Summary There are few data on the skeletal health of Hispanic men. We observed differences in vitamin D deficiency and low BMD between Hispanic ethnic subgroups that persisted with adjustment for ...risk factors. Our data indicate a substantial burden of low BMD and vitamin D deficiency among Hispanic men. Introduction Disparities within ethnic groups are generally ignored, but in evolving populations they may have implications for public health. We examined ethnic variation in serum 25-hydroxyvitamin D 25(OH)D and bone mineral density (BMD) among Hispanic American men. Methods Three hundred and fifty-eight Hispanic males 30 to 79 years of age were studied. Logistic regression models assessed variation in odds of vitamin D deficiency (<20 ng/mL) and low BMD (T-score<-1) by ethnicity, with and without adjustment for risk factors (age, smoking, occupation, physical activity, body mass index, and sunlight exposure). Results Vitamin D deficiency was most common among Puerto Rican (26%), compared with Dominican (21%), Central American (11%), and South American (9%) men. Percentages with low BMD were: South American (44%), Puerto Rican (34%), Dominican (29%), and Central American (23%). Adjustment for age and risk factors failed to account for Hispanic subgroup differences in vitamin D deficiency and low BMD. Population estimates indicate a substantial burden of low BMD and vitamin D deficiency among Hispanic men. Conclusions Our findings underscore the importance of examining the skeletal health of Hispanic subgroups, and suggest that a considerable number of Hispanic men may be at elevated risk of fracture and vitamin D deficiency.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Obesity is suspected to confer protection against fracture, but evidence is mixed. We examined proximal femur geometry and body composition measures in a diverse group of 1171 men (30–79 yr of age). ...Analyses showed that nonbone lean mass, but not fat mass, is independently associated with measures of proximal femur density, axial and bending strength, and resistance to buckling.
Introduction: Obesity is often said to confer protection against fracture, but the mechanisms driving such an association remain poorly understood. We hypothesized that the effect of increased body mass on bone structure would be accounted for by total and/or appendicular nonbone lean mass, and that once these trends were removed, fat mass would show no protective influence. To test this hypothesis, we examined body composition and geometric indices of proximal femur strength in an ethnically diverse (black, Hispanic, and white) sample of randomly selected men, 30–79 yr of age.
Materials and Methods: Data were obtained from N = 1171 community‐dwelling subjects enrolled in the cross‐sectional Boston Area Community Health/Bone study. Body composition was obtained by DXA. Hip geometry parameters at the narrow neck, intertrochanter, and shaft were obtained using Hip Structural Analysis of DXA images. These measures included BMD, bone material in cross‐sections (cross‐sectional area), bending strength (section modulus), and propensity to buckle under compression (average buckling ratio). Analyses controlled for age, race/ethnicity, height, and physical activity.
Results: In exploratory analyses, lean mass, fat mass, and BMI were each positively associated with hip strength. However, controlling for lean mass was sufficient to remove the positive, and induce a negative, association for fat mass or BMI. Associations between lean mass and hip strength were strongest and resistant to control for other measures. Lean mass alone was sufficient to account for a substantial proportion of racial/ethnic difference in hip strength measures, whereas fat mass exhibited no comparable explanatory power.
Conclusions: The positive association between relative weight and proximal femur strength is accounted for by lean mass, suggesting that, in men, the protective effect of BMI in preventing fracture is mediated not by adipose tissue but by the influence of increased muscle mass accompanying elevated BMI.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Summary
We examined BMC and body composition in 1,209 black, Hispanic, and white men. Weight, BMI, waist circumference, and fat mass were associated with BMC only up to certain thresholds, whereas ...lean mass exhibited more consistent associations. The protective influence of increased weight appears to be driven by lean mass.
Introduction
Reduced body size is associated with decreased bone mass and increased fracture risk, but associations in men and racially/ethnically diverse populations remain understudied. We examined bone mineral content (BMC) at the hip, spine, and forearm as a function of body weight, body mass index (BMI), waist circumference, fat mass (FM), and nonbone lean mass (LM).
Methods
The design was cross-sectional; 363 non-Hispanic black, 397 Hispanic, and 449 non-Hispanic white residents of greater Boston participated (N = 1,209, ages 30–79 y). BMC, LM, and FM were measured by DXA. Multiple linear regression was used to describe associations.
