JRSM >
Volume 97, Number 3 >
Pp. 124-125
Department of Rheumatology, Harrogate District Hospital, Harrogate, North Yorks, UK
Correspondence to: Dr Jane Freeston, 5 Eller Close, 50 North Lane, Leeds LS8 2QW, UK E-mail: jefreeston{at}yahoo.com
In a patient with myopathy and renal impairment, a cause to be excluded is thyroid dysfunction.
CASE HISTORY
A man aged 39 was referred in March 1998 to our otolaryngology service with a new symptom of snoring, which was treated unsuccessfully by uvulopalatopharyngoplasty a year later. Subsequently, in December 2000, he was referred to the regional renal unit with anorexia and lethargy associated with renal impairment. He was slightly short of breath and had experienced a change in his vision, necessitating glasses. On examination, he was normotensive. Creatinine was 189 µmol/L, urea 7.5 mmol/L, cholesterol 8.4 mmol/L. Other blood and urine tests, renal tract ultrasound and renal biopsy were normal. By May 2001, his creatinine had increased to 220 and his cholesterol to 10. A renal scan and doppler study were unrevealing but a glomerular filtration rate of 55 mL/min confirmed that renal function was subnormal. He was started on atorvastatin but within a week experienced new-onset myalgia and weakness. His creatine phosphokinase (CPK) was 3700 IU/L (normal range 24–195), so the atorvastatin was stopped. The CPK continued to increase, reaching 4200 a month later. Renal function was unchanged.
With a possible diagnosis of polymyositis in mind, the patient, now 43, was referred to the rheumatology service. On examination, proximal and distal muscle power seemed normal but periorbital oedema was noted. Thyroid function tests indicated hypothyroidism and treatment was started with levothyroxine 50 µg daily. By March 2002, at which time the levothyroxine dose was 100 µg daily, indices were all normal (Table 1) and the patient had returned to his premorbid state.
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COMMENT
In a Medline review from 1979 to the present we found three cases of renal impairment and primary hypothyroidism associated with a raised CPK. In all three patients the raised CPK was associated with myopathy on electromyography or muscle histology, and two had rhabdomyolysis.1–3 All three responded dramatically to thyroid replacement therapy with improvement in renal function and a decline in CPK. Our patient in addition had lipid abnormalities (a feature of dysthyroid states4) and these too were reversed by treatment of the hypothyroidism. Muscle enzymes in serum seem to correlate with the severity of the hypothyroidism rather than the extent of the myopathy.2 Electromyographic abnormalities and muscle biopsy histological changes are usually minor and non-specific, making the condition hard to differentiate from polymyositis. Progression to rhabdomyolysis in hypothyroidism is very rare, and most previously reported cases have been associated with precipitating factors such as trauma, exercise and lipid-lowering medication.1
The presentation of hypothyroid-related myopathy can be further masked by other co-existent autoimmune disease such as Addison's disease. Interestingly, in such cases, the myalgic symptoms did not improve until levothyroxine was added to the steroid replacement therapy.5
Hypothyroidism is not only a recognized cause of de novo renal failure but can also precipitate deterioration in patients with stable chronic renal failure, with levothyroxine replacement resulting in up to 50% improvement in renal function. It is important to detect, especially in the elderly, since hypothyroid symptoms may be masked in patients with known renal failure and the condition is easily treatable.6,7
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