Bone mass in totally thyroidectomized patients. Role of calcitonin deficiency and exogenous thyroid treatment

Calcitonin has an uncertain role in the preservation of bone mass. Since surgical thyroidectomy abolishes the calcitonin secretion in response to calcium, the bone mineral density at the radius shaft and lumbar spine was measured in 60 patients (5 men, 16 premenopausal, 34 postmenopausal euparathyroid and 5 postmenopausal hypoparathyroid women) who had undergone near total thyroidectomy for thyroid cancer 8.4 +/- 0.7 years before the study. All patients were maintained on suppressive doses of thyroid hormones. Bone mineral density values of the radius shaft (expressed as Z-score) of 34 postmenopausal euparathyroid women was significantly below the normal average (mean +/- SEM = -0.59 +/- 0.2; p = 0.01). Bone mineral density of the lumbar spine was also below the normal average although the difference only approached statistical significance (-0.36 +/- 0.2; 0.05 less than p less than 0.1). The bone mineral density of neither the radius nor the spine differed from normal levels in the premenopausal women and the postmenopausal hypoparathyroid women. Unexpectedly, the bone mineral density of the spine was significantly increased in the 5 thyroidectomized men. The results indicate that thyroidectomized women have a diminished bone mass after the menopause only if parathyroid function is normal. Since the patients were receiving thyroid hormone at suppressive doses, the present study is not able to separate the relative contributions of calcitonin deficit and exogenous thyroid on bone mass loss.     

Bone metabolism in patients with differentiated thyroid carcinoma receiving suppressive levothyroxine treatment.

AIM: Patients with differentiated thyroid carcinoma (DTC) must receive suppressive levothyroxine (LT(4)) therapy for the rest of their lives. The literature, however, presents conflicting results on how this affects bone metabolism. The aim of this study was to assess the influence of the estrogen status and LT(4) therapy, in particular LT(4) dosage in micrograms per kilograms (microg/kg), on bone metabolism in female patients with DTC. MATERIAL AND METHODS: Three markers of bone metabolism (C-terminal telopeptide of type I collagen in serum [SCTx]; N-terminal telopeptide of type I collagen in urine [U-NTx]; and osteocalcin [OC]) were investigated in four groups: group REF (healthy premenopausal female controls), group DTC-ES (premenopausal women with DTC and normal estrogen levels), group DTC-ED (postmenopausal women with DTC and estrogen deficiency), and group DTC-HRT (postmenopausal women with DTC undergoing hormone replacement therapy [HRT]). All patients with DTC were on a well-adjusted suppressive LT(4) therapy with TSH levels 0.1 mU/L or less. RESULTS: In group DTC-ES bone turnover was comparable to group REF, whereas in group DTC-ED, all three markers were significantly increased as compared to groups REF and DTC-ES. In group DTC-HRT, the HRT normalized U-NTx and OC. However, in this group S-CTx was not completely normalized by HRT in all patients, although also significantly lowered compared to group DTC-ED. The analysis of LT(4 )dosage per kilogram showed that premenopausal DTC-patients had increased markers of bone metabolism if LT(4) dosage exceeded 2.6 microg/kg. Estrogen-deficient patients with DTC, however, had a much lower critical LT(4) dosage, above which increased markers of bone metabolism were seen. CONCLUSION: A well-adjusted suppressive LT(4) therapy of less than 2.6 microg/kg and normal estrogen levels do not seem to increase bone metabolism in estrogen-sufficient patients with DTC. The normalization of an estrogen deficiency by HRT or other antiresorptive therapies and minimal suppressive dosages of LT(4) are attempts to optimize the care of patients with DTC. In postmenopausal patients with DTC and patients with DTC who require LT(4) dosages in excess of 2.6 microg/kg, the information provided by markers of bone metabolism may help to prevent bone damage.     

