Hormones and disorders of mineral metabolism:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
2000
|
| Schriftenreihe: | Endocrinology and metabolism clinics of North America
29,3 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XI S., S. 451 - 655 Ill., graph. Darst. |
Internformat
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| 650 | 7 | |a Deficiëntieziekten |2 gtt | |
| 650 | 7 | |a Hormonen |2 gtt | |
| 650 | 4 | |a Hormones | |
| 650 | 2 | |a Maladies de la parathyroïde | |
| 650 | 2 | |a Maladies métaboliques | |
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| 650 | 4 | |a Endocrine glands |x Diseases |x Complications | |
| 650 | 4 | |a Hormones | |
| 650 | 4 | |a Metabolic Diseases | |
| 650 | 4 | |a Metabolism |x Disorders |x Complications | |
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| 650 | 4 | |a Minerals |x metabolism | |
| 650 | 4 | |a Parathyroid Diseases | |
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Datensatz im Suchindex
| _version_ | 1804128190099095552 |
|---|---|
| adam_text | HORMONES AND DISORDERS OF MINERAL METABOLISM
CONTENTS
Preface ix
Gordon J. Strewler
Natural History of Primary Hyperparathyroidism 451
Shonni J. Silverberg
Primary hyperparathyroidism has evolved into a disorder that is
largely asymptomatic. Nevertheless, there is ample evidence of
target organ effects even in asymptomatic patients. Recent data
suggest that the disease is stable in most asymptomatic patients.
Little change is observed in biochemical parameters or bone min¬
eral density over time. A subgroup of asymptomatic patients
shows biochemical evidence of disease progression, although, in
the author s series, no overt clinical complications developed.
Surgical cure is associated with biochemical normalization and
increased bone density.
Primary Hyperparathyroidism: When to Observe and
When to Operate 465
John P. Bilezikian
The decision to operate or not on a patient with primary hyper¬
parathyroidism depends on how the disorder presents clinically.
Symptomatic patients should undergo parathyroid surgery.
Asymptomatic patients may or may not be candidates for surgery
depending on the presence of features of the disease that may
place these patients at increased risk for complications. Recent
observations have expanded the potential indications for parathy¬
roid surgery among those who are asymptomatic. This article
reviews classic and newer indications for surgery, and presents
results of the decision for or against surgery in the context of the
natural history of the disease.
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
Surgical Approaches to Primary Hyperparathyroidism 479
Monica S. Eigelberger and Orlo H. Clark
Primary hyperparathyroidism (HPT) is a common disease that
can be diagnosed with nearly 100% accuracy. Surgical therapy is
the only definitive cure for this disease, and normocalcemia can
be achieved in 95% of patients who are cared for by an experi¬
enced surgeon at initial operation. Although a debate exists re¬
garding the need for surgery in asymptomatic patients, the au¬
thors believe that the benefits of surgery, including improvement
in symptoms and associated complications, warrant surgical in¬
tervention in nearly all patients; nonoperative therapy is reserved
for older patients with multiple comorbid conditions and minimal
hypercalcemia and clinical manifestations. In this article, the au¬
thors discuss the natural history of primary HPT, a cost effective
method of diagnosis, the indications for surgical therapy, the
appropriate use of preoperative localization studies, the surgical
approaches, and the long term benefits versus risks of surgery.
Familial Hypocalciuric Hypercalcemia and Other
Disorders with Resistance to Extracellular Calcium 503
Edward M. Brown
An extracellular calcium (Ca2t) sensing receptor (CaR) recently
cloned from the parathyroid gland mediates the direct actions of
Ca2 o on parathyroid, kidney, and other tissues, playing key roles in
systemic Ca2+ homeostasis. Disorders in which there is generalized
resistance to the usual actions of Ca2t, on these latter issues results
from inactivating mutations in the CaR. In the heterozygous state,
inactivating mutations usually cause a generally asymptomatic
condition characterized by mild parathyroid hormone (PTH) de
pendent hypercalcemia accompanied by relative hypocalciuria,
known as familial hypocalciuric hypercalcemia (FHH). A much
more severe form of hypercalcemia in neonates, neonatal severe
hyperparathyroidism (NSHPT), arises from homozygous inactivat¬
ing mutations of the CaR, or in occasional cases, from heterozygous
mutations—perhaps because specific mutations exert a dominant
negative action on the wild type CaR in the latter cases. In primary
hyperparathyroidism (PHPT) and in some cases of severe uremic
secondary hyperparathyroidism (SHPT), there is selective resis¬
tance of pathological parathyroid glands to Ca2+ in the absence of
inactivating the CaR mutations, that occurs in part because the
level of expression of the receptor is reduced. Thus PTH dependent
forms of hypercalcemia can result from either inherited, general¬
ized Ca2+O resistance ranging in severity from mild to severe, as
in FHH or NSHPT, respectively, or from acquired, tissue (i.e.,
parathyroid) specific resistance to Ca2+0 in PHPT and SHPT.