Results
Weight, BMI, waist circumference, and FM were associated with BMC only up to certain thresholds. LM, by contrast, displayed strong and consistent associations; in multivariate models, femoral neck BMC exhibited a 13% increase per 10 kg cross-sectional increase in LM. In models controlling for LM, positive associations between BMC and other body composition measures were eliminated. Results did not vary by race/ethnicity.
Conclusions
The protective effect of increased body size in maintaining bone mass is likely due to the influence of lean tissue. These results suggest that maintenance of lean mass is the most promising strategy in maintaining bone health with advancing age.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Summary
Data on bone architecture in diverse male populations are limited. We examined proximal femur geometry in 1,190 black, Hispanic, and white men. Cross-sectional analyses indicate greatest bone ...strength among black men, and greater age-related differences in bone strength among Hispanic men than other subjects at the narrow neck and intertrochanter regions of the proximal femur.
Introduction
Although race/ethnic differences in bone mass are well-documented, less is known about differences in bone architecture. We examined proximal femur geometry in a diverse, randomly-sampled population of 1,190 community-dwelling men (age 30–79 y).
Methods
Dual X-ray absorptiometry scans were obtained for 355 black, 394 Hispanic, and 441 white subjects. Measures were obtained for the narrow neck (NN), intertrochanter (IT) and shaft regions of the proximal femur via hip structural analysis. Analyses considered bone mineral density (BMD, g/cm
2
), outer diameter (cm), cross-sectional area (CSA, cm
2
), section modulus (Z, cm
3
), and buckling ratio (BR). Results were adjusted for height, weight and physical activity level.
Results
Black subjects exhibited greater age-specific BMD, CSA and Z, than their white counterparts. For instance, at age 50 y, NN BMD was approximately 11% higher among black men (
p
< 0.001). Hispanic men exhibited sharper age-related differences in NN and IT BMD than did others. IT BMD, for instance, decreased by 2.4% with 10 y age among Hispanic subjects, but had virtually no age trend in others (
p
< 0.001).
Conclusions
These results imply greater bone strength among black American men than among their white counterparts, and may indicate elevated fracture risk among older Hispanic American subpopulations.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
To determine the time course of histologic resolution of prostate cancer following radiotherapy (RTj and to correlate biopsy results with clinical outcome.
Since July 1990, all patients treated with ...radical external beam RT for prostate cancer at the General Division of the Ottawa Regional Cancer Centre have had systematic transrectal ultrasound (TRUS) and TRUS-guided biopsies beginning 12 months after RT and then every 6 months until negative or until clinical failure. Thus, 226 patients have had 375 TRUS with four to seven specimens per examination. Stage distribution was T1b: 32, T1c: 11, T2a: 45, T2b: 82, T3: 50, and T4: 6. Median follow-up was 33 months.
Biopsy results were negative in 69.5% of patients by 30 months of follow-up. Thirty-two (14%) had local failure (T1b: 12.5%, T1c: 0%, T2a: 11 %, T2b: 15%, T3: 18%, T4: 33%). Seven (3%) had chemical failure, and 47 (21%) had biopsy-only failure. Median follow-up for the biopsy-only failure group is only 19.5 months and mean prostate-specific antigen (PSA) is 1.0 ng/mL Thirty-nine patients, initially with biopsyonly failure, have converted to negative biopsies at a median of 26 months. Nadir PSA for patients with local failure was 3.9 ng/mL at 14 months versus 0.7 ng/mL at 23 months for those without failure. Patients with late conversion to negative biopsy results had a later nadir PSA of 1.3 ng/mL at 27.3 months.
Routine prostate biopsy specimens after RT in an unselected population show tumor clearance that is in agreement with long-term clinical follow-up, although tumor may take more than 30 months to resolve. Nadir PSA can be used to predict outcome.
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IJS, IMTLJ, KILJ, KISLJ, NUK, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Objectives. A reference range of prostate-specific antigen (PSA) values compatible with cure following radiotherapy (RT) for prostate cancer (PCa) has yet to be established. Various thresholds, as ...low as 0.5 ng/mL, have been used to define biochemical disease-free status. We report PSA profiles in 118 patients who were systematically biopsied following standard RT, with a minimum 4-year follow-up.
