of villous atrophy (silent CD), while 13 had no detectable atrophy (latent CD) on duodenal biopsies. Latent CD patients had significantly less osteopenia/osteoporosis (1/9 (11%) vs 23/33 (70%), p,0.001)), and lower T cell receptor (TCR) ab+ intraepithelial T cell counts (38¡20 vs 55¡15, p,0.01) than silent CD patients. The mean age at diagnosis and first GFD was lower in latent than in silent patients (14.4¡5 vs 40.1¡47 months, p,0.05). Latent patients did not differ significantly from the seven control patients on a long-term GFD, except for a higher frequency of CD-specific serum antibodies. However, two latent patients relapsed clinically and histologically during subsequent follow-up. Conclusions: Long-term latency developed in about 20% of CD patients who remained symptom free after gluten reintroduction. This latency can be transient and thus a regular follow-up is mandatory. In silent patients, the increased risk of osteoporosis substantiates the need for a GFD.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Long-term follow-up of 61 coeliac patients diagnosed in childhood: evolution toward latency is possible on a normal diet

Matysiak‐Budnik

Malamut

Serre

et al. 2007

Gut

124

View full text Add to dashboard Cite

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“…Some concern could be raised about the benefit of blocking lymphocyte homing to the intestine, and potential long-term adverse consequences, also because beneficial immunosuppressive regulatory T cells are equally inhibited. Since its demonstration, the possibility to develop tolerance to gluten in certain patients affected by celiac disease has gained more attractiveness as another potential immunomodulatory approach[116,117]. An alternative method studied for induction of tolerance to gluten is oral administration of a genetically modified Lactococus lactis bacterium, capable of secreting deamidated DQ8-restricted gliadin epitope.…”

Section: Current Treatments Of Celiac Diseasementioning

confidence: 99%

Celiac disease: From pathophysiology to treatment

Parzanese

Qehajaj

Patrinicola

et al. 2017

WJGP

218

169

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Celiac disease, also known as “celiac sprue”, is a chronic inflammatory disorder of the small intestine, produced by the ingestion of dietary gluten products in susceptible people. It is a multifactorial disease, including genetic and environmental factors. Environmental trigger is represented by gluten while the genetic predisposition has been identified in the major histocompatibility complex region. Celiac disease is not a rare disorder like previously thought, with a global prevalence around 1%. The reason of its under-recognition is mainly referable to the fact that about half of affected people do not have the classic gastrointestinal symptoms, but they present nonspecific manifestations of nutritional deficiency or have no symptoms at all. Here we review the most recent data concerning epidemiology, pathogenesis, clinical presentation, available diagnostic tests and therapeutic management of celiac disease.

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“…The role of oats as a part of GFD has been controversial, but consumption of pure oats is nonetheless considered safe and well tolerated [108,109]. The need for dietary treatment is currently considered to be lifelong, even though there are a few reports of celiac and dermatitis herpetiformis patients developing gluten tolerance and being able to reintroduce gluten to their diet [110][111][112].…”

Section: Gluten-free Diet Is Currently the Only Treatmentmentioning

confidence: 97%

Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review

Rauhavirta

Hietikko

Salmi

et al. 2016

Clinic Rev Allerg Immunol

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Celiac disease is a common inflammatory disorder with a prevalence of 1-2 % in which a distinct dietary wheat, rye, and barley component, gluten, induces small-bowel mucosal villous atrophy, crypt hyperplasia, and inflammation. The small-bowel mucosal damage can be reversed by a strict lifelong gluten-free diet, which is currently the only effective treatment for the condition. A key player in the pathogenetic process leading to the enteropathy is played by a protein called transglutaminase 2 (TG2), which is able to enzymatically modify gluten-derived gliadin peptides. The TG2-catalyzed deamidation of the gliadin peptides results in their increased binding affinity to the disease-predisposing human leukocyte antigen (HLA) DQ2 and DQ8 molecules, thus enabling a strong immune response to be launched. Blocking the enzymatic activity of TG2 has thus been suggested as a suitable novel pharmacological approach to treat celiac disease. By virtue of its transamidation capacity, TG2 is also able to cross-link gliadin peptides to itself, this resulting in the generation of TG2-gliadin peptide complexes whose presence might provide an explanation for the generation of the TG2 autoantibodies characteristic of celiac disease. Due to their excellent specificity for the disorder, the TG2-targeted autoantibodies are widely used in the diagnostics as a first-line test to select patients for gastrointestinal endoscopy. More recently, it has come to be appreciated that these autoantibodies and also the TG2-specific B cells might play an active role in the disease pathogenesis. In this review, we assess the role of TG2, TG2-specific B cells, and autoantibodies in celiac disease.

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Long-term remission in patients with dermatitis herpetiformis on a normal diet

Cited by 41 publications

References 14 publications

Long-term follow-up of 61 coeliac patients diagnosed in childhood: evolution toward latency is possible on a normal diet

Long-term follow-up of 61 coeliac patients diagnosed in childhood: evolution toward latency is possible on a normal diet

Celiac disease: From pathophysiology to treatment

Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review

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