Autoimmune endocrine disorders:
Gespeichert in:
| Weitere Verfasser: | |
|---|---|
| Format: | Buch |
| Sprache: | English |
| Veröffentlicht: |
Philadelphia, Pa.
Saunders
2009
|
| Schriftenreihe: | Endocrinology and metabolism clinics of North America
38,2 |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XVIII S., S. 265 - 470 Ill. |
| ISBN: | 9781437704716 1437704719 |
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| 245 | 1 | 0 | |a Autoimmune endocrine disorders |c guest ed. Simon H. S. Pearce |
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Datensatz im Suchindex
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| adam_text | Titel: Autoimmune endocrine disorders
Autor: Pearce, Simon H. S.
Jahr: 2009
Autoimmune Endocrine Disorders
Contents
Foreword xiii
Derek LeRoith
Preface xvii
Simon H.S. Pearce
Regulatory T Cells: Key Players in Tolerance and Autoimmunity 265
Talal A. Chatila
CD4 + CD25 + regulatory T (TR) lymphocytes are essential to the mainte¬
nance of immunologic tolerance in the host. The discovery of Foxp3 as
a transcription factor essential to the differentiation of TR ushered in
detailed studies of the molecular mechanisms of TR cell development,
peripheral homeostasis, and effector functions. In humans, loss of function
mutations in genes that regulate T-cell development and function have
been associated with TR cell deficiency or dysfunction and syndromes
of autoimmunity and immune dysregulation. Augmentation of TR cells by
immunotherapy and pharmacologic agents is a promising strategy for
the treatment of allergic and autoimmune diseases.
Clearing the AIRE: On the Pathophysiological Basis of the Autoimmune
Polyendocrinopathy Syndrome Type-1 273
Noriko Shikama, Gretel Nusspaumer, and Georg A. Hollander
Autoimmune polyendocrine syndrome type-1 clinically manifests as the
triad of hypoparathyroidism, primary adrenocortical insufficiency, and
chronic mucocutaneous candidiasis. Mutations in the gene that encodes
the autoimmune regulator protein, AIRE, have been identified as the cause
of the autoimmune polyendocrine syndrome type-1. The loss of immuno¬
logic tolerance to tissue-restricted antigens consequent to an absence of
AIRE expression in the thymus results in the thymic export of autoreactive
T cells that initiate autoimmunity. In this article, we discuss the role of AIRE
in autoimmune polyendocrine syndrome type-1 and identify issues that
still need to be addressed to fully understand the molecular pathophysiol-
ogy of this complex syndrome.
Genetics of Type 1 Diabetes and Autoimmune Thyroid Disease 289
Simon H.S. Pearce and Tony R. Merriman
The search for the susceptibility alleles for the complex genetic conditions
of type 1 diabetes and autoimmune thyroid diseases has gained momen¬
tum in recent years. Studies have revealed several novel disease suscep¬
tibility alleles of relevance to both conditions, which brings the total
number of genetic variants contributing to type 1 diabetes to ten. Addi¬
tional genetic loci remain to be discovered, particularly in the autoimmune
thyroid diseases. In the future, the density and coverage of single
viii Contents
nucleotide polymorphisms available for high throughput genotyping will
improve, and detailed analysis of the role of copy number variants in these
diseases will shed new light on the pathogenesis of these common
endocrinopathies.
Advances in Type 1 Diabetes Therapeutics: Immunomodulation and fi-Cell Salvage 303
Frank Waldron-Lynch and Kevan C. Herold
Refinements in our understanding of the pathogenic mechanisms of Type
1 diabetes from studies of animal models and clinical observation have led
to new clinical trials to prevent disease progression and restore the loss of
3-cells that defines the disease. Antigen-specific agents have shown initial
promise and non-antigen-specific agents now have improved safety com¬
pared with older agents. In addition, preclinical studies with other agents
have shown efficacy. Ultimately, a combination of immunologic and cellu¬
lar therapies may be needed to restore metabolic control. Agents that aug¬
ment recovery of dysfunctional (3-cells, and other compounds that may be
able to induce p-cell replication, are logical additions once immune toler¬
ance is achieved.
The Thyroid-Stimulating Hormone Receptor: Impact of Thyroid-Stimulating
Hormone and Thyroid-Stimulating Hormone Receptor Antibodies
on Multimerization, Cleavage, and Signaling 319
Rauf Latif, Syed A. Morshed, Mone Zaidi, and Terry F. Davies
The thyroid-stimulating hormone receptor (TSHR) has a central role in thy-
rocyte function and is also one of the major autoantigens for the autoim¬
mune thyroid diseases. We review the post-translational processing,
multimerization, and intramolecular cleavage of TSHR, all of which may
modulate its signal transduction. The recent characterization of monoclo¬
nal antibodies to the TSHR, including stimulating, blocking, and neutral an¬
tibodies, have also revealed unique biologic insights into receptor
activation and the variety of these TSHR antibodies may help explain the
multiple clinical phenotypes seen in autoimmune thyroid diseases. Knowl¬
edge of the structure/function relationship of the TSHR is beginning to
provide a greater understanding of thyroid physiology and thyroid
autoimmunity.
Toward Better Models of Hyperthyroid Graves Disease 343
Sel^uk Dagdelen, Yi-chi M. Kong, and J. Paul Banga
Graves disease affects only humans. Although it is a treatable illness,
medical therapy with antithyroid drugs is imperfect, showing high rates
of recurrence. Furthermore, the etiology and treatment of the associated
ophthalmopathy still represent problematic issues. Animal models could
contribute to the solution of such problems by providing a better under¬
standing of the underlying pathogenesis and could be used for evaluating
novel therapeutic strategies. This article discusses the pursuit of a better
experimental model for hyperthyroid Graves disease and outlines how
this research has clarified the immunology of the disease.
