Captopril-associated agranulocytosis in hypertension of lupus nephritis

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Captopril (SQ 14225), the first orally active inhibitor of angiotensin-coverting enzyme, is a promising drug for the treatment of arterial hypertension. Side-effects include rashes, fever, transient loss of taste and proteinuria, and 4 cases of agranulocytosis in the patients with renal impairment have been reported in Caucasians. However, in Japan there are no reports on captopril-associated agranulocytosis due to lack of clinical usage. We have seen a case of agranulocytosis in a patient with lupus nephritis being treated with captopril.This 30-year-old woman was known to have had systemic lupus erythematosus (SLE) since 1968, the diagnosis being based on clinical findings (skin lesion, arthritis, and glomerulonephritis) and laboratory investigations (antinuclear antibodies, LE cell, anti-DNA antibodies, and reduced level of serum complement). She was treated with high doses of steroid hormone, immunosuppressive drugs, and dipyridamole. Nevertheless, her renal function deteriorated and hypertension with fluid overload became a major problem in May, 1979. Treatment of frusemide, propranolol, α-methyldopa, and hydralazine was unsuccessful in controlling hypertension, as was regular hemodialysis on May 18, 1979. Cephalothin was given for treatment of urinary tract infection, then drug eruption and agranulocytosis appeared. Cephalothin was withdrawn, and over the next 3 days leukocyte-counts rapidly returned to normal. Hypertension in this patient was refractory to conventional therapy. In July, 1979, captopril was given, all the other antihypertensive therapy being discontinued. A prompt and persistent fall in blood pressure ensued. Nearly 2 weeks after the start of the captopril treatment she had transiently reduced leukocyte-count and a pruritic and pustular rash. Twenty-four days later, when on a maintenance dose of 250mg captopril, agranulocytosis was seen again. Bone-marrow cytology showed a slightly increased number of granulocytic cells and a marked left shift. Anti-leukocyte agglutinating antibodies could not be demonstrated. Since no clinical or laboratory evidence for increased SLE activities was found, drug-induced agranulocytosis was suspected. Captopril was withdrawn and prednisolone was transiently increased. Over the next 9 days Ieukocytecounts gradually returned to normal.Captopril effectively controlled the hypertension in our patient, who had been resistant to conventional management. The agranulocytosis was probably related to captopril because of its clinical course. Agranulocytosis has not been described in any other patients taking captopril treatment in Japan. The underlying disease, renal insufficiency and hypersensitivities to drugs, were relevant in this case.
日本臨床免疫学会の論文

Captopril-associated agranulocytosis in hypertension of lupus nephritis

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