WCIM 2014 SEOUL KOREA 233
Poster Session
The Korean Journal of Internal Medicine Vol. 29, No. 5 (Suppl. 1)
PS 0716 Rheumatology
Ocular Toxicity of Hydroxychloroquine is More Fre- quent in Male Patients
Omer KARADAG1, Abdulsamet ERDEN1, Levent KILIC1, Umut KALYONCU1, Ali AKDOGAN1, Sule APRAS BILGEN1, Sedat KIRAZ1, Ihsan ERTENLI1
Department of Rheumatology, Faculty of Medicine, Hacettepe University, Turkey1
Background: Hydroxychloroquine(HQ) is widely used to treat for rheumatoid arthri- tis(RA) and connectice tissue disorders.Due to the potential of ocular toxicity,routine ophtalmological assessment(ROA) is essential for sight safety.
Methods: In our outpatient clinic, patients with RA and connective tissue disorders such as systemic lupus erythematosus (SLE), sjogren syndorme (SS) and overlap were assessed consecutively for drug status of HQ by a standard questionnaire between December 2013 and January 2014. Patients who used HQ less than 1 year (13.6%) were excluded from study.Ocular toxicity was taken from patients’ reported.If ophthalmologist advised to cease HQ due to ocular toxicity,we accepted as ocular side effect. Patients with ocular toxicity were not reevaluated by an ophthalmologist. Cumulative HQ dosage and risk factors for ocular toxicity were assessed by using Mann-Whitney U test.
Results: A total of 266 patients(90.6% female) were enrolled.Mean age was 50±13.5 years and median disease duration was 8 years(1-50).Median duration of HQ treat- ment was 6 years(1-28) and median dose was 400 mg/day.Of 46(17.3%) patients were ceased HQ.The reasons of cease of HQ were ocular toxicity 22(47.8%), patient non-adherence 9(19.6%),dermatological side effect 3(6.5%),others 12(26.1%).22 of all 266(%8.3) patients developed ocular toxicity.Ocular toxicity was found more fre- quently in male 5/20(20%) vs 17/241(7%),p=0.025). Median cumulative HQ dosage in patients with ocular toxicity was 864 gram (108-2160) in other words 12.9 gr per kilo- gram(1.2-40).Older age (58±10 vs 50±13,p=0.008),longer disease duration (14.8±11.5 vs 9.2±7.1 years,p=0.013), and longer HQ duration (10±6.3 vs 7.1±5.6 years,p=0.023) were associated with ocular toxicity.
Conclusions: Among regularly follow-up patients, ocular toxicity of HQ was not rare in a rheumatology outpatient clinic.Cumulative toxicity for ocular toxicity was 13 gram/kilogram;however, certain patients developed toxicity in 1 gram/kg/day.Although, important part of our patients was female, ocular toxicity was seen more frequently in male patients. Other risk factors such as longer disease duration,longer HQ usage and older age were also demonstrated in our patients.
PS 0717 Rheumatology
Toxic Hepatitis in Patients with Systemic Lupus Erythe- matosus
Nayoung PARK1, Minyoung HER1, Dongyook KIM1 Inje University Busan Paik Hospital, Korea1
Background: Subclinical liver disease is common in SLE, but strikingly high levels of liver enzymes are rare. Our aim was to fi nd the cause of liver enzyme abnormalities in lupus patients, particularly with toxic hepatitis.
Methods: We performed a retrospective chart review of SLE patients treated at the Inje University Hospital between 2001 and 2013. We defi ned liver enzyme abnormality as a = 2 fold increase in 2 or more of 4 components:bilirubin, AST, ALT and LDH or ALP.
Toxic hepatitis was diagnosed by a score 5 in the Roussel Uclaf Causality Assessment Method (RUCAM) and classifi ed according to their pattern of liver enzyme.
Results: Clinical and laboratory fi ndings was reviewed in 301 SLE patients. Of 301 pa- tients, 74 (24.6%) met strict criteria for liver enzyme abnormality. Toxic hepatitis (n = 20), viral hepatitis (n = 3), autoimmune hepatitis (n = 5), elevated enzyme associated with infection (n = 4) and an indeterminate clinical diagnosis, presumably associated with lupus activity (n=42) were diagnosed. Among 20 patients with toxic hepatitis, herbal medicines (n = 8), anti-tuberculosis drug (n = 4), antibiotics (n = 5), NSAIDS (n = 1), or anticonvulsant drug (n = 2) were the cause of toxic hepatitis. There were striking abnormalities in 20 patients (mean peak values: AST 610 ±551 U/L, ALT 369±
352 U/L, ALP 598±387 U/L, LDH 1,128±761 U/L). 5 had a cholestatic pattern, 9 had a hepatocellular pattern, 3 had a mixed pattern and 3 were undetermined. 17 patients were found to have active lupus (SLEDAI=4). After cessation of the suspected medica- tion and subsequent steroids treatment, liver enzyme were improved.
