Related Experiment Video
Updated: Jan 11, 2026

Mouse Model of Pressure Ulcers After Spinal Cord Injury
Published on: March 9, 2019
Essential amino acid supplementation for pressure ulcers: pathophysiological rationale and results from a pilot study
Maciej Świątkiewicz1, Andrzej Lejczak2, Piotr Foltyński3
1Department of Experimental Pharmacology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawinskiego 5, Warsaw, 02-106, Poland. mswiatkiewicz@imdik.pan.pl.
None:
Pressure ulcers (PU) are a major and serious problem affecting millions of people. Malnutrition, frequently co-occurring with PU, is considered modifiable risk factor, and dietary supplements currently recommended for supporting PU healing contain a high amount of protein and some additives (zinc, vitamin C, arginine). Unfortunately, many patients with PU suffer from chronic kidney disease and would not tolerate a high-protein diet. Amino acid profiling of the blood serum of PU patients has shown decreased concentrations of exogenous amino acids histidine, tryptophan and threonine. Their common feature is a low daily requirement, 4 to 15 mg/kg body weight. In animal experiments, various types of stress increase metabolic demand for these amino acids. On the other hand, stress significantly slows down wound healing, both in animals and in humans. Considering these observations, a pilot clinical trial in the quasi-experimental design has been performed to assess the effect of Pellicar-F, a proprietary food composition containing histidine in the form of carnosine, plus tryptophan and threonine on PU control. After six weeks patients receiving daily doses of the aforementioned food composition, compared to control patients, displayed statistically significant reduction of the pressure ulcer area. Further evaluation of this product in pressure ulcers and other chronic wounds is indicated.
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Peptic Ulcer Disease IV: Management
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...

