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Objective: Gastroesophageal reflux disease (GERD) is one of the most common comorbidity in many diseases, but the frequency in rheumatic disease has not been well understood., Methods: We investigated the prevalence of GERD by GerdQ in 530 rheumatic patients [systematic lupus erythematosus (SLE; n = 120), rheumatoid arthritis (RA; n = 117), polymyalgia rheumatica (PMR; n = 40), dermatomyositis and polymyositis (PM/DM; n = 38), systemic scleroderma (SSc; n = 37), mixed connective tissue disease (MCTD; n = 18), Behçet disease (BD; n = 17), adult onset still disease (AOSD; n = 14), and other rheumatic diseases (n = 129)]., Results: The mean GerdQ scores of patients was 6.2 ± 1.8, respectively, and no significant differences were observed between all patients. However, the GERD prevalence in SSc and BD was increased compared to that in SLE, RA, PMR, PM/DM, MCTD, and AOSD. In no medication of proton pump inhibitors (PPIs), a significant increase in the risk of GERD symptoms was 2.5 times compared with that in the medication of PPIs in all patients by multivariable regression analysis. On the other hand, there were no increased risks of GERD symptoms with corticosteroids., Conclusion: In rheumatic diseases, GerdQ would be the useful tool of diagnosis GERD, regardless whether the patients complain or not about gastrointestinal (GI) symptoms.

Nephrotoxicity is a frequent complication of cisplatin-induced chemotherapy, in which T cells are known to promote acute kidney injury (AKI). Apoptosis and necrosis of tubules and inflammatory events also contribute to the nephrotoxicity. A delineation of the mechanisms that underlie the inappropriate renal and tubular inflammation can thus provide important insights into potential therapies for cisplatin-induced AKI. Rho-kinases are known to act as molecular switches controlling several critical cellular functions, including cell migration, cytokine production, and apoptosis. Here, we show that the Rho-kinase inhibitor fasudil attenuated cisplatin nephrotoxicity, resulting in less histological damage, improved renal function, and the infiltration of fewer leukocytes into the kidney. Renal nuclear factor-κB activation and apoptosis were reduced, and the expressions of proinflammatory renal cytokine and chemokine mRNA were decreased. Urinary and renal kidney injury molecule-1 (Kim-1) expression was also reduced, a finding that is consistent with diminished kidney injury. In the current study, we also showed that fasudil could be protective of the impaired tubules. In vitro, fasudil reduced the apoptosis (annexin-V+PI cells) and cytokine production (tumor necrosis factor+ cells) in T cells and the apoptosis (annexin-V+PI cells) and tubular damage (Kim-1+ cells) in proximal tubular cells by flow cytometric analysis. As Rho-kinase plays an important role in promoting cisplatin nephrotoxicity, inhibiting Rho-kinase may be a therapeutic strategy for preventing cisplatin-induced AKI., (Copyright © 2015 the American Physiological Society.)

To predict the response of patients with rheumatoid arthritis (RA) to infliximab, patient profile and laboratory findings were compared to determine whether there was any association with the clinical course of the disease, and the clinical significance of serum rheumatoid factor (RF) in the response to this treatment was considered. Sixty-two RA patients were treated with infliximab, 87.9% of whom were positive for RF. At baseline and 12 months after the start of treatment, RF titers were significantly lower in the low-CRP group (CRP at 12 months<0.3 mg/dl) compared with that in the high-CRP group (CRP at 12 months >1.5 mg/dl). Furthermore, at baseline and 12 months, RF titers were significantly lower in the good-CRP-response group (DeltaCRP>or=1.5 mg/d) compared with the poor-CRP-response group (DeltaCRP