Effect of alcohol ingestion on bone and mineral metabolism in rats

1980 ◽  
Vol 238 (6) ◽  
pp. E507-E510 ◽  
Author(s):  
D. T. Baran ◽  
S. L. Teitelbaum ◽  
M. A. Bergfeld ◽  
G. Parker ◽  
E. M. Cruvant ◽  
...  
Keyword(s):  
Mineral Metabolism ◽  
Serum Levels ◽  
Urinary Calcium ◽  
Alcohol Ingestion ◽  
Ethanol Administration ◽  
Calcium Excretion ◽  
Hydroxyvitamin D ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Circulating Levels

Chronic ethanol administration to growing rats for 56 days resulted in circulating levels of 140 mg/dl, approximating concentrations that characterize alcoholic intoxication in man. This degree of alcohol ingestion, although without gross or histological effect on the liver or testicles, was attended by decreased trabecular bone volume despite a normal rate of skeletal mineralization as measured by time-spaced tetracycline labeling. Concomitant serum levels of calcium, phosphate, magnesium, creatinine, glutamic oxalacetic transaminase, alkaline phosphatase, testosterone, and 25-hydroxyvitamin D were normal. Although alcohol treatment was associated with a significant decrease in urinary calcium excretion, it had no effect on phosphate excretion nor on its renal tubular reabsorption. The data reveal that circulating levels of alcohol that do not result in hepatic or testicular injury are toxic for bone.

Contrasting effects of intravenous and oral etidronate on vitamin D metabolism in man

1988 ◽  
Vol 74 (1) ◽  
pp. 101-106 ◽  
Author(s):  
P. J. Lawson-Matthew ◽  
D. F. Guilland-Cumming ◽  
A. J. P. Yates ◽  
R. G. G. Russell ◽  
J. A. Kanis
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Progressive Increase ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Renal Tubular Reabsorption ◽  
Early Effects ◽  
Renal Tubular

1. We have studied the early effects of intravenously and orally administered etidronate on vitamin D metabolism and indirect indices of calcium and skeletal metabolism in 17 patients with Paget's disease of bone. 2. Administration of etidronate by mouth (700–1400 mg daily for 1 month) or its intravenous infusion (300 mg daily for 5 days) decreased bone resorption as judged by urinary excretion of hydroxyproline and significantly increased renal tubular reabsorption of phosphate. No significant change in serum activity of alkaline phosphatase was noted with either regimen. 3. When etidronate was given by mouth there was a progressive decrease in fasting urinary calcium excretion and a rise in serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. In contrast, intravenous etidronate decreased serum values of l,25-(OH)2D3 and was associated with a progressive increase in fasting calcium excretion, suggesting a decrease in the net influx of calcium from the extracellular compartment to bone. Significant inverse correlations were noted between the change induced in 1,25-(OH)2D3 values at 2 weeks and the changes in serum calcium, phosphate and fasting urinary excretion of calcium. 4. These observations suggest that the different effects of intravenous and oral etidronate on l,25-(OH)2D3 values are a consequence of different doses of etidronate used and the different effects of these regimens on the accretion of calcium into bone.

CA 15.3 with Urinary Calcium Excretion is Useful in the Diagnosis and Monitoring of Bone Metastases from Breast Cancer

1993 ◽  
Vol 8 (4) ◽  
pp. 208-214
Author(s):  
G.C. Yadav ◽  
A. Rao ◽  
M.M. Motawy ◽  
N. Safadi ◽  
M. Jameel Ahmed
Keyword(s):  
Breast Cancer ◽  
Bone Metastasis ◽  
Bone Metastases ◽  
Serum Levels ◽  
Urinary Calcium ◽  
Response To Therapy ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Diagnostic Efficacy ◽  
Ca 15.3

