Bone Density and Mineral Metabolism in Thyroidectomized Patients Treated with Long-Term l-Thyroxine

1994 ◽  
Vol 87 (5) ◽  
pp. 593-597 ◽  
Author(s):  
Sandro Giannini ◽  
Martino Nobile ◽  
Leonardo Sartori ◽  
Pierluigi Binotto ◽  
Matteo Ciuffreda ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Density ◽  
Bone Mass ◽  
Mineral Metabolism ◽  
Menopausal Status ◽  
Bone Alkaline Phosphatase ◽  
Thyroid Stimulating Hormone ◽  
Control Subjects ◽  
And Control

1. A decreased bone mass has been reported in patients with endogenous hyperthyroidism, but the effect on bone density and mineral metabolism of thyroxine administration in thyroidectomized patients is still controversial. To further contribute to this debate, we studied 25 women thyroidectomized for thyroid cancer on long-term treatment with thyroid-stimulating hormone-suppressive doses of L-thyroxine. Twenty-one sex- and age-matched normal subjects were also studied as a control group. 2. The bone density of the spine and serum calcitonin, calcitriol and parathyroid hormone concentrations were not different when the whole patient group was compared with the control subjects, nor when the patients and control subjects were compared according to their menopausal status. However, postmenopausal thyroidectomized patients showed significantly lower bone mass (P < 0.001) than premenopausal patients. 3. L-Thyroxine-treated patients showed significantly higher levels of bone alkaline phosphatase and urine hydroxyproline excretion than control subjects (P < 0.003 and P < 0.001, respectively). These differences were still present when patients and control subjects were analysed according to their menopausal status. However, bone alkaline phosphatase was significantly higher in postmenopausal than in premenopausal women only in L-thyroxine-treated patients (P < 0.05). In postmenopausal L-thyroxine-treated patients a negative correlation between time since menopause and bone mass (P < 0.05) and a positive correlation between bone alkaline phosphatase and hydroxyproline excretion (P < 0.03) were also found. 4. We conclude that long-term thyroid-stimulating hormone-suppressive treatment with L-thyroxine in thyroidectomized women is not associated with a decrease in spinal bone mass nor with calcitonin deficiency, and that L-thyroxine treatment may increase skeletal sensitivity to menopause-related bone loss.

Decreased responsiveness to chronic salmon calcitonin treatment in rat kidney and calvaria studied using quantitative enzyme cytochemistry

1985 ◽  
Vol 108 (4) ◽  
pp. 570-576
Author(s):  
D. Michael Salmon ◽  
M. Azria ◽  
Joan M. Zanelli
Keyword(s):  
Alkaline Phosphatase ◽  
Salmon Calcitonin ◽  
Mineral Metabolism ◽  
Bone Alkaline Phosphatase ◽  
Term Treatment ◽  
Target Tissue ◽  
Intracellular Enzyme ◽  
Long Term Treatment ◽  
And Control

Abstract. Growing rats were treated with daily im doses of salmon calcitonin (sCT) (2, 15 and 100 IU/kg) for various times (1, 4 and 24 weeks). The effects on intracellular enzyme activities in bone and kidney were monitored using quantitative cytochemical methods previously developed for the identification of specific target tissue responses to calcitonins. The basal alkaline phosphatase activities in both kidney and bone were decreased by long-term treatment at all time periods and doses tested. No change was noted in basal Ca ATPase activities in kidney after treatment. The capacity of target tissues in chronically treated and control rats to respond to an acute iv dose of sCT was also compared. Acute provocation tests in treated and control rats showed that the renal alkaline phosphatase response was decreased in the rats receiving long-term treatment. Moreover, the direction of response was reversed in chronically treated rats when bone alkaline phosphatase and renal Ca-dependent ATPase activity was measured after acute provocation with sCT, i.e. bone alkaline phosphatase was stimulated instead of being inhibited and renal Ca ATPase was inhibited instead of being stimulated. The application of quantitative cytochemial techiques has demonstrated intracellular changes in enzyme activites in both kidney and bone. The impaired sCT responsiveness can be detected at shorter times of treatment (1 week) and lower doses (2 IU/kg) than has previously been possible by measurement of indices of mineral metabolism in plasma or urine.

scholarly journals Bone-Derived Serum Enzymes and Bone Density in Perimenopausal Caucasian Women

