Transaminase Changes in Korean Rheumatoid Arthritis Patients with Chronic Hepatitis C after Biologic Therapy

OBJECTIVE: Coexisting chronic hepatitis C can be problematic when treating rheumatoid arthritis (RA). This study examined the changes in the transaminase and viral load in hepatitis C virus (HCV)-infected RA patients after initiating biologic agents. METHODS: A multicenter retrospective study was conducted at 12 University Hospitals in Korea between November 2014 and November 2015, and 78 RA patients, who met the 2010 American College of Rheumatology and European League Against Rheumatism classification criteria for RA and were concomitantly infected with HCV, were identified. The baseline and longitudinal clinical data, changes in liver function, and viral RNA titers were evaluated. RESULTS: Seventeen (21.8%) patients were treated with biologic agents, including etanercept (n=8), adalimumab (n=8), infliximab (n=2), tocilizumab (n=2), abatacept (n=1), and golimumab (n=1) (median 1.5 patient-years). Four patients experienced marked increases in transaminase during treatment with adalimumab (n=2) and tocilizumab (n=2). Two patients (one using adalimumab, the other using tocilizumab) were treated with anti-viral agents and showed dramatic improvement in both the viral RNA and transaminase. One patient discontinued adalimumab due to the repeated elevated transaminase levels along with a twofold increase in the viral RNA titer, and the transaminase level subsequently normalized. No case of overt viral reactivation was identified. CONCLUSION: The data support that changes in transaminase and/or viral load associated with biologic agents in HCV-infected RA patients are possible. Therefore, the liver function and viral RNA titer should be followed regularly during biologic therapy.

Four Cases of Polyarteritis Nodosa Presenting Initially as Pain and Pitting Edema in Both Lower Extremities

Polyarteritis nodosa (PAN) has a broad spectrum of clinical presentation, since it affects small and medium-sized muscular arteries with microaneurysm formation, aneurysmal rupture with hemorrhage, thrombosis, and, consequently, organ ischemia or infarction. Although skeletal muscle involvement is well documented in patients with PAN, it can mimic more common diseases, and cause confusion and delays in diagnosis. PAN muscular involvement may have limited or early systemic forms with a benign course and excellent clinical response to corticosteroid therapy. Herein, we describe the clinical course and outcome of four unusual cases of PAN manifested by acute onset of pain and pitting edema in both lower extremities; in addition, we reviewed the relevant literature.

Risk of Herpes Zoster in Patients with Rheumatoid Arthritis Undergoing Biologic Disease-Modifying Therapy

OBJECTIVE: Rheumatoid arthritis (RA) patients suffer from an increased risk of herpes zoster (HZ) partially due to immunosuppressant medications. This study investigated HZ in RA patients treated with biologic disease-modifying antirheumatic drugs (bDMARDs), as compared with conventional DMARDs (cDMARDs). METHODS: This retrospective case series study assembled record information of 277 RA patients who received bDMARDs after failure of at least one cDMARDs at Seoul National University Hospital between August 2003 and February 2015. Following capture of baseline information and identification of HZ episodes, crude HZ incidence rates per 100 patient-years (95% confidence intervals) were calculated. RESULTS: For 718 treatment courses, 277 (38.6%) comprised cDMARDs, 66 (9.2%) infliximab, 175 (24.4%) etanercept, 95 (13.2%) adalimumab, 9 (1.3%) golimumab, 41 (5.7%) rituximab, 31 (4.3%) abatacept, and 24 (3.3%) tocilizumab. There were 37 HZ episodes, 16 during cDMARD treatment courses, and 21 accompanying bDMARDs, two with infliximab, eight with etanercept, five with adalimumab, and three each with rituximab and abatacept. The crude HZ incidence rate per 100 patient-years was 2.4 (1.4∼3.9) for cDMARDs, 2.2 (0.3∼7.9) for infliximab, 1.8 (0.8∼3.6) for etanercept, 3.7 (1.2∼8.4) for adalimumab, 3.9 (0.8∼11.0) for rituximab, and 8.5 (1.8∼23.1) for abatacept. CONCLUSION: We conclude that bDMARDs do not always increase the risk of HZs in RA patients, although HZ rates vary for different bDMARDs.

