Two cases of Ticlopidine-induced neutropenia in patients with cardiovascular disease

Ticlopidine is an antiplatelet agent used as a drug to prevent the recurrence of cerebral infarction or ischemic heart disease. Close attention has recently been paid to the superiority of this drug to aspirin in the prevention of stroke. Its mechanism of action differs from aspirin, dipyridamole, and sulfinpyrazone. Inhibition of the adenosine diphosphate induced pathway of platelet aggregation, along with the activation of adenylate cyclase and suppression of platelet-activating factor and thromboxane A2, are the postulated mechanisms of action of ticlopidine. Because ticlopidine causes neutropenia and agranulocytosis in roughly 1% of treated patients, usually within the first 3 months of treatment, this drug has been reserved for patients intolerant to aspirin therapy. We reported two cases of ticlopidine-induced neutropenia and one patient hospitalized with severe neutropenia and pneumonia.

Two cases of Ticlopidine-induced neutropenia in patients with cardiovascular disease

Ticlopidine is an antiplatelet agent used as a drug to prevent the recurrence of cerebral infarction or ischemic heart disease. Close attention has recently been paid to the superiority of this drug to aspirin in the prevention of stroke. Its mechanism of action differs from aspirin, dipyridamole, and sulfinpyrazone. Inhibition of the adenosine diphosphate induced pathway of platelet aggregation, along with the activation of adenylate cyclase and suppression of platelet-activating factor and thromboxane A2, are the postulated mechanisms of action of ticlopidine. Because ticlopidine causes neutropenia and agranulocytosis in roughly 1% of treated patients, usually within the first 3 months of treatment, this drug has been reserved for patients intolerant to aspirin therapy. We reported two cases of ticlopidine-induced neutropenia and one patient hospitalized with severe neutropenia and pneumonia.

Avanços terapêuticos em cardiologia: parte 4. Antiplaquetários em cardiologia / Terapeutic advances in cardiology: Part 4. Antiplatelets in cardiology

Os autores fazem uma revisäo dos antiagregantes plaquetários disponíveis. Chamam a atençäo que a hirudina é inibidora da trombina, o verapamil é antagonista da adrenalina, o ridogrel e o ômega 3 bloqueiam os endoperóxidos bem como a sulfinpirazona, a aspirina, dipiridamol e ticlopidina. Existem antiagregantes com açäo do fator de ativaçäo plaquetária como a ginkgo-biloba e o diltiazem. Fazem uma revisäo das indicaçöes clínicas destas drogas à luz dos conhecimentos atuais

Clinical profile, therapeutic approach and outcome of gouty arthritis in northern India.

Thirty patients with gouty arthritis were studied over 3 years. The diagnosis was established with the help of polarised light microscopy. All the patients were males, with a median age of 45 years. They belonged to the middle or upper socio-economic class and were obese (mean body mass index 29.7). Chronic alcoholism, diabetes mellitus and hypertension were present in one patient each. No patient had symptomatic coronary artery disease. Although 6 patients had a history of renal colic, only one had gouty nephropathy with chronic renal failure. Six patients had a positive family history of gout. The disease involved mostly the joints of the lower extremity and podagra was observed in 70% of patients. Eight patients had tophi at various sites. There were 17 'over producers' and 13 'under excretors' of uric acid. The treatment consisted of patient education, symptomatic control with non steroidal anti-inflammatory drugs and/or colchicine and antihyperuricaemic therapy. The overproducers were treated with allopurinol while the under excretors were treated with [corrected] sulfinpyrazone. In general, there was a good response to therapy as indicated by lowering of serum uric acid and the number of painful episodes per year. The overall profile of the disease appears similar to that seen in the West.

Estado actual de la terapia antiplaquetaria / Current status of antiplatelet therapy

Se definen los mecanismos de acción y el efecto preventivo de las drogas anti-plaquetarias en padecimientos cardiovasculares y cerebrales, a partir de estudios bibliográficos. Se concluye que el dipiridamol y la sulfinpirazona no superan al ácido acetíl salicílico como antiagregante plaquetario y que este último continúa como droga de elección para este tipo de profilaxis. Se hace énfasis en estudios con ácido acetíl salicílico en bajas dosis como antiagregante plaquetario

Prostaglandinas, ácido acetilsalicílico, dipiridamol e sulfinpirazona na doença coronária / Prostaglandins acetylsalicylic acid, dipyridamol and sulfinpyrazone in coronary disease

As prostaglandinas säo substâncias existentes em todos os tecidos do organismo. Säo atuantes à pequena distância do sítio de produçäo. Têm efeitos biológicos marcantes, sobretudo na circulaçäo coronária, com grandes implicaçöes na doença arterial coronária. Drogas como ácido acetilsalicílico, dipiridamol e sulfinpirazona exercem seus benefícios porque têm efeitos farmacológicos nas prostaglandinas

Efectos de sulfinpirazona sobre tejidos miocárdicos con estimulación eléctrica o sin ella / Effects of sulfinpyrazone on myocardial tissues with or without electrical stimulation

Se estudiaron in vitro los efectos del ácido arquidónico (AAq) y sulfinpirazona (SP) sobre miocardio de rata "suquía" de 240+ ou - 10g. Bandas auriculares y ventriculares fueron instaladas en solución Krebs-bicarbonato a 36 + ou- 1-C, registrado tensión contráctil isométrica (TC) y niveles de malonato (MDA), con electroestimulación o sin ella (1,6 Hz), AAq (2,5 microng/ml) y SP (375, 750, 1.500 y 3.000 microng/ml). AAq deprimió 100% de la TC de ambos preparados, registrándose en tiempos variables (9 a 17 min.) recuperación espontánea en la mayoría de los casos, aunque sin recuperar los valores iniciales. La reactividad eléctrica aumentó en el tejido auricular, pero no en el ventricular. Los efectos de SP dependen de la concentración; 375 microng/ml bajan la TC auricular 87 + ou - 7,3%. La respuesta ventricular a esa dosis fue variable, aunque la TC disminuyó en 61,5% de los preparados; 3 mg/ml son homogéneamente estimulantes. La reactividad eléctrica disminuye con SP. La concentración de MDA en los preparados auriculares cayó muy significativamente (p<0,001) después de SP. En los ventriculares se observó disminución de menor magnitud, también significativa (p<0,02). La suma algebraica de caída y recuperación de TC de los preparados auriculares después de dar SP, da un porcentaje de pérdida similar al descenso del malonato (+ ou - 25%). Se sugiere que: a) AAq deprime el miocardio por acción directa sin descartar alguna transformación inmediata en derivados activos. b) La SP inhibiría distintas enzimas en función de las dosis. c) El MDA parece ser consumido por el tejido miocárdico o metabolizado en el medio. Se plantean explicaciones alternativas para este fenómeno y su relación con el mecanismo de acción de la sulfinpirazona