1993 ◽  
Vol 30 (2) ◽  
pp. 191-194 ◽  
Author(s):  
J D Johnston ◽  
S Koneru ◽  
T Kuwana ◽  
S B Rosalki
Keyword(s):  
Alkaline Phosphatase ◽  
Acid Phosphatase ◽  
Bone Density ◽  
Femoral Neck ◽  
Serum Levels ◽  
Bone Alkaline Phosphatase ◽  
Serum Enzymes ◽  
Tartrate Resistant Acid Phosphatase ◽  
Vertebral Bone ◽  
Caucasian Women

Serum levels of bone-origin alkaline phosphatase and of tartrate-resistant acid phosphatase were measured in Caucasian women aged 41–69 years who had volunteered for bone densitometry. Bone alkaline phosphatase and tartrate-resistant acid phosphatase were inversely correlated with vertebral bone density and with femoral neck bone density. Bone alkaline phosphatase and acid phosphatase were also significantly correlated, consistent with the concept of ‘coupling’ between osteoblast and osteoclast activity.

Decreased Bone Density in Adolescent Girls With Anorexia Nervosa

PEDIATRICS ◽  
1990 ◽  
Vol 86 (3) ◽  
pp. 440-447 ◽  
Author(s):  
Laura K. Bachrach ◽  
David Guido ◽  
Debra Katzman ◽  
Iris F. Litt ◽  
Robert Marcus
Keyword(s):  
Bone Mineral Density ◽  
Body Mass Index ◽  
Anorexia Nervosa ◽  
Bone Density ◽  
Bone Mass ◽  
Body Mass ◽  
Bone Mineral ◽  
Whole Body ◽  
Mineral Density ◽  
Control Subjects

Osteoporosis develops in women with chronic anorexia nervosa. To determine whether bone mass is reduced in younger patients as well, bone density was studied in a group of adolescent patients with anorexia nervosa. With single- and dual-photon absorptiometry, a comparison was made of bone mineral density of midradius, lumbar spine, and whole body in 18 girls (12 to 20 years of age) with anorexia nervosa and 25 healthy control subjects of comparable age. Patients had significantly lower lumbar vertebral bone density than did control subjects (0.830 ± 0.140 vs 1.054 ± 0.139 g/cm2) and significantly lower whole body bone mass (0.700 ± 0.130 vs 0.955 ± 0.130 g/cm2). Midradius bone density was not significantly reduced. Of 18 patients, 12 had bone density greater than 2 standard deviations less than normal values for age. The diagnosis of anorexia nervosa had been made less than 1 year earlier for half of these girls. Body mass index correlated significantly with bone mass in girls who were not anorexic (P &lt; .05, .005, and .0001 for lumbar, radius, and whole body, respectively). Bone mineral correlated significantly with body mass index in patients with anorexia nervosa as well. In addition, age at onset and duration of anorexia nervosa, but not calcium intake, activity level, or duration of amenorrhea correlated significantly with bone mineral density. It was concluded that important deficits of bone mass occur as a frequent and often early complication of anorexia nervosa in adolescence. Whole body is considerably more sensitive than midradius bone density as a measure of cortical bone loss in this illness. Low body mass index is an important predictor of this reduction in bone mass.

Rickets Associated With Long-Term Anticonvulsant Therapy in a Pediatric Outpatient Population

PEDIATRICS ◽  
1975 ◽  
Vol 56 (1) ◽  
pp. 52-57 ◽  
Author(s):  
Carl J. Crosley ◽  
Claire Chee ◽  
Peter H. Berman
Keyword(s):  
Alkaline Phosphatase ◽  
Alkaline Phosphatase Activity ◽  
Serum Alkaline Phosphatase ◽  
Pediatric Population ◽  
Anticonvulsant Therapy ◽  
Control Population ◽  
Serum Alkaline Phosphatase Activity ◽  
Calcium And Phosphorus ◽  
And Control

Over a 12-month period, an ambulatory pediatric population receiving long-term anticonvulsants was surveyed for the presence of biochemical and radiologic rickets. There were 74 treated children and 95 matched controls. Elevations of serum alkaline phosphatase activity occurred in 31 of the 74 (42%) treated children (23 of 47 children between 2 and 10 years and 8 of 21 children between 10 and 16 years). This frequency of abnormal values was significantly greater than that which occurred in our control population. Calcium and phosphorus abnormalities were minimal in both treated and control populations. Radiologic rickets occurred in 6 of the 74 (8%) of the treated children and in none of the control population. Neither the severity of the rickets nor the degree of hyperalkaline phosphatasemia were correlated with age of the patient, duration, and/or dose of anticonvulsant therapy.

