Faculty Bibliography

Establishing the presence of adenocarcinoma of the small bowel is exceedingly difficult. Survival is contingent on prompt diagnosis. We describe a patient with an atypical presentation of jejunal adenocarcinoma visualized via small bowel enteroclysis. She was referred with 'gastroparesis,' based on both a radionucleotide scan that revealed markedly delayed gastric emptying and a 'normal' small bowel series. A markedly abnormal scintigraphic study and a negative small bowel series does not exclude disease of the small intestine and should provide the impetus to further pursue the possibility of an obstructing lesion. The enteroclysis is a relatively safe and effective study in the preoperative diagnosis of small bowel tumors

OBJECTIVE: To determine whether there are any unusual patterns of transmission of susceptibility to inflammatory bowel disease (IBD) within multiplex families. METHODS: Individuals with IBD were recruited for genome-wide screening of susceptibility genes. The extent of familial aggregation and blood relationships in multiplex families were determined by questionnaires given to participants followed up by confirmation of disease diagnosis by participants' physicians. RESULTS: Of 135 families identified in which both a parent and a child had IBD, 93 involved transmission of susceptibility to disease from mother to child versus 42 examples of transmission from father to child (p = 0.00001, exact two-tailed binomial test). This distortion in transmission on the basis of the sex of the parent was observed only among non-Jewish pairs with Crohn's disease (CD), in which, of 33 parent-child pairs with CD, disease susceptibility was transmitted from the mother 28 times (p = 0.00007). CONCLUSION: Susceptibility to CD in a subset of patients may involve a gene that is imprinted

Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation whose cellular components are capable of oxidative respiratory bursts that may result in tissue injury. Mucosal biopsies were analyzed for protein carbonyl content (POPs), DNA oxidation products [8-hydroxy-2'-deoxyguanosine (8-OHdG)], reactive oxygen intermediates (ROIs), trace metals (copper, zinc, and iron) and superoxide dismutase (Cu-Zn SOD). In Crohn's disease biopsies, there was an increase in ROIs, POPs, 8-OHdG, and iron, while decreased copper and Cu-Zn SOD activity were found in inflamed tissues compared to controls. For ulcerative colitis, there was an increase in ROIs, POPs, and iron in inflamed tissue compared to controls, while decreased zinc and copper were observed. An imbalance in the formation of reactive oxygen species and antioxidant micronutrients may be important in the pathogenesis and/or perpetuation of the tissue injury in IBD and may provide a rationale for therapeutic modulation with antioxidants

: Crohn's disease (CD) and ulcerative colitis (UC) are idiopathic inflammatory bowel diseases (IBD) that are characterized by chronic intestinal inflammation and are associated with abnormalities of peripheral and mucosal immune function. The aim of our study was to determine whether CD or UC is characterized by discrete profiles of intestinal lymphokine production. Total cellular RNA was isolated from biopsies of healthy controls and from patients with IBD. Messenger RNA transcript levels in biopsies were determined for interleukin-2 (IL-2), IL-4, IL-5, and interferon-gamma (IFN-gamma), using a quantitative reverse transcriptase polymerase chain reaction method. Compared with inflamed UC mucosa and controls, CD mucosal lesions contained higher IL-2 and IFN-gamma mRNA (p < 0.05), which is consistent with a T-helper cell 1 (Th1)-like pattern. In UC, IL-5 mRNA content was higher in involved areas compared with controls (p < 0.05) and inflamed CD lesions (p < 0.05), suggestive of a Th2 pattern. We conclude that the intestinal mucosa of CD and UC have inflammatory responses characterized by discrete T-helper profiles of lymphokines. This strongly suggests that the immunopathogenesis of these two forms of IBD are different.