The reduction of bone mineral density in postmenopausal women with primary hyperparathyroidism is higher in the presence of concomitant GH secretion impairment

OBJECTIVE: To investigate, in a large group of postmenopausal primary hyperparathyroidism (PHP) women, whether the concomitance of GH deficiency (GHD) may contribute to the development of changes in bone mineral density (BMD). DESIGN: GH secretion, bone status and metabolism were investigated in 50 postmenopausal women with PHP and in a control group of 60 women with no evidence of PHP, matched for age, age at menopause and body mass index (BMI). METHODS: GH response to growth hormone-releasing hormone (GHRH)+arginine (Arg), femoral neck BMD (g/cm2) by dual energy X-ray absorptiometry, BMI, serum-ionized calcium, parathyroid hormone (PTH) and markers of bone remodelling were evaluated in all patients and controls. RESULTS: Among PHP patients, GH secretion was reduced (8.8 +/- 4.2 microg/l, range 1.1-16.5 microg/l) in 34 patients and normal (28.7 +/- 11.8 microg/l, range 17.9-55.7 microg/l) in the remaining 16 (P < 0.05), no women in the control group had GHD (peak GH 33.8 +/- 10.9 microg/l, range 21.7 +/- 63.2 microg/l). Osteoporosis (T-score < - 2.5) and osteopenia (T-score > -2.5 and < -1) were found in 73.5 and 17.6% of GHD patients, in 37.5 and 43.7% of patients with normal GH secretion and 3.1 and 27% of controls. T-score and BMD were not correlated with ionized calcium, age, age at menopause, BMI, GH peak and IGF-I but were correlated with serum PTH levels in both groups. T-score was correlated with serum levels of markers of bone remodelling only in PHP patients with GHD. CONCLUSIONS: Concomitant impairment of GH secretion may play a pathogenetic role in the occurrence of changes in bone mass observed in PHP and contribute to make them more severe.     

Bone risk of hormone-suppressing therapy in differentiated thyroid epithelioma. Study by dual photon absorptiometry]

A decreased bone mineral density is a well known complication of thyrotoxicosis. If bone is also adversely affected by a subclinical hyperthyroidism is still debated. Such a situation is deliberately induced for treatment of thyroid differentiated carcinoma. We compared bone mineral measurements in case of thyroid carcinoma exposed to prolonged suppressive hormonal treatment (288 patient year, LT3 in 87%) and in age and weight matched controls. We did not find any difference in both sexes between the two populations in term of fracture rate and vertebral mineral density measured by dual photon absorptiometry, nor any influence of gonadal status in women.     

A therapeutic dilemma: suppressive doses of thyroxine significantly reduce bone mineral measurements in both premenopausal and postmenopausal women with thyroid carcinoma

We measured lumbar spine, femoral neck, and forearm bone mineral (BMD) in 24 women (14 premenopausal and 10 postmenopausal) who had been treated with total thyroidectomy and 131 Iodine ablation therapy for nonanaplastic thyroid carcinoma and 24 case controls. At the time of the study, all patients were free of cancer (negative 131 Iodine whole body scan and serum thyroglobulin levels less than 0.3 micrograms/L) and all were receiving doses of T4 sufficiently high to prevent a rise in a serum thyroid-stimulating hormone concentration after an iv bolus of TRH. Femoral neck BMD were significantly reduced in both the premenopausal women (89 +/- 3.8% of case controls, 95% CI, 81 to 98) and postmenopausal women (77 +/- 3.9% of case controls; 95% CI, 68 to 86) receiving T4. Lumbar spine BMD and forearm BMD were unaffected in the premenopausal women, but significantly reduced in the postmenopausal women receiving T4 (lumbar spine BMD = 84 +/- 6.2% of case controls; 95% CI, 70 to 98 and forearm BMD = 89 +/- 5.6% of case controls; 95% CI, 76 to 101). Serum bone Gla-protein, a marker of bone turnover, was significantly increased in both the premenopausal and the postmenopausal women receiving T4 compared to case controls (P less than 0.001 for the difference between patient groups and controls). Whereas the cumulative dose of T4 was highly correlated with the femoral neck BMD in the premenopausal patients (r = 0.528; P less than 0.05); the presence of hypogonadism was the main determinant of the lumbar spine and forearm BMD. This data confirms that premenopausal and postmenopausal women receiving suppressive doses of T4 for thyroid carcinoma have diminished bone mineral measurements and are at risk for osteoporosis.     

