Allergic purpura, including purpura due to foods, drugs and infections

Ackroyd, J F

doi:10.1016/0002-9343(53)90377-5

Cited by 196 publications

(40 citation statements)

References 121 publications

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“…Our results rather favor the early hypothesis by Ackroyd (1), who suggested that the interaction of the drug and platelets generates an antigenic complex. However, Shulman also has suggested that a plasma component with a special affinity for the platelet membrane may react with the drug (5) and indeed we have shown that a plasma or serum component is required for the formationi of the antigen.…”

Section: Discussionsupporting

confidence: 79%

“…In thrombocytopenia induced by various drugs immunoglobulin (Ig)G antibodies have been shown to cause platelet damage in the presence of the offending drug (1). Formation of an antigen-antibody complex evidenced by complement fixation only occurs in the presence of drug, antibody and platelet (2,3).…”

Section: Introductionmentioning

confidence: 99%

“…Two hypotheses have been postulated to explain the pathology of the disorder. Ackroyd (1) suggested that the drug reacts with platelets to form a complex which acts as antigen for antibody synthesis. However, synthesis of antibodies against the drug alone and subsequent nonspecific interaction of the resulting immune complex with platelets which act as "innocent bystanders" have been favored by others (4,5).…”

Section: Introductionmentioning

confidence: 99%

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Study of the factors that cause specific transformation in cultures of lymphocytes from patients with quinine- and quinidine-induced immune thrombocytopenia.

Hosseinzadeh¹,

Firkin²,

Pfueller³

1980

J. Clin. Invest.

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A B S T R A C T Quinine-or quinidine-induced thrombocytopenic purpura is caused by synthesis of an immunoglobulin (Ig)G antibody, which causes platelet damage in the presence of the offending drug. The nature of the antigenic stimulus has been examined by measuring incorporation of [3H]thymidine into DNA during lymphocyte transformation to blast cells in the presence of the drug. Although patients' lymphocytes responded normally to the nonspecific mitogen, phytohemagglutinin P, they did not respond to either drug or platelets alone. However, significant transformation occurred when patients' lymphocytes were cultured for 7 d with homologous or autologous platelets in the presence of therapeutic concentrations of the drugs (0.39-39 ,M). Platelet membranes were more active than intact platelets on the basis of protein content, whereas platelets from a patient with Bernard-Soulier syndrome were inactive. Washed platelets pretreated with the drugs were inactive when cultured with lymphocytes in the absence of the drugs, whereas platelets pretreated similarly in plasma caused transformation. Control lymphocytes from 20 normal patients and 6 patients with nondrug-induced thrombocytopenia were not transformed by drugs and platelets in the presence of normal serum or serum containing drug-dependent antibody, showing that the observed response was specific for presensitized lymphocytes. Thus lymphocytes of patients with drug-induced thrombocytopenia are transformed by an antigen that forms after interaction ofplasma, specific platelet membrane components and the drug.A preliminary report of this work appeared as an abstract in 1979. Thromb. Haemostasis. 42: 1.

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Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Study of the factors that cause specific transformation in cultures of lymphocytes from patients with quinine- and quinidine-induced immune thrombocytopenia.

Hosseinzadeh¹,

Firkin²,

Pfueller³

1980

J. Clin. Invest.

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“…Recently, Hosseinzadeh et al (7) provided new evidence to support Ackroyd's hypothesis (2) by showing that lymphocytes from patients who had experienced quinine-or quinidine-induced thrombocytopenia could be stimulated by platelets previously exposed to drug in the presence of plasma and then washed, but not by drug or platelets alone. They suggested that the stimulating antigen was formed by drug complexed to the platelet membrane with the aid of a plasma cofactor.…”

mentioning

confidence: 99%

“…Two mechanisms have been suggested to explain the etiology of drug-induced immunologic thrombocytopenia. Ackroyd (2) proposed that drug, acting as a hapten, modifies some platelet constituent to produce an antigen that stimulates antibody production. Subsequent challenge of a sensitized individual by the same drug would lead to drug-coated platelets that bind antibody and are destroyed.…”

mentioning

confidence: 99%

Drug-Antibody-Platelet Interaction in Quinine- and Quinidine-induced Thrombocytopenia

Christie¹,

Aster²

1982

J. Clin. Invest.

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A B S T R A C T Binding of quinine-and quinidine-dependent antibodies to platelets was studied using an electroimmunoassay to measure platelet-bound IgG. Antibodies from four patients with drug-induced thrombocytopenia differed significantly in their interaction with platelets: association constants for binding to platelets at high drug concentrations ranged from 0.29 to 2.6 X 107 M-1, the maximum number of antibody molecules bound ranged from 36,000 to 161,000/platelet, the amount of drug necessary to achieve half-maximum binding of antibodies to platelets ranged from 2 to 60 ,tM, and only one of the antibodies cross-reacted with the stereoisomer of the drug to which the patient was sensitized. Binding of the antibodies to platelets was enhanced at the highest achievable molar ratio of drug:antibody, 10,000:1, rather than being inhibited, as would be expected in a conventional, hapten-dependent reaction. The drugantibody-platelet reaction was unaffected by Factor VIII/von Willebrand protein, nonspecifically aggregated IgG, or heat-labile complement components. After pretreatment with tritiated quinine, platelets retained several hundred thousand molecules of drug each, but failed to bind detectable amounts of antibody. However, platelets treated simultaneously with quinine-dependent antibody and tritiated quinine retained significantly more drug after repeated washes than platelets treated with drug and normal serum.These findings support the proposition that in quinine-and quinidine-induced thrombocytopenia, drug and antibody combine first in the soluble phase to form a complex, which then binds with high affinity to a receptor on the platelet surface (innocent bystander reaction), and demonstrate that these antibodies are A preliminary report was presented at the VlIIth International Congress on Thrombosis and Haemostasis, Toronto, Canada, 1981. Thromb. Haemostasis. 46: 296.

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Nonthrombocytopenic Purpura Due to Carbromal Ingestion

Rosenthal¹

1964

Arch Dermatol

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Allergic purpura, including purpura due to foods, drugs and infections

Cited by 196 publications

References 121 publications

Study of the factors that cause specific transformation in cultures of lymphocytes from patients with quinine- and quinidine-induced immune thrombocytopenia.

Study of the factors that cause specific transformation in cultures of lymphocytes from patients with quinine- and quinidine-induced immune thrombocytopenia.

Drug-Antibody-Platelet Interaction in Quinine- and Quinidine-induced Thrombocytopenia

Nonthrombocytopenic Purpura Due to Carbromal Ingestion

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