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  Vol. 120 No. 3, March 2002 TABLE OF CONTENTS
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  Mechanisms of Ophthalmologic Disease
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Insights Into the Pathogenesis of Thyroid-Associated Orbitopathy

Evolving Rationale for Therapy

Michael Kazim, MD; Robert A. Goldberg, MD; Terry J. Smith, MD

Arch Ophthalmol. 2002;120:380-386.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Attempts to understand the pathogenesis of thyroid-associated orbitopathy (TAO) have failed, in part because of confounding features associated with its variable clinical presentation. In the absence of a more complete insight into disease mechanisms, no specific and effective therapy can be developed. It is our view that much of the information necessary to unravel the complexities of TAO and therefore formulate rational therapy has already been gathered.


CLINICAL FEATURES OF TAO

Thyroid-associated orbitopathy varies widely in its pattern of presentation. Generalizations about this disease are not particularly useful when treatment plans are developed for an individual patient, but the following description will serve as a point of reference for the subsequent discussion. Thyroid-associated orbitopathy is identified in approximately 20% of those seen with Graves disease on initial examination. A far larger group manifests subclinical, self-limited forms of TAO. The prevalence of these milder . . . [Full Text of this Article]

SOME UNANSWERED QUESTIONS

RECENT INSIGHTS INTO THE PATHOGENESIS OF TAO

DIFFERENCES BETWEEN ORBITAL FIBROBLASTS AND THOSE IN OTHER ANATOMIC REGIONS

CLINICAL AND THERAPEUTIC CONSEQUENCES OF THE ORBITAL FIBROBLAST PHENOTYPE

TREATMENT RECOMMENDATIONS

CONCLUSION

From the Department of Ophthalmology, College of Physicians and Surgeons, Columbia University, New York, NY (Dr Kazim); Jules Stein Eye Institute, Los Angeles, Calif (Drs Goldberg and Smith); Division of Molecular Medicine, Department of Medicine, Harbor-UCLA Medical Center, Torrance, Calif (Dr Smith); and School of Medicine, University of California, Los Angeles (Drs Goldberg and Smith).



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Arch Ophthalmol 2007;125:1652-1656.
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B Cell Depletion in Graves' Disease: The Right Answer to the Wrong Question?
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Interleukin-4 Induces 15-Lipoxygenase-1 Expression in Human Orbital Fibroblasts from Patients with Graves Disease: EVIDENCE FOR ANATOMIC SITE-SELECTIVE ACTIONS OF Th2 CYTOKINES
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J. Biol. Chem. 2006;281:18296-18306.
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T Helper Type 1 and Type 2 Cytokines Exert Divergent Influence on the Induction of Prostaglandin E2 and Hyaluronan Synthesis by Interleukin-1{beta} in Orbital Fibroblasts: Implications for the Pathogenesis of Thyroid-Associated Ophthalmopathy
Han and Smith
Endocrinology 2006;147:13-19.
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IL-1{beta} Induces IL-6 Expression in Human Orbital Fibroblasts: Identification of an Anatomic-Site Specific Phenotypic Attribute Relevant to Thyroid-Associated Ophthalmopathy
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J. Immunol. 2005;175:1310-1319.
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Induction by IL-1{beta} of Tissue Inhibitor of Metalloproteinase-1 in Human Orbital Fibroblasts: Modulation of Gene Promoter Activity by IL-4 and IFN-{gamma}
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J. Immunol. 2005;174:3072-3079.
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Thyroid associated ophthalmopathy: evidence for CD4+ {gamma}{delta} T cells; de novo differentiation of RFD7+ macrophages, but not of RFD1+ dendritic cells; and loss of {gamma}{delta} and {alpha}{beta} T cell receptor expression
Eckstein et al.
Br. J. Ophthalmol. 2004;88:803-808.
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Current Perspective on the Pathogenesis of Graves' Disease and Ophthalmopathy
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