Risk of osteoporosis in men with chronic bronchitis

Praet, Jean Philippe; Peretz, Anne; Rozenberg, Serge; Famaey, Jean Pierre; Bourdoux, Pierre

doi:10.1007/bf01624152

Cited by 50 publications

(28 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Primers and TaqMan probes were designed using the Primer Express 1.0 (Applied Biosystems) software to amplify Ͻ 150 base pairs. Probes were labeled at the 5Ј end with the reporter dye molecule 6-carboxy-fluorescein (FAM) (22) and at the 3Ј end with the quencher dye molecule 6-carboxytetramethyl-rhodamine (TAMRA). The target gene and the housekeeping gene (glyceraldehyde-3-phosphate dehydrogenase [GAPDH]) were simultaneously tested in duplicate or triplicate.…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

Thrombin and TNF-α/IL-1β Synergistically Induce Fibroblast-Mediated Collagen Gel Degradation

Fang

Liu

Al-Mugotir

et al. 2006

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Degradation of preexisting and newly synthesized extracellular matrix is thought to play an important role in tissue remodeling. The current study evaluated whether thrombin and TNF-␣/IL-1␤ could collaboratively induce collagen degradation by human fetal lung fibroblasts (HFL-1) and adult bronchial fibroblasts cultured in threedimensional collagen gels. TNF-␣/IL-1␤ alone induced production of matrix metalloproteinases (MMPs)-1, -3, and -9, which were released in latent form. With the addition of thrombin, the latent MMPs were converted into active forms and this resulted in collagen gel degradation. Part of the activation of MMPs by thrombin resulted from direct activation of MMP-1, MMP-2, MMP-3, and MMP-9 in the absence of cells. In addition, tissue inhibitor of metalloproteinase-1 production was inhibited by the combination of thrombin and TNF-␣/ IL-1␤. These results suggest that thrombin and TNF-␣/IL-1␤ synergize to induce degradation of three-dimensional collagen gels through increasing the production and activation of MMPs, and that this effect is mediated through both direct activation of MMPs by thrombin and indirectly by thrombin activation of fibroblasts. Through such mechanisms, thrombin could contribute to many chronic lung disorders characterized by tissue remodeling.

show abstract

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

Thrombin and TNF-α/IL-1β Synergistically Induce Fibroblast-Mediated Collagen Gel Degradation

Fang

Liu

Al-Mugotir

et al. 2006

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

show abstract

“…Cross-sectional studies have revealed that bone mass is reduced in patients with COPD (3,4). Bone mass loss is caused by malnutrition, immobility, and hormonal imbalance.…”

Section: Introductionmentioning

confidence: 99%

Relationship between Changes of Bone Mineral Content and Twelve-Minute Walking Distance in Men with Chronic Obstructive Pulmonary Disease: A Longitudinal Study.

et al. 1997

View full text Add to dashboard Cite

Cross-sectional studies have revealed that bone mass is reduced in patients with chronic obstructive pulmonary disease (COPD). To elucidate the factors influencing bone mass in COPD, we measured whole body bone mineral content (BMC) by dual energy X-ray absorptiometry (DXA), pulmonary function, and twelve-minute walking distance (TMD) in men with COPD, who had been monitored for at least one year. Westudied the body composition in 22 male patients with COPDand 19 age-matched male controls (age 72.6 ± 7.2 vs 67.5 ± 10.1 years, mean ± SD). COPD patients showed a significantly lower body weight (49.3 ± 5.7 vs 57.9 ± 3.5 kg, respectively), body mass index (18.9 ± 2.1 vs 22.1 ± 1.3 kg/m2) and BMC(1.9 ± 0.4 vs 2.2 ± 0.4 kg) than controls. The changes in BMCwere significantly correlated with TMD(r=0.53, p<0.02). These results demonstrate that decreased exercise capacity, at least in part, accounts for acceleration of bone mass loss in COPDpatients.

show abstract

“…This programme included spinal radiography and, in some centres, measurements of BMD by dual-energy X-ray absorptiometry. Since both COPD and smoking are themselves risk factors for osteoporosis [1,14], EUROSCOP provided a valuable opportunity to evaluate the impact of long-term inhaled corticosteroid therapy on bone density and metabolism in a population at risk of osteoporosis. The radiographical and BMD data from patients who completed the study are presented in this paper.…”

mentioning

confidence: 99%

Bone mineral density in patients with chronic obstructive pulmonary disease treated with budesonide Turbuhaler(R)

Johnell

Pauwels²,

Löfdahl

et al. 2002

European Respiratory Journal

View full text Add to dashboard Cite

There is a need for studying the effects of long-term inhaled corticosteroid therapy on bone mineral density (BMD) and vertebral fracture rates in patients with mild chronic obstructive pulmonary disease (COPD).Patients (n=912, mean age 52 yrs) with mild COPD (mean forced expiratory volume in one second (FEV1) 77% of predicted; mean FEV1/slow vital capacity ratio 62%) were randomized to receive budesonide 400 mg, or placebo twice daily via Turbuhaler1. BMD was measured at the L2-L4 vertebrae and the femoral neck, trochanter and Ward9s triangle by dual-energy X-ray absorptiometry at baseline and after 6, 12, 24 and 36 months (n=161). Radiographs of the thoracic and lumbar spine were obtained at the beginning and end of treatment (n=653).Previous fractures were present at baseline in 43 budesonide-treated patients (13.4%) and 38 placebo-treated patients (11.5%). New fractures occurred in five budesonidetreated patients, compared with three in the placebo group (p=0.50). There were no significant changes in BMD at any site in budesonide-treated patients, compared with the placebo group, during the course of the study. Budesonide treatment was associated with a slight but statistically significant decrease in the area under the concentrationtime curve for serum osteocalcin.In the present study, involving a large group of patients with chronic obstructive pulmonary disease, long-term treatment with budesonide 800 mg?day -1 via Turbuhaler1 had no clinically significant effects on bone mineral density or fracture rates.

show abstract

Risk of osteoporosis in men with chronic bronchitis

Cited by 50 publications

References 34 publications

Thrombin and TNF-α/IL-1β Synergistically Induce Fibroblast-Mediated Collagen Gel Degradation

Thrombin and TNF-α/IL-1β Synergistically Induce Fibroblast-Mediated Collagen Gel Degradation

Relationship between Changes of Bone Mineral Content and Twelve-Minute Walking Distance in Men with Chronic Obstructive Pulmonary Disease: A Longitudinal Study.

Bone mineral density in patients with chronic obstructive pulmonary disease treated with budesonide Turbuhaler(R)

Contact Info

Product

Resources

About