Serum levels of breast carcinoma antigen (CA 15.3) and urinary calcium excretion (UCa) were determined in 73 patients with breast cancer: 36 without bone metastases (stage I-IV) and 37 with bone metastases. The patients in the latter group were further investigated at 2,4 and 6 months from the start of treatment. Both markers showed significant elevations in the group with bone metastases (CA 15.3: P = 1.0×10–6, UCa: P = 8.6×10–9). The bone metastasis index (BMI), which represents the combination of the markers, had better diagnostic efficacy (90%) than CA 15.3 alone (84%) or UCa alone (82%). During treatment of bone metastasis, the longitudinal levels of the markers showed a highly significant association with the therapeutic response assessed by the UICC criteria. For identifying progression of disease, the diagnostic efficacy of CA 15.3, UCa and a combination of both, the so-called Biochemical Index of Response (BIR), was 65%, 70% and 79%, respectively, at two months and 89%, 84% and 92% at four months. Application of the tandem, CA 15.3 with UCa, was very useful for the detection of bone metastases and the prediction of response to therapy.

Thyroparathyroidectomy exaggerates calciuric action of ammonium chloride in rats

1984 ◽  
Vol 246 (1) ◽  
pp. F54-F58 ◽  
Author(s):  
A. Goulding ◽  
D. R. Campbell
Keyword(s):  
Bone Resorption ◽  
Ammonium Chloride ◽  
Chronic Administration ◽  
Urinary Calcium ◽  
Urinary Hydroxyproline ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Hydroxyproline Excretion ◽  
Calcium Loss ◽  
Intact Rats

The effects of chronic ammonium chloride (NH4Cl) administration on urinary calcium, urinary hydroxyproline, and calcium and phosphate balances were studied in intact and thyroparathyroidectomized (TPTX) rats. NH4Cl (2 g/100 g diet) was administered for 16 days to growing rats consuming a low calcium (0.1% Ca) diet. NH4Cl increased urinary calcium and hydroxyproline. NH4Cl caused greater urinary calcium loss in TPTX than in intact rats, but hydroxyproline excretion in these groups was similar. Compensatory increases in net alimentary absorption of calcium and phosphate occurred in intact but not in TPTX rats. Urinary cAMP was depressed by thyroparathyroidectomy but was unaffected by NH4Cl. It is concluded that NH4Cl depresses renal tubular reabsorption of calcium and increases bone resorption in the presence and absence of the thyroid and parathyroid glands. However, our results suggest that parathyroid hormone plays an important calcium-sparing role, while calcitonin may act to limit the rate of bone resorption, in intact rats during chronic administration of NH4Cl.

Urinary calcium excretion in severe preeclampsia and eclampsia

2006 ◽  
Vol 44 (1) ◽  
Author(s):  
Metin Ingec ◽  
Hakan Nazik ◽  
Sedat Kadanali
Keyword(s):  
Serum Levels ◽  
Urinary Calcium ◽  
Severe Preeclampsia ◽  
Urinary Calcium Excretion ◽  
Control Group ◽  
Calcium Excretion ◽  
Total Calcium ◽  
Group 4 ◽  
Mild Preeclampsia ◽  
Group 2

AbstractUrinary calcium levels in women with mild preeclampsia, severe preeclampsia and eclampsia were evaluated in this study. We collected 24-h urine samples from 35 mild preeclamptic (Group 1), 30 severe preeclamptic (Group 2), and 17 eclamptic patients (Group 3). The control group (Group 4) consisted of 35 healthy pregnant women. Serum levels of total calcium and creatinine, and urinary calcium were measured. These values were compared in the four groups. The mean maternal age and parity were similar in all groups. There were no statistically significant differences in the serum levels of total calcium and creatinine (p>0.05). Urinary calcium excretion in patients with preeclampsia and eclampsia was significantly lower than in controls (p<0.0001). Urinary calcium levels between mild preeclampsia and severe pre-eclampsia, and severe preeclampsia and eclampsia were similar (p>0.05), but were lower in eclampsia than in mild preeclampsia (p<0.05). In conclusion, urinary calcium excretion is reduced in patients with severe preeclampsia or eclampsia. However, the decrease in urinary calcium excretion cannot be used to identify the severity of preeclampsia, or to predict impending eclampsia.

