B. Zamani, H. R. Golkar, S. Farshbaf, M. Emadi-Baygi, M. Tajabadi-Ebrahimi, P. Jafari, R Akhavan, M. Taghizadeh, M. R. Memarzadeh, and Z. Asemi, Clinical and metabolic response to probiotic supplementation in patients with rheumatoid arthritis: A randomized, double-blind, placebo-controlled trial, International Journal of Rheumatic Diseases 19, no. 9 (2016): 869–879, https://doi.org/10.1111/1756-185X.12888. This Expression of Concern is for the above article, published online on 02 May 2016 in Wiley Online Library (wileyonlinelibrary.com), and has been published by agreement between the journal Editor-in-Chief, James Cheng-Chung Wei, and John Wiley & Sons Australia, Ltd. The Expression of Concern has been agreed due to concerns raised regarding the integrity of the research and discrepancies in reporting. An investigation has been conducted by the National Committee for Ethics in Biomedical Research Iran, in coordination with Kashan University of Medical Sciences (KAUMS). However, without the verification of clinical records there remain sufficient doubts about the feasibility and integrity of the research undertaken. As a result, the journal has decided to issue an Expression of Concern to alert readers.
Sjögren's disease is one of the most common systemic autoimmune diseases with hallmark features of sicca (dryness) symptoms of the eyes and mouth. There are a variety of ways to quantify xerostomia. α-Amylase is an enzyme secreted by the pancreas and salivary glands. While not specific to salivary glands, it may be measured as a surrogate marker of their output. Therefore, in this short investigation, we determined if there were any associations of serum α-amylase with subjective and objective markers of xerostomia. This investigation found a correlation between objective and subjective markers of xerostomia and α-amylase which suggests that measuring this analyte is a novel adjunct to qualifying xerostomia in the clinic.
The cardiovascular risk of JAK inhibitors (JAKi) is a contentious issue. The ORAL surveillance study—a randomized, non-inferiority, safety endpoint trial—demonstrated that the JAKi tofacitinib (TOF) was not non-inferior to tumor necrosis factor inhibitor (TNFi) regarding major adverse cardiovascular events (MACE) in patients with rheumatoid arthritis (RA).1 Since patients in ORAL surveillance were older with cardiovascular risk factors, it is difficult to generalize this result to other patients. To clarify this issue, we performed a systematic literature search of the Cochrane library and MEDLINE (Ovid) databases with key terms related to JAKi, MACE, and rheumatic diseases. We included English studies investigating adults with RA, psoriatic arthritis (PsA), or axial spondyloarthritis (axSpA) who were receiving TOF, baricitinib (BARI), or upadacitinib (UPA), which involved MACE or changes in cardiometabolic factors as outcome parameters (Table 1). While most studies explored TOF and RA, some explored the impact of JAKi on cardiometabolic factors, and how this may subsequently alter cardiovascular risk.2-5
One review explored hypothetical mechanisms through which JAKi may alter MACE.2 In both a mouse model and human studies, blockade of interleukin 6 downstream pathways (which plays a pivotal role in RA pathogenesis) may positively or negatively modify cardiovascular outcomes, depending on the surrounding pathophysiological milieu. However, regarding PsA and axSpA, JAKi may provide cardioprotective effects via blockade of JAK2, which is involved in the pathogenesis of these diseases. JAKi may also modulate LDL catabolism, which seems consistent with observations in early JAKi studies.3
In 2013, TOF use in RA was associated with a mean rise in LDL, with LDL serum levels stabilizing from the third month.3 Nevertheless, strong associations between serum lipid level and increased risk of cardiovascular events cannot be demonstrated through early JAKi trials alone. Firstly, such studies were of shorter duration and would only detect MACE that occurred within 1 year. Additionally, cardiovascular safety is rarely a primary endpoint in these trials; high-risk patients are often excluded from such studies.
These challenges are partly what prompted the ORAL surveillance study. Here, fasting LDL and HDL levels rose and stabilized from the second month for patients receiving TOF 5 mg and TOF 10 mg relative to TNFi.1 However, increased numerical incidence of MACE in TOF users relative to TNFi users may be partially attributable to background cardiovascular risk rather than changes in lipid levels alone.4 Therefore, the link between JAKi, serum lipid levels, and cardiovascular risk requires further enquiry.
The impact of JAKi on other cardiometabolic parameters has also
Ankylosing spondylitis (AS) predominantly affects the spine and sacroiliac joints, with rare renal involvement. We investigated the incidence rate and risk factors for chronic kidney disease (CKD) in patients with AS and its relationship with long-term nonsteroidal anti-inflammatory drug (NSAID) use.
We retrospectively analyzed data of patients diagnosed with AS from the Korean National Health Insurance service. The 3-month, 6-month, and 1-year Assessment of SpondyloArthritis International Society (ASAS) NSAID Intake Scores were categorized into four groups, as follows: =0, >0 and ≤33.3, 33.3–66.6, and >66.6.
Of the 12 000 patients with AS, 150 were identified with CKD, and the incidence rate was 4.64 per 10 000 patient-years. Factors significantly associated with CKD included age ≥60 years, Charlson Comorbidity Index, hypertension, and diabetes mellitus. In the nested case–control analysis, among the ASAS NSAIDs Intake Scores for 0–365 days from diagnosis, the ≥66.6 group had a significantly lower odds ratio than those of the =0 group.
The present study established the incidence rate of CKD in Korean patients with AS. Though older age and comorbidities were found to be associated with a higher CKD risk, long-term NSAID use was associated with a lower risk. Therefore, the optimal use of NSAIDs in inflammatory diseases requires extensive research.
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