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