International Journal of Rheumatic Diseases最新文献

Objective: Despite advancements in pharmacological treatments, living with inflammatory arthritis (IA) (including rheumatoid arthritis (RA), psoriatic arthritis (PsA), and axial spondyloarthritis (axSpA)) can make it challenging to engage in social activities, which may increase the risk of loneliness. Although loneliness is predominantly prevalent in IA, its origin and impact on mental health status on daily life with IA remain unexplored. Therefore, the objective of this study was to describe the experiences of people with IA in relation to loneliness.

Methods: Semi-structured telephone interviews were conducted with purposefully sampled participants who reported loneliness. Reflexive thematic analysis was applied to analyze data.

Results: The interviews included fourteen participants (RA (n = 5), PsA (n = 5), and AxSpA (n = 4)) with median age of 47 (range 25-76). We developed three themes: (1) "Loneliness amplifies the negative impact of IA," illustrating the experience of loneliness as an integrated part of the participants' struggles; (2) "Excluding myself from what I need the most," detailing participants' awareness of their need but inability to engage in social activities; and (3) "Longing for loneliness to be addressed," expressing unfulfilled wishes for health professionals to address loneliness.

Conclusion: Participants in our study reported that loneliness had a profound impact on their overall well-being and self-management. Overall, there is a critical need to address loneliness as an essential issue for people with IA, highlighting the necessity for increased support and recognition. By addressing loneliness, health professionals can protect patients' mental health and help them navigate social connections, enhancing their self-management and overall well-being.

A 19-year-old male patient with phenylketonuria (PKU) was presented to our clinic with complaints of left hip pain and fever for one week. Physical examination and MRI examination showed findings compatible with pyogenic sacroiliitis and an abscess in the left iliopsoas muscle. The patient's clinical and radiological findings improved markedly with empirical antibiotic treatment. Although immune system disorders associated with PKU have been reported previously, to our knowledge, a direct link between PKU and rheumatological diseases has not yet been demonstrated. This case suggests that further research is needed to understand the potential effects of PKU on the immune system and susceptibility to infections.

Background: Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.

Methods: In the current study, IL-1β-induced C28/I2 cells were used to establish an in vitro model of OA. The expression of HCP5 in OA cartilage tissue and in the in vitro model of OA was detected by RT-qPCR. Cell viability and apoptosis were assessed by CCK-8 and Annexin V-PI double staining. Western blotting was employed to detect the protein expression of MMP-13 and aggrecan.

Results: The results showed that the findings suggested that HCP5 was downregulated in OA cartilage tissue and IL-1β-induced C28/I2 cells. HCP5 overexpression greatly enhanced IL-1β-induced proliferation of C28/I2 cells, as well as prevented cell apoptosis and degradation of extracellular matrix (ECM). Besides, we have shown that HCP5 is a ceRNA that regulates KLF5 by sponging miR-375. Furthermore, KLF5 is also regulated by m6A regulation induced by HCP5. Finally, overexpression of miR-375, the m6A modification inhibitor, as well as KLF5 inhibition reversed the impact of HCP5 on IL-1β-induced C28/I2 cells.

Conclusion: In summary, the present study demonstrated that the HCP5/KLF5 axis inhibited the progression of osteoarthritis.

Background: γδT cells have been implicated in the pathogenesis of autoimmune diseases. The study aims to investigate the abundance of γδT cells in MRL/lpr mice.

Methods: MRL/lpr mice were used as lupus models, while C3H/HeJ mice served as normal controls. The abundance of γδT cells in different organs was examined by flow cytometry. Plasma double-stranded DNA antibody levels, blood urea nitrogen, creatinine, and urinary protein levels were measured. Renal histopathology was observed via H&E staining. The correlations between the abundance of γδT cells and lupus manifestations were analyzed.

Results: Compared with C3H/HeJ mice, the number of γδT cells and Vγ6⁺γδT cell subset in the peripheral blood of MRL/lpr mice was significantly reduced. However, in the kidney, the number of γδT cells and Vγ6⁺γδT cell subset was significantly increased. Additionally, the number of Vγ6⁺γδT cells in the kidney was positively correlated with the urinary protein level. The number of IFN-γ⁺Vγ6⁺γδT cells in the kidney was positively correlated with urinary protein level.

Conclusion: In MRL/lpr mice, it is likely that peripheral γδT cells, especially the Vγ6 subset, infiltrate the kidney and secrete IFN-γ, which contributes to the development of lupus nephritis.

Objective: To analyze the diagnostic value of a combined test of anti-cyclic citrullinated peptide antibody (CCP), anti-keratin antibody (AKA), anti-carbamylated protein antibody (Carp antibody), and rheumatoid factor (RF) in the early diagnosis of rheumatoid arthritis (RA).

Methods: Sixty cases of RA admitted to our hospital from 2021 to 2022 (observation group) were selected, along with 50 cases of healthy physical examiners (control group). The results of CCP antibody, AKA antibody, Carp antibody, and rheumatoid factor in both groups were analyzed: the concentration of CCP antibody, AKA antibody, Carp antibody, and rheumatoid factor in each group at different levels; the comparison of various testing methods with the "gold standard" test; and the ROC curve analysis of CCP antibody, AKA antibody, Carp antibody, and rheumatoid factor in each group.

Results: The concentrations of CCP antibody, AKA antibody, Carp antibody, and rheumatoid factor were significantly higher in the observation group than in the control group (p < 0.05). Furthermore, there was a significant increase in the concentrations of CCP antibody, AKA antibody, Carp antibody, and rheumatoid factor from the mild to moderate group (p < 0.05), as well as from the moderate to severe group (p < 0.05). Additionally, when comparing the mild and severe groups, there was a significant elevation in the concentrations of CCP antibody, AKA antibody, Carp antibody (p < 0.05), and rheumatoid factor (p < 0.05).

