Discussion
There is no comprehensive consensus about the origin and etiology of UC however it does fulfill the criteria for an autoimmune disease [4 5]. some of the characteristics of UC are precisely autoimmune. The fact that certain human leukocyte antigens (HLAs) are in association with UC [5], certain autoantibodies are found to be involved as well, and most importantly the response to immunosuppressive therapy has led to this conclusion [4 5]. Our patient had previously been diagnosed and was under treatment for the disease and her medical history was consistent with our findings as well. However, her early workup was unsuccessful in diagnosing the underlying cause for pancytopenia. This phenomenon is thought to be related to the early stages of SLE in which it had no clinical manifestation [4 6].
A wide variety of disorders are also thought to have an autoimmune basis such as celiac disease, ankylosing spondylitis, primary sclerosing cholangitis, etc. one of such disorders that is rarely concurrent with UC is SLE [7]. In a case-control study conducted by Shor et al. UC was more prevalent in patients diagnosed with SLE [8]. However, in multivariate regression models, SLE was not in association with UC. There is a certain problem that also makes establishing the relation between the two even more difficult and that is the fact that certain medications, 5-aminosalicylic acid (5-ASA) compounds, in particular, can cause drug-induced lupus [2]. And sometimes it’s hard to distinguish between these two. Even though lupus can be both idiopathic and drug-induced, there are certain differences between the two. While anti-dsDNA antibodies and more importantly hypocomplementemia are common findings among idiopathic cases and they are rarely associated with drug-induced type [2]. Even though our patient had been on 5-ASA medication for a considerable amount of time we believe that her SLE diagnosis was true and accurate as she fulfilled the EULAR/ACR criteria.
In a study conducted by Snook Ja, the association between autoimmune diseases and inflammatory bowel disease had been studied and it turns out that 6.6 % of the patients with UC had another autoimmune disease [4 9]. However, the gastrointestinal manifestations of both UC and SLE are similar and common in both, and might be difficult to distinguish between the two; particularly in lupus colitis which is caused by inflammation, vasculitis, and necrosis in vessels of the intestine. Kurlander and Kisner described the involvement in patients with concurrent SLE and UC to be mostly in 2 forms [10]; 1) a predominating vasculitis with bleeding and perforation usually associated with a clinical picture suggestive of SLE; or 2) non-specific ulcerative or granulomatous colitis.
Although many cases have been suggestive for the association between UC and SLE, the link between the two needs more study and more investigation as to its too rare.
Another disease manifestation of our patient which was interesting was monoclonal gammopathy. This phenomenon is rarely associated with SLE however several mechanisms have been proposed to be involved; polyclonal B-cell activation both peripheral and in the bone marrow, abnormal B-cell clones, And immunosuppressive agents prescribed for SLE patients that disposes them to malignancies especially multiple myeloma, are some of these mechanisms [1 3]. In a study conducted by YM Ali, et al at the University of Toronto they concluded that the prevalence of monoclonal gammopathy in SLE patients (5.4%) is higher than the general population (1–2%) [3]. In this study, it’s also suggested that this disorder is not associated with any malignancies. Our patient had a very high ESR level this inflammatory factor had prompted us to obtain a serum protein electrophoresis. As the pathogenicity of gammopathy in such patients has not been discovered we suggest that all patients go through malignancy workup.