Heath / Marx Calcium Disorders

Butterworths International Medical Reviews: Clinical Endocrinology
1. Auflage 2013
ISBN: 978-1-4831-9210-9
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 298 Seiten

Clinical Endocrinology 2: Calcium Disorders presents an extensive examination of the treatment of postmenopausal and senile osteoporosis. It discusses the acquired disorders of vitamin D metabolism. It addresses the prevention of osteoporosis. Some of the topics covered in the book are the classification of rickets; mechanisms of homeostasis; transepithelial transport of phosphate anion; definition of mendelian rickets; treatment of; classification of androgens and synthetic anabolic agents; and assessment of parathyroid function. The measurement of parathyroid hormone is fully covered. An in-depth account of the indirect assessment of parathyroid activity is provided. The acquired disorders of Vitamin D metabolism are completely presented. A chapter is devoted to the aetiological views of rickets and osteomalacia. Another section focuses on the treatment and prevention of rickets and osteomalacia. The analysis of renal osteodystrophy, hypercalcemia, and familial hypocalciuric hypercalcemia are briefly covered. The book can provide useful information to doctors, endocrinologists, students, and researchers.

Autoren/Hrsg.

Heath, David

Marx, Stephen J.

Inhaltsverzeichnis

1;Front Cover;1
2;Calcium Disorders;4
3;Copyright Page;5
4;Table of Contents;12
5;Preface;6
6;List of Contributors;8
7;Chapter 1. Hereditary rickets;14
7.1;INTRODUCTION;14
7.2;THE COMPONENTS OF MINERAL METABOLISM: THE EVOLUTIONARY PERSPECTIVE;15
7.3;CLASSIFICATION OF RICKETS;17
7.4;MECHANISMS OF HOMEOSTASIS;18
7.5;MENDELIAN RICKETS/OSTEOMALACIA;28
8;Chapter 2. The prevention of osteoporosis;60
8.1;LOCALIZED OSTEOPOROSIS;63
8.2;GENERALIZED OSTEOPOROSIS;66
8.3;References;75
9;Chapter 3. The treatment of postmenopausal and senile osteoporosis;82
9.1;INTRODUCTION;82
9.2;CALCIUM;82
9.3;ESTROGEN;83
9.4;ANDROGENS AND SYNTHETIC ANABOLIC AGENTS;86
9.5;PROGESTOGENS;87
9.6;FLUORIDE;87
9.7;VITAMIN D AND VITAMIN D METABOLITES;89
9.8;CALCITONIN;90
9.9;DIPHOSPHONATES;91
9.10;PARATHYROID HORMONE;92
9.11;INORGANIC PHOSPHATE;92
9.12;GROWTH HORMONE;93
9.13;AN APPROACH TO TREATMENT OF THE INDIVIDUAL PATIENT;93
9.14;References;96
10;Chapter 4. The assessment of parathyroid function;105
10.1;INTRODUCTION;105
10.2;PARATHYROID HORMONE;105
10.3;MEASUREMENT OF PARATHYROID HORMONE;108
10.4;INDIRECT ASSESSMENT OF PARATHYROID ACTIVITY;110
10.5;PHOSPHATE EXCRETION;110
10.6;CALCIUM EXCRETION;111
10.7;CYCLIC AMP EXCRETION;112
10.8;STEROID SUPPRESSION TEST;113
10.9;MULTIVARIANT ANALYSIS;113
10.10;PARATHYROID FUNCTION IN HYPERCALCAEMIA;113
10.11;PARATHYROID FUNCTION IN CHRONIC RENAL FAILURE;115
10.12;PARATHYROID FUNCTION IN HYPOCALCAEMIA;116
10.13;CONCLUSIONS;120
10.14;Acknowledgements;120
10.15;References;120
11;Chapter 5. Bisphosphonates;127
11.1;INTRODUCTION;127
11.2;BONE SCANNING;129
11.3;MEDICAL USES OF BISPHOSPHONATES;129
11.4;OTHER BISPHOSPHONATES;133
11.5;References;134
12;Chapter 6. Acquired disorders of vitamin D metabolism;138
12.1;INTRODUCTION;138
