Anti-Annexin V Antibodies: Association with Vascular Involvement and Disease Outcome in Patients with Systemic Sclerosis

Background: Systemic Sclerosis (SSc) is characterized by skin thickening, fibrosis and vascular obliteration. The onset and course are heterogeneous. Prominent features include autoimmunity, inflammation and vascular damage. Aim of study: To measure the level of serum Anti-Annexin V antibodies in SSc patients and to study its significance in relation to vascular damage in these patients. Patients and methods: Twenty patients with SSc (12 with diffuse SSc and 8 with the limited form) and 10 healthy age and sex matched volunteers as controls were all subjected to routine laboratory testing and immunological profiling including antinuclear, anti-Scl-70, anticentomere, anticardiolipin antibodies and anti-annexin V antibodies titres. Vascular damage was assessed by clinical examination and assessment of the disease activity score, nailfold capillaroscopy and colour flow Doppler of the renal arteries; Doppler echocardiography was used for assessing pulmonary hypertension. Results: Anti-annexin V antibodies were detected in 75% of patients. Comparisons between anti-annexin V in diffuse and limited subgroups showed no significance; however a statistically significant positive correlation was found between Anti-annexin V titre and the degree of vascular damage in SSc patients. Anti-annexin V increased significantly in patients with severe vascular damage in comparison with those less affected (15.3 ± 6.6 vs. 11.25 ± 3.6, P , 0.05). A significant positive correlation was found between Anti-annexin V titre and both the ACL titre (r = 0.79, P , 0.001) and the resistive index of the main renal artery (r = 0.42, P , 0.05). Conclusion: Anti-annexin V antibodies were significantly present in sera of patients with SSc. Patients with more severe forms of vascular damage had higher titres of these antibodies. Anti-annexin V antibodies are a sensitive predictor of vascular damage in SSc and could serve as a useful parameter in discriminating patients with a higher risk of vascular affection from those without

Type 2 diabetes raises serum sclerostin levels and disturbs the relation between sclerostin and bone mineral density: a call for caution with antisclerostin therapy in osteoporosis

Background Sclerostin is an osteocyte-secreted protein that negatively regulates osteoblasts. Wnt signaling may be crucial in the pathogenesis of impaired bone quality in type 2 diabetes mellitus (T2DM). The possibility that currently studied antisclerostin bone-forming agents could be useful to T2DM patients with osteoporosis needs further investigations. Aim The aim of this study was to investigate the relationship between serum sclerostin and bone mineral density in T2DM patients, in comparison with nondiabetic individuals. Patients and methods This study was conducted on 21 T2DM patients and 22 nondiabetic individuals. All participants were 60 years or older. They underwent history taking, clinical examination, routine lab investigations, and glycated hemoglobin assessment. Serum sclerostin was measured by ELISA. Bone mineral density (BMD) was measured at the left femoral neck and lumbar spine. Results Serum sclerostin level was significantly higher in T2DM patients compared with nondiabetic individuals. Male participants showed significantly higher sclerostin levels among the nondiabetic individuals, whereas this difference was not significant among T2DM patients. The Bone mineral density (BMD) and t-values of T2DM patients and the nondiabetic group were not significantly different. We found a significant positive correlation between sclerostin level and lumbar spine BMD among nondiabetic individuals, whereas among T2DM patients, this correlation was not significant. Sclerostin levels did not show a significant difference between diabetic osteoporotic and diabetic nonosteoporotic patients. Conclusion Patients with T2DM have raised sclerostin levels that, unlike those in nondiabetic individuals, are not correlated with BMD. This pathological condition that is specific to diabetes necessitates further study, careful assessment of the role of antisclerostin therapy, and probable dose adjustment for osteoporosis in T2DM patients

The Interplay between Zinc, Vitamin D and, IL-17 in Patients with Chronic Hepatitis C Liver Disease

Objectives. To assess zinc (Zn) and vitamin D (Vit. D) status in chronic Hepatitis C virus- (HCV) infected patients and their relationship to interleukin- (IL-) 17 and disease severity and then investigate whether Zn and Vit. D3 modulate IL-17 expression in chronic HCV patients. Methods. Seventy patients and fifty healthy subjects were investigated. Serum levels of Zn, Vit. D, and IL-17 were assessed in the patients group and subgroups. Patients lymphocytes were activated in vitro in the presence or absence of Zn or Vit. D3 and then intracellular IL-17 production was assessed using flow cytometry. Results. Zn and Vit. D were significantly decreased in HCV patients. Increasing disease severity leads to more reduction in Zn level opposed by increasing IL-17 level. Zn potently reduced IL-17 production in a dose-related fashion; however it did not exert any toxic effects. Although Vit. D apparently increases IL17 expression, it is unclear whether it is due to its toxic effect on cell count or lack of definite association between Vit. D and both IL-17 and disease severity. Conclusions. This study demonstrates that Zn modulates IL-17 expression and provides a rationale for evaluating this compound as a supplementary agent in the treatment of chronic HCV

Role of cartilage oligomeric matrix protein (COMP) as a prognostic biomarker in follow-up of early rheumatoid arthritis patients: Correlation to musculoskeletal ultrasonographic findings

Aim of the work: To assess the level of serum cartilage oligomeric matrix protein (COMP) in early rheumatoid arthritis (RA) patients and study its relation to disease activity and musculoskeletal ultrasound (MSUS) findings. Patients and methods: The study included 40 early RA patients. Disease activity score (DAS28) was assessed. Serum COMP level was measured and MSUS findings of the small joints of hands done at base line and after 6 months of follow up.20 age and sex matched control were included. Results: Patients age was 38.8 ± 9.3 years; 36 females and 4 males and disease duration 6.7 ± 3.5 years. Serum COMP was significantly higher in patients (median 190 U/L; 90–750 U/L) compared to control (90 U/L; 80–130 U/L)(p < .001) being higher in more active (250 U/L) (p = .001) and significantly correlated with baseline synovial inflammation (p = .009). COMP levels were lowered after 6 months of receiving treatment (110 U/L; 30–180 U/L) (p < .001). The presence of bony erosions increased with more active disease (p =  .003). There was a significant reduction in the erythrocyte sedimentation rate and COMP at follow up (p < .0001 and p = .001 respectively). No correlation was found between the COMP level with C-reactive protein, ESR, MSUS score or bony erosions at follow up. Conclusions: COMP significantly correlated with disease activity in early RA and could be used as a marker of activity. It correlates significantly with synovial inflammation detected by power Doppler. COMP may reflect the outcome and could be used as a prognostic marker in RA patients. COMP did not significantly correlate with bone erosions. Keywords: COMP, Rheumatoid arthritis, Joint ultrasonograph