PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12803064

[Thyroid orbitopathy].

Iftach Yassur·Guy J Ben Simon·Nachum Rosen
View original source ↗Export metadata ↓

Abstract

Thyroid Orbitopathy (T.O) is the most common orbital disease caused by a systemic illness. The clinical manifestations of T.O are a result of inflammation, edema and scarring of orbital tissue, and include exophthalmos, soft tissue edema, lid retraction, chemosis, exposure keratitis that can lead to corneal ulceration and perforation, ocular motility disorders and strabismus, and compressive optic neuropathy. T.O is an autoimmune disease but the exact etiology is yet to be revealed. Most cases resolve spontaneously without the need for medical or surgical intervention, but more severe cases may result in devastating visual and cosmetic results. In recent years, there has been a significant progress in the understanding of the disease and the medical and surgical treatment of T.O. This work reviews new aspects of T.O and it's surgical treatment, and include clinical photographs of patients operated on in our department.

Explore related subjects

Autoimmune DiseasesDiagnosis, DifferentialExophthalmosGraves DiseaseHumansRemission, SpontaneousEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Iftach Yassur, Guy J Ben Simon, Nachum Rosen. 2003. [Thyroid orbitopathy].. https://pubmed.ncbi.nlm.nih.gov/12803064/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

The kinetics of binding to p38MAP kinase by analogues of BIRB 796.

BIRB 796, a member of the N-pyrazole-N'-naphthly urea class of p38MAPK inhibitors, binds to the kinase with both slow association and dissociation rates. Prior to binding, the kinase undergoes a reorganization of the activation loop exposing a critical binding domain. We demonstrate that, independent of the loop movement, association rates are governed by low energy conformations of the inhibitor and polar functionality on the tolyl ring. As anticipated, the dissociation rates of the inhibitors from the kinase are slowed by lipophilic and hydrogen bond interactions. The value of structure-kinetic relationships (SKR) in drug design is discussed.

Autoimmune Diseases↗
PubMed2003

Autoimmune subepidermal bullous skin diseases: the impact of recent findings for the dermatopathologist.

In recent years improved knowledge of the mechanisms of intercellular and cell-matrix adhesion has led to better understanding of the blistering process in many bullous dermatoses. The wide characterisation of adhesion molecules has partially changed some traditional views and invariably has made the routine work of the pathologist more complex. If understanding cell-cell cohesion structures such as desmosomes and adherens junctions is complex enough, the cell-matrix adhesion structures, such as hemidesmosomes and their structural analogues on the basement membrane and superficial dermis, are even more complex. Defects of such structures cause the subepidermal bullous diseases in which there has been most characterisation of the adhesion molecules and has also led to the discovery of new diseases (e.g. p200 pemphigoid). Most of the antigens are also the targets for mutations seen in patients with the inherited type of epidermolysis bullosa, a group of rare blistering genodermatoses. Another important aspect of bullous skin conditions is the more accurate definition of the role of the different inflammatory cells involved in triggering, development and maintenance of these diseases. Recent studies have outlined the important role of T-cell lymphocytes and their cytokines in their pathogenesis. All these studies, based mainly on highly sophisticated ultrastructural and molecular biology techniques, have updated our knowledge of the pathogenesis of blistering diseases. Nevertheless, the diagnostic characterisation of bullous diseases remains sometimes difficult, and some pathological features and mechanisms still represent an enigma. Diseases such as bullous pemphigoid and cicatricial pemphigoid, or anti-laminin cicatricial pemphigoid and acquired bullous epidermolysis share the same molecular target but have very different clinical manifestations. Explaining this phenomenon, probably linked to different expressions of MHC, is one of the challenges for the future.

Autoimmune Diseases↗