Medical Approaches to Primary Hyperparathyroidism 523
Gordon J. Strewler
Medical therapy is useful in cases of acute primary hyperparathy¬
roidism, patients with recurrent disease, and parathyroid card
noma. Among the therapeutic agents that have been employed,
oral phosphate, bisphosphonates, and estrogens have been suc¬
cessful. The newly described calcimimetic agents directly block
secretion of parathyroid hormone from the glands and offer an
important new approach to medical therapy of primary hyper
parathyroidism.
Multiple Endocrine Neoplasia Type 1 541
Rajesh V. Thakker
Multiple Endocrine Neoplasia Type 1 (MEN 1) is an autosomal
dominant disorder characterized by the combined occurrence of
tumors of the parathyroids, pancreatic islet cells, and anterior
pituitary. Other MEN 1 associated tumors include angiofibromas,
collagenomas, lipomas, carcinoids, and adrenal cortical tumors.
The MEN1 gene, which represents a putative tumor suppressor
gene, was identified in 1997, and more than 340 mutations have
been reported in MEN 1 families, patients with nonfamilial MEN
1, families with isolated primary hyperparathyroidism, and spo¬
radic non MEN 1 endocrine tumors. The mutations have been
scattered throughout the nine exons that encode a 610 amino acid
nuclear protein, MENIN, which interacts with the rranscriptional
factor, JunD. These recent developments have made it possible to
consider genetic screening for this inherited disorder.
Pseudohypoparathyroidism: New Insights into an Old
Disease 569
Murat Bastepe and Harald Jiippner
The complex GNAS1 gene (chromosome 20ql3.3) encodes the
stimulatory G protein (Gs a) and at least three additional, alterna¬
tively spliced transcripts, XLas, NESP55, and AS, which are de¬
rived either from the paternal or the maternal allele, or from
both. Pseudohypoparathyroidism type la (PHP la) and pseudo
pseudohypoparathyroidism (pPHP) are caused by heterozygous
mutations in the coding exons of GNAS1, but the endocrine
abnormalities occur only if the genetic defect is inherited from an
obligate female carrier. Recent linkage studies have shown that
the genetic defect responsible for pseudohypoparathyroidism
type Ib (PHP Ib) maps also to the GNAS1 locus and that this
disorder is paternally imprinted just as PHP Ia/pPHP. It therefore
appears likely that mutations in distinct regions of the GNAS1
gene are the cause of at least three different forms of PHP.
Disorders of Phosphate Metabolism 591
Linda A. DiMeglio, Kenneth E. White, and
Michael J. Econs
Phosphate is essential for skeletal mineralization and for multiple
cellular functions. Several inherited and acquired disorders dis
rupt phosphate homeostasis, resulting in conditions of hypo
and hyperphosphatemia. Unfortunately, these disorders are often
misdiagnosed and are inappropriately treated. This article re¬
views isolated phosphate wasting disorder and tumoral calcino
sis, a disorder that results in increased phosphate reabsorption.
Identification of these disorders is important because optimal
therapy varies. Additionally, insight gained from studying these
disorders provides a better understanding of the complex but
fascinating process of maintenance of phosphate homeostasis.
Vitamin D Deficiency and Disorders of Vitamin D
Metabolism 611
Melissa K. Thomas and Marie B. Demay
The disorders of vitamin D metabolism are inherited metabolic
abnormalities involving mutations of the vitamin D receptor or
enzymes involved in the metabolism of vitamin D to its biologi¬
cally active form 1,25 dihydroxyvitamin D. Although these muta¬
tions are rare, studies in affected patients and animal models
have helped to identify critical actions of vitamin D and the
mechanism by which it exerts its effects. Vitamin D deficiency,
however, is an increasingly recognized problem among the el¬
derly and in the general population. Screening for vitamin D
deficiency only in those patients with known risk factors will
result in a large proportion of unrecognized affected patients.
