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Solve Pexidartinib Issues Rapidly

The finding that a decreasing BMI is associated with an increasing risk of osteoporosis is in line with several other studies in COPD patients.24, 31, 38�C42 The link between low BMI and osteoporosis in COPD patients is not entirely clear yet. It might be decreased physical activity, increased inflammation, or other mechanisms leading to proteolysis.43�C45 More studies are needed investigating this link. Increasing PTH significantly increased Pexidartinib the OR for osteoporosis. Patients with high PTH levels all had normal calcium levels; hence they had secondary hyperparathyroidism. Secondary hyperparathyroidism is caused by vitamin D deficiency.46 Indeed, we found a significant negative correlation between vitamin D and PTH in our study population (r?=??0.28, p?<?.001). This is in line with Kuchuc and colleagues, who found an increasing vitamin D level significantly decreasing PTH.19 In addition, markers of bone turnover decreased significantly. Combined with our results, <a href="http://www.selleckchem.com/products/chir-99021-ct99021-hcl.html">GSK-3 inhibitor a decreasing PTH level may cause decreasing speed of bone turnover, resulting in a better microarchitecture and hence less osteoporosis. Because there is still a lot of discussion about the best cutoff value for vitamin D deficiency, we also used 80 nmol/L as the cutoff, which is used in postmenopausal women with osteoporosis. The prevalence of vitamin D deficiency increased to 86%. The significant difference between GOLD stages disappeared (GOLD I 87%, GOLD II 84%, GOLD III 89%, GOLD IV 85%; p?=?.829); however, the possible correlation with osteoporosis was still not found. There was no significant influence of FEV1 on osteoporosis. Indeed, the prevalence of osteoporosis did not differ between GOLD stages. This result suggests that there are more factors involved in the prognosis and morbidity Y 27632 of COPD patients than airflow limitation.47 This cross-sectional study has some methodologic considerations. Interpretation of clinical correlates of osteoporosis should be with caution in a cross-sectional design. Second, there could be a selection bias because we included COPD outpatients treated by chest physicians and not patients treated by family physicians. However, the current consecutive sample of clinically stable COPD patients has been collected prospectively in a general hospital, including all GOLD stages. Consequently, it can be considered to be a representative sample of Dutch COPD outpatients attending a regular outpatient COPD clinic. Half the patients with clinically stable COPD attending a regular outpatient COPD clinic have osteoporosis, as determined by local DXA and spinal X-ray independent of GOLD classification. Correlates of osteoporosis in COPD are age, BMI, and PTH level. Given the current definition of COPD as a multicomponent disease, the awareness of a high prevalence of osteoporosis should be raised.
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