Eye changes, in particular UER, are common in patients with Hashimoto's thyroiditis. Since thyroid stimulating hormone-receptor antibodies are not usually associated with Hashimoto's thyroiditis, autoimmune mediated damage of the levator palpebrae superioris (eyelid) muscle cannot be due to these antibodies. Although eyelid abnormalities may be a minor problem for most patients, for some there are major cosmetic implications requiring surgical management.
BackgroundHeart failure is common in the elderly and is associated with high rates of hospitalisation, readmission and mortality. International guidelines however are not frequently implemented in this population.MethodsWe retrospectively studied the clinical profile, investigations, treatment on discharge, length of hospital stay, readmission rate and mortality in 261 patients, aged ≥75 years, with a discharge diagnosis of heart failure. Clinical frailty was estimated using the Canadian Study of Health and Aging clinical frailty scale.ResultsHypertension (64%), atrial fibrillation (50.6%) and ischaemic heart disease (46%) were common, and 75.6% of patients were clinically vulnerable or frail. 23.5% of admitters had an inpatient echocardiogram and 20% of patients had at least one readmission episode for heart failure. On discharge, 64.6% of admissions were treated with an ACE inhibitor or angiotensin II receptor antagonist, 49.3% with a β blocker and 28.7% with an aldosterone receptor antagonist (ARA). Patients discharged from cardiology wards were more likely to receive a β blocker (p<0.05) versus care of elderly (COE) wards and readmitters were more likely to receive an ARA (p<0.05) versus patients with a single admission. In total, 34 inpatient deaths were recorded (13%) and 80 deaths (30.7%) were recorded long-term (median follow-up 337 days). Long-term mortality was significantly lower in single admitters versus readmitters (p<0.0001) and in those managed on cardiology wards versus COE wards (p<0.05).ConclusionsCompared with patients hospitalised on geriatric wards, those admitted to cardiology units were discharged more frequently with recommended medications and had a lower long-term mortality.
Thyroid-associated ophthalmopathy (TAO), or thyroid eye disease, is a complex inflammatory disorder of the eye that, as its name implies, is associated with thyroid disease. TAO can be divided into three subtypes: ocular myopathy, congestive myopathy and mixed congestive and myopathic ophthalmopathy. Although the precise pathophysiology of TAO remains unclear it is likely to reflect an autoimmune reaction involving sensitized T-cells and autoantibodies directed against a thyroid and orbital tissue shared antigen. One well studied candidate in this immune reaction is the thyroid-stimulating hormone receptor (TSH-r), expressed in the orbital fibroblast and pre adipocyte. In our studies of TAO, we have investigated the nature and significance of antibodies targeting other eye muscle and orbital connective tissue (OCT) antigens. Our findings suggest that autoimmunity against the eye muscle antigen calsequestrin and the OCT antigen collagen XIII plays a role in the pathogenesis of TAO. We propose that ocular myopathy and chronic eyelid retraction are due to autoimmunity against skeletal muscle calsequestrin in the extraocular and eyelid muscles, respectively. This may be initiated in the thyroid where calsequestrin expression is upregulated, possibly due to a stimulatory effect of TSH-r antibodies. We also propose that congestive ophthalmopathy results from a reaction against the TSH-r or collagen XIII in orbital fibroblast cell membranes. Further insight into the role of eye muscle and OCT antigens in the pathogenesis of TAO may allow for the development of new therapies to treat the eye disorder and reduce patient morbidity.Note: LATS = long-acting thyroid stimulator, TSH-r = thyroid-stimulating hormone receptor.Box 1 Timeline of discoveries related to thyroid-associated ophthalmopathy (TAO). reproduced with the permission from Tani J, wall Jr. Autoimmunity against eye-muscle antigens may explain thyroid-associated ophthalmopathy.
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