Osteoporosis (OP) is one of the signs of bone damage in rheumatoid arthritis (RA). The 14-3-3η protein is an inflammatory protein, which has been reported to be associated with rheumatoid arthritis (RA). This is to determine the serum levels of 14-3-3η protein, evaluate its diagnostic value in early RA, and clear out its significance in RA with secondary osteoporosis. Two hundred fifty-nine RA patients and 80 age and sex-matched healthy controls were included. Assays of serum 14-3-3η protein were done for all participants by enzyme-linked immunosorbent assay (ELISA). Dual-energy X-ray absorptiometry (DEXA) was used to measure bone mineral density (BMD). Serum 14-3-3η protein level was significantly high in RA (2.49/4.72), compared with controls (P < 0.0001). Positive rate of 14-3-3η protein in RA was 97.3%, which was higher than that in controls (χ = 276.641, P< 0.0001). Serum 14-3-3η protein level in early RA was significantly higher than that in established RA (3.91/4.82 vs 2.01/3.29, Z = 2.624, P < 0.05). The positive rate among three groups (normal control, early RA group, established RA group) differed from each other (χ = 131.396, P< 0.0001). Results of ROC curve indicated the cutoff point of 14-3-3η protein for diagnosis of early RA was 0.879 ng/ml (P < 0.0001). Linear correlation analysis found that serum 14-3-3η protein positively correlated with VAS and HAQ (P < 0.0001), negatively correlated with BMD at lumbar spine and femur in RA (P < 0.0001). Serum 14-3-3η protein among groups of bone mass normal (2.73/3.79), osteopenia (3.15/4.86), and osteoporosis (6.34/6.42) was different in early RA patients (χ = 7.974, P< 0.05). Serum 14-3-3η protein levels increase significantly in patients with RA (especially in early RA). There are close relationships between serum 14-3-3η protein and clinical symptoms and osteoporosis in patients with RA.

GIOP exists generally in Chinese patients with RA, which relates to treatment course not daily dosage of GC. Usage of GC is also the risk factor for the happening of OPF in Chinese patients with RA.

Objective: Lipid mediators have been suggested to have a role in pain sensitivity and response; however, longitudinal data on lipid metabolites and persistent multisite musculoskeletal pain (MSMP) are lacking. This study was to identify lipid metabolic markers for persistent MSMP. Methods: Lipidomic profiling of 807 lipid species was performed on serum samples of 536 participants from a cohort study. MSMP was measured by a questionnaire and defined as painful sites ≥4. Persistent MSMP was defined as having MSMP at every visit. Logistic regression was used with adjustment for potential confounders. The Benjamini–Hochberg method was used to control for multiple testing. Results: A total of 530 samples with 807 lipid metabolites passed quality control. Mean age at baseline was 61.54 ± 6.57 years and 50% were females. In total, 112 (21%) of the participants had persistent MSMP. Persistent MSMP was significantly associated with lower levels of monohexosylceramide (HexCer)(d18:1/22:0 and d18:1/24:0), acylcarnitine (AC)(26:0) and lysophosphatidylcholine (LPC)(18:1 [sn1], 18:2 [sn1], 18:2 [sn2], and 15-MHDA[sn1] [104_sn1]) after controlling for multiple testing. After adjustment for age, sex, body mass index, comorbidities, and physical activity, HexCer(d18:1/22:0 and d18:1/24:0) and LPC(15-MHDA [sn1] [104_sn1]) were significantly associated with persistent MSMP [Odds Ratio (OR) ranging from 0.25–0.36]. Two lipid classes—HexCer and LPC—were negatively associated with persistent MSMP after adjustment for covariates (OR = 0.22 and 0.27, respectively). Conclusions: This study identified three novel lipid signatures of persistent MSMP, suggesting that lipid metabolism is involved in the pathogenesis of persistent pain.

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BackgroundLipid mediators have been suggested to have a role in pain sensitivity and response; however, longitudinal data on lipid metabolites and persistent multisite musculoskeletal pain (MSMP) are lacking.ObjectivesThis study was to identify lipid metabolic markers for persistent MSMP.MethodsLipidomic profiling of 807 lipid species was performed on serum samples of 536 participants from a cohort study. MSMP was measured by a questionnaire and defined as painful sites ≥4. Persistent MSMP was defined as having MSMP at every visit. Logistic regression was used with adjustment for potential confounders. The Benjamini Hochberg method was used to control for multiple testing.ResultsA total of 530 samples with 807 lipid metabolites passed quality control. Mean age at baseline was 61.54±6.57 years and 50% were females. One hundred and twelve (21%) of the participants had persistent MSMP. Persistent MSMP was significantly associated with lower levels of monohexosylceramide (HexCer)(d18:1/22:0 and d18:1/24:0), acylcarnitine (AC)(26:0) and lysophosphatidylcholine (LPC)(18:1 [sn1], 18:2 [sn1], 18:2 [sn2], and 15-MHDA[sn1] [104_sn1]) after controlling for multiple testing. After adjustment for age, sex, body mass index, diabetes status, and physical activity, HexCer(d18:1/22:0 and d18:1/24:0) and LPC(18:1 [sn1] and 15-MHDA [sn1] [104_sn1]) were significantly associated with persistent MSMP [Odds Ratio (OR) ranging from 0.24 - 0.32]. Two lipid classes -- HexCer and LPC were negatively associated with persistent MSMP after adjustment for covariates (OR=0.19 and 0.21, respectively).ConclusionThis study identified four novel lipid signatures of persistent MSMP, suggesting that lipid metabolism is involved in the pathogenesis of persistent pain.Disclosure of InterestsNone declared