Primary biliary cirrhosis is not an additional risk factor for bone loss in women receiving regular calcium and vitamin D supplementation: a controlled longitudinal study

BACKGROUND AND GOALS: Alterations in bone metabolism in primary biliary cirrhosis (PBC) are generally considered to be highly prevalent and severe, but no data are available from prospective studies with adequate control groups. The aims of this study were: (1) to measure changes in bone mineral density (BMD) over time; (2) to correlate the degree of bone loss with the severity of liver disease; and (3) to characterize bone disease in PBC patients receiving regular calcium and vitamin D supplementation. STUDY: We enrolled 118 women with PBC (mean age+/-SD: 56+/-11 y; 72% postmenopausal; 43% with cirrhosis), and measured BMD (lumbar spine, DXA-Hologic) at entry and serially over the following 5 years. The controls were 472 healthy women selected from a large observational group matched for age and menopausal status (mean age+/-SD: 55+/-10 y; 73% postmenopausal). RESULTS: Mean BMD was 0.851+/-0.142 g/cm2 in the PBC group and 0.857+/-0.158 g/cm2 in the control group; the prevalence of osteoporosis was 28% and 29%, respectively. BMD significantly correlated with age and postmenopausal status, but not with liver cirrhosis or serum bilirubin levels. The biochemical markers of bone turnover were high in about 50% of the patients. The yearly bone loss in the PBC group was 0.008 g/cm2 (95% confidence interval: 0.014-0.003) similar to that calculated in the control group. CONCLUSIONS: Among patients with PBC, the prevalence of osteoporosis and the yearly rate of BMD loss are similar to those observed in the general population, and are not associated with the severity of liver disease.     

REDUCED FOREARM BONE MINERAL CONTENT AND BIOCHEMICAL EVIDENCE OF INCREASED BONE TURNOVER IN WOMEN WITH EUTHYROID GOITRE TREATED WITH THYROID HORMONE

We used single-photon absorptiometry to assess forearm bone mineral content (BMC/BW) (arbitrary units normalized for bone width) at a proximal site (PBMC/BW) and at a more distal site (DBMC/BW) in 60 women treated with 25-50 micrograms T3 or 50-100 micrograms T4 for euthyroid goitre, in 13 untreated goitre patients, and in 2 controls matched for age and menopausal state for each goitre patient. BMC/BW was not significantly different between untreated goitre patients and controls. In 36 premenopausal patients, treated for 5.8 +/- 5.4 years (mean +/- SD) a slight decrease in PBMC/BW of about 5% compared to controls to controls was observed (PBMC/BW 1.42 +/- 0.19 vs 1.49 +/- 0.13, P less than 0.05). In 24 postmenopausal patients, treated for 10.0 +/- 5.8 year, a 20% deficit in BMC/BW compared to controls was found (DBMC/BW 0.80 +/- 0.18 vs 1.06 +/- 0.20, P less than 0.001 and PBMC/BW 1.14 +/- 0.20 vs 1.42 +/- 0.19, P less than 0.001). Biochemical indices of bone metabolism in 43 pre and post-menopausal patients and 43 controls showed in the patients a higher serum alkaline phosphatase activity (AP) (P less than 0.01 and P less than 0.05 and serum osteocalcin (NS and P less than 0.05). AP was negatively correlated with TSH levels and, in postmenopausal patients, with DBMC/BW and PBMC/BW. Our results suggest that treatment of euthyroid women with moderate doses of thyroid hormone increases bone turnover with clear adverse effects on bone mineral status in postmenopausal patients.     

Relationship between bone mineral density and angiotensin converting enzyme polymorphism in hypertensive postmenopausal women

BACKGROUND: The purpose of this study was to assess the relationship between bone mineral density and insertion/deletion (I/D) angiotensin converting enzyme polymorphism (ACE) in hypertensive postmenopausal women. METHODS: Blood and urine samples from the study subjects were analyzed for calcium metabolism related parameters. Densitometry studies were conducted in the lumbar spine (L2 to L4). The ACE polymorphism was analyzed by polymerase chain reaction. RESULTS: Women with II genotype showed a higher intact parathyroid hormone (76 +/- 33 v 55 +/- 27 pg/mL and 52 +/- 26 pg/mL, P =.034) without a decrease in calciuria, and higher bone mineral density than women with ID and homozygotus deletion genotype (1.138 +/- 0.08 v 1.051 +/- 0.16 pg/mL and 1.053 +/- 0.16 pg/mL). CONCLUSIONS: The ACE polymorphism could be one of the factors causing bone mass variations.     

The effects of thyrotropin-suppressive therapy on bone metabolism in patients with well-differentiated thyroid carcinoma.

