title: Long-term follow-up of 61 coeliac patients diagnosed in childhood: evolution toward latency is possible on a normal diet.
abstract: OBJECTIVE
  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) alphabeta+ 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.
authors.affiliation: INSERM, U793, Faculté de Médecine René Descartes, IFR94, Paris, France.
authors.forename: Tamara
authors.initials: T
authors.lastname: Matysiak-Budnik
authors.forename: Georgia
authors.initials: G
authors.lastname: Malamut
authors.forename: Natacha Patey-Mariaud
authors.initials: NP
authors.lastname: de Serre
authors.forename: Etienne
authors.initials: E
authors.lastname: Grosdidier
authors.forename: Sylvie
authors.initials: S
authors.lastname: Seguier
authors.forename: Nicole
authors.initials: N
authors.lastname: Brousse
authors.forename: Sophie
authors.initials: S
authors.lastname: Caillat-Zucman
authors.forename: Nadine
authors.initials: N
authors.lastname: Cerf-Bensussan
authors.forename: Jacques
authors.initials: J
authors.lastname: Schmitz
authors.forename: Christophe
authors.initials: C
authors.lastname: Cellier
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001284:Atrophy; D001323:Autoantibodies / Q000097:blood; D015519:Bone Density; D002446:Celiac Disease / Q000178:diet therapy* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D004386:Duodenum / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005983:Glutens / Q000008:administration & dosage*; D006650:Histocompatibility Testing; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009752:Nutritional Status; D011379:Prognosis; D012189:Retrospective Studies; D000637:Transaminases / Q000097:blood
chemical_list: D001323:Autoantibodies; D005983:Glutens; D000637:Transaminases