Mucin depletion in inflammatory bowel disease

Article Abstract:

The management of patients with inflammatory bowel disease frequently depends on differentiating between Crohn's disease (chronic inflammation of the lower ileum, or small intestine) and ulcerative colitis (inflammation of the colon with tissue ulceration). This distinction can be made by examining rectal biopsy specimens. Granulomata (granular growths) are frequently seen in the bowel tissues of patient's with Crohn's disease, but not with sufficient frequency to make this feature the basis of diagnosis. Consequently, researchers have used other factors, such as mucin depletion and mucosal gland atrophy, to distinguish between the two inflammatory bowel diseases. (Mucin is a glycoprotein found in mucous that forms a protective coating.) To explore whether mucin depletion can reliably be used to differentiate between Crohn's disease and ulcerative colitis, rectal biopsies from 5 normal controls, 11 patients with Crohn's disease, and 10 patients with ulcerative colitis were examined. The classification of patients was made on the basis of a thorough evaluation of the case records accompanying tissue specimens. The results of the study revealed that there was less mucin in the tissues of ulcerative colitis cases than in the controls or cases of Crohn's disease. There was a significant difference in mucosal gland content between the controls and the ulcerative colitis cases. There was no significant difference in mucosal gland content between the ulcerative colitis and Crohn's disease cases. These findings suggest that mucin content may be used as a qualitative diagnostic determinant. (Consumer Summary produced by Reliance Medical Information, Inc.)

Ulcerative colitis, Mucins

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The pathological concept of diffuse axonal injury; its pathogenesis and the assessment of severity

Article Abstract:

The severity of head injury determines the neurological status of patients. The nerve cells are examined microscopically for the extent of diffuse axonal injury (DAI), damage to the axons of the brain. Axons are the parts of the nerve cells that carry impulses from the nerve to other components of the body. The degree of DAI is used as an indicator of the severity of injury. Various forms of DAI can occur, including: axonal ballooning; hypertrophied microglia; long tract degeneration and diffuse gliosis of the white matter. The forms of injury seen in patients can be correlated with survival. Axonal balloonings are seen in patients who survive only for a short time after injury (12 to 24 hours). Hypertrophied microglia are seen in patients who survive several days to weeks after injury. Patients with long tract degeneration and diffuse gliosis of the white matter can survive for years. Focal lesions are another type of microscopic damage. They are thought to occur due to deformation of the brain by shear forces at the time of injury. They are filled with blood at first and then become cyst-like in time. A grading system is used to evaluate the extent of the DAI in various areas of the brain and to correlate the microscopic injury with the clinical assessment of severity of injury. (Consumer Summary produced by Reliance Medical Information, Inc.)

Injuries, Nerves, Brain, Brain injuries

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Axonal damage in Crohn's disease is frequent, but non specific

Article Abstract:

Previous investigators have reported widespread, severe necrosis (death) of autonomic nerves of the bowel in cases of Crohn's disease. Confirmation of these findings could be used to distinguish Crohn's disease from other chronic inflammatory bowel diseases. Therefore, to confirm these findings, two ileostomy biopsies each were taken from 13 cases of Crohn's disease, 4 of ulcerative colitis, 1 of diverticulitis, and 1 of fecal incontinence. A large number of damaged nerves were observed, as were other damaged tissue structures that could be mistaken for damaged axons. Three axonal damage categories were established; focal damage, diffuse damage and empty axons. In 13 cases of Crohn's disease, about 30 percent of the axons were abnormal; 21.25 percent were abnormal in the 4 cases of ulcerative colitis; in the two control cases, 12.11 and 10.63 percent of the axons were damaged, respectively. There was no significant difference in the damaged axon percentages between the cases of Crohn's disease and ulcerative colitis. Thus, these findings do not confirm previous reports identifying axonal damage as specific evidence of Crohn's disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

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