Search

Introduction: This study aimed to investigate the associations of digital ulcers (DUs) in patients with systemic sclerosis (SSc). Methods: This retrospective study investigated the demographic characteristics, specific autoantibodies, organ involvement, and laboratory tests in patients with SSc from our hospital. Results: This study enrolled 144 patients with SSc. The DU+ group consisted of 15 (10.4%) patients. Patients with SSc having DUs have longer disease duration, higher fibrinogen, higher fibrin degradation product, and lower cholesterol. None of the patients used cholesterol-lowering drugs before onset of DUs. The study also demonstrated a higher prevalence of anti-dsDNA and anti-histone antibodies in patients with SSc with DUs. Anti-dsDNA antibody is a specific antibody for SLE with a specificity of 96–99%. A total of 86.1% (124/144) of patients suffered from diffuse cutaneous SSc, and 28.5% (41/144) of patients suffered from overlap syndrome. Conclusion: Our study indicated that patients with SSc with fibrinogen of >2.895 g/L (p = 0.043) and cholesterol of <3.340 mmol/L (p = 0.036), which is equal to 129.258 mg/dL, are at high risk of developing DUs. [ABSTRACT FROM AUTHOR]

Objective: CD4+CD25+Foxp3+ regulatory T (Treg) cell-mediated immunosuppression is an essential mechanism of rheumatoid arthritis (RA). However, little is known regarding the specific role of CD4+CD25−Foxp3+ Treg cells in RA. This study aimed to investigate the frequency of circulating CD4+CD25−Foxp3+ Treg cells and their role in RA. Methods: Sixty-one untreated RA patients and 40 healthy controls (HCs) were enrolled in this study. The proportion of CD4+CD25−Foxp3+ T cells and CD4+CD25+Foxp3+ Tregs; the levels of CTLA4, GITR, Helios, and ICOS; and the production of IL-17A, IFN-γ, and IL-10 were assessed by flow cytometry. The correlation of CD4+CD25–Foxp3+ T cells and CD4+CD25+Foxp3+ Tregs with the clinical indicators was conducted by Spearman correlation analysis. Results: The proportion of CD4+CD25–Foxp3+ T cells was elevated in RA and positively correlated with disease activity. CD4+CD25–Foxp3+ T cells expressed less Helios and produced more IFN-γ than conventional Tregs in RA. Additionally, the proportion of CD4+CD25–Foxp3+ T cells was positively correlated with DAS28 score, IgG titer, and anti-CCP titer. Conclusions: These data indicate that CD4+CD25−Foxp3+ T cells in RA exhibit several different functional properties from conventional Tregs and are correlated with RA disease activity. Highlights: The proportion of CD4+CD25−Foxp3+ T cells was elevated in untreated RA. CD4+CD25−Foxp3+ T cells expressed decreased Helios compared with Treg cells in both RA patients and HCs. CD4+CD25−Foxp3+ T cells produced increased IFN-γ compared with Tregs in RA patients. Elevated CD4+CD25−Foxp3+ T cells were positively correlated with DAS28 score, anti-IgG titer and anti-CCP titer. [ABSTRACT FROM AUTHOR]

Background: Osteoporosis (OP) is a systemic osteopathy with increased bone fragility and increased risk of fracture. Osteoclasts (OC) are the key target cells in the treatment of osteoporosis. We aimed to research the role of L‐type calcium channel protein Cav1.3 in OC differentiation in this study. Methods: OP rat model was established to detect the expression level of Cav1.3. Tartrate‐resistant acid phosphatase assay was used to measure the differentiation of osteoclast during receptor activator of nuclear factor κ‐Β ligand (RANKL)‐induced osteoclasts formation. The expression of bone differentiation‐related proteins were detected by western blot analysis. Results: Cav1.3 is upregulated in OP rats. Knockdown of Cav1.3 inhibits the differentiation of RAW264.7. Cav1.3 regulates the cell differentiation and bone resorption of RAW264.7 during RANKL‐induced osteoclasts formation, which is accompanied by upregulation of CaMK II, p‐CERB, AP‐1, NFATC1, and NF‐κB. Conclusion: Cav1.3 plays an important role in osteoporosis and the differentiation of osteoclast, which might be involved with the bone differentiation‐related proteins. [ABSTRACT FROM AUTHOR]

Idiopathic juvenile osteoporosis (IJO) is a rare primary form of osteoporosis of unknown etiology that develops in a previously healthy child. IJO is characterized by repeated fractures, including vertebral compression fractures. It is usually a self-limiting disease that spontaneously resolves after puberty, but in some cases it may result in severe deformities and functional impairment. There are probably the following reasons about etiological factors and pathogenesis in IJO: 1) Imbalance between bone formation and bone resorption; 2) Adolescent growth burst and bone mass increase; 3) Abnormal metabolic regulation factors of bone; 4) Abnormal collagen synthesis. IJO runs an acute course, usually over a period of 2 to 4 years, during which time there is growth arrest and multiple fractures, and then the disease remits. Both the axial and the appendicular skeleton are affected. The severe cases may have fractures of the vertebrae and the long bones, particularly in the metaphyses, that lead to pain in the back, foot, hip and extremities, muscle weakness, limitation of free movement, deformity, and unique gait because of difficulty in walking. The diagnosis of IJO is based both on the exclusion of other diseases and on its own positive features. The diagnosis of IJO is best made from its X-ray features, which include multiple vertebral compression fractures and fractures of the long bones, especially around the weight-bearing joints. Treatment of IJO is extremely complicated. The basic strategy of treatment is to protect the spine and to avoid the occurring of fractures and deformity until remission occurs. Supportive care is instituted promptly in anticipation of spontaneous recovery with the onset of puberty. [ABSTRACT FROM AUTHOR]