Patients with differentiated thyroid carcinoma (DTC) are commonly treated long-term with thyrotropin (TSH)- suppressive thyroxine replacement therapy resolving in a state of subclinical hyperthyroidism. The relationship between subclinical hyperthyroidism and osteoporosis is not clear. In this review, we systematically selected and analyzed 21 studies addressing this issue. Although multiple methodological differences between studies prevented a structured meta-analysis, our data suggest that postmenopausal women with subclinical hyperthyroidism are most at risk, whereas no increased risk was observed in men and premenopausal women. Based on these findings we believe that measurement of bone mineral density is recommended in postmenopausal women with DTC starting TSH suppressive therapy. This should be subsequently regularly measured to enable timely intervention with bone protective agents.     

Oral alendronate increases bone mineral density in postmenopausal women with primary hyperparathyroidism

The effect of biphosphonate therapy on bone mineral density (BMD) in patients with primary hyperparathyroidism (PHP) is unknown. Forty postmenopausal women (mean age, 70 yr) with PHP were randomized to receive alendronate 10 mg/d or placebo for 48 wk, followed by treatment withdrawal for 24 wk. The mean (+/-SD) changes in BMD at femoral neck (+4.17 +/- 6.01% vs. -0.25 +/- 3.3%; P = 0.011) and lumbar spine (+3.79 +/- 4.04% vs. 0.19 +/- 2.80%; P = 0.016) were significantly higher with alendronate at 48 wk. Serum calcium was reduced with alendronate but not placebo (-0.09 vs. +0.01 mmol/liter; P = 0.018). Serum bone-specific alkaline phosphatase activity was lower with alendronate from 12 wk onward and increased 24 wk after treatment withdrawal (21.1 +/- 12.8 to 7.3 +/- 4.9 IU/liter at 48 wk, and 15.0 +/- 14.8 IU/liter 24 wk after withdrawal; P = 0.002 for trend). Osteocalcin concentration decreased at 48 wk and increased 24 wk after alendronate withdrawal (P = 0.019 for trend of change over time) but not with placebo. Urinary N-telopeptide/creatinine ratio decreased with alendronate at 48 wk and increased 24 wk after treatment withdrawal (P = 0.008 for trend). N-telopeptide/creatinine ratio did not change with placebo. Alendronate improves BMD and reduces bone turnover markers in postmenopausal women with PHP.     

High dietary phytoestrogen intake is associated with higher bone mineral density in postmenopausal but not premenopausal women.

Animal studies demonstrated that phytoestrogen had a protective effect against bone loss after ovariectomy. However, data on dietary phytoestrogen intake as well as its relationship with bone mineral density (BMD) in human are not available. Six hundred fifty southern Chinese women, aged 19 to 86 yr, were recruited to determine their dietary phytoestrogen intake by a food frequency questionnaire. BMDs at the lumbar spine and hip region were measured using dual energy x-ray absorptiometry. The subjects were analyzed according to various tertiles of phytoestrogen intake. Among the postmenopausal women (n = 357), significant differences in the lumbar spine (L2-4) BMD (0.820 +/- 0.145 vs. 0.771 +/- 0.131 g/cm2, P < 0.05) and Ward's triangle BMD (0.450 +/- 0.151 vs. 0.415 +/- 0.142 g/cm2; P < 0.05) were found between the highest and lowest intake of isoflavone after adjusting for age, height, weight, years since menopause, smoking, alcohol consumption, HRT usage, and daily calcium intake. Women with the highest intake of isoflavone had significantly lower levels of serum PTH (19.38 +/- 14.61 vs. 26.56 +/- 11.19 pg/ml; P < 0.05), osteocalcin (4.95 +/- 3.61 vs. 6.69 +/- 5.05 mg/liter; P = 0.05), and urinary N-telopeptide (34.18 +/- 25.31 vs. 49.66 +/- 41.00 nmol bone collagen equivalents/mmol creatinine; P < 0.05) when compared with those with the lowest intake of isoflavone. No association between dietary phytoestrogen intake and BMDs was seen in the premenopausal women with high endogenous E (n = 293). In conclusion, postmenopausal women with habitually high intake of dietary isoflavone are associated with higher BMD values at both the spine and hip region. Customarily high isoflavone intake may help to reverse the state of secondary hyperparathyroidism associated with E withdrawal and hence lower the rate of bone turnover in postmenopausal women.     

