Agranulocytosis Caused by Chlorpropamide

Stein, Julie

doi:10.1001/archinte.1964.00280080022005

Cited by 14 publications

(4 citation statements)

References 19 publications

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“…7., 1966, 1, 148 Chlorpropamide is widely used for the control of late onset nonketotic diabetes mellitus, and is classed as an arylsulphonylurea. Among its many side-effects are blood dyscrasias, which include thrombocytopenia (Fitzpatrick, 1963), leucopenia, low-grade anaemia, eosinophilia (Rothfeld et al, 1960), aplastic anaemia (Erslev, 1964), and agranulocytosis (Stein, 1964). Transient gastrointestinal disturbances, intolerance of alcohol, hypoglycaemia (sometimes prolonged), impairment of liver function (Rothfeld et al, 1960), foetal damage (Campbell, 1963), and neuropathy have been reported.…”

Section: Casementioning

confidence: 99%

Familial incidence of cerebral aneurysms.

Chakravorty¹,

Gleadhill²

1966

BMJ

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Section: Casementioning

confidence: 99%

Familial incidence of cerebral aneurysms.

Chakravorty¹,

Gleadhill²

1966

BMJ

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Section: Fatal Case Of Toxic Erythema Aftermentioning

confidence: 99%

Fatal case of toxic erythema after chlorpropamide (Diabinese).

Tullett¹

1966

BMJ

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Chlorpropamide is widely used for the control of late onset nonketotic diabetes mellitus, and is classed as an arylsulphonylurea. Among its many side-effects are blood dyscrasias, which include thrombocytopenia (Fitzpatrick, 1963), leucopenia, low-grade anaemia, eosinophilia (Rothfeld et al., 1960), aplastic anaemia (Erslev, 1964), and agranulocytosis (Stein, 1964). Transient gastrointestinal disturbances, intolerance of alcohol, hypoglycaemia (sometimes prolonged), impairment of liver function (Rothfeld et al., 1960), foetal damage (Campbell, 1963), and neuropathy have been reported.Purely dermatological toxicity often shows itself as an erythematous rash of varying severity which disappears on withdrawal of the drug. Photosensitivity (Hitselberger and Fosnaugh, 1962), erythema nodosum, erythema multiforme (Stewart et al., 1959), and the Stevens-Johnson syndrome (Yaffee, 1960) have occurred, but hitherto no fatal reaction has been reported in the literature. These skin manifestations are paralleled closely by those due to the sulphonamides, and the fatal effects of some long-acting preparations have recently been reviewed in these columns (B.M.7., 1964). CASE REPORTA lady of 71 consulted her doctor about a scaly rash on her knees and excessive thirst. Psoriasis and diabetes mellitus were diagnosed and Diabinese (chlorpropamide) prescribed, 250 mg. twice daily being given for three days, then increased to 500 mg. twice daily for two days, and-lowered to 250 mg. twice daily as glycosuria was controlled. A few days later she developed an extensive purplish skin eruption, while mouth lesions rendered swallowing painful.The drug was withdrawn on the third day of this reaction and antihistamine given.She was admitted to hospital on the tenth day of the rash, and examination showed perhaps 85% of the skin involved by purpuric lesions, some of which could be recognized as target-like. Marked crusting was present on her face and lips, there was severe conjunctivitis and chemosis, and the oral mucosae were denuded. Large intact bullae were present on the feet and ankles. Her blood-pressure was 150/70 mm. Hg, and no abnormality was found in the heart, lungs, or abdomen. Though a diagnosis of severe drug eruption was made at this time, her general condition gave no cause for alarm. Plasma electrolytes, alkali reserve, and urea were normal, while the blood sugar was 296 mg./100 ml. A radiograph of the chest showed slight cardiac enlargement, a clean sample of urine revealed 20 leucocytes per high-power field, and culture yielded a moderate growth of Staph. pyogenes. Her white cell count was 5,000, and E.S.R. was 27 mm./hour.However, after a further 48 hours her condition deteriorated, the eruption had become more extensive, and a staphylococcus was isolated from the mouth and conjunctivae which was sensitive to a wide range of antibiotics, though untypable by phages. Her blood sugar rose to 520 mg./100 ml. and urine became strongly positive for ketones. Treatment with soluble insulin controlled this moderate ketosis, but sh...

