ADVERSE REACTIONS ASSOCIATED WITH CLOFIBRATE

... in Chronic Renal Failure A syndrome of muscle pain and elevated serum-creatinine-kinase has been reported in association with clofibrate therapy.

It has been suggested that chronic renal failure is a pathogenic factor in the development of this syndrome. The

following case illustrates these points and raises the question of the role of hypothyroidism in this reaction to clofibrate.

Hypothryoidism could, theoretically, interfere with the excretion of clofibrate and, thus, result in higher plasma levels.

A 34-year-old woman with juvenile diabetes mellitus, chronic renal failure and unrecognised primary hypothyroidism

was started on clofibrate l.Sg/ d. Ten days later she was unable to walk because of severe muscle pain and weakness

in her legs. Serum-creatine-kinase and SGOT were elevated. Withdrawal of clofibrate resulted in rapid relief of

muscle pain and a gradual fall in serum enzymes. Serum-creatine-kinase remained somewhat elevated until the patient was treated with thyroid replacement.

Rumpf, K.W. eta!.: Lancet 1: 249 (31 Jan 1976)

... Further Reports During clofibrate treatment of hyperlipidaemia, 2 patients with pre-existing renal disease (a 31-year-old woman with

chronic pyelonephritis and a 37-year-old man with progressive glomerulonephritis) developed incapacitating muscle symptoms

and severe vomiting. Muscle enzyme values were elevated. Both patients experienced a sudden deterioration in renal

function, which was thought to be secondary to the severe vomiting and subsequent salt depletion. The patients had first

experienced malaise and muscle tenderness after having been on clofibrate for 7 days in one case and 7 months in the

other. Recovery followed peritoneal dialysis and discontinuation of clofibrate.

Chronic renal failure should be regarded as a contraindication to clofibrate therapy and the use of clofibrate should be extremely cautious in possibly progressive renal disease. Even when the impairment is mild and the bio­

chemistries normal, a further asymptomatic decrease in renal function could precipitate clofibrate toxicity.

Dosa, S. eta!.: Lancet I: 250 (31 Jan 1976)

INPHARMA 14th February,1976p6