Paradoxical ulcerative colitis during treatment with secukinumab for psoriasis

EJD, vol. 29, n◦ 4, July-August 2019 say (CLEIA: index > 850 U/mL) (MBL, Nagoya, Japan), and negative for another ELISA (Phadia, Uppsala, Sweden) and a double immunodiffusion assay (MBL). Since it is uncommon for a patient with localized scleroderma (LSc) to test positive for anti-topo I Abs, we conducted an immunoprecipitation assay using the K562 cell extract as an antigen in order to confirm the existence of an anti-topo I Ab. The patient’s sera precipitated a 100-kd protein which was identical to the prototype sera of anti-topo I Abs (figure 1C). The patient did not have any organ involvement, including interstitial lung disease, oesophageal dysfunction, renal disease, arthritis, and myositis. Based on these findings, the patient was diagnosed with generalized morphea with anti-topo I Abs. Oral administration of corticosteroids (10 mg/day) was initiated and skin thickness gradually improved. After a year, oral corticosteroids were discontinued, and thickening of the skin decreased, but pigmentation remained. The patient was still positive for anti-topo I Ab at one and two years after the discontinuation of oral corticosteroids (MBL ELISA index: 145.8 and 129.2, respectively). LSc is a disease that causes fibrosis in the dermis and subcutaneous tissue. In contrast to systemic sclerosis (SSc), LSc does not exhibit microvascular abnormalities, such as Raynaud’s phenomenon and capillary changes, or internal organ involvement. LSc rarely progresses to SSc. Although there are currently no autoAbs specific for LSc, anti-nuclear Ab is often positive. Takehara et al. previously reported that anti-nuclear Ab was present in 72.7% of patients with LSc [1]. Anti-ssDNA Ab [2] and anti-histone Ab [3] have also frequently been detected (50% and 47%, respectively). However, SSc-specific autoAbs are rarely detected in patients with LSc. Two juvenile LSc patients with antitopo I Abs were reported without progression to SSc, based on a final observation [4]. Also, a 12-year-old patient with LSc tested positive for anti-Ku Ab and her LSc progressed to systemic disease two years after initial presentation [5]. In our case, there are currently no findings to indicate SSc, however, the patient is being carefully followed due to potential transition from LSc to SSc in the future. In the present case, anti-topo I Ab results were inconsistent among the different detection assays. Differences in protein purification systems may account for the difference in reactivities observed: MBL utilises the E. coli protein expression system, while Phadia utilizes the baculoviral cell expression system. Alternatively, a specific region of >52 amino acids (512-563) of topo I has been reported to be necessary for recognition by anti-topo I Ab of SSc patients [6], and the antigen epitope that recognised the anti-topo I Ab in our case may have differed in this respect.