Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 60-year-old man who presented with fever, weight loss, generalized aching, left temporal and ear pain, and an erythrocyte sedimentation rate of 125 mm/hour. Due to the presumed diagnosis of giant cell arteritis (GCA), the patient was treated with prednisone (60 mg daily), with immediate improvement in his symptoms. Biopsy of the temporal arteries revealed no significant inflammatory infiltrate. Further evaluation included assessments of thyroid function, which revealed an elevated T4 level, low thyroid-stimulating hormone level, and suppressed radioactive iodine uptake on thyroid scintigraphy. A diagnosis of subacute thyroiditis was made, prednisone therapy was tapered over 3 weeks, and treatment with beta blockers was instituted. The patient remained asymptomatic and returned to a euthyroid state. This case illustrates that subacute thyroiditis should be considered in the differential diagnosis of GCA.
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PMID:Occult subacute thyroiditis mimicking classic giant cell arteritis. 798 Jun 73

We previously demonstrated that the O-linked beta-N-acetylglucosamine (O-GlcNAc) posttranslational modification confers cardioprotection at least partially through mitochondrial-dependent mechanisms, but it remained unclear if O-GlcNAc signaling interfered with other mechanisms of cell death. Because ischemia/hypoxia causes endoplasmic reticulum (ER) stress, we ascertained whether O-GlcNAc signaling could attenuate ER stress-induced cell death per se. Before induction of ER stress (with tunicamycin or brefeldin A), we adenovirally overexpressed O-GlcNAc transferase (AdOGT) or pharmacologically inhibited O-GlcNAcase [via O-(2-acetamido-2-deoxy-d-glucopyranosylidene) amino-N-phenylcarbamate] to augment O-GlcNAc levels or adenovirally overexpressed O-GlcNAcase to reduce O-GlcNAc levels. AdOGT significantly (P < 0.05) attenuated the activation of the maladaptive arm of the unfolded protein response [according to C/EBP homologous protein (CHOP) activation] and cardiomyocyte death (reflected by percent propidium iodide positivity). Moreover, pharmacological inhibition of O-GlcNAcase significantly (P < 0.05) mitigated ER stress-induced CHOP activation and cardiac myocyte death. Interestingly, overexpression of GCA did not alter ER stress markers but exacerbated brefeldin A-induced cardiomyocyte death. We conclude that enhanced O-GlcNAc signaling represents a partially proadaptive response to reduce ER stress-induced cell death. These results provide new insights into a possible interaction between O-GlcNAc signaling and ER stress and may partially explain a mechanism of O-GlcNAc-mediated cardioprotection.
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PMID:O-GlcNAc signaling attenuates ER stress-induced cardiomyocyte death. 1973 55