Association of Serum Vitamin D (25OHD) Level with Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Acute exacerbations of COPD is characterized by a change in the patients baseline dyspnoea, cough and/or sputum that is beyond normal day to day differences and guides to a change in standard medications in a patient with COPD. Vitamin D influences the innate & adaptive immune system, and exerts pleiotropic antimicrobial and anti-inflammatory responses. Vitamin D deficiency is frequent among COPD patients but its contributory role in disease exacerbations is widely debated. This study was aimed to assess relationship between reduced serum vitamin D (25-OHD) level with COPD severity and acute exacerbation. This observational cross-sectional study was carried out in the department of Respiratory Medicine, NIDCH, Mohakhali, Dhaka, Bangladesh from October 2016 to September 2017. Consecutive 80 hospital admitted patients with acute exacerbation of chronic obstructive pulmonary disease diagnosed on the basis of clinical history & pulmonary function tests and 78 age & sex matched controls were investigated for serum vitamin D (25-OHD) level. Among the COPD patients, 37% had Vitamin D deficiency (<20ng/ml) and 28.75% had Vitamin D insufficiency (20-29ng/ml). Mean vitamin D (25-OHD) level of COPD patients (25.82±10.62ngm/ml) was found to be significantly lower than healthy controls (32.57±11.32ngm/ml). Vitamin D deficiency was found, by Pearson correlation test, to be significantly associated with severity of COPD. Multivariate analysis showed that age (in years), FEV1 (percent predicted), frequent exacerbators (≥2 in the last year), and smoking (>40 pack year) were significantly associated with Vitamin D deficiency. Acute exacerbation of chronic obstructive pulmonary disease patients was found to have vitamin D deficiency and vitamin D deficiency was significantly associated with severity of COPD. Vitamin D deficiency was also associated with frequent disease exacerbation.

Bone turnover and body weight relationships differ in normal-weight compared with heavier postmenopausal women.

Low body weight is associated with increased risk for fractures, whereas higher body weight has been shown to be protective against osteoporosis. This study evaluated whether body weight plays a role regulating bone turnover and mass in normal-weight (body mass index (BMI) <25 kg/m2), overweight (BMI 25-29.9 kg/m2) and obese (BMI> or =30 kg/m2) postmenopausal women who were either receiving hormone replacement therapy [HRT(+)] or not [HRT(-)] (total of six groups). Body weight, BMI, total body bone mineral content (TBBMC), and markers of bone formation (serum osteocalcin) and bone resorption (urinary pyridinoline (PYD) and deoxypyridinoline) were retrospectively analyzed in 210 postmenopausal women. The mean age was 67+/-6 years, with mean body weight of 70.8+/-14.2 kg, ranging from 45.0 to 115.5 kg. Body weight was positively correlated with TBBMC ( r=0.50, p<0.0001). There was a lower TBBMC and higher bone formation rate in normal-weight than obese HRT(-) women, but in women taking HRT there were no differences between BMI categories. In addition, in normal-weight HRT(-) women only, PYD and body weight showed a negative correlation (r=-0.39, p=0.01). Among normal-weight, but not overweight or obese subjects, we observed higher TBBMC and lower bone turnover in the HRT(+) compared with the HRT(-) group. Regression models explained 36% of the variance in TBBMC, mainly through body weight. Additional models could only explain 11-15% of the variance in bone turnover. Taken together, these data suggest that among normal-weight but not obese postmenopausal women, higher bone turnover is associated with lower bone mass, and that only normal-weight women show a different bone turnover profile with HRT treatment. Body weight should be considered an important factor in bone metabolism with relevant clinical implications.

Moderate energy restriction increases bone resorption in obese postmenopausal women.

BACKGROUND: Weight reduction reduces bone mineral density (BMD) and increases the risk of osteoporosis. OBJECTIVE: We investigated whether bone is mobilized in postmenopausal women during energy restriction and whether hormones regulate bone turnover and mass. DESIGN: Twenty-seven obese postmenopausal women with a mean (+/-SD) age of 55.9 +/- 7.9 y and body mass index (in kg/m(2)) of 33.0 +/- 3.8 completed the 6-mo study. Fourteen women followed a moderate energy-restricted diet (WL group) and 13 control subjects maintained their body weight (WM group). Body weight, bone turnover markers, serum parathyroid hormone (PTH), and dietary intake were measured throughout the study. Total-body BMD, sex hormone binding globulin, leptin, and estrone were measured at baseline and at week 25. RESULTS: In the WL group, body weight decreased by 10.2 +/- 5.5% (P < 0.001), body fat mass decreased by 18.7 +/- 11.3% (P < 0.001), and total-body BMD decreased by 1.2 +/- 1.2%; these changes were significantly different from those in the WM group (P < 0.05). Serial measurements showed chronically elevated rates of bone resorption and formation during energy restriction that were greater than in the WM group (P < 0.05). Serum sex hormone binding globulin increased and leptin decreased with weight loss (P < 0.05). Serum PTH tended to increase in the WL group but not in the WM group (P < 0.06). The reduction in fat mass with weight loss was directly associated with a decrease in serum estrone (P < 0.01, R(2) = 0.50). CONCLUSIONS: Moderate energy restriction increases bone turnover in obese postmenopausal women and may be regulated in part by alterations in serum PTH and estrone.