The Parathyroid Hormone Related Protein 629
Gordon J. Strewler
This article focuses on recent studies that add several new types
of cancer to the range of tumors that have parathyroid hormone
related protein (PTHrP) as part of their repertoire. Topics include
a new modus operandi for PTHrP as a mediator of local osteolysis
around bone metastases, and tentative conclusions on the ap¬
proach to using assays for PTHrP to aid in the differential diagno¬
sis of hypercalcemia. PTHrP is vital to the normal functioning of
mammals. Its role in adults and as a remarkably versatile regula¬
tor of development is apparently more ancient than the role of
PTH and certainly more protean in action.
Index 647
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| spelling | Hormones and disorders of mineral metabolism Gordon J. Strewler guest ed. Philadelphia [u.a.] Saunders 2000 XI S., S. 451 - 655 Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Endocrinology and metabolism clinics of North America 29,3 Deficiëntieziekten gtt Hormonen gtt Hormones Maladies de la parathyroïde Maladies métaboliques Mineralen gtt Minéraux - Métabolisme Métabolisme minéral, Troubles du Stofwisselingsziekten gtt Endocrine glands Diseases Complications Metabolic Diseases Metabolism Disorders Complications Mineral metabolism Complications Minerals in the body Minerals metabolism Parathyroid Diseases Parathyroid glands Diseases Complications Hormon (DE-588)4025864-6 gnd rswk-swf Mineralstoffwechsel (DE-588)4039464-5 gnd rswk-swf Mineralstoffwechselstörung (DE-588)4039465-7 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Mineralstoffwechselstörung (DE-588)4039465-7 s DE-604 Mineralstoffwechsel (DE-588)4039464-5 s Hormon (DE-588)4025864-6 s Strewler, Gordon J. Sonstige oth Endocrinology and metabolism clinics of North America 29,3 (DE-604)BV000625447 29,3 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=009146685&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Hormones and disorders of mineral metabolism Endocrinology and metabolism clinics of North America Deficiëntieziekten gtt Hormonen gtt Hormones Maladies de la parathyroïde Maladies métaboliques Mineralen gtt Minéraux - Métabolisme Métabolisme minéral, Troubles du Stofwisselingsziekten gtt Endocrine glands Diseases Complications Metabolic Diseases Metabolism Disorders Complications Mineral metabolism Complications Minerals in the body Minerals metabolism Parathyroid Diseases Parathyroid glands Diseases Complications Hormon (DE-588)4025864-6 gnd Mineralstoffwechsel (DE-588)4039464-5 gnd Mineralstoffwechselstörung (DE-588)4039465-7 gnd |
| subject_GND | (DE-588)4025864-6 (DE-588)4039464-5 (DE-588)4039465-7 (DE-588)4143413-4 |
| title | Hormones and disorders of mineral metabolism |
| title_auth | Hormones and disorders of mineral metabolism |
| title_exact_search | Hormones and disorders of mineral metabolism |
| title_full | Hormones and disorders of mineral metabolism Gordon J. Strewler guest ed. |
| title_fullStr | Hormones and disorders of mineral metabolism Gordon J. Strewler guest ed. |
| title_full_unstemmed | Hormones and disorders of mineral metabolism Gordon J. Strewler guest ed. |
| title_short | Hormones and disorders of mineral metabolism |
| title_sort | hormones and disorders of mineral metabolism |
| topic | Deficiëntieziekten gtt Hormonen gtt Hormones Maladies de la parathyroïde Maladies métaboliques Mineralen gtt Minéraux - Métabolisme Métabolisme minéral, Troubles du Stofwisselingsziekten gtt Endocrine glands Diseases Complications Metabolic Diseases Metabolism Disorders Complications Mineral metabolism Complications Minerals in the body Minerals metabolism Parathyroid Diseases Parathyroid glands Diseases Complications Hormon (DE-588)4025864-6 gnd Mineralstoffwechsel (DE-588)4039464-5 gnd Mineralstoffwechselstörung (DE-588)4039465-7 gnd |
| topic_facet | Deficiëntieziekten Hormonen Hormones Maladies de la parathyroïde Maladies métaboliques Mineralen Minéraux - Métabolisme Métabolisme minéral, Troubles du Stofwisselingsziekten Endocrine glands Diseases Complications Metabolic Diseases Metabolism Disorders Complications Mineral metabolism Complications Minerals in the body Minerals metabolism Parathyroid Diseases Parathyroid glands Diseases Complications Hormon Mineralstoffwechsel Mineralstoffwechselstörung Aufsatzsammlung |
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