Endocrine Abstracts

Introduction: Symptoms of hypothyroidism in childhood include tiredness, poor growth, weight gain, dry skin and constipation. Whilst muscular manifestations including myalgia, muscle weakness, aches and cramps, stiffness and delayed tendon jerk relaxation are common, rhabdomyolysis has also rarely been reported.

Case presentation: An 11-year-old female presented to her GP with a history of tiredness and poor growth. Initial blood tests performed by the GP showed: TSH >100 mU/l, fT4 <5 pmol/l, ALT 198, creatinine 137, glucose 2.9 mmol/l. On review she described several months of low energy levels, muscle cramps, back pain and feeling cold. On examination, her weight was on the 90th centile and height between the 3rd and 10th centiles with historical heights tracking along the 50th centile. She was pale with dry skin, periorbital puffiness and bilateral non-pitting leg oedema and was bradycardic but normotensive. Further investigation revealed an elevated creatine kinase (CK) of 9830 U/l (0–300 U/l), normal cortisol and blood glucose. She had positive thyroid peroxidase antibodies 1237.1 U/ml (0–50). On starting levothyroxine, her musculoskeletal symptoms resolved and renal function, ALT and CK normalised. Her height velocity improved and weight decreased to 10th centile. There was no recurrence of hypoglycaemia.

Conclusion: Rhabdomyolysis is characterized by muscular symptoms and elevated levels of CK, lactate dehydrogenase and ALT and can cause acute renal failure. The pathogenesis of rhabdomyolysis in hypothyroidism is unclear but may occur as a consequence of abnormal glycogenolysis, impaired mitochondrial oxidative metabolism and triglyceride turnover which impair muscle function. Rhabdomyolysis should be considered in patients with hypothyroidism presenting with muscular symptoms and unexplained deranged renal function. Hypoglycaemia has also been reported as a very rare complication of hypothyroidism and although the cause is unknown, altered glucose-insulin homeostasis and altered hypothalamic–pituitary–adrenal axis activity have been suggested as potential mechanisms.