12.2;AETIOLOGICAL VIEWS OF RICKETS AND OSTEOMALACIA;138
12.3;THE EPIDEMIOLOGY OF RICKETS AND OSTEOMALACIA;141
12.4;THE PREVALENCE OF RICKETS AND OSTEOMALACIA IN THE PAST;147
12.5;RISK FACTORS FOR THE DEVELOPMENT OF RICKETS AND OSTEOMALACIA;147
12.6;THE ROLE OF DIETARY FACTORS AND DAYLIGHT OUTDOOR EXPOSURE IN THE AETIOLOGY OF ASIAN RICKETS;152
12.7;ENDOGENOUS RISK FACTORS FOR THE DEVELOPMENT OF RICKETS AND OSTEOMALACIA;155
12.8;POSSIBLE MECHANISMS INVOLVED IN THE AETIOLOGY OF RICKETS AND OSTEOMALACIA;155
12.9;THE RELATIONSHIP OF GASTROINTESTINAL DISEASE TO VITAMIN D DEFICIENCY;156
12.10;THE TREATMENT OF RICKETS AND OSTEOMALACIA;157
12.11;THE PREVENTION OF RICKETS AND OSTEOMALACIA;158
12.12;CONCLUSION;158
12.13;References;159
13;Chapter 7. Renal osteodystrophy;164
13.1;INTRODUCTION;164
13.2;SKELETAL PATHOLOGY IN RENAL OSTEODYSTROPHY;164
13.3;PATHOPHYSIOLOGY OF ALTERED CALCIUM HOMEOSTASIS;166
13.4;CLINICAL FEATURES OF RENAL OSTEODYSTROPHY;171
13.5;BIOCHEMICAL FEATURES OF RENAL OSTEODYSTROPHY;180
13.6;RADIOGRAPHIC FEATURES OF RENAL OSTEODYSTROPHY;182
13.7;MANAGEMENT OF RENAL OSTEODYSTROPHY;188
13.8;References;195
14;Chapter 8. Asymptomatic hypercalcemia and primary hyperparathyroidism;202
14.1;STATEMENT OF THE PROBLEM;202
14.2;DEFINITIONS;203
14.3;THE PROBLEM OF CALCIUM MEASUREMENT;204
14.4;THE DIFFERENTIAL DIAGNOSIS OF HYPERCALCEMIA;206
14.5;DIAGNOSTIC TESTING IN ASYMPTOMATIC HYPERCALCEMIA;208
14.6;EPIDEMIOLOGY, AND THE BIOLOGICAL AND MEDICAL CONSEQUENCES OF PRIMARY HYPERPARATHYROIDISM;213
14.7;THERAPEUTIC DECISIONS IN ASYMPTOMATIC HYPERCALCEMIA;219
14.8;COST-BENEFIT CONSIDERATIONS IN DIAGNOSIS AND TREATMENT OF ASYMPTOMATIC PRIMARY HYPERPARATHYROIDISM;221
14.9;AN ARGUMENT FOR SURGICAL THERAPY IN MOST CASES OF WELL-DOCUMENTED PRIMARY HYPERPARATHYROIDISM;222
14.10;QUESTIONS IN NEED OF ANSWERS;223
14.11;SUMMARY;224
14.12;References;225
15;Chapter 9. Familial hypocalciuric hypercalcemia;230
15.1;INTRODUCTION;230
15.2;RECOGNITION AND CLINICAL FEATURES OF FAMILIAL HYPOCALCIURIC HYPERCALCEMIA;230
15.3;RADIOGRAPHIC FEATURES;232
15.4;COMPOSITION OF SERUM;232
15.5;URINARY EXCRETION OF CALCIUM AND CREATININE;233
15.6;PARATHYROID FUNCTION;234
15.7;RESPONSE TO PARATHYROID SURGERY;235
15.8;GENETICS;236
15.9;EPIDEMIOLOGY;236
15.10;PATHOPHYSIOLOGY;237
15.11;DIAGNOSIS;239
15.12;RELATION TO THE FAMILIAL MULTIPLE ENDOCRINE NEOPLASIA SYNDROMES;240
15.13;MANAGEMENT;241
15.14;SUMMARY;242
15.15;References;243
16;Chapter 10. Hypercalcaemia of malignancy;246
16.1;MALIGNANT STATES ASSOCIATED WITH HYERCALCAEMIA;246
16.2;HYPERCALCAEMIA ASSOCIATED WITH SPECIFIC NEOPLASTIC CONDITIONS;249
16.3;THE MECHANISM OF HYPERCALCAEMIA IN MALIGNANCY;251
16.4;BIOCHEMICAL CHANGES IN MALIGNANT HYPERCALCAEMIA;255
16.5;MANAGEMENT OF MALIGNANT HYPERCALCAEMIA;255
16.6;References;257
17;Chapter 11. Hypocalcemia and other abnormalities of mineral homeostasis during the neonatal period;261
17.1;INTRODUCTION AND IN UTERO CONDITIONS;261
17.2;NORMAL POSTNATAL CHANGES;263
17.3;EARLY NEONATAL HYPOCALCEMIA;265
17.4;LATE NEONATAL HYPOCALCEMIA;269
17.5;HYPOMINERALIZATION AND LATE-LATE HYPOCALCEMIA;272
17.6;SUMMARY;282
17.7;References;283
18;Index;290