scholarly journals Recombinant human parathyroid hormone (1–84) is effective in CASR-associated hypoparathyroidism

2020 ◽  
Vol 183 (6) ◽  
pp. K13-K21
Author(s):  
Colin Patrick Hawkes ◽  
Dorothy I Shulman ◽  
Michael A Levine
Keyword(s):  
Parathyroid Hormone ◽  
Traditional Approach ◽  
Calcium Supplementation ◽  
Case Series ◽  
Calcium Sensitivity ◽  
Serum Levels ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Human Parathyroid Hormone

Introduction Gain-of-function mutations in the CASR gene cause Autosomal Dominant Hypocalcemia Type 1 (ADH1), the most common genetic cause of isolated hypoparathyroidism. Subjects have increased calcium sensitivity in the renal tubule, leading to increased urinary calcium excretion, nephrocalcinosis and nephrolithiasis when compared with other causes of hypoparathyroidism. The traditional approach to treatment includes activated vitamin D but this further increases urinary calcium excretion. Methods In this case series, we describe the use of recombinant human parathyroid hormone (rhPTH)1–84 to treat subjects with ADH1, with improved control of serum and urinary calcium levels. Results We describe two children and one adult with ADH1 due to heterozygous CASR mutations who were treated with rhPTH(1–84). Case 1 was a 9.4-year-old female whose 24-h urinary calcium decreased from 7.5 to 3.9 mg/kg at 1 year. Calcitriol and calcium supplementation were discontinued after titration of rhPTH(1–84). Case 2 was a 9.5-year-old male whose 24-h urinary calcium decreased from 11.7 to 1.7 mg/kg at 1 year, and calcitriol was also discontinued. Case 3 was a 24-year-old female whose treatment was switched from multi-dose teriparatide to daily rhPTH(1–84). All three subjects achieved or maintained target serum levels of calcium and normal or improved urinary calcium levels with daily rhPTH(1–84) monotherapy. Conclusions We have described three subjects with ADH1 who were treated effectively with rhPTH(1–84). In all cases, hypercalciuria improved by comparison to treatment with conventional therapy consisting of calcium supplementation and calcitriol.

A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men

1997 ◽  
Vol 83 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
Noriko Ashizawa ◽  
Rei Fujimura ◽  
Kumpei Tokuyama ◽  
Masashige Suzuki
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Bone Resorption ◽  
Resistance Exercise ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Osteoclastic Bone Resorption ◽  
Calcium Excretion ◽  
Repetition Maximum ◽  
Renal Tubular

Ashizawa, Noriko, Rei Fujimura, Kumpei Tokuyama, and Masashige Suzuki. A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men. J. Appl. Physiol. 83(4): 1159–1163, 1997.—Metabolic acidosis increases urinary calcium excretion in humans as a result of administration of ammonium chloride, an increase in dietary protein intake, and fasting-induced ketoacidosis. An intense bout of exercise, exceeding aerobic capacity, also causes significant decrease in blood pH as a result of increase in blood lactate concentration. In this study we investigated changes in renal calcium handling, plasma parathyroid hormone concentration, and osteoclastic bone resorption after a single bout of resistance exercise. Ten male subjects completed a bout of resistance exercise with an intensity of 60% of one repetition maximum for the first set and 80% of one repetition maximum for the second and third sets. After exercise, blood and urine pH shifted toward acidity and urinary calcium excretion increased. Hypercalciuria was observed in the presence of an increased fractional calcium excretion and an unchanged filtered load of calcium. Therefore, the observed increase in urinary calcium excretion was due primarily to decrease in renal tubular reabsorption of calcium. Likely causes of the increase in renal excretion of calcium are metabolic acidosis itself and decreased parathyroid hormone. When urinary calcium excretion increased, urinary deoxypyridinoline, a marker of osteoclastic bone resorption, decreased. These results suggest that 1) strenuous resistance exercise increased urinary calcium excretion by decreasing renal tubular calcium reabsorption, 2) urinary calcium excretion increased independently of osteoclast activation, and 3) the mechanism resulting in postexercise hypercalciuria might involve non-cell-mediated physicochemical bone dissolution.

