Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 74-year-old patient sought treatment for visual obscuration and clinically had signs of Graves orbitopathy. Past medical history was unremarkable except for the use of antihypertensive medication. During the hospital admission, a fluorescent treponemal antibody absorption test was reactive, indicating infection with syphilis at some time in the past. Visual deterioration despite oral corticosteroid therapy prompted orbital decompression. At the time of surgery, she sustained a globe rupture. Presumably, syphilitic scleritis was responsible, in part, for scleral thinning and weakening, predisposing her to this complication. To the authors' knowledge, globe rupture has not been previously reported during orbital decompression.
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PMID:Ruptured globe during orbital decompression surgery. 978 85

We immunized BALB/c mice with M12 cells (H-2d) expressing either mouse (mM12 cells) or human thyrotropin receptor (TSHR) (hM12 cells). Immunized mice developed autoantibodies to native TSHR by day 90 and, by day 180, showed considerable stimulatory Ab activity as measured by their ability to enhance cAMP production (ranging from 6. 52 to 20.83 pmol/ml in different treatment groups relative to 1.83 pmol/ml for controls) by TSHR-expressing Chinese hamster ovary cells. These mice developed severe hyperthyroidism with significant elevations in both tetraiodothyronine and triiodothyronine hormones. Tetraiodothyronine levels in different experimental groups ranged from a mean of 8.66-12.4 microg/dl, relative to 4.8 microg/dl in controls. Similarly, mean triiodothyronine values ranged from 156.18 to 195.13 ng/dl, relative to 34.99 ng/dl for controls. Next, we immunized BALB/c mice with a soluble extracellular domain of human TSHR (TBP), or TBP expressed on human embryonic kidney cells (293 cells) (293-TBP cells). These mice showed severe hyperthyroidism in a manner very similar to that described above for mice immunized with the mouse TSHR or human TSHR, and exhibited significant weight loss, with average weight for treatment groups ranging from 20.6 to 21.67 g, while controls weighed 24.2 g. Early after onset of the disease, histopathological examination of thyroids showed enlargement of colloids and thinning of epithelial cells without inflammation. However, later during disease, focal necrosis and lymphocytic infiltration were apparent. Our results showed that conformationally intact ectodomain of TSHR is sufficient for disease induction. Availability of a reproducible model in which 100% of the animals develop disease should facilitate studies aimed at understanding the molecular pathogenesis of Graves' disease.
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PMID:Induction of experimental autoimmune Graves' disease in BALB/c mice. 1052 22

An euthyroid patient was referred for compressive optic neuropathy in Graves' disease. Under prednisone therapy the right and left visual acuities were 1.0 and 0.4, with a profound decrease in color vision on the left. Bilateral anterior orbital decompressions were performed. When prednisone was withdrawn postoperatively, the visual acuity of the right eye dropped to 0.32 with bilateral complete failure on the Ishihara color test. A biopsy of the inferior oblique muscle of the left eye confirmed Graves' disease and additional transantral decompression of the right orbital apex was performed. Under intravenous methylprednisolone therapy, the visual acuity dropped postoperatively to 0.2 and 0.4, respectively. 15 U botulinum toxin were given by retrobulbar injection between the inferior and lateral rectus muscles. Four days later the patient called and said that the visual acuity in the right eye had improved tremendously. Two weeks after the injection the visual acuity was 0.7 in both eyes, although prednisone had been reduced to 20 mg by that time. The convergent strabismus had increased but the already severely restricted motility of the right eye had been little affected by the retrobulbar injection, and adduction not at all. Orbital CT-scan showed thinning of the inferior and lateral rectus muscles, but not of the medial rectus.
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PMID:Botulinum toxin as adjunct for refractory compressive optic neuropathy in Graves' disease. 1204 25

Female Chinese hamsters (n = 10) were immunized with Chinese hamster ovary (CHO) cells that expressed the human TSH receptor (TSHR) to generate a model of Graves' disease. TSHR-autoantibodies (TSHR-Ab) were determined by CHO-TSHR. Two hamsters with stimulating TSHR-Ab showed thyrocyte hypertrophy associated with a focal lymphocytic infiltration. CHO-TSHR were then stimulated with interferon gamma to enhance major histocompatibility complex class II expression. However, after immunization no stimulating TSHR-Ab were detected, but blocking TSHR-Ab were found in three of five animals. The thyroid glands from these hamsters showed marked thinning of thyroid epithelial cells, indicative of early thyroid atrophy consistent with a TSHR blocking antibody, but no lymphocytic infiltration. Lastly, female Armenian hamsters were immunized with an adenovirus construct incorporating wild-type TSHR. High titers of TSHR-Ab were induced effectively, but the thyroid hypertrophy observed was not associated with a lymphocyte infiltration. In summary, we demonstrated that the hamster could serve as a model of TSHR autoimmunity and that an adenoviral vector produced higher levels of TSHR-Ab than more conventional immunization with cells. The data also indicated that the intrathyroidal cellular immunity in this model was not related to TSHR-Ab formation and was an independent reflection of the T-cell immune response to TSHR antigen.
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PMID:Induction of thyroid-stimulating hormone receptor autoimmunity in hamsters. 1253 30