Conclusion: Anti-cyclic citrullinated peptide antibody, AKA antibody, Carp antibody, and rheumatoid factor combined tests have high sensitivity and specificity in the diagnosis of RA.

Objectives: To determine the prevalence of self-reported delayed adverse events (DAEs), major AEs, and flares following COVID-19 vaccinations among patients with autoimmune rheumatic diseases (AIRDs) in Malaysia.

Methodology: An electronically validated survey from the COVID-19 vaccination in autoimmune diseases (COVAD) study group was distributed in July 2021 to patients with autoimmune diseases and healthy controls (HCs). The survey collected data on DAEs (any AE that persisted or occurred after 7 days of vaccination), any early or delayed major adverse events (MAEs), and flares following COVID-19 vaccination. Generalized estimating equation (GEE) models were performed to determine the factors associated with repeated events of DAEs, MAEs, and flares.

Results: A total of 556 vaccines were administered to 204 subjects (150 AIRDs and 54 HCs), with 72.1% completing 3 doses. In multivariate GEE analysis, there was a greater frequency of minor DAEs among AIRDs versus HCs (OR 5.65, p = 0.052). The occurrence of MAEs was higher in AIRDs versus HCs (4.9% vs. 1.3%, p = 0.052), but it was no longer significant in the GEE model. In the AIRDs group, the BNT162b2 vaccine increased the risk for minor DAEs (OR4.68, p = 0.02) while patients with autoimmune multimorbidity showed a greater risk for MAEs (OR 8.25, p = 0.007). The rate of flare was 10.6% and multivariate GEE analysis revealed that The rate of flare was 10.6% and multivariate GEE analysis revealed that systemic lupus erythematosus (SLE) (OR0.31, p = 0.03) and hydroxychloroquine (HCQ) (OR 0.16, p < 0.001) were protective against flare.

Conclusion: The rates of minor DAEs, major AEs, and flares were comparable with other reported studies. Different types of vaccines, underlying AIRDs, and treatments may influence the symptoms of AEs and flares postvaccination against COVID-19.

Objective: Serum uric acid (SUA) may play positive roles in diseases associated with oxidative stress, such as osteoporosis (OP). Nevertheless, the specific impact of SUA levels on both bone mineral density (BMD) and the risk of OP remains uncertain. Considering such information crucial for clinicians when making decisions about urate-lowering therapy (ULT), we sought to fill this gap by conducting dose-response meta-analyses.

Methods: PubMed, EMBASE, and Cochrane Library were searched for studies that met the inclusion criteria. Pooled standardized mean difference (SMD) for BMDs and the odds ratio (OR) for OP between the highest and lowest SUA categories as well as the nonlinear dose-response relationships were estimated.

Results: Pooled SMDs indicate that participants in the highest category of SUA have greater BMDs at the lumbar spine (SMD = 0.37; 95% CI: 0.27, 0.46), femoral neck (SMD = 0.25; 95% CI: 0.21, 0.29), total hip (SMD = 0.34; 95% CI: 0.26, 0.42), and lower risk of OP (OR = 0.59, 95% CI: 0.52, 0.67) compared with the lowest. The nonlinear dose-response relationships were also observed. However, when the SUA level exceeded 6 mg/dL, the dose-response curve between SUA levels and the risk of OP tended to be flattened.

Conclusion: Nonlinear dose-response relationships were found that higher SUA levels are associated with greater BMDs and lower risk of OP. For patients receiving ULT, maintaining SUA level at around 6 mg/dL may be appropriate from the perspective of bone metabolism.

Objectives: Limited studies reported the correlation between Sjögren's syndrome (SS) and vitiligo. This study explores the association between SS and the risk of developing vitiligo and assesses comorbidity profiles and medication impacts.

Methods: We conducted a retrospective, population-based analysis using data from Taiwan's National Health Insurance Research Database, spanning 2008 to 2019. The primary outcome was the incidence of vitiligo, which was analyzed using Cox proportional hazards models, with additional subgroup and sensitivity analyses conducted.

Results: The study incorporated 223 582 individuals with SS and 9 775 363 controls. A total of 208 942 pairs of the SS and controls were analyzed following propensity score matching. Non-matched and matched cohort analyses have consistent results. In matched analysis, individuals with SS had a 1.90-fold increased risk of developing vitiligo compared to those without SS after adjustment (95% confidence interval [Cl], 1.67-2.15; p < 0.001). Age-related risk was evident, particularly in those aged 40-59 years and 60-79 years. Males had a lower risk of vitiligo than females. Comorbidities such as hyperlipidemia, chronic liver disease, hyperthyroidism, and spondylarthritis further increase the risk. During the first year following diagnosis, individuals with SS exhibited a significantly elevated risk of developing vitiligo compared to those without SS (aHR, 2.15; 95% Cl, 1.54-3.00; p < 0.001). Over a decade of follow-up, the SS cohort showed a markedly higher cumulative risk of vitiligo than the non-SS cohort (log-rank p < 0.001). Subgroup analysis revealed that systemic corticosteroid administration significantly mitigated the risk of developing vitiligo in SS patients (aHR, 0.67; 95% CI, 0.53-0.86; p < 0.001) compared to patients who did not receive systemic corticosteroids.

Conclusion: SS is significantly associated with an increased risk of developing vitiligo. Further research is warranted to elucidate the underlying mechanisms.