Safety and efficacy of estrogen therapy in preventing bone loss in primary biliary cirrhosis

OBJECTIVE: Estrogen therapy has been found to be useful in the treatment of postmenopausal osteoporosis. However, concern about its potential for worsening cholestasis has limited its use in postmenopausal women with primary biliary cirrhosis. The aim of the present study was to determine the safety as well as the efficacy of estrogen replacement therapy with respect to bone mass in postmenopausal women with primary biliary cirrhosis. METHODS: Bone mineral density of the lumbar spine (measured using dual energy x-ray absorptiometry) of 46 unselected postmenopausal women with primary biliary cirrhosis receiving estrogen replacement therapy was compared with 46 age-matched women with primary biliary cirrhosis not receiving estrogen replacement therapy, and with the expected normal bone mineral density adjusted for age and ethnic group. RESULTS: The mean duration of follow-up was 4.8 +/- 0.4 yr. Treatment with estrogens resulted in a significantly lower rate of bone loss (0.002 g/cm(2)/yr +/- 0.028 vs 0.009 g/cm(2)/yr +/- 0.020, p = 0.05). Worsening cholestasis attributable to estrogen replacement therapy did not occur in any patient. One patient (2%) discontinued therapy because of side effects. CONCLUSIONS: Estrogen replacement therapy in postmenopausal patients with primary biliary cirrhosis is safe and may be effective in decreasing the rate of bone loss.     

Bone density and bone metabolism are normal after long-term gluten-free diet in young celiac patients

OBJECTIVES: Osteoporosis and alterations of bone metabolism are frequent complications of celiac disease. We evaluated the impact of long-term gluten-free diet (GFD) initiated during childhood and adolescence on bone mineralization and bone metabolism. METHODS: We studied 30 celiac patients on GFD for > or = 5 yr. The mean age at diagnosis was 11.4+/-5.0 yr, and the mean duration of GFD was 10.7+/-4.3 yr. Results were compared with those obtained in 240 healthy controls. Bone mineral density (BMD) was measured in the lumbar spine and in the whole skeleton by dual-energy x-ray absorptiometry. Serum levels of bone-specific alkaline phosphatase (BALP) and N-terminal propeptide of type I procollagen (PINP) were measured as bone formation indices, and urine levels of N-telopeptide of type I collagen (NTx) as bone resorption index. RESULTS: BMD measurements of celiac patients (lumbar spine: 1.131+/-0.121 g/cm2; total body: 1.145+/-0.184 g/cm2) did not differ from those of control subjects (lumbar spine: 1.131+/-0.184 g/cm2; total body: 1.159+/-0.118 g/cm2). The levels of BALP, PINP, and NTx of celiac patients did not differ from those of controls. Patients who started GFD before puberty had BMD and bone metabolism measurements comparable to those of patients who started GFD during puberty. CONCLUSIONS: Our data show that long-term dietary treatment ensures normal mineralization and bone turnover.     

Clinical significance of alendronate in postmenopausal type 2 diabetes mellitus

OBJECTIVES: To examine early changes in biochemical markers of bone turnover and bone mineral density (BMD) in a clinical trial of anti-resorptive agent alendronate versus alfacalcidol in postmenopausal women with type 2 diabetes mellitus. METHODS: 12 subjects (mean age; 73.1 +/- 6.3 yrs, duration of diabetes; 13.2 +/- 3.7 yrs) were administered alendronate sodium (5 mg/day) and 12 subjects (mean age; 70.7 +/- 7.8 yrs, duration of diabetes; 12.8 +/- 2.0 yrs) were administered alfacalcidol (0.5 microg/day) for 12 months. Urinary N-telopeptide cross-linked collagen type I (NTx), one of biochemical markers, and radial bone mineral density (BMD) were measured as a marker of bone turnover. RESULTS: After 12 months, urinary NTx did not change in women with alfacalcidol treatment, however urinary NTx significantly decreased after alendronate treatment. The BMD significantly decreased by 3.33% (p<0.05) in women with alfacalcidol treatment, while the BMD did not decrease in women with alendronate treatment. CONCLUSION: Alendronate that produces reduction in urinary NTx and inhibition of decrease in BMD may have a clinical significance to reduce the risk of bone fracture in postmenopausal type 2 diabetic women.     

