Effectiveness of administering zinc acetate hydrate to patients with inflammatory bowel disease and zinc deficiency: a retrospective observational two-center study.
Crohn disease
Inflammatory bowel diseases
Ulcerative colitis
Zinc acetate
Zinc deficiency
Journal
Intestinal research
ISSN: 1598-9100
Titre abrégé: Intest Res
Pays: Korea (South)
ID NLM: 101572802
Informations de publication
Date de publication:
Jan 2022
Jan 2022
Historique:
received:
07
10
2020
accepted:
19
12
2020
pubmed:
22
1
2021
medline:
22
1
2021
entrez:
21
1
2021
Statut:
ppublish
Résumé
Inflammatory bowel disease (IBD) patients frequently have zinc deficiency. IBD patients with zinc deficiency have higher risks of IBD-related hospitalization, complications, and requiring surgery. This study aimed to examine the effectiveness of zinc acetate hydrate (ZAH; Nobelzin) in IBD patients with zinc deficiency. IBD patients with zinc deficiency who received ZAH from March 2017 to April 2020 were registered in this 2-center, retrospective, observational study. Changes in serum zinc levels and disease activity (Crohn's Disease Activity Index [CDAI]) before and after ZAH administration were analyzed. Fifty-one patients with Crohn's disease (CD, n = 40) or ulcerative colitis (UC, n = 11) were registered. Median serum zinc level and median CDAI scores significantly improved (55.5-91.0 μg/dL, P< 0.001; 171.5-129, P< 0.001, respectively) in CD patients 4 weeks after starting ZAH administration. Similarly, median serum zinc levels and CDAI scores significantly improved (57.0-81.0 μg/dL, P< 0.001; 177-148, P= 0.012, respectively) 20 weeks after starting ZAH administration. Similar investigations were conducted in groups where no treatment change, other than ZAH administration, was implemented; significant improvements were observed in both serum zinc level and CDAI scores. Median serum zinc levels in UC patients 4 weeks after starting ZAH administration significantly improved from 63.0 to 94.0 μg/dL (P= 0.002), but no significant changes in disease activity were observed. One patient experienced side effects of abdominal discomfort and nausea. ZAH administration is effective in improving zinc deficiency and may contribute to improving disease activity in IBD.
Sections du résumé
BACKGROUND/AIMS
OBJECTIVE
Inflammatory bowel disease (IBD) patients frequently have zinc deficiency. IBD patients with zinc deficiency have higher risks of IBD-related hospitalization, complications, and requiring surgery. This study aimed to examine the effectiveness of zinc acetate hydrate (ZAH; Nobelzin) in IBD patients with zinc deficiency.
METHODS
METHODS
IBD patients with zinc deficiency who received ZAH from March 2017 to April 2020 were registered in this 2-center, retrospective, observational study. Changes in serum zinc levels and disease activity (Crohn's Disease Activity Index [CDAI]) before and after ZAH administration were analyzed.
RESULTS
RESULTS
Fifty-one patients with Crohn's disease (CD, n = 40) or ulcerative colitis (UC, n = 11) were registered. Median serum zinc level and median CDAI scores significantly improved (55.5-91.0 μg/dL, P< 0.001; 171.5-129, P< 0.001, respectively) in CD patients 4 weeks after starting ZAH administration. Similarly, median serum zinc levels and CDAI scores significantly improved (57.0-81.0 μg/dL, P< 0.001; 177-148, P= 0.012, respectively) 20 weeks after starting ZAH administration. Similar investigations were conducted in groups where no treatment change, other than ZAH administration, was implemented; significant improvements were observed in both serum zinc level and CDAI scores. Median serum zinc levels in UC patients 4 weeks after starting ZAH administration significantly improved from 63.0 to 94.0 μg/dL (P= 0.002), but no significant changes in disease activity were observed. One patient experienced side effects of abdominal discomfort and nausea.
CONCLUSIONS
CONCLUSIONS
ZAH administration is effective in improving zinc deficiency and may contribute to improving disease activity in IBD.
Identifiants
pubmed: 33472340
pii: ir.2020.00124
doi: 10.5217/ir.2020.00124
pmc: PMC8831780
doi:
Types de publication
Journal Article
Langues
eng
Pagination
78-89Références
Gastroenterology. 1979 Oct;77(4 Pt 2):843-6
pubmed: 467941
Am J Clin Nutr. 1982 May;35(5):981-7
pubmed: 7081095
Sci Rep. 2017 Feb 24;7:43126
pubmed: 28233796
Inflamm Bowel Dis. 2017 Jan;23(1):152-157
pubmed: 27930412
Clin Ter. 2008 Sep-Oct;159(5):329-46
pubmed: 18998036
Inflamm Bowel Dis. 2006 Mar;12(3):185-91
pubmed: 16534419
J Biol Chem. 2012 Aug 31;287(36):30485-96
pubmed: 22736759
Gut. 1980 May;21(5):387-91
pubmed: 7429301
Clin Exp Dermatol. 1982 Nov;7(6):629-32
pubmed: 6891297
Dig Dis Sci. 1981 Oct;26(10):865-70
pubmed: 7285724
Digestion. 1977;16(1-2):87-95
pubmed: 615740
J Gastroenterol Hepatol. 2019 Oct;34(10):1703-1710
pubmed: 30821862
Gastroenterology. 1979 Oct;77(4 Pt 2):898-906
pubmed: 381094
Gastroenterology. 1980 Feb;78(2):272-9
pubmed: 7350050
Scand J Gastroenterol. 2014 Feb;49(2):164-72
pubmed: 24286534
Scand J Gastroenterol. 1998 May;33(5):514-23
pubmed: 9648992
Gastroenterology. 1976 Mar;70(3):439-44
pubmed: 1248701
Postgrad Med J. 1983 Nov;59(697):690-7
pubmed: 6359105
Inflamm Bowel Dis. 2001 May;7(2):94-8
pubmed: 11383597
JPEN J Parenter Enteral Nutr. 2007 Jul-Aug;31(4):311-9
pubmed: 17595441
Gut. 2019 Dec;68(Suppl 3):s1-s106
pubmed: 31562236
Proc R Soc Med. 1971 Feb;64(2):166-70
pubmed: 5548941
Environ Health Perspect. 1994 Jun;102 Suppl 2:5-46
pubmed: 7925188
Inflamm Bowel Dis. 2012 Oct;18(10):1961-81
pubmed: 22488830
Br J Surg. 1972 Oct;59(10):817-9
pubmed: 5077895
N Engl J Med. 1987 Dec 24;317(26):1625-9
pubmed: 3317057
J Gastroenterol. 2018 Mar;53(3):305-353
pubmed: 29429045