ABSTRACT
Spinal cord injury-induced hyponatremia is an under-recognized entity, without a mention in the European hyponatremia guidelines. We present a case of a 56-year-old female quadraplegic patient with cervical cord injury, presenting with severe hyponatremia and tonic-clonic seizures. This case highlights the challenges in medical management; action mechanisms are further discussed.
ABSTRACT
Subclinical hypothyroidism (also known as compensated hypothyroidism or mild hypothyroidism) is a condition associated with a raised serum concentration of thyroid stimulating hormone (TSH) but a normal serum free thyroxine (FT4). It is common, affecting about 10% of women above the age of 55 years. Autoimmunity is the commonest cause of subclinical hypothyroidism. About 2.5% of patients with subclinical hypothyroidism progress to clinically overt hypothyroidism each year; the rate of progression is higher in patients with thyroid autoantibodies and higher thyroid stimulating hormone levels. However, thyroid function normalises spontaneously in up to 40% cases. Only a small minority of patients with subclinical hypothyroidism have symptoms, and the evidence to support that levothyroxine ameliorate the symptoms in these patients is weak. Subclinical hypothyroidism in younger patients (<65 years) is associated with an increased risk of coronary heart disease, heart failure and cerebrovascular disease. The risk increases with increasing levels of thyroid stimulating hormone, and is particularly high in patients with TSH levels ≥10.0 mu/L. There is lack of evidence from randomised controlled trials as to whether levothyroxine treatment can prevent these risks, although a large observational study of the UK general practice research database has shown that levothyroxine may reduce the risk of coronary heart disease in younger patients (<70 years). Therefore, the decision whether to treat or not to treat subclinical hypothyroidism should be made after careful consideration of the patient's age, the presence of symptoms, the presence of thyroid antibodies and other risk factors such as cardiovascular disease.
Subject(s)
Asymptomatic Diseases/therapy , Hypothyroidism/complications , Hypothyroidism/drug therapy , Thyroxine/therapeutic use , Cardiovascular Diseases/etiology , Humans , Hypothyroidism/diagnosis , Mental Disorders/etiology , Metabolic Diseases/etiology , Practice Guidelines as Topic , Symptom AssessmentABSTRACT
The title compound, [RuCl(C(6)H(7)N)(2)(C(27)H(35)N(3))]PF(6)·C(3)H(6)O, was obtained unintentionally as the product of the reaction of 1,1'-methyl-enebis(4-methyl-pyridinium) hexa-fluoriso-phos-phate and RuCl(3)(tpy*) (tpy* is 4,4',4''-tri-tert-butyl-2,2':6',2''-terpyridine) in the presence of triethyl-amine and LiCl. The mol-ecular structure of the complex displays an octa-hedral geometry around the Ru(II) ion and the unit cell contains an acetone solvent mol-ecule and one orientationally disordered PF(6) (-) anion (occupancy ratio 0.75:0.25) which is hydrogen bonded to two H atoms of the tpy* ligand of the nearest [RuCl(pic)(2)(tpy*)](+) cation (pic is 4-methyl-pyridine). One of the tert-butyl groups of the tpy* ligand is also disordered over two sets of sites in a 0.75:0.25 ratio.