Leseproben

2 The prevention of osteoporosis
J.M. Aitken Publisher Summary
This chapter describes the prevention of osteoporosis, that is, the most common abnormality of the adult skeleton. The diagnosis of osteoporosis initially rests upon establishing adequate radiological criteria to substantiate a deficiency of bone substance. The appearance of radio translucency of the skeleton is not enough and the diagnosis must be backed up by a quantitative measurement at an appropriate skeletal site. When osteoporosis is generalized, bone mass measurements on peripheral bone sites, where cortical bone predominates, are preferable to measurements on the axial skeleton, where there is a higher proportion of trabecular bone, because the former are amenable to a much greater degree of precision and reproducibility. Hence, trabecular bone, with its high metabolic activity, is lost to a much greater extent than cortical bone in the early stages of generalized skeletal wasting. However, in spite of this initial lack of synchronism between bone loss at trabecular and cortical sites, there is a surprisingly good in vitro correlation in the aging population between measurements of bone mass at sites of widely varying structural composition. The use of synthetic anabolic steroids, such as androgens and anabolic, are used for the treatment of osteoporosis, but they are considerably less effective than oestrogens in the prevention of further spinal collapse in postmenopausal women. However, the prevention of osteoporosis caused by sex hormone deficiency could be theoretically simple if all postmenopausal women are to be assessed for sex hormone replacement therapy. Osteoporosis is the most common abnormality of the adult skeleton and this abnormality becomes increasingly prevalent as people age. Osteoporotic bone is structurally weak and prone to fracture as a result of relatively trivial trauma. The female skeleton becomes osteoporotic much more readily than the male skeleton and after middle age Colles' fracture, vertebral body compression and fracture of the femoral neck occur at an almost exponential rate in the ageing female population. It would therefore be a distinct socioeconomic advantage to be able to prevent the development of osteoporosis and thereby remove a potential cause of considerable suffering in the elderly. However, in order to be able to prevent osteoporosis it is important to know how osteoporosis develops and the way in which different variables may affect this. The term osteoporosis is interpreted in different ways by different people, but for the purpose of this chapter it will be defined as a significant reduction in skeletal mass. This reduction in skeletal mass may be localized or generalized, but the bony tissue present is assumed to show no qualitative differences from normal bone. A significant reduction in bone mass is defined by a value more than 2 SD below the mean value found in a normal population of either men or women at a time when skeletal mass is at its peak value. In both men and women skeletal mass reaches this peak value somewhere between the ages of 30 and 40 years. This sort of information has in the past been obtained from cross-sectional population surveys and the results of one of these is shown in Figure 2.1. Figure 2.1 Relationship between metacarpal mineral content (SAE) and age in women. Mean ± 2SD (3rd–97th percentile). (After Smith et al.89) In this survey the parameter of bone mass was the Standardized Aluminium Equivalent (SAE) measured at the midpoint of the third metacarpal from a plain X-ray of the hand alongside an aluminium step wedge12. Using this method for measuring bone mass, the critical value 2 SD below the mean at the age of 35 years in women is 2.8mmA1 cm–1, and hence any woman with a SAE of 2.8mmA1cm–1 or less would be said to have osteoporosis. Although this definition is somewhat empirical it has been shown that the prevalence of vertebral crush fractures increases progressively as the SAE falls further below this critical value88. Similar observations have been made by other investigators using different methods and different skeletal reference sites36. Johnston et al.48 studied 526 normal Caucasian women using a ?