Gastrointestinal mucosal injury

Soluble TNF-ot receptors bind to TNF-a (a pro-inflammatory cytokine), limiting its activity (Buescher and Williams-Koeppen, 1998). Plateletactivating factor acetylhydrolase (PAF-AH) degrades PAP, thereby limiting the gastrointestinal mucosal injury caused by PAP (Furukawa et al, 1993). 

Rainsford et al. (2003) described gastrointestinal mucosal injury following repeated daily oral administration of conventional formulations of indomethacin and other non-steroidal anti-inflammatory drags to Landrace pigs as a model for human gastrointestinal... 

Gastrointestinal Mucosal Injury Liver Damage (Continued)... 

Delacruz V, Weppler D, Island E, Gonzalez M, Tryphonopoulos P, Moon J, Smith L, Tzakis A, Ruiz P. Mycophenolate mofetil-related gastrointestinal mucosal injury in multivisceral transplantation. Transplant Proc 2010 42(1) 82-4. 

Basic Mechanisms of Gastrointestinal Mucosal Cell Injury and Protection" Harmon, J.W., Ed. Williams Wilkins ... 

Figure 3-4. Adrian Allen s "Bottle Brush" structure for each of the four subunits of hog gastric mucus. This figure is from a late publication, but an essentially similar one was shown and published before 1975. (From Allen A, The structure and function of gastrointestinal mucus, in Harmon JW, ed Basic Mechanisms of Gastrointestinal Mucosal Cell Injury and Protection. Baltimore Williams Wilkins, 1981, pp 351-365. Copyright 1981 reproduced by permission.)...

Following ingestion of the substance, the gastrointestinal (GI) tract is the site of initial or phase I toxicity to the mucosal surfaces. This toxicity is manifested by swelling, edema, and painful ulceration of the mouth, pharynx, esophagus, stomach, and intestine. With higher levels, other GI toxicity includes centrizonal hepatocellular injury, which can cause elevated bilirubin, and hepatocellular enzyme levels such as AST, ALT, and LDH. 

Although the exact mechanism by which mustard produces tissue injury is not known, the mechanism of action has been suggested to be its ability to directly alkylate DNA. This DNA alkylation and cross-linking in rapidly dividing cells such as basal keratinocytes, mucosal epithelium, and bone marrow precursor cells leads to cellular death and inflammatory reactions. Systemic effects with extensive exposures include bone marrow inhibition, with a drop in the white blood cell count, and gastrointestinal tract damage. 

IV. Diagnosis is based on a history of exposure to a corrosive agent and characteristic findings of skin, eye, or mucosal irritation or redness and the presence of injury to the gastrointestinal tract. Victims with oral or esophageal injury nearly always have drooling or pain on swallowing. 

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