Eggshell membrane in the treatment of pain and stiffness from osteoarthritis of the knee: a randomized, multicenter, double-blind, placebo-controlled clinical study

Natural Eggshell Membrane (NEM®) is a new novel dietary supplement that contains naturally occurring glycosaminoglycans and proteins essential for maintaining healthy articular cartilage and the surrounding synovium. The randomized, multicenter, double-blind, placebo-controlled Osteoarthritis Pain Treatment Incorporating NEM® clinical study was conducted to evaluate the efficacy and safety of NEM® as a treatment for pain and stiffness associated with osteoarthritis of the knee. Sixty-seven patients were randomly assigned to receive either oral NEM® 500 mg (n = 34) or placebo (n = 33) daily for 8 weeks. The primary endpoint was the change in overall Western Ontario and McMasters Universities (WOMAC) Osteoarthritis Index as well as pain, stiffness, and function WOMAC subscales measured at 10, 30, and 60 days. The clinical assessment was performed on the intent-to-treat population. Supplementation with NEM® produced an absolute rate of response that was statistically significant (up to 26.6%) versus placebo at all time points for both pain and stiffness, but was not significantly improved for function and overall WOMAC scores, although trending toward improvement. Rapid responses were seen for mean pain subscores (15.9% reduction, P = 0.036) and mean stiffness subscores (12.8% reduction, P = 0.024) occurring after only 10 days of supplementation. There were no serious adverse events reported during the study and the treatment was reported to be well tolerated by study participants. Natural Eggshell Membrane (NEM®) is an effective and safe option for the treatment of pain and stiffness associated with knee osteoarthritis. Supplementation with NEM®, 500 mg taken once daily, significantly reduced both joint pain and stiffness compared to placebo at 10, 30, and 60 days. The Clinical Trial Registration number for this study is NCT00750477

A model of human lung fibrogenesis for the assessment of anti-fibrotic strategies in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with limited therapeutic options. KCa3.1 ion channels play a critical role in TGFβ1-dependent pro-fibrotic responses in human lung myofibroblasts. We aimed to develop a human lung parenchymal model of fibrogenesis and test the efficacy of the selective KCa3.1 blocker senicapoc. 2 mm3 pieces of human lung parenchyma were cultured for 7 days in DMEM ± TGFβ1 (10 ng/ml) and pro-fibrotic pathways examined by RT-PCR, immunohistochemistry and collagen secretion. Following 7 days of culture with TGFβ1, 41 IPF- and fibrosis-associated genes were significantly upregulated. Immunohistochemical staining demonstrated increased expression of ECM proteins and fibroblast-specific protein after TGFβ1-stimulation. Collagen secretion was significantly increased following TGFβ1-stimulation. These pro-fibrotic responses were attenuated by senicapoc, but not by dexamethasone. This 7 day ex vivo model of human lung fibrogenesis recapitulates pro-fibrotic events evident in IPF and is sensitive to KCa3.1 channel inhibition. By maintaining the complex cell-cell and cell-matrix interactions of human tissue, and removing cross-species heterogeneity, this model may better predict drug efficacy in clinical trials and accelerate drug development in IPF. KCa3.1 channels are a promising target for the treatment of IPF.This work was supported by The Dunhill Medical Trust, project grant R270/1112, the MRC, project grant MR/K018213/1, and The British Lung Foundation, grant PPRG15-8. The work was also supported in part by the National Institute for Health Research Leicester Respiratory Biomedical Research Unit

The Utility of Urine Desmosine as a Marker of Lung Injury in Spine Surgery

The objective of this prospective observational study was to determine if urine desmosine levels, a marker of lung injury, increase in response to the periopreative insults of anterior and posterior spine surgery. Desmosine, a stable breakdown product of elastin, has been proposed as a surrogate marker of lung injury in patients with COPD, tobacco use, and ARDS. We recently evaluated this marker in patients undergoing knee surgery, but the utility of desmosine as a marker of lung injury in patients undergoing spine surgery remains unstudied. In this study, we enrolled ten consecutive patients, who underwent anterior/posterior spine surgery. Patient demographics and perioperative data were recorded. Urine samples were collected at baseline, 1 day, and 3 days postoperatively and analyzed for levels of desmosine using a previously validated radioimmunoassay. Desmosine levels were 35.9 ± 18.2 pmol/mg creatinine at baseline, 38.7 ± 11 pmol/mg creatinine on postoperative day 1, and 70.5 ± 49.1 pmol/mg creatinine on postoperative day 3, respectively. Desmosine/creatinine ratios measured on day 3 postoperatively were significantly elevated compared to levels at baseline, and represented a 96.3% increase. No difference was seen between levels at baseline and day 1 postoperatively. In conclusion, we were able to show a significant increase in urine desmosine levels associated with anterior/posterior spine surgery. In the context of previous studies, our findings suggest that desmosine may be a marker of lung injury in this setting. However, further research is warranted for validation and correlation of desmosine levels to clinical markers and various degrees of lung injury