-ray photon absorptiometric technique to measure bone mass at the midpoint of the radius. In their study a value 2 SD below the mean at the age of 35 years was found to be about 0.70 g bone mineral/cm. They found that there was a considerable overlap in the radius bone mass values between women with vertebral crush fractures and those without. However Mazess et al.65 found that a mid-radius bone mineral value of 0.68 g/cm discriminated between 50 white women without evidence of skeletal failure, and 50 white women with spontaneous fractures of the vertebrae, femoral neck or radius. The implicit assumption that osteoporotic bone is qualitatively indistinguishable from normal bone may not necessarily be wholly true, for although the ratio of calcium to phosphorus remains constant as skeletal mass declines, the ratios of calcium to zinc and calcium to magnesium fall both with age and bone mass4 (Figure 2.2), It is therefore quite possible, if one were to look critically at other constituents of osteoporotic bone and compare these with those present in normal bone, that further biochemical differences would be found. Figure 2.2 Relationship between trabecular bone calcium/zinc ratio and age in 12 female () and 16 male (•) cadavers. (After Aitken4) When one uses histomorphometric techniques to study osteoporotic bone obtained from the iliac crest, it is apparent that in about 10% of patients the resorption surfaces and the surface area covered by osteoid are increased. This suggests that in these patients there is increased bone turnover. Likewise, when bone samples from osteoporotic patients are examined after double tetracycline labelling, it has been found that about 37% have a low osteoblastic appositional rate70. Whereas serum calcium and phosphorus concentrations and urinary hydroxyproline excretion are within the normal range in patients with osteoporosis, there is a tendency for these values to be at the upper end of the normal range. Furthermore, using whole body retention of technetium-labelled (99mTc) diphosphonate as a measure of skeletal metabolic activity, patients with osteoporosis as a whole tend to have higher than normal values, although lower than those found in patients with osteomalacia, hyperparathyroidism and Paget’s disease19. In spite of these minor differences, the diagnosis of osteoporosis is still made on the basis of a significantly reduced bone mass in association with normal values for serum calcium, phosphorus and alkaline phosphatase, normal urinary hydroxyproline excretion and normal bone histology using routine laboratory techniques. It is therefore important to exclude all other causes of metabolic bone disease associated with rarefaction of the skeleton including osteomalacia, hyperparathyroidism, multiple myeloma and carcinomatosis, since all these conditions occur with increasing frequency in the ageing population. In patients with these diseases radiotranslucency of the bone may be the result of the underlying condition or, in view of the increasing prevalence of osteoporosis with age, merely coincidental. The diagnosis of osteoporosis initially rests upon establishing adequate radiological criteria to substantiate a deficiency of bone substance. The appearance of radiotranslucency of the skeleton is not enough and the diagnosis must be backed up by a quantitative measurement at an appropriate skeletal site. When osteoporosis is generalized bone mass measurements on peripheral bone sites, where cortical bone predominates, are preferable to measurements on the axial skeleton, where there is a higher proportion of trabecular bone, because the former are amenable to a much greater degree of precision and reproducibility. This is in spite of the fact that not all types of bone share the same degree of metabolic activity, and thus at the inception of a period of generalized bone loss, those parts of the skeleton with the most rapid turnover will be affected to a greater degree before the more slowly metabolizing parts. Hence trabecular bone, with its high metabolic activity, is lost to a much greater extent than cortical bone in the early stages of generalized skeletal wasting. However, in spite of this initial lack of synchronism between bone loss at trabecular and cortical sites, there is a surprisingly good in vitro correlation in the ageing population between measurements of bone mass at sites of widely varying structural composition9. Unfortunately this correlation is not good enough for one to be able to predict bone mass at a critical site, such as a vertebral body, from measurements at a non-critical but easily quantifiable site such as the midshaft of the radius. In this respect Madsen61 found that about 15% of subjects with low in vivo spinal bone mass measurements had normal midshaft radius values. However, serial bone mass measurements at a peripheral site amenable to good reproducibility will give a reliable indication of the progress of generalized skeletal wasting provided that the effects of localized disorders can be excluded. LOCALIZED OSTEOPOROSIS
On occasions osteoporosis is a local...