Methods. One hundred eighteen patients were treated with standard external beam RT from May 1987 to October 1991, and were followed prospectively with transrectal ultrasound (TRUS)-guided biopsies and measurement of serum PSA levels. Stage distribution was as follows: T1b: 25 patients, T2a: 27 patients, T2b/c: 42 patients, T3: 23 patients, T4: 1 patient. Median follow-up for patients without clinical failure is 68 months (range 48 to 108). Treatment failures were categorized as biochemical (biochemical failure chemF: PSA level of 2.0 ng/mL or more and greater than 1 ng/mL over nadir), local (local failure LF: positive biopsy and PSA level greater than 2.0), and distant failure (DF).
Results. PCa recurred in 55% of patients: 38% LF (n = 45; 30 isolated and 15 with DF), 25% DF (n = 30; 15 isolated and 15 with LF), and 4% chemF (n = 5). Mean PSA nadir was 0.4 for patients with no evidence of disease (NED) and occurred at 33 months, 3.2 for LF at 17 months, 7.7 for DF at 12 months, and 1.4 for chemF at 24 months. After reaching the nadir, PSA in patients with recurrence followed first-order kinetics, rising exponentially over time. The mean PSA doubling time was 12.6 months for LF, 5.2 months for DF, and 21.8 months for chemF (
P = 0.004). At last follow-up, the median PSA for patients without evidence of disease is 0.5 ng/mL. Four such patients had PSA values that rose to between 1 and 2 ng/mL for 5 to 38 months, but these eventually fell again to less than 1 ng/mL. Three patients had PSA values between 2 and 3 ng/mL, but 2 now have decreasing levels and the third has a rising level. All patients whose PSA levels rose to greater than 3 ng/mL exhibited a persistently rising pattern and ultimate tumor recurrence.
Conclusions. There is a range of PSA values following RT for PCa that is compatible with cure. A definition of biochemical disease-free status at any absolute threshold of PSA level less than 3 ng/mL will overdiagnose failure in a significant proportion of patients. Patients with a PSA level between 1.5 and 3 ng/mL should be observed until there is unequivocal evidence of disease recurrence. In the absence of known biopsy status, PSA doubling time can be a useful indicator of whether failure is local or distant.
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IJS, IMTLJ, KILJ, KISLJ, NUK, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
8.
Prevalence of Symptomatic Androgen Deficiency in Men Araujo, Andre B; Esche, Gretchen R; Kupelian, Varant ...
The journal of clinical endocrinology and metabolism,
2007-November, Volume:
92, Issue:
11
Journal Article
Peer reviewed
Open access
Context: Despite recognition that androgen deficiency in men should be defined according to biochemical and clinical criteria, most prevalence estimates are based on low testosterone levels alone.
...Objective: The objective of this study was to examine the association between symptoms of androgen deficiency and low total and calculated free testosterone levels and estimate the prevalence of symptomatic androgen deficiency in men.
Design: This study was a population-based, observational survey.
Participants: A total of 1475 Black, Hispanic, and white men, between the ages of 30–79 yr, with complete data on testosterone, SHBG, and symptoms of androgen deficiency, and who are not taking medications that impact sex steroid levels were randomly selected from the Boston Area Community Health Survey.
Outcome: Outcomes were measured as symptomatic androgen deficiency, defined as low total (<300 ng/dl) and free (<5 ng/dl) testosterone plus presence of low libido, erectile dysfunction, osteoporosis or fracture, or two or more of following symptoms: sleep disturbance, depressed mood, lethargy, or diminished physical performance.
Results: Mean age of the sample was 47.3 ± 12.5 yr. Approximately 24% of subjects had total testosterone less than 300 ng/dl, and 11% of subjects had free testosterone less than 5 ng/dl. Prevalence of symptoms were as follows: low libido (12%), erectile dysfunction (16%), osteoporosis/fracture (1%), and two or more of the nonspecific symptoms (20%). Low testosterone levels were associated with symptoms, but many men with low testosterone levels were asymptomatic (e.g. in men 50+ yr, 47.6%). Crude prevalence of symptomatic androgen deficiency was 5.6% (95% confidence interval: 3.6%, 8.6%), and was not significantly related to race and ethnic group. Prevalence was low in men less than 70 yr (3.1–7.0%) and increased markedly with age to 18.4% among 70 yr olds. Projection of these estimates to the year 2025 suggests that there will be as many as 6.5 million American men ages 30–79 yr with symptomatic androgen deficiency, an increase of 38% from 2000 population estimates.
Conclusions: Prevalence of symptomatic androgen deficiency in men 30 and 79 yr of age is 5.6% and increases substantially with age. The aging of the U.S. male population will cause a large increase in the burden of symptomatic androgen deficiency. Future work should address the clinical significance of low testosterone levels in asymptomatic men.