Effects of alendronate on bone mineral density and bone metabolic markers in postmenopausal asthmatic women treated with inhaled corticosteroids

We have recently shown that long-term use of inhaled corticosteroids decreases bone mineral density (BMD) of the lumbar spine in postmenopausal asthmatic women. The present study aimed to evaluate the efficacy of alendronate in comparison with that of alfacalcidol (1-alpha-hydroxyvitamin D(3)) for the treatment of BMD reduction in postmenopausal asthmatic patients who had inhaled corticosteroid therapy without regular use of systemic corticosteroids. Twenty-eight postmenopausal asthmatic patients with BMD T score of -1.0 or less were randomized to receive alendronate (5 mg/d) or alfacalcidol (1 microg/d). Bone mineral density was determined at baseline and 12 months after the treatment, and biochemical markers of bone metabolism were measured at baseline and after 6 and 12 months of treatment. The mean (+/-SD) BMD values at the lumbar spine, the total hip, and the Ward's triangle significantly increased by 4.9 +/- 4.5% (P = .0005), 2.4 +/- 2.2% (P = .0005), and 3.6 +/- 5.2% (P = .02) at 12 months in the alendronate group, whereas the corresponding values did not significantly change in the alfacalcidol group. In the alendronate group, urinary N-telopeptide (NTx), serum osteocalcin, and serum alkaline phosphatase concentrations significantly decreased, and serum intact parathyroid (PTH) level significantly increased, from baseline at both 6 and 12 months. In the alfacalcidol group, urinary NTx showed modest but significant decrease, although the extent of the change was smaller than that in the alendronate group. We concluded that alendronate was effective to improve reduced BMD in postmenopausal asthmatic patients on inhaled corticosteroid therapy through the mechanism of inhibiting bone resorption.     

Plasma leptin concentrations in postmenopausal women with osteoporosis

BACKGROUND: The obese are usually protected against osteoporosis and have increased bone mineral density and plasma leptin concentrations. A recent in vitro study demonstrated that leptin acts on human marrow stromal cells to enhance differentiation to osteoblasts, suggesting an influence of leptin on bone mass. However, little is known about the relationship between plasma leptin and bone mass in postmenopausal women with osteoporosis. OBJECTIVE: To investigate plasma leptin concentrations in postmenopausal women with osteoporosis to improve the understanding of the role of leptin in determining bone mass. METHODS: Fifty postmenopausal women with osteoporosis (ages 61.18+/-6.51 years; body mass index (BMI) 28. 91+/-3.44kg/m(2), mean+/-s.d.) and 30 age- and BMI-matched healthy postmenopausal women were included in the study. Bone mineral densities (BMD) were measured by dual energy X-ray absorptiometry. Plasma leptin concentrations were determined using an immunoradiometric assay. RESULTS: The median spine BMD value in the patient group (0.695+/-8.26g/cm(2), median+/-s.e.m.) was significantly lower than that in the control group (1.006+/-1. 29g/cm(2), median+/-s.e.m.; z=-7.454, P<0.001). The median plasma leptin concentration in the patient group (18.70+/-1.78ng/ml, median+/-s.e.m.) was not significantly different from that in the control group (22.35+/-2.20ng/ml, median+/-s.e.m.; z=-1.630, P=0. 103). Plasma leptin concentrations were correlated with BMI in both groups (r(s)=0.394, P=0.031 in controls and r(s)=0.404, P=0.004 in the patient group). There was no correlation between plasma leptin concentrations and BMD values in controls (r(s)=-0.107, P=0.575) but a weak correlation was observed in the patient group (r(s)=0.285, P=0.045). CONCLUSION: Our data suggest that circulating plasma leptin does not have a significant direct influence on bone mass in postmenopausal women.     

亚临床甲状腺功能减退症与绝经后女性骨代谢指标的相关性分析

目的探讨亚临床甲状腺功能减退症(SCH)与绝经后女性骨密度及骨代谢相关指标的关系。方法选取2015年1月至2018年6月在空军军医大学西京医院老年病科就诊的138例绝经后女性临床资料,根据患者是否患SCH分为SCH组(68例)和正常对照组(70例)。检测并比较2组患者骨密度相关指标[碱性磷酸酶(ALP)、Ca~(2+)、骨化三醇、骨密度T值(T -1.0为骨密度异常)]以及甲状腺功能相关指标[甲状旁腺激素(PTH)、促甲状腺激素(TSH)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、甲状腺过氧化物酶抗体(TPOAb~+)比例]。采用SPSS 18.0统计软件对数据进行分析。相关性采用Spearman相关分析。结果 SCH组及对照组患者骨密度异常率分别为50.0%(34/68)和25.7%(18/70),2组比较差异有统计学意义(P=0.003)。与对照组比较,SCH组患者TSH水平和TPOAb~+比例显著升高(P0.05),但FT3、FT4、PTH及骨代谢相关指标比较,差异无统计学意义(P0.05)。Spearman相关分析显示,TSH、TPOAb~+与ALP、骨化三醇、骨密度T值呈负相关,其中TSH与T值呈高度负相关(r=-0.804,P0.01)。结论 SCH可能引起绝经后女性骨量异常和骨密度测定值降低,这可能与血清TSH水平升高和TPOAb呈阳性有关。     

