Content area
Full Text
Background
Statins and ciprofloxacin are both commonly prescribed drugs. 1 2 While the interactions between statins and other antibiotics are well documented, 3 the interaction between statins and ciprofloxacin is less so. 4-6 The consequences of this interaction can have potentially serious outcomes and be detrimental to patient well-being.
Case presentation
A 62-year-old woman presented to hospital, on general practitioner (GP) advice, with a 15-day history of slowly progressing muscle weakness and a 10-day history of dark brown, frothy urine. The patient had attended her GP a day before, who took routine blood tests (including creatine kinase, CK) and on receipt of results (including CK=16 070 U/L), advised seeking urgent medical advice.
Medical history includes previous myocardial infarction (MI) and recurrent urinary tract infection. Four days prior to the onset of muscle weakness, the patient developed typical urinary tract infection symptoms (including foul smelling urine, dysuria and haematuria) and was treated with ciprofloxacin. The patient had been taking simvastatin (40 mg nocte) for 13 years and had never previously taken ciprofloxacin. She is a non-smoker and drinks alcohol occasionally. There was no history of recreational drug use. Other medication includes nicorandil (10 mg BD), aspirin (75 mg OD), bisoprolol (5 mg OD) and glycerol trinitrate (400 [mu]g PRN) with no recent changes.
Four days after starting ciprofloxacin therapy, the patient noted increased weakness in her limbs (lower limbs>upper limbs) and progressive difficultly completing activities of daily living. Limb weakness progressed over the antibiotic course and continued following its completion. At the time of initial GP presentation, antibiotic course had been completed. A change in urine colour from red to darker brown was noted, and as urine colour became darker, limb weakness became more severe, leading her to seek medical advice in the community. There was no history of injury or immobilisation. On arrival to hospital, CK had risen to 24 514 U/L and liver function was deranged (AST 870 U/L, ALT 240 U/L). Calcium level was normal. There were no infective symptoms to suggest viral aetiology. On examination, there was markedly reduced power, especially in the lower limbs (proximal>distal) with no evidence of compartment syndrome.