Thyroid Nodules in Patients with Acromegaly: Frequency According to the ACR TI-RADS Classification and its Relationship with Disease Activity

2021 ◽  
Author(s):  
Mustafa Can ◽  
Muhammet Kocabaş ◽  
Melia Karakose ◽  
Hatice Caliskan Burgucu ◽  
Zeliha Yarar ◽  
...  
Keyword(s):  
Disease Activity ◽  
Thyroid Nodules ◽  
Thyroid Volume ◽  
Thyroid Stimulating Hormone ◽  
Control Group ◽  
Control Subjects ◽  
Number Of Patients ◽  
Significant Difference ◽  
The Mean ◽  
And Control

Abstract Purpose: In our study, we aimed to determine the frequency of thyroid nodules in patients with acromegaly according to the American College of Radiology (ACR) Thyroid Imaging, Reporting and Data System (TI-RADS) classification and its relationship with acromegaly disease activity. Methods: A total of 56 patients with acromegaly and age, sex, and body mass index matched with 56 healthy control subjects were included in our study. Thyroid-stimulating hormone, free thyroxine, and anti-thyroperoxidase antibody levels of patients and control subjects were measured. In addition, patients and healthy controls were evaluated by ultrasonography to determine thyroid structure, thyroid volume, and thyroid nodules and to make ACR TI-RADS classification. Results: Thyroid nodules were present in 31 (55.4%) of 56 patients in the acromegaly group and 20 (35.7%) of 56 subjects in the control group, and the frequency of thyroid nodules was significantly higher in the acromegaly group (p=0.038). The mean number of nodules in the acromegaly group and control group was 1.27±1.43 and 0.48±0.73, respectively, and the mean number of nodules was significantly higher in the acromegaly group (p=0.003). The number of patients with TI-RADS 1, TI-RADS 2, and TI-RADS 4 nodules in the acromegaly group was higher than the control group (p=0.026, p=0.049, p=0.007, respectively). No difference was found in terms of cytological findings between those who have undergone FNAB in the acromegaly group and control group. Conclusion: In our study, we found that the frequency of thyroid nodules, the number of thyroid nodules, and the number of TI-RADS 1, TI-RADS 2, and TI-RADS 4 nodules increased in patients with acromegaly. There was no significant difference between acromegaly disease activity and thyroid nodule frequency, number of thyroid nodules, and TI-RADS classifications.

Comparison Between DEXA and Finite Element Studies in the Long-Term Bone Remodeling of an Anatomical Femoral Stem

2009 ◽  
Vol 131 (4) ◽  
Author(s):  
A. Herrera ◽  
J. J. Panisello ◽  
E. Ibarz ◽  
J. Cegoñino ◽  
J. A. Puértolas ◽  
...  
Keyword(s):  
Finite Element ◽  
Bone Density ◽  
Bone Mass ◽  
Simulation Model ◽  
Load Transfer ◽  
Fe Simulation ◽  
Femoral Stem ◽  
Mineral Density ◽  
Biomechanical Behavior

The implantation of a cemented or cementless femoral stem changes the physiological load transfer on the femur producing an effect on the bone called adaptative remodeling. The patterns of this remodeling are attributed to mechanical and biological factors, and those changes in bone mineral density have been determined in long-term densitometry studies. This technique has proved to be a useful tool able to quantify small changes in bone density in different femoral areas, and it is considered to be ideal for long-term studies. On the other hand, the finite element (FE) simulation allows the study of the biomechanical changes produced in the femur after the implantation of a femoral stem. The aim of this study was to contrast the findings obtained from a 5 year follow-up densitometry study that used a newly designed femoral stem (73 patients were included in this study), with the results obtained using a finite element simulation that reproduces the pattern of load transfer that this stem causes on the femur. In this study we have obtained a good comparison between the results of stress of FE simulation and the bone mass values of the densitometry study establishing a ratio between the increases in stress (%) versus the increases in bone density (%). Hence, the changes in bone density in the long term, compared with the healthy femur, are due to different load transfers after stem implantation. It has been checked that in the Gruen zone 7 at 5 years, the most important reduction in stress (7.85%) is produced, which coincides with the highest loss of bone mass (23.89%). Furthermore, the simulation model can be used with different stems with several load conditions and at different time periods to carry out the study of biomechanical behavior in the interaction between the stem and the femur, explaining the evolution of bone density in accordance to Wolff’s law, which validates the simulation model.