Conclusions: In our study, herbal medicines were the most common cause of toxic hepatitis in Korean lupus patients. Antibiotics and anti-Tb drugs also could lead to toxic hepatitis in lupus patients.
PS 0718 Rheumatology
Autoimmune Hepatitis in Systemic Lupus Erythemato- sus
Doo-Ho LIM1, Seung-Hyeon BAE1, Soo Min AHN1, SeokChan HONG1, Yong-Gil KIM1, Chang-Keun LEE1, Bin YOO1
Asan Medical Center, Korea1
Background: Autoimmune hepatitis(AIH) is chronic progressive liver disease of un- known cause, characterized by circulating autoantibodies and hyperglobulinemia.
Patients with AIH often have other autoimmune diseases. However, AIH accompanied by SLE(AIH-SLE overlap) is relatively rare. The aims of study were to identify distinct features of AIH-SLE overlap compared with primary AIH(PAIH) and to evaluate factors related with outcome of AIH-SLE overlap.
Methods: From May. 1995 to Feb. 2014, the clinical data of 164 patients with PAIH and 23 patients with AIH-SLE overlap in a tertiary referral center were reviewed retro- spectively. AlH was diagnosed if pretreatment or posttreatment score was above 9 or 11, according to AIH diagnostic scoring system of American Association for the Study of Liver Disease in 2002. Liver biopsy was performed in all AIH patients. SLE patients fulfi lled at least 4 of the 1997 revised ACR criteria. Progression was defi ned as occur- rence of liver cirrhosis(LC), hepatocellular carcinoma(HCC), liver transplantation(LT) or death from hepatic failure.
Results: Mean follow-up duration of AIH-SLE overlap and PAIH were 7.62±4.13 years and 6.23±4.21, respectively(Table1). Age at AIH diagnosis was younger and initial serum IgG level was higher in AIH-SLE overlap(P<0.005). There were no signifi cant differences of histological findings and treatment strategy. Although proportion of overall progression was not different, severe progression such as HCC, LT or death only happened in PAIH. Among 23 patients of AIH-SLE overlap, 8 with progression showed higher serum IgG level(4077.38±1641.02mg/dl) compared to 15 without progression(2560.71±932.24) (p=0.017). Furthermore, progression in AIH-SLE overlap was associated with serum IgG level of above 2 folds upper limit of normal(OR=11.00, 95%CI=1.420–85.201, P=0.026).
Conclusion: Clinical course of AIH might be expected less aggressively in AIH-SLE overlap than PAIH. In addition, we could suggest that initial high level of serum IgG is a poor prognostic factor in AIH-SLE overlap.
PS 0719 Rheumatology
Panenteritis as The Initial Presentation of Systemic Lupus Erythematosus
Han Ah LEE1, Jae Hoon KIM2, Hye Gi SHIM3, Young Ho SEO4, Beom Jae LEE5, Sung Jae CHOI6, Young Ho LEE7, Jong Dae JI8, Gwan Gyu SONG9
Korea University Anam Hospital, Korea University College of Medicine, Korea1, Korea University Guro Hospital, Korea University College of Medicine, Korea2, Alpert Medical School of Brown University, USA3, Korea University Ansan Hospital, Korea University College of Medicine, Korea4, Korea University Guro Hospital, Korea University College of Medicine, Korea5, Korea University Ansan Hospital, Korea University College of Medicine, Korea6, Korea University Anam Hospital, Korea University College of Medicine, Korea7, Korea University Anam Hospital, Korea University College of Medicine, Korea8, Korea University Guro Hospital, Korea University College of Medicine, Korea9
Introduction: Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that can affect almost any organ system. Lupus enteritis is rare and serious compli- cation of SLE. It presents as abdominal pain, diarrhea, and vomiting. Lupus enteritis usually affects the small and large bowels, and rectum is rarely involved, because of collateral circulation. Here, we describe a 25-year-old woman who presented with panenteritis as the fi rst manifestation of SLE.
Case Description: The patient is a 25-year-old woman who had multiple hospital- izations at an outside hospital for prolonged abdominal pain, nausea, and diarrhea without any evidence of SLE. Malar rash and history of oral ulcer were observed. Lab- oratory investigations showed a positive antinuclear antibody (1:320) with speckled pattern, positive IgM anti-ß2 glycoprotein I and IgM anti-cardiolipin antibody, low complement (C3/C4 59/5 mg/dl) and proteinuria (1426mg per 24 hours). In hospital, seizure developed. The brain magnetic resonance imaging showed high signal intensity in both temporo-parieto-occipital area and the electroencephalogram findings are suggestive of partial seizure disorder in left occipital area. A computed tomography showed ascites and diffuse hypodense submucosal thickening involving the stomach lower body, small and large bowel. A colonoscopic biopsy was nonspecifi c. A kidney biopsy showed WHO class IIa lupus nephritis. This patient was diagnosed as SLE with extensive lupus enteritis. Treatment was commenced with high-dose corticosteroids
234 32nd World Congress of Internal Medicine (October 24-28, 2014) WCIM 2014
followed by mycophenolate mofetil, hydroxychloroquine, and azathioprine.
