P151 Ulcerative colitis patients with zinc deficiency are at higher risk for disease-related complications
S. S. Siva*1, D. T. Rubin1, G. Gulotta1, K. Wroblewski2, J. Pekow1
1The University of Chicago Inflammatory Bowel Disease Centre, Inflammatory Bowel Disease, Chicago, Illinois, United States, 2The University of Chicago, Public Health Sciences, Chicago, Illinois, United States
Zinc acts as an important mediator during immune response and may enhance inflammation in the pathogenesis of ulcerative colitis (UC). In animal models of colitis, zinc deficiency is associated with more severe disease activity, whereas zinc supplementation improves markers of inflammation. Little data exist, however, on the effect of zinc deficiency on disease course in patients with UC.
Using our single-institution inflammatory bowel disease (IBD) cohort, we identified UC patients who had multiple measurements of plasma zinc levels. Zinc deficiency was defined as serum level < 0.66 ng/dl. IBD-associated hospitalisations, surgeries, and disease-related complications (anaemia and malnutrition) were compared using a logistic regression model between patients who were zinc deficient and those who had normal zinc levels, as well as in those whose zinc deficiency was corrected.
In total, 223 UC patients were included in the analysis (low zinc, n = 86; normal zinc, n = 137). Small bowel surgery (ostomy or J-pouch) (odds ratio [OR] 3.05 [1.20–7.74], colon surgery (OR 3.72 [1.46–9.48]), malnutrition (OR 5.51 [1.85–16.36]), and anaemia (OR 2.92 [1.46–5.85]) were significantly associated with zinc deficiency. After adjusting for age, sex, race, disease duration, anti-tumour necrosis factor- (TNF) biologics, and immunomodulators, zinc deficiency was associated with increased risk of UC-related hospitalisations (OR 3.05 [1.52–6.13]), surgeries (OR 3.32 [1.42–7.80]), and disease-related complications (OR 2.18 [1.16–4.10]).
Table 1 Zinc deficiency and IBD-related clinical outcomes in UC
|At least 1 UC-related hospitalisation||P-value||At least 1 UC-related surgery||P-value||At least 1 UC-related complication||P-value|
|Odds ratio for low zinc vs normal zinc (95% confidence interval [CI])|
|Unadjusted||2.93 (1.61, 5.35)***||P < 0.001||3.48 (1.65, 7.51)**||P < 0.01||1.94 (1.12, 3.37)*||P < 0.05|
|Adjusted 1||3.05 (1.52, 6.13)**||P < 0.01||3.32 (1.42, 7.80)**||P < 0.01||2.18 (1.16, 4.10)*||P < 0.05|
|Adjusted 2||2.07 (0.98, 4.36)||0.055||2.22 (0.91, 5.44)||0.081||1.75 (0.90, 3.42)||0.10|
|1 Adjusted for gender, race, use of anti-tumour necrosis factor (TNF) or immunomodulators, age, and duration of disease||2 Adjusted for gender, race, use of anti-TNF or immunomodulators, age, duration of disease, and albumin|
These associations were insignificant after adjusting for serum albumin, as zinc levels correlated with albumin levels in the cohort (R = 0.48, p < 0.001). UC patients who normalised their zinc within 12 months (n = 18) had reduced odds of IBD-related hospitalisation (OR 0.21 [0.07–0.69]) and IBD-related complications (OR 0.19 [0.05–0.67]) compared with those who remained deficient (n = 56).
Zinc deficiency is commonly seen in patients with UC who have low serum albumin levels. As such, poor outcomes associated with zinc deficiency in patients with UC likely reflect more severe disease activity or changes in nutritional status. These findings support close monitoring and replacement of zinc levels in patients low albumin levels with active UC.
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