scholarly journals Bone and Mineral Metabolism in Patients with Primary Aldosteronism

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Luigi Petramala ◽  
Laura Zinnamosca ◽  
Amina Settevendemmie ◽  
Cristiano Marinelli ◽  
Matteo Nardi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Primary Aldosteronism ◽  
Mineral Metabolism ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Mineral Density ◽  
Lower Serum ◽  
Functional Link ◽  
The Impact

Primary aldosteronism represents major cause of secondary hypertension, strongly associated with high cardiovascular morbidity and mortality. Aldosterone excess may influence mineral homeostasis, through higher urinary calcium excretion inducing secondary increase of parathyroid hormone. Recently, in a cohort of PA patients a significant increase of primary hyperparathyroidism was found, suggesting a bidirectional functional link between the adrenal and parathyroid glands. The aim of this study was to evaluate the impact of aldosterone excess on mineral metabolism and bone mass density. In 73 PA patients we evaluated anthropometric and biochemical parameters, renin-angiotensin-aldosterone system, calcium-phosphorus metabolism, and bone mineral density; control groups were 73 essential hypertension (EH) subjects and 40 healthy subjects. Compared to HS and EH, PA subjects had significantly lower serum calcium levels and higher urinary calcium excretion. Moreover, PA patients showed higher plasma PTH, lower serum 25(OH)-vitamin D levels, higher prevalence of vitamin D deficiency (65% versus 25% and 25%;P<0.001), and higher prevalence of osteopenia/osteoporosis (38.5 and 10.5%) than EH (28% and 4%) and NS (25% and 5%), respectively. This study supports the hypothesis that bone loss and fracture risk in PA patients are potentially the result of aldosterone mediated hypercalciuria and the consecutive secondary hyperparathyroidism.

Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis

2007 ◽  
Vol 292 (1) ◽  
pp. F66-F75 ◽  
Author(s):  
Elaine M. Worcester ◽  
Daniel L. Gillen ◽  
Andrew P. Evan ◽  
Joan H. Parks ◽  
Katrina Wright ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Serum Magnesium ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Stone Formers ◽  
Calcium Reabsorption ◽  
Renal Tubular ◽  
Filtered Load

Idiopathic hypercalciuria (IH) is common among calcium stone formers (IHSF). The increased urinary calcium arises from increased intestinal absorption of calcium, but it is unclear whether increased filtered load or decreased renal tubular reabsorption of calcium is the main mechanism for the increased renal excretion. To explore this question, 10 IHSF and 7 normal subjects (N) were studied for 1 day. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, and calories. Fasting and fed, ultrafiltrable calcium levels, and filtered load of calcium did not differ between N and IHSF. Urine calcium rose with meals, and fractional reabsorption fell in all subjects, but the change was significantly higher in IHSF. The changes in calcium excretion were independent of sodium excretion. Serum parathyroid hormone levels did not differ between N and IHSF, and they could not account for the greater fall in calcium reabsorption in IHSF. Serum magnesium and phosphorus levels in IHSF were below N throughout the day, and tubule phosphate reabsorption was lower in IHSF than N after meals. The primary mechanism by which kidneys ferry absorbed calcium into the urine after meals is via reduced tubule calcium reabsorption, and IHSF differ from N in the magnitude of the response. Parathyroid hormone is not likely to be a sufficient explanation for this difference.

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