The objective of this study was to correlate the failure pattern of localized prostate carcinoma after radiotherapy (RT) with pretreatment (preTx) PSA and post-RT nadir PSA, using systematic biopsies ...and serum PSA in the assessment of outcome.
From January 1990 to February 1994, 207 patients treated with external beam RT were followed prospectively with systematic transrectal ultrasound-guided biopsies and measurements of serum PSA levels. Three hundred forty-three biopsies were performed, with 4-7 samples taken per session. The distribution of T classification was as follows: 19 patients had T1b, 15 had T1c, 34 had T2a, 79 had T2b/c, 53 had T3, and 7 had T4. Median follow-up was 36 months (range, 12-70 months). Failures were categorized as biochemical (chemF) (PSA > 2.0 ng/mL and > 1 ng/ mL over nadir), local (LF) (positive biopsy and PSA > 2), and distant (DF). The Cox proportional hazards model was used for multivariate analysis (MVA).
Overall, failures were seen in 68 of 207 patients: 20 LF, 24 DF, 7 LF + DF, and 17 chemF. In univariate analysis, failures correlated significantly with preTx PSA, post-RT nadir PSA, T classification, and Gleason's score (GS). The total failure rate was 12% for T1b, T1c, and T2a; 39% for T2b and T2c; and 60% for T3 and T4 (P < 0.0001). By evaluation with preTx PSA, at 36 months the total failure rate was 3% for preTx PSA < or = 5 ng/mL 16% for 5.1-10 ng/mL, 32% for 10.1-15 ng/mL, 42% for 15.1-20 ng/mL, 63% for 20.1-50 ng/mL, and 88% for > 50 ng/mL (P < 0.0001). By evaluation with post-RT nadir PSA, at 36 months the total failure rate was 4% for nadir PSA < or = 0.5 ng/ mL, 26% for 0.6-1 ng/mL, 33% for 1.1-2 ng/mL, and 92% for > 2 ng/mL (P < 0.0001). In MVA, nadir PSA (P < 0.0001) and T classification (P < 0.0005) were independent predictors for any failure. LF occurred in 13% of patients (27 of 207). For these 27 patients, the categorization of T classification was: T1b/T1c/T2a, 7%; T2b/T2c, 16%; and T3/T4, 15% (P = not significant). In MVA, only nadir PSA (P = 0.0004) predicted for LF. DF occurred in 15% of patients (31 of 207). In MVA, nadir PSA (P < 0.0001) and T classification (P < 0.0001) predicted for DF, with pretreatment PSA of borderline significance (P < 0.05). To assess preTx predictors of outcome, post-RT nadir PSA was removed from the model. PreTx PSA then became the dominant variable to predict any failure (P < 0.0001), LF (P = 0.05), chemF (P = 0.0001), and DF (P < 0.003), while T classification also predicted for any failure (P = 0.03), chemF (P = 0.05), and DF (P < 0.0001).
Systematic prostate biopsies, performed as part of the rigorous followup of prostate carcinoma after RT, define the patterns of failure and confirm the prognostic value of preTx PSA, post-RT nadir PSA, and T classification. Prior to treatment, preTx PSA is the overwhelming independent predictor of failure, but it is surpassed by post-RT nadir PSA when this is added to the model.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Preliminary interventional data suggest that a reduction of dietary acid load raises renal uric acid excretion and decreases serum uric acid (SUA). In line with this, in a recent cross-sectional ...analysis of a representative adult population sample, a higher potential renal acid load (PRAL) was found to associate with higher SUA levels. Against this background, we re-examined the relationship of the body's acid load with SUA and hyperuricemia using nutrition-derived estimates of renal net acid excretion (NAE). After adjusting for relevant confounders, eNAE.sub.PRAL+OA (p = 0.0048) and eNAE.sub.Prot/K (p = 0.0023) were positively associated with SUA. In addition, participants with a higher eNAE.sub.PRAL+OA or eNAE.sub.Prot/K had higher ORs for having hyperuricemia (OR: 1.73, 95% CI: 1.24-2.40, OR: 1.51, 95% CI: 1.10-2.08, respectively). The results substantiate findings of a previous analysis that dietary acid load is a potential influencing factor on SUA. This implicates that a lower dietary acid load may have beneficial effects on SUA.
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DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, VSZLJ, ZAGLJ
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