A Case of Relapsing Polychondritis Improved by Infliximab Treatment

Relapsing polychondritis is an episodic, systemic inflammation of the cartilage with unknown autoimmune etiology. It leads to the destruction of cartilaginous structures of the ear, eye, nose, respiratory tract, joints, skin, and heart valve, and its presented symptoms are diverse. It can be improved mainly by corticosteroid or immunosuppressive agents. Recently, the use of biologic agents (TNF inhibitors, rituximab, tocilizumab et al) was reported from abroad. However, there is no reported case of relapsing polychondritis, which is treated by biologic agents in Korea. We report this first case of refractory relapsing polychondritis, which was improved with a treatment of Infliximab.

Rituximab Treatment for the Patients with Refractory Inflammatory Myopathy

OBJECTIVE: To assess the efficacy and safety of rituximab (RTX) on disease activity and muscle strength in patients with inflammatory myopathies refractory to conventional therapy. METHODS: Four inflammatory myopathy patients who had been refractory to glucocorticoids, one or more immunosuppressive therapies and intravenous immunoglobulin were treated on an open-label basis. Each patient received two 500 mg doses of RTX 2 weeks apart in one cycle. In one patient who did not respond after the first cycle of RTX, the infusion schedule was modified by the physician. We measured muscle enzyme including CPK, LDH and assessed muscle strength individually to evaluate RTX response. Additionally anti-CD19 antibody was measured. RESULTS: Three patients responded to the first cycle of RTX treatment with improvements in muscle enzyme and muscle strength, and then maintained physical function over the duration of several infusion cycles. In one patient, muscle enzyme did not decrease after the first cycle of RTX, and a high dose glucocorticoid was given. After modifying the treatment schedule with monthly RTX infusion, his muscle enzyme level and muscle strength improved. Anti-CD19 antibody decreased after RTX generally, but responses were variable. Herpes zoster infection occurred in two patients. CONCLUSION: Rituximab may be a therapeutic choice in refractory inflammatory myopathy. However a further trial is needed to confirm the efficacy and prove the safety.

Rituximab Treatment in a Case of Dermatomyositis Accompanied by Thrombotic Thrombocytopenic Purpura / 대한내과학회지

Thrombotic thrombocytopenic purpura (TTP) is an uncommon, serious disease known to be related with infection, toxin, pregnancy and autoimmune disease. Autoimmune disease-related TTP is rare, difficult to diagnose and can rapidly become fatal if left untreated. We report the case of a 59 year-old Korean female with TTP associated with dermatomyositis flare. The patient was suspected to have amyopathic dermatomyositis and was treated with moderate doses of oral glucocorticoids. One month later, muscle weakness developed with dermatomyositis flare, and the patient showed confusion, acute renal failure, thrombocytopenia and microangiopathic hemolytic anemia. She was diagnosed with TTP associated with dermatomyositis flare. After prompt plasmapheresis treatment with high dose glucocorticoid therapy, her confusion, thrombocytopenia and anemia were improved. However, oliguric renal failure and myopathy remained, and thrombocytopenia and anemia recurred. After starting additional rituximab treatment, the clinical manifestation of dermatomyositis and TTP improved markedly.

A Case of Ankylosing Spondylitis Accompanied by Henoch-Schonlein Purpura and Chronic Inflammatory Demyelinating Polyneuropathy / 대한내과학회지

Peripheral nervous system dysfunction is a rare complication in Henoch-Schonlein purpura, but it tends to recover spontaneously without treatment. A 78-year-old man who had ankylosing spondylitis presented with Henoch-Schonlein purpura associated with progressive sensorimotor polyneuropathy. He was diagnosed with chronic inflammatory demyelinating polyneuropathy, which did not improve despite intravenous immunoglobulin therapy. We describe a case of Henoch-Schonlein purpura, accompanied by chronic inflammatory demyelinating polyneuropathy in a patient with ankylosing spondylitis.