Plasma Calcitonin in Paget's Disease of Bone

1977 ◽  
Vol 52 (3) ◽  
pp. 329-332 ◽  
Author(s):  
J. A. Kanis ◽  
G. Heynen ◽  
R. J. Walton
Keyword(s):  
Alkaline Phosphatase ◽  
Plasma Levels ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Paget's Disease Of Bone ◽  
Control Subjects ◽  
Plasma Alkaline Phosphatase ◽  
And Control ◽  
Age And Sex

1. Plasma levels of immunoreactive calcitonin were measured in 22 patients with untreated Paget's disease of bone and in 22 control subjects matched for age and sex. 2. No significant differences in plasma calcitonin were found between patients and control subjects, and hormone levels did not correlate significantly with activity of plasma alkaline phosphatase. 3. These results suggest that Paget's disease of bone is not due to deficient secretion of endogenous calcitonin.

scholarly journals Bone Formation Markers in Adults with Mild Osteogenesis Imperfecta

2007 ◽  
Vol 53 (6) ◽  
pp. 1109-1114 ◽  
Author(s):  
Tim Cundy ◽  
Anne Horne ◽  
Mark Bolland ◽  
Greg Gamble ◽  
James Davidson
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Formation ◽  
Bone Mass ◽  
Osteogenesis Imperfecta ◽  
Plasma Concentrations ◽  
Bone Alkaline Phosphatase ◽  
Type I ◽  
Low Bone Mass ◽  
Bone Formation Markers ◽  
Discriminant Ability

Abstract Background: Plasma concentrations of procollagen peptides are decreased in osteogenesis imperfecta (OI), whereas other bone formation markers may be increased. We examined the utility of combining these markers in the diagnosis of OI in adults. Methods: We measured plasma concentrations of procollagen-1 N-peptide (P1NP), osteocalcin, and bone alkaline phosphatase in 24 patients with nondeforming OI, 25 patients with low bone mass due to other causes, and 38 age- and sex-matched controls. The discriminant ability of various test combinations was assessed by the construction of ROC curves. Results: The median (range) ratio of osteocalcin to P1NP was significantly greater in patients with type I OI [1.75 (0.80–3.86)] than in controls [0.59 (0.34–0.90)] and patients with other causes of low bone mass [0.48 (0.05–1.38); P &lt;0.0001]. This ratio allowed nearly complete differentiation between healthy controls and patients with type I OI, but not patients with type IV OI. With a cutoff of 0.97 for osteocalcin:P1NP, the sensitivity and specificity were maximized at 95% (95% CI 76%–100%) and 88% (69%–97%), respectively, for patients with other causes of low bone mass vs those with type I OI only. For patients with other causes of low bone mass vs all OI patients, sensitivity and specificity were 83% (63%–95%) and 88% (69%–97%), respectively. The addition of bone alkaline phosphatase data did not improve the discriminant ability of the osteocalcin:P1NP ratio. Conclusions: The osteocalcin:P1NP ratio is a sensitive and specific test for type I OI in adults, but it has less utility in the diagnosis of other types of nondeforming OI.

Altered Bone and Mineral Metabolism in Patients Treated with Imatinb.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4668-4668
Author(s):  
Ellin Berman ◽  
Maria Nicolaides ◽  
Nicolas Sauter ◽  
Suzanne Chanel ◽  
Brianne Wilson ◽  
...  
Keyword(s):  
Vitamin D ◽  
Alkaline Phosphatase ◽  
Bone Formation ◽  
Mineral Metabolism ◽  
Fractional Excretion ◽  
Bone Alkaline Phosphatase ◽  
Hypophosphatemic Rickets ◽  
Common Side Effect ◽  
Time Interval ◽  
Low Levels