131I联合左旋甲状腺素对分化型甲状腺癌术后患者骨代谢的影响

观察^131I联合左旋甲状腺素（LT4）替代治疗或抑制治疗对120例分化型甲状腺癌（DTC）术后患者部分骨代谢生化指标及骨密度的影响。替代组、抑制组与健康对照组血钙、血磷、血碱性磷酸酶（ALP）、骨密度（BMD）的差异无统计学意义，不同^131I累积剂量组间血钙、血磷、ALP、BMD的差异亦无统计学意义。观察期内所有患者无一例发生骨折。对DTC术后患者给予^131I联合替代或抑制剂量的LT4治疗是安全和必要的，该策略在短期内不会引起骨代谢生化指标和BMD的明显异常。     

The relationship of swimming exercise to bone mass in men and women

Exercise appears to be capable of exerting a positive effect on bone mass, but how exercise can be used to best advantage in the prevention and therapy of osteopenia is unclear. Weight-bearing activity has been commonly considered to be essential for the beneficial effects of exercise on the skeleton, and, therefore, swimming has been considered valueless in the maintenance of bone mass. To examine this issue we measured radial and vertebral bone mineral density in a group of subjects aged 40 to 85 years who had been swimming regularly for at least 3 years as well as in a similar group of nonexercising control subjects. The swimmers engaged in no other forms of regular exercise, and no subject had other conditions known to affect bone or mineral metabolism. Dietary calcium and protein intakes were similar in the two groups. At both radial (0.84 +/- 0.08 vs 0.81 +/- 0.09 g/cm2) and vertebral (123 +/- 27 vs 108 +/- 31 mg/cm3) sites the male swimmers had significantly greater bone mineral density than did the nonexercisers. In women, however, no relationship of swimming to bone mineral density could be identified. These results suggest that swimming exercise may be beneficial in the prevention or therapy of osteopenia and that its usefulness in this regard should be further investigated.     

Sex hormones and bone metabolism in postmenopausal rheumatoid arthritis treated with two different glucocorticoids.

To investigate the effect of low doses of 2 different glucocorticoids on bone mass, sex hormone status and bone metabolic indices, a study was undertaken in 16 postmenopausal women with rheumatoid arthritis (RA) receiving < 15 mg/day of deflazacort and in 16 patients with RA matched for age, years postmenopause and disease duration, receiving < 10 mg/day of prednisone. Sixteen healthy postmenopausal women and 16 nonsteroid treated patients with RA were also studied as control groups. Vertebral bone density (vBMD) was lower (mean +/- SD: 0.65 +/- 0.07 vs 0.73 +/- 0.09 g/cm2; p < 0.02) in prednisone treated patients than in deflazacort treated patients, whose vBMD values were similar to those of nonsteroid treated RA. No significant difference was found as for radial bone mineral content. Circulating levels of estradiol, dehydroepiandrosterone sulfate, androstenedione and progesterone were low in all patient groups with RA when compared with healthy controls. The prednisone treated patients showed significantly lower values of all sex hormones with respect to deflazacort treated patients. Osteocalcin values were also lower (3.0 +/- 1.4 vs 3.9 +/- 1.6 ng/ml; p < 0.05) in prednisone treated patients with respect to deflazacort treated group. Glucocorticoid treated patients showed a direct correlation (r2 = 0.39) between vBMD and plasma estradiol levels, while no correlation was found with osteocalcin values. In conclusion, our postmenopausal patients with RA treated with low dose prednisone had reduced levels of sex hormones and osteocalcin and reduced vertebral bone mass. Comparable doses of deflazacort showed only a mild inhibitory effect on sex hormones and osteocalcin, and did not show any detectable effect on bone mass.