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Pancreatic enzymes, primarily consisting of lipase, protease (trypsin and chymotrypsin), and amylase, are essential biocatalysts secreted by the exocrine pancreas into the duodenum to facilitate the breakdown of fats, proteins, and carbohydrates [1, 2]. In healthy individuals, these enzymes are largely inactivated or degraded as they pass through the gastrointestinal tract; however, significant residual activity can be found in the stool, particularly in conditions of rapid transit or altered gut pH [4, 5]. These stool enzymes play a dual role in clinical medicine: their deficiency leads to malabsorption and exocrine pancreatic insufficiency (EPI), while their presence in feces can cause severe skin irritation and breakdown, leading to incontinence-associated dermatitis (IAD) and diaper rash [1, 4]. Therapeutically, pancreatic enzymes are administered as replacement therapy (pancrelipase) to treat EPI associated with cystic fibrosis, chronic pancreatitis, or pancreatectomy [StatPearls]. Conversely, in the management of dermatitis, the goal is to neutralize or provide a barrier against these enzymes to prevent epidermal damage [4]. Zinc oxide is a notable agent that acts by inhibiting the activity of fecal proteases and lipases [1, 4]. Monitoring of stool enzyme levels, such as fecal elastase-1, serves as a critical diagnostic biomarker for assessing pancreatic function [StatPearls].
Enzyme replacement therapy (for insufficiency); Inhibition of enzymatic activity on skin (for dermatitis); Barrier protection against enzymatic damage; pH modulation to reduce enzyme activation.
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