Anemia in a 66-Year-Old Woman

Jun H. Lee, MD; Marc D. Basson, MD, PhD

Disclosures

December 02, 2015

The location of the lesion is important as it helps to determine the best route of administration for therapeutic intervention in patients with UC. Lesions are found in the rectum (proctitis) in 30%-35% of patients, extend up to the splenic flexure (left-sided colitis) in 30%-45% of patients, and involve the whole colon (pancolitis) in 20%-25% of patients.[11,12] In addition, the severity of the disease also plays a role in choosing the right treatment.

Classification is as follows:

  • Mild—<4 stools/day, no systemic signs of toxicity, normal erythrocyte sedimentation rate (ESR)

  • Moderate—>4 stools/day, minimal signs of toxicity

  • Severe—> 6 stools/day, signs of toxicity (eg, fever, increased blood pressure), increased ESR

Table 1. Management According to Severity and Site of Disease

5-ASA = 5-aminosalicylic acid; TNF = tumor necrosis factor; IV = intravenous. Data from Kornbluth A, et al.[13]

A newer formulation of mesalazine, which has replaced sulfasalazine as the mainstay of treatment for IBD, reaches the commonly affected left colon better than previous formulations. It has been engineered so that the drug does not get absorbed until it reaches the left colon. Furthermore, because the compound is released slowly over 24 hours, patients only have to take the drug once a day, increasing compliance with the medication regimen.[14]

Unlike what was observed in the past, recent studies have shown that elderly patients were more likely to be in clinical remission and successfully tapered off of steroids within the first year. This may reflect a relative decrease in immunocompetence with age. As the immune system weakens, the overall cell-mediated immune response declines, which makes elderly patients more susceptible to developing UC. However, the relatively immunodeficient state leads to aberrant immune response that normally leads to flare ups, ultimately facilitating more frequent and stable clinical remission than observed in younger cohorts who are able to mount a full immune response.[3]

Additional studies on the pathogenesis of UC are beginning to suggest that enteric microbiota dysbiosis may contribute to the development of the disease. The presence of normal pathogens within the gut is disrupted, which, in turn, prevents these organisms from protecting against nonresident pathogens. This may lead to the development of IBD. Some researchers have proposed replacing fecal microbiota from a healthy donor as a form of treatment. So far, the results of fecal transplantation are mixed and require further testing.[15]

When the patient does not respond to medical treatment, then surgery is required. Unlike in CD, surgery is curative for UC. Surgeons most often perform a proctocolectomy with ileal pouch anal anastomosis, although very ill patients may receive lesser procedures, including proctocolectomy with ileostomy or even total abdominal colectomy with ileostomy, leaving the rectal stump behind in the pelvis.[1,4,13] Surgery is more commonly used as a first-line treatment for complications secondary to UC, such as fulminant colitis, toxic megacolon, strictures, or colon cancer. Although all are potentially quite serious, guidelines are set up specifically to monitor for colonic dysplasia. The risk for colon cancer increases up to 30% after 30 years of disease. Early onset, greater extent of disease, and family history of colon cancer all increase the risk. Current guidelines recommend annual colonoscopy 8 years from the time of diagnosis and every 1-3 years thereafter, depending on the findings.[4,13] However, it is not certain that screening actually improves survival rates.[16]

The patient in this case was treated with oral mesalazine, to which she responded well, and she went into remission without the need for steroid treatment.

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