Contents ix
Treatment of Graves Hyperthyroidism: Evidence-Based and Emerging Modalities 355
Laszlo Hegedus
Currently there are three well-established treatment options for hyperthy-
roid Graves disease (GD): antithyroid drug therapy with thionamides
(ATD), radioactive iodine treatment with 131I, and thyroid surgery. This ar¬
ticle reviews the current evidence so the reader can evaluate advantages
and disadvantages of these treatment modalities. Surgery is rarely used,
except for patients who have a large goiter or ophthalmopathy. Fewer
than 50% of patients treated with ATD remain in long-term remission.
Therefore, radioactive iodine is used increasingly. No data as yet support
the routine use of biologic therapies (eg, rituximab). Prospective, random¬
ized studies comparing available and any novel therapeutic options for GD
are needed. The focus of these studies should include, but not be limited
to, cost and quality of life.
Thyroid-Associated Orbitopathy: Who and How to Treat 373
Jane Dickinson and Petros Perros
Thyroid-associated orbitopathy is the most frequent and troublesome
nonthyroidal complication of Graves disease. It is mandatory to determine
whether sight-threatening orbitopathy is present, as this requires prompt
and aggressive treatment. Therapies for non-sight-threatening disease
range from supportive measures only to medical therapies for active eye
disease and surgical rehabilitation for burnt-out disease. Intravenous ste¬
roids and orbital radiotherapy are the mainstays of medical therapy. Reha¬
bilitative surgery is frequently a staged process that may involve
sequentially: orbital decompression, strabismus surgery, and eyelid pro¬
cedures. Smoking cessation is recommended at all disease stages. Treat¬
ment within a multidisciplinary team consisting of both endocrinologists
and ophthalmologists may lead to optimal patient outcomes.
Immunology of Addison s Disease and Premature Ovarian Failure 389
Eystein S. Husebye and Kristian Lovas
Autoimmune Addison s disease and autoimmune ovarian insufficiency are
caused by selective targeting by T and B lymphocytes to the steroidogenic
apparatus in these organs. Autoantibodies toward 21-hydroxylase are
a clinically useful marker for autoimmune Addison s disease. Autoanti¬
bodies to 21-hydroxylase are found in premature ovarian insufficiency,
but others also can be present, notably antibodies against side-chain
cleavage enzyme. The autoimmune response primarily targets the theca
cells, yielding elevated concentrations of inhibin, which is emerging as
a useful diagnostic marker for autoimmune etiology of ovarian insuffi¬
ciency. Little is known about its immunogenetics, but in contrast to Addi¬
son s disease, several experimental models of autoimmune premature
ovarian insufficiency are available for study.
Fine Tuning for Quality of Life: 21st Century Approach to Treatment
of Addison s Disease 407
Nicole Reisch and Wiebke Arlt
Despite treatment with glucocorticoids and mineralocorticoids, the ability
to work and quality of life of patients who have adrenal insufficiency
x Contents
remains low. There are no helpful objective measures of optimal glucocor-
ticoid replacement, so this is best achieved by careful clinical assessment.
Adequacy of mineralocorticoid replacement may be judged by assessing
postural change in blood pressure, serum electrolytes, and plasma renin
activity. Novel delayed-release and sustained-release formulations of hy-
drocortisone seem to more closely mimic diurnal serum cortisol rhythms
than conventional hydrocortisone tablets. Such preparations are currently
being evaluated and may play a role in management of patients who have
adrenal insufficiency.
Diagnosis and Management of Polyendocrinopathy Syndromes 419
Catherine J. Owen and Tim D. Cheetham
The autoimmune polyendocrinopathy syndromes are variable in presenta¬
tion and can be challenging to diagnose and manage. Diagnosis of the
type 1 autoimmune polyendocrinopathy syndrome can be difficult at an
early age when often only one manifestation is present, and it may take
years for others to appear. Increased awareness of polyendocrinopathy
syndromes, combined with analysis of specific autoantibodies and molec¬
ular genetics, should help earlier diagnosis of these conditions and prevent
serious complications. Further definition of susceptibility genes and auto-
antigens, as well as a better understanding of the pathogenesis, is required
to improve the diagnosis and management of these patients.
Anti-Parathyroid and Anti-Calcium Sensing Receptor Antibodies
in Autoimmune Hypoparathyroidism 437
Edward M. Brown
The parathyroid glands are an infrequent target for autoimmunity, the ex¬
ception being autoimmune polyglandular syndrome type 1, in which auto¬
immune hypoparathyroidism is the rule. Antibodies that are directed
against the parathyroid cell surface calcium-sensing receptor (CaSR)
have recently been recognized to be present in the serum of patients
with autoimmune hypoparathyroidism. In some individuals, these anti-
CaSR antibodies have also been shown to produce functional activation
of the receptor, suggesting a direct pathogenic role in hypocalcemia. Ad¬
ditionally, a few hypercalcemic patients with autoimmune hypocalciuric
hypercalcemia owing to anti-CaSR antibodies that inhibit receptor activa¬
tion have now been identified. Other novel parathyroid autoantigens are
starting to be elucidated, suggesting that new approaches to treatment,
such as CaSR antagonists or agonists (calcilytics/calcimimetics), may be
worthwhile.
Index 447
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| dewey-ones | 616 - Diseases |
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| dewey-sort | 3616.4079 |
| dewey-tens | 610 - Medicine and health |
| discipline | Medizin |
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