Calcium supplementation suppresses bone turnover during weight reduction in postmenopausal women.

Bone mobilization, lowering of bone mineral density (BMD), and osteoporotic fractures are recognized in postmenopausal women with weight loss. Because a high-calcium intake suppresses bone loss in peri- and postmenopausal women, the present randomized, double-blind, placebo-controlled study was designed to test the hypothesis that calcium supplementation prevents net bone mobilization and consequent bone mineral loss during voluntary weight reduction in obese postmenopausal women. Subjects were placed on a moderate energy-restricted diet and either calcium supplementation (1 g/day) or placebo for 6 months. Body weight, bone turnover markers (pyridinium cross-links), osteocalcin, and parathyroid hormone (PTH) were measured at treatment weeks 1-5, 7, 10, 13, 16, 20, and 25. Total body BMD, insulin-like growth factor, 25-hydroxyvitamin D, and sex hormone binding globulin (SHBG) were measured at baseline and week 25. The calcium supplemented (n = 15; age 60.9 +/- 9.4 years, body mass index [BMI] 33.2 +/- 4.6 kg/m2) and placebo (n = 16; age 55.8 +/- 8.3 years, BMI 32.9 +/- 4.5 kg/m2) groups lost similar amounts of weight over the study interval (10.2 +/- 5.3% vs. 10.0 +/- 5.2%) and both groups increased SHBG (p < 0.001). There was a statistical effect of calcium supplementation during weight loss to suppress pyridinium cross-links, osteocalcin, and PTH (p < 0.05, < 0.01, and < 0.05, respectively). Loss of BMD tended to be greater in the placebo group by 1.4% (p < 0.08) after weight loss. One gram per day calcium supplementation normalizes the increased calcium-PTH axis activity and the elevated bone turnover rate observed during moderate voluntary energy restriction in postmenopausal women.

Longitudinal study of urinary hydroxy-pyridinium cross-links and growth in healthy infants: higher values with breastfeeding and after daytime sleep.

Urinary pyridinoline and deoxypyridinoline crosslinks (crosslink) are excreted when bone is resorbed. The aims of this study in healthy infants were to determine whether crosslinks a) could predict growth velocity, b) are variable due to circadian rhythm, and c) differ in infants who were either breast-fed or formula-fed. In 78 healthy infants (48 male; 30 female) urine samples were collected and anthropometric measurements were taken at 2, 3, 4, 5, 6, 8, 10 and 12 months of age. In addition, a total of 25 samples were collected during the day (0700-2000) in 5 of the infants to determine circadian rhythm of crosslink excretion. Crosslink excretion decreased (p < 0.001) with age between 2 and 12 months. Pyridinoline excretion showed a significant, but weak correlation (r > or = 0.21; p < 0.05) with linear growth velocity and weight velocity in the subsequent month until 6 months of age, and no correlation thereafter. Infants studied for circadian rhythm showed a 63% greater (p < 0.05) rate of pyridinoline excretion after a nap as compared to the 13-hour mean value. In a subset of infants whose energy intake was exclusively from breast milk (BF, n = 23) or formula (FF, n = 10), crosslink excretion was greater in BF infants at 3 months of age (p < 0.05). The correlations between crosslink excretion and growth parameters indicate that crosslinks may be useful as a marker of growth in infant populations. However sources of variation in crosslink excretion, such as circadian rhythm and diet may limit their utility to predict growth in an individual infant. These factors should be considered in future studies examining markers of bone turnover in infants.

Urinary pyridinium cross-link excretion is increased in critically ill surgical patients.

OBJECTIVES: To determine: a) the rate of pyridinium cross-links of collagen excretion, breakdown products of bone, in critically ill surgical patients in the intensive care unit (ICU); and b) the relationship between cross-link excretion and nitrogen excretion and balance to ascertain whether collagen breakdown products contribute to protein losses during a hypercatabolic state. DESIGN: Observational study starting on the first postoperative day to 20 days or until discharge. SETTING: A surgical ICU in a University hospital. PATIENTS: Nine mechanically ventilated, postoperative surgical patients (73 +/- 3 [SD] yrs), receiving routine parenteral nutrition (18% protein) and 17 age-matched healthy subjects. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Resting energy expenditure was determined daily for < or = 5 days after admission, and energy intake was set at 1.04 times the initial energy expenditure; thereafter, values of intake were reset weekly. Daily 24-hr urine samples were analyzed for cross-links, total and urea nitrogen, calcium, and creatinine for 20 days or until discharge. Two urine samples were also analyzed for cross-links in the healthy subjects. The excretion of cross-links from the surgical patients was markedly higher (p < .001) than in the healthy subjects, and calcium balance was significantly negative (p < .05). Patients who were discharged from the ICU within 5 days showed a lower rate of cross-link excretion (p < .02) and less day-to-day variability, compared with those patients who stayed longer, whether calculated over the course of the study or over the first 2 days in the ICU. There was no correlation between cross-links and energy expenditure, nitrogen excretion, or balance. CONCLUSIONS: The rate of cross-link excretion in critically ill patients: a) is markedly increased; b) is greater within the first two postoperative days in those patients who have an extended stay (> 5 days) in the ICU; and c) is independent of the rate of nitrogen excretion. These findings suggest that critically ill postoperative patients experience an acute breakdown of collagen, which is likely due to resorption of bone or possibly comes from other collagen sources.