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“…Gastrointestinal symptoms, skin reactions, and blood dyscrasias constitute the major groups (Stein et al, 1964;Dinsdale et al, 1968;Aecker and Hynes, 1969;Norman et al, 1970). The anaphylactic reaction to chlorpropamide as described in the following case has, to the best of our knowledge, not been hitherto reported.…”

mentioning

confidence: 99%

Anaphylactic reaction to chlorpropamide.

Ravid¹,

Rubinstein²,

Cabili³

1971

BMJ

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The total incidence of untoward reactions to chlorpropamide is about 6% (Sayers and Travis, 1965). Gastrointestinal symptoms, skin reactions, and blood dyscrasias constitute the major groups (Stein et al., 1964;Dinsdale et al., 1968;Aecker and Hynes, 1969;Norman et al., 1970). The anaphylactic reaction to chlorpropamide as described in the following case has, to the best of our knowledge, not been hitherto reported. Case HistoryA 46-year-old sanitation worker was admitted to hospital after sudden onset of nausea, retrosternal pressure, and confusion. Diabetes mellitus had been found two months earlier and treated for three weeks by 500 mg of chlorpropamide daily. The patient then stopped the medication. No history of untoward reaction to the drug could be elicited in retrospect. Polydipsia and polyuria made him seek medical help and he was again given chlorpropamide. On the morning of admission he ingested his first two chlorpropamide tablets and then had breakfast; a few minutes later he complained of nausea and increasing retrosternal pressure. He became confused and collapsed and was rushed to hospital.Examination showed pallor, cyanosis, tachypnoea, and tachycardia; the systolic blood pressure was 30-40 mm Hg. Blood was drawn for glucose determination, and 40 ml of 50% glucose solution was injected intravenously. When his condition failed to improve 400 mg of hydrocortisone followed by 1,500 ml of isotonic saline and 46 mEq of sodium bicarbonate were rapidly administered intravenously. Blood pressure then rose to 140/80, he regained consciousness, and the cyanosis subsided. The E.C.G. was normal. The initial blood glucose level (drawn before the intravenous injection of glucose) was 278 mg/100 ml. The hyperglycaemia was subsequently controlled on tolbutamide and he was discharged.Two weeks later he was readmitted because of urticaria. Treatment with tripelennamine and prednisolone for four days brought no relief. Tolbutamide was then withdrawn and the hyperglycaemia was controlled on 24 units of NPH (isophane) insulin. Less than 24 hours after the withdrawal of tolbutamide the urticaria disappeared. The presence of reaginic antibodies to chlorpropamide was tested by means of the Prausnitz-Kiistner reaction: 0-2 ml of the patient's serum was injected intracutaneously into the forearms of three physicians. Twenty-four hours later a similar volume of chlorpropamide solution in isotonic saline (containing about 5 mg of chlorpropamide) was injected into the prepared site and into the contralateral forearm. A typical weal and flare reaction 40 by 20 mm in diameter appeared within 5 to 15 minutes at the prepared sites in all three volunteers, while no reaction occurred at the control sites. CommentThe Prausnitz-Kustner reaction is a time-honoured, reliable procedure for the demonstration of reaginic antibodies. The positive test for anaphylaxis, together with the clinical signs of vascular collapse about half an hour after ingestion of 500 mg of chlorpropamide and in the presence of high blood glucose, leave little...

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Agranulocytosis Caused by Chlorpropamide

Cited by 14 publications

References 19 publications

Familial incidence of cerebral aneurysms.

Familial incidence of cerebral aneurysms.

Fatal case of toxic erythema after chlorpropamide (Diabinese).

Anaphylactic reaction to chlorpropamide.

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