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.