e rather than a reciprocal response between Th1- and Th2-helper cell function. Prostaglandins are needed to maintain gut tolerance as well, agents that interfere with this activity, such as nonsteroidal anti-inflammatory drugs, are a causative factor for IBD symptom initiation (1:1).
Environmental factors may contribute to relapse rates. Seasonal variations affect UC, with highest relapses found from September to February, and decreases found in the summer. Stress is also implicated as a causative factor. Chronic and current stressors have negative effects on the neuroendocrine system and inflammatory responses, however, exact mechanisms related to UC remain unclear. Smoking has been linked to multifocal gastrointestinal infarction and may be a pathogenic mechanism in UC (5:810).
Immunology/Pathophysiology, Clinical Presentation, & Diagnosis
UC can be differentiated from CD by its pathological presentation. UC includes recurrent diffuse inflammation in the colon and rectum, while CD can include any portion of the gastrointestinal tract from mouth to anus. Associated characteristics of UC include persistent mucosal inflammation and glandular architecture contortion (5:858-9).
Diagnosis of UC includes accurate and detailed history taking, endoscopy, and radiography (5:858-9). Patient history helps determine ranges in symptom intensity from mild to severe, and from infrequent to continuous. The presence or absence of symptoms is a primary indication of disease categorization. Symptom severity scales can be used to specify pain levels, frequency and intensity, with changes and relief, gastrointestinal location, and effects (3:81S).
Endoscopic examinations include flexible sigmoidoscopy, colonoscopy, and esophagogastrocluodenoscopy. Abdominal computed tomography scan can identify abscesses, masses, fistulas, or strictures. Barium enemas help identify colon inflammation (4:60-61).
To distinguish UC from CD, a ...