Ulcerative Colitis Blog

One of the most common questions posed by patients about their disease is: Why did I get UC?

Our current understanding is that inflammatory bowel disease (IBD) develops in genetically susceptible individuals when they are exposed to an environmental trigger that sets off an exuberant inflammatory cascade. Although most people with a new diagnosis of IBD do not have a family history, there is compelling evidence for a genetic contribution to this disease, further supported by the discovery of genes associated with IBD in the last five years. Approximately 5-25% of patients with IBD report having a family member who also has IBD (either Crohn’s disease or UC). Siblings of patients with UC are 5-15 times more likely to develop IBD than individuals without an affected brother or sister. Studies of identical twins have shown that if one twin has UC, there is a 10-20% probability of the other twin also developing UC. With regard to fraternal twins, however, the risk is the same as that for non-twin siblings. If one parent has UC, the chance of his/her child developing IBD is about 5%. In the special instance that both parents have IBD, the likelihood of their children having IBD increases to about 30% by age 28. Research has shown that there is concordance (similarity) of disease type among family members. That is, within families with one or more family members affected by IBD, individuals are likely to have the same form of disease as one another (Crohn’s disease or UC). Some studies have suggested that individuals with a family history of IBD may have earlier disease onset compared to individuals without affected family members.

Other factors influencing genetic risk include ethnic/racial background. The highest rates of IBD are found in Caucasian individuals, especially those of Jewish heritage. Among Jewish sub-groups, Ashkenazi Jews have a 2 to 9 fold greater prevalence over non-Jewish counterparts. African Americans and Asians are believed to have a lower risk of IBD, although there appears to be a trend towards growing prevalence rates in these populations.

While investigators have identified a handful of genes which may play a role in UC, no single gene alone has been established as a cause. Research has shown that the genetics of IBD are complex, most likely involving interactions of multiple genes and environmental factors. It is hoped that a better understanding of the interplay between genes and the environment will help identify what triggers IBD and how we may either prevent or treat it more effectively.

Extraintestinal Manifestations of Ulcerative Colitis Part I
Ulcerative colitis and Crohns disease are chronic inflammatory conditions primarily involving the intestine. The systemic nature of these diseases, however, may result in pathological processes involving other organ systems. The constellation of disease associated, non-gastrointestinal symptoms experienced by patients are referred to as extraintestinal manifestations (EMs) of IBD. The reason why some IBD patients develop EMs and others do not is not known. It is suspected that both genetics and autoimmunity play a role in the development of symptoms outside the gastrointestinal tract.

Estimates suggest that 20-40% of IBD patients have EMs, with a slightly greater prevalence among individuals with Crohns disease than UC. The most common EMs of UC involve the musculoskeletal system, skin, eyes, and liver. While the vast majority of EMs develop after the diagnosis of UC, 10% of patients may experience non-gastrointestinal symptoms as the first sign of their UC.

Musculoskeletal Manifestations
Arthritis - The arthritis associated with UC is typically described as an aching or stiffness in the knees, hips, ankles, wrists, or elbows. Unlike other forms of arthritis (ie; rheumatoid arthritis/osteoarthritis) the joints tend not to swell or become deformed. It has been suggested that the severity of arthritis correlates with disease extent and activity in the bowel.
Sacroiliitis - Inflammation of the joints of the tailbone is a common cause of low back pain among patients with UC.
Ankylosing spondylitis - Ankylosing spondylitis is a rheumatologic condition of the spine which can exist by itself or in association with UC. Inflammation and fusion of spinal joints results in back pain and stiffness. For further information click on the link below.– http://www.wheelessonline.com/ortho/ankylosing_spondylitis

Skin Manifestations
Erythema nodosum – Erythema nodosum presents with red, painful, warm, raised nodules symmetrically distributed on the legs, and sometimes arms. The appearance of the nodules is often associated with underlying bowel activity and arthritis. For photos and further information - http://www.aafp.org/afp/20070301/695.html
Pyoderma gangrenosum – Pyoderma gangrenosum begins as a pustular or nodular lesion which subsequently ulcerates and erodes surrounding tissue. These lesions are often seen on the front of the legs, at sites of prior trauma, and around ostomies. Their evolution tends to be independent of bowel activity. For photos and further information click on the link below.– http://postgradmed.com/.../12_02/puzzles_answer.htn