Abstract Imatinib is a tyrosine kinase that effectively inhibits the bcr-abl fusion protein in Philadelphia (Ph) chromosome positive CML and c-kit, which is overexpressed in gastrointestinal stomal tumors (GIST). We identified a group of patients treated with Imatinib at Memorial Hospital who developed low phosphate (PO4) levels and studied metabolic bone and mineral parameters associated with this finding. A total of 61 patients who received a prescription for Imatinib from the hospital pharmacy were screened to determine whether a PO4 level had ever been drawn. Of these, 26 had at least one PO4 level, and 10 of these (38%) had a low value (&lt;2.5 mg/dL).Patients samples were then studied for calcium (Ca++), parathyroid horme (PTH), 25-(OH)-vitamin D and 1,25-(OH)2-vitamin D, as well as serum markers of bone formation (bone alkaline phosphatase and osteocalcin) and resorption (N-telopeptide). Urinary calcium and PO4 were measured and fractional excretion of PO4 (FEPO4) was calculated as well. A total of 10 patients (8 men, 2 women) median age 47 (range 32–60) with CML (n=8) or GIST (n=2) were studied. The median time interval between diagnosis and starting Imatinib was 3.8 mos (range 0.4–161) and the median interval between starting Imatinib and first low PO4 was 3.9 mos (range 0.3–23). Results of Bone Metabolism UPIN PO4 Calcium PTH FePO4 N-Telopep Osteocalcin Bone Alk phos ND: Not done: NMA: No measurable amount; 25-(OH)-vitD levels were low to mid-normal, and 1,25-(OH)2 vit D levels were typically borderline high or elevated (data not shown) 2.5–4.2mg/dL 8.5–10.5mg/dL 10–65pg/mL &lt; 5% 5.5–19.5nM 3.1–12.7ng/ml 15–441U/L 1 2.0 8.7 84 25 ND ND ND 2 1.7 8.6 97 24 ND ND ND 3 2.3 9.4 68 44 ND ND ND 4 1.9 9.5 84 25 7.1 3.7 18 5 1.8 8.9 85 17 6.2 NMA 15 6 2.1 9.3 83 23 ND ND ND 7 1.7 8.7 57 16 5.6 NMA 17 8 1.3 8.1 136 38 10.1 NMA 53 9 2.3 9.2 81 10 13.4 NMA 17 10 2.1 8.9 41 17 5.8 2.6 15 Two patients who temporarily stopped Imatinib had normalization of their PO4, which again decreased upon resumption of the drug. In summary, patients who develop hypophosphatemia while on Imatinib have low-normal to mildly low serum Ca++ but elevated PTH, elevated FEPO4, low-normal levels of N-telopeptide, very low levels of osteocalcin, and low levels of bone alkaline phosphatase. These values distinctly differ from patients with either inherited or tumor induced forms of hypophosphatemia with renal phosphate wasting (X-linked hypophosphatemic rickets, adult dominant hypophosphatemic rickets, and tumor-induced osteomalacia). Our preliminary data suggest that in some patients, Imatinib results in profound suppression of bone formation and mild suppression of bone resorption, leading to a state of hypodynamic bone remodeling. Further investigation is planned comparing patients on Imatinib who become hypophosphatemic and those who do not. Better characterization of bone and mineral metabolism in this setting is important for several reasons: (1) myalgias from Imatinb, a common side effect, may be related to hyphophosphatemia and correctible with appropriate replacement; (2) while these data are premature, it is conceivable that Imatinib might be useful in situations where suppression of bone formation and turnover is desirable, such as in osteoblastic bone metastases, osteopetrosis, and other diseases of abnormally increased bone formation.

Abnormal Bone Mineral Metabolism after Long-Term Anticonvulsant Treatment

1994 ◽  
Vol 28 (1) ◽  
pp. 47-48 ◽  
Author(s):  
Christopher P. Alderman ◽  
Catherine L. Hill
Keyword(s):  
Alkaline Phosphatase ◽  
Serum Concentration ◽  
Bone Mineral ◽  
Serum Alkaline Phosphatase ◽  
Mineral Metabolism ◽  
Bone Mineral Metabolism ◽  
Hepatic Microsomal Enzyme ◽  
Grand Mal ◽  
Anticonvulsant Treatment

OBJECTIVE: To present a case of anticonvulsant-induced disturbances of bone mineral metabolism associated with long-term phenytoin treatment. CASE SUMMARY: An 87-year-old woman was hospitalized with generalized acroparesthesia. Her medical history was significant for grand mal epilepsy, which had been treated with phenytoin for more than ten years. On admission she was found to be hypocalcemic, and her alkaline phosphatase concentration was markedly elevated. DISCUSSION: Further investigations revealed that the patient's serum concentration of 25-hydroxycalciferol was well below the expected range. Phenytoin treatment was withdrawn, and calcitriol supplementation commenced. Ten weeks later she was normocalcemic, and the calcitriol dosage was reduced. Radiologic investigations at this time revealed an ununited hip fracture, as well as widespread evidence of bone demineralization. CONCLUSIONS: Minor elevations of liver enzymes observed in association with anticonvulsant treatment may reflect hepatic microsomal enzyme induction. Marked elevation of serum alkaline phosphatase, particularly when seen in concert with hypocalcemia, may be markers of anticonvulsant-induced bone disease. Under these circumstances, further radiologic investigations and measurement of the vitamin D serum concentration should be undertaken.

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