Conclusion: Lupus enteritis is rare and serious complication, and rectum is rarely in- volved. It is important for clinicians to be aware that lupus enteritis could be the fi rst presentation of SLE in the young woman with no history of SLE, but with a prolonged course of abdominal pain, diarrhea, vomiting and with computed tomography fi ndings showed marked bowel edema involving the small and large bowel.
PS 0720 Rheumatology
Adalimumab-Induced Systemic Lupus Erythematosus in a Patient with Rheumatoid Arthritis
Tae-Han LEE1, Ji-Min LEE1, Hye-Jin JEONG1, Chang-Nam SON1, Ji-Min KIM1, Sang- Hyon KIM1
Keimyung University Dongsan Medical Center, Korea1
Introduction: Anti tumor necrosis factor alpha (TNFα) is widely used in the manage- ment of patients with rheumatic disease, including rheumatoid arthritis (RA). However, anti TNFα has a number of rare but serious adverse effects, including infection, tu- berculosis, and drug induced systemic lupus erythematosus (SLE).
Case: A 42-year-old woman with RA treated with methotrexate, sulfasalazine, and bucillmaine over 6 months presented to our outpatient clinic with multiple joint pain.
The patient’s RF was elevated to 141 IU/mL, and anti-CCP to 111 U/mL, while ESR was 85 mm/hr, and CRP was 1.10 mg/dL. Since the patient had continued active joint infl ammation, adalimumab was added to treatment with methotrexate and predni- solone. Her arthritic symptoms improved signifi cantly with adalimumab. The RF, ESR, and CRP levels declined to 43.2 IU/mL, 26mm/hr, and 0.02 mg/dL, respectively. After 9 months of treatment, the patient noticed cutaneous lesions, multiple infl amed tender nodules, and plaque on her face, arms, legs, and buttock. ESR and CRP were elevated to 90 mm/hr and 0.69 mg/dL, respectively. The serology of the ANA was positive at a titer of 1:2560. It was also positive for anti-dsDNA antibodies. The C3 level was 69.5 mg/dL, the C4 level was 14.6 mg/dL, and the patient was positive for anti-histone antibodies. The histopathology of a biopsy from a lesion on the left forearm showed nodular panniculitis with vasculitis. Based on the clinical, laboratory, and histopatho- logical findings, this case was consistent with a diagnosis of drug-induced SLE, so adalimumab was discontinued.
Conclusion: Although a case of etanercept-induced SLE in a patient with RA was re- ported in Korea, adalimumab-induced SLE had not been reported previously. Therefore, we report the fi rst case of adalimumab-induced SLE in a patient with RA.
PS 0721 Rheumatology
Acute Disseminated Encephalomyelitis After Enteroviral Infection as a First Manifestation of Systemic Lupus Erythematosus
Ji-Min KIM1, Chang-Nam SON1, Hyuk Won CHANG2, Sang-Hyon KIM1
Keimyung University Dongsan Medical Center, Korea1, Keimyung University Dongsan Medical Center, Korea2
Acute disseminated encephalomyelitis (ADEM) is a rare demyelinating disease of the central nervous system that is thought to be caused by an abnormal immune response as a result of an infection or a vaccination. ADEM as a complication of systemic lu- pus erythematosus (SLE) has not been proven in the literature. Herein, we present an unusual case of 17-year-old girl who developed ADEM after enterovirus infection as a fi rst manifestation of SLE. A 17-year-old Asian girl was admitted to the hospital with severe headache and double vision for a week. Ten days prior to admission, she had suffered from abdominal pain and diarrhea after traveling to the seaside. On admis- sion, she was somewhat lethargic with a temperature of 37.8℃. Cerebrospinal fl uid analysis showed unremarkable fi ndings and negative results for microorganism. Brain magnetic resonance imaging (MRI) showed multifocal hyperintensity lesions in both basal ganglia, right thalamus, midbrain, pons, cortical and subcortical regions of both cerebellum (Figure). Serum neutralizing antibody titer of 1:64 against enterovirus 71 was observed. On hospital day 3, vasculitic rash appeared on both palms and arthralgia of the left ankle occurred. Laboratory fi ndings showed leukopenia, thrombocytopenia, hypocomplementemia, and proteinuria. The autoimmune profi le demonstrated positive antinuclear antibody (1:1280, speckled pattern), positive anti-double-stranded DNA antibody, and positive anti-SSA/anti-Ro antibody. Lupus anticoagulant and anti-cardi- olipin antibodies (IgG, IgM) were also present while there were no clinical signs of ar- terial or venous thrombosis. We diagnosed SLE presenting with ADEM associated with enterovirus infection as an initial manifestation. After steroid and cyclophosphamide pulse therapy, brain MRI revealed nearly complete resolution of most of high signal in- tensity lesions. In conclusion, this case suggests that ADEM after enterovirus infection may arises, although rarely, as a fi rst manifestation of SLE.
