Lily Gillette
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Lily Gillette has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
- Jocelyn Anne Silvester
Boston Children's Hospital Boston Massachusetts USA
2 shared publications - Abigail Plone
Division of Gastroenterology, Hepatology and Nutrition, Boston Children’s Hospital, Harvard Medical School , Boston, MA
1 shared publication - Alka Goyal
Department of Pediatric Gastroenterology, Hepatology and Nutrition, Stanford University , Stanford, CA
1 shared publication - Amelie Therrien
Celiac Center, Department of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
1 shared publication - Casey R. Johnson
Division of Gastroenterology, Hepatology and Nutrition, Boston Children’s Hospital, Harvard Medical School , Boston, MA
1 shared publication Ciaran P. Kelly
Celiac Center, Department of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
1 shared publication
Latest Publications
- Open Access
- 11 July 2026
- Published by Oxford University Press (OUP) in Inflammatory Bowel Diseases
- Vol. 32 (9) , 1849-1853
Novel SLC10A2 variants induce primary bile acid malabsorption and dysbiosis with IBD-like features
Lay summary: We describe biochemically and functionally validated primary bile acid malabsorption caused by novel biallelic SLC10A2 variants in a child initially diagnosed with Crohn’s disease. Pediatric IBD cohort reanalysis identified PBAM-compatible genotypes, supporting selective testing when clinical features are suggestive.
- 11 July 2026
- Published by Oxford University Press (OUP) in Inflammatory Bowel Diseases
- Vol. 32 (9) , 1849-1853
Open AccessNovel SLC10A2 variants induce primary bile acid malabsorption and dysbiosis with IBD-like features
Lay summary: We describe biochemically and functionally validated primary bile acid malabsorption caused by novel biallelic SLC10A2 variants in a child initially diagnosed with Crohn’s disease. Pediatric IBD cohort reanalysis identified PBAM-compatible genotypes, supporting selective testing when clinical features are suggestive.
- 14 May 2025
- Published by Wolters Kluwer Health in American Journal of Gastroenterology
- Vol. 121 (2) , 517-525
Hereditary Alpha-Tryptasemia Is Associated With Ongoing Symptoms in Individuals With Celiac Disease Despite Following a Gluten-free Diet
INTRODUCTION: Hereditary alpha-tryptasemia (HαT) is caused by the increased copy number of TPSAB1 when encoding for alpha-tryptase, resulting in elevated basal serum tryptase (BST). Many affected individuals report irritable bowel syndrome–like and reflux symptoms. We aimed to assess the prevalence of HαT in celiac disease (CeD) and whether this genetic trait modifies disease course. METHODS: This study included a prospective cohort of subjects with CeD or nonceliac gluten sensitivity (NCGS) either at diagnosis (Dx), with persisting symptoms on a gluten-free diet, or in clinical remission. BST levels were determined by immunoassay, and tryptase genotyping was performed on genomic DNA using digital droplet polymerase chain reaction (PCR) [ddPCR]. Duodenal and gastric biopsies were stained for c-KIT, and mast cell (MC) counts were averaged over 5 high power field (hpf). RESULTS: There were 153 eligible subjects: 13 with NCGS and 140 with CeD (8 patients with new Dx, 66 with persisting symptoms, 66 in remission). HαT was found in 9 subjects, all symptomatic with CeD (6.4%). One was new Dx, and the others had persisting symptoms (12.3% of subgroup). Excluding HαT, BST levels were higher among patients with CeD vs NCGS (median 5.4 vs 3.9 mcg/L P < 0.05). Duodenal MC counts were higher in CeD vs controls ( P < 0.05) and 24% higher in those with HαT (median HαT CeD 27.3/hpf, non-HαT CeD 22.0/hpf, controls 18.4/hpf). MC counts did not differ based on villous atrophy or clinical presentation. DISCUSSION: The prevalence of HαT in CeD is similar to the general population; however, all participants with CeD and HαT had ongoing gastrointestinal (GI) symptoms. Evaluation for HαT should be considered in the management of patients with CeD and persisting symptoms.
- 14 May 2025
- Published by Wolters Kluwer Health in American Journal of Gastroenterology
- Vol. 121 (2) , 517-525
Hereditary Alpha-Tryptasemia Is Associated With Ongoing Symptoms in Individuals With Celiac Disease Despite Following a Gluten-free Diet
INTRODUCTION: Hereditary alpha-tryptasemia (HαT) is caused by the increased copy number of TPSAB1 when encoding for alpha-tryptase, resulting in elevated basal serum tryptase (BST). Many affected individuals report irritable bowel syndrome–like and reflux symptoms. We aimed to assess the prevalence of HαT in celiac disease (CeD) and whether this genetic trait modifies disease course. METHODS: This study included a prospective cohort of subjects with CeD or nonceliac gluten sensitivity (NCGS) either at diagnosis (Dx), with persisting symptoms on a gluten-free diet, or in clinical remission. BST levels were determined by immunoassay, and tryptase genotyping was performed on genomic DNA using digital droplet polymerase chain reaction (PCR) [ddPCR]. Duodenal and gastric biopsies were stained for c-KIT, and mast cell (MC) counts were averaged over 5 high power field (hpf). RESULTS: There were 153 eligible subjects: 13 with NCGS and 140 with CeD (8 patients with new Dx, 66 with persisting symptoms, 66 in remission). HαT was found in 9 subjects, all symptomatic with CeD (6.4%). One was new Dx, and the others had persisting symptoms (12.3% of subgroup). Excluding HαT, BST levels were higher among patients with CeD vs NCGS (median 5.4 vs 3.9 mcg/L P < 0.05). Duodenal MC counts were higher in CeD vs controls ( P < 0.05) and 24% higher in those with HαT (median HαT CeD 27.3/hpf, non-HαT CeD 22.0/hpf, controls 18.4/hpf). MC counts did not differ based on villous atrophy or clinical presentation. DISCUSSION: The prevalence of HαT in CeD is similar to the general population; however, all participants with CeD and HαT had ongoing gastrointestinal (GI) symptoms. Evaluation for HαT should be considered in the management of patients with CeD and persisting symptoms.