Ulcerative Colitis

Clinical Manifestations, Pathology, and Diagnosis

The principal symptoms of ulcerative colitis are rectal bleeding, constipation early (in ulcerative proctitis), diarrhea usually, abdominal cramping pain, rectal urgency, fever, anorexia, fatigue, and weight loss. The physical findings depend upon the severity of the colitis, ranging from normal in mild disease, to fever, pallor from loss of blood, dehydration and malnutrition, and the signs of associated complications. X-ray and endoscopic examinations demonstrate diffuse inflammation and ulceration of the rectum and colon in 50 percent of patients, and the adjoining terminal ileum. Ulcerative colitis begins in the mucosa and submucosa of the colon (the inner bowel surface); in severe colitis the entire bowel wall may be involved. The principal histological features are the following: vascular congestion, diffuse cellular infiltration with polymorphonuclear cells, lymphocytes, plasma cells, mast cells, eosinophils, and macrophages; multiple crypt abscesses; and shallow ulcerations. Chronic ulcerative proctitis is the same disease as ulcerative colitis, except for its restriction to the rectum and its milder course.

The laboratory findings reflect the severity of the colitis. The white blood cell count usually is normal except in the presence of complications. The hemoglobin, red cell, and hematocrit are decreased in propor tion to the loss of blood. The sedimentation rate may be elevated but frequently is normal. Blood proteins including serum albumin often are diminished. The stools contain blood. Cultures are negative for known pathogenic bacteria.

Complications are numerous. In the colon, they include pericolitis, toxic dilatation, perforation, peritonitis, hemorrhage, obstruction, polyps, carcinoma, and lymphoma. The many systemic complications include iron-deficiency anemia, hemolytic anemia, protein loss, malnutrition, retardation of growth in children, arthritis, iritis, sacroileitis, metabolic bone disease, skin problems (erythema nodosum, pyoderma gangrenosum), pyelonephritis, nephrolithiasis, liver disease (fat infiltration, hepatitis, pericholangitis, sclerosing cholangitis), and vascular thromboses.

The differential diagnosis includes specific bacterial infections, ischemic colitis, diverticulitis, and Crohn's disease of the colon.


The therapeutic emphasis in ulcerative colitis involves a general program of nutritional restoration, emotional support, sulfasalazine, 5-aminosalicylic acid, antispasmodics, antibacterial drugs, adrenocor-ticotropin (ACTH), and adrenal corticosteroids. Proctocolectomy and ileostomy is a highly successful operation for ulcerative colitis. The Kock continent pouch, and total colectomy together with ileoanal anastomoses, with and without ileal pouch, offer useful surgical alternatives in selected patients. The prognosis of ulcerative colitis has improved considerably, and the mortality has diminished to less than 1 percent as a result of the many medical and surgical therapeutic advances.


Ulcerative colitis is common among young people, especially below the age of 40 years, but no age range is exempt and the number of older patients is increasing. There is no sex predominance. The circumstances of onset of ulcerative colitis in most instances are not known. Patients usually appear to be in good health; occasionally, symptoms appear after visits to countries such as Mexico and Saudi Arabia, implicating an enteric infection. Initial thoughts as to etiology emphasized a microbial infection, and this possibility continues today. Many organisms have been implicated and discarded, including diplostreptococ-cus, Streptococcus, Escherichia coli, Pseudomonas aeruginosa, Clostridium difficile, Sphaerophorus nec-rophorus, Morgan's bacillus, Shigella organisms,

Salmonella paratyphi, Proteus organisms, viruses (e.g., lymphopathia venereum), parasites, and fungi (Histoplasma, Monilia). Immunologic mechanisms have been implicated on the basis of clinical, morphological, and experimental observations. The immunologic disorder may be one of defective immunoregula-tion, as in an altered response to a microbial infection or to usual bowel organisms. Nutritional deficiencies are common but are secondary developments.

Various circumstances such as acute respiratory illness, enteric infections, and antibiotics may act as a "trigger mechanism," precipitating the disease in genetically "vulnerable" persons. Genetic influences may be expressed through the immune response genes and the mucosal immune system of the bowel. Emotional disturbances are common in patients with ulcerative colitis, but they probably do not initiate the disease. The important interactions among the central nervous system, the gut, and the endocrine and immune systems now under investigation may clarify these issues.

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