Inherited and/or acquired thrombophilic defects can result in venous or arterial thrombosis. This case report describes arterial thrombotic episodes triggered by the ingestion of an aphrodisiac remedy containing cantharidin in a 46-year-old female patient later discovered to be heterozygous for prothrombin G20210A mutation and seropositive for anti-
The association between the risk of clinically apparent thrombosis and seropositivity for anti-phospholipid (aPL) antibodies including lupus anticoagulant (LA), anti-cardiolipin (aCL), anti-
Cantharidin, the main active component in preparations of
This paper aims to present a temporal association of thrombotic episodes with the ingestion of an aphrodisiac remedy containing cantharidin in an adult female patient later discovered to be heterozygous for prothrombin G20210A mutation and seropositive for anti-
A 46-year-old female patient was admitted to our outpatient clinic for further investigation of arterial thrombotic episodes. She had symptoms of dyspnea and chest pain which started two months ago, and prior evaluation with pulmonary computed tomography (CT) angiography had revealed acute thrombosis of right bronchial artery. Pain and weakness developed in the right arm within a few days, and the Doppler ultrasound demonstrated thrombosis of right radial artery. Two days after starting treatment with subcutaneous enoxaparin at a dose of 1 mg/kg bid and acetylsalicylic acid at a dose of 100 mg/day, she presented with severe abdominal pain, nausea, and vomiting. The abdominal CT scan revealed splenic infarction, which necessitated splenectomy.
Her past medical history was unremarkable for any chronic condition or medication use except a commercially manufactured solution of Spanish fly or
Laboratory tests were as follows: white blood count: 12.05 × 109/L; hemoglobin: 12.9 g/dL; platelet: 500 × 109/L; blood urea nitrogen: 8 mg/dL; creatinine: 0.71 mg/dL; alanine aminotransferase: 29 U/L; aspartate aminotransferase: 22 U/L; lactate dehydrogenase: 167 U/L; prothrombin time (PT): 23.6 sec; activated partial thromboplastin time (aPTT): 34.9 sec; INR: 2.09 (secondary to warfarin); d-dimer: 71 ng/mL; plasma fibrinogen: 2.92 g/L; protein C: 71%; protein S: 83%; activated protein C resistance (APC): 2.74 R. During the follow-up, the patient had persistent mild thrombocytosis, which was presumed to be postsplenectomy thrombocytosis. Antinuclear antibody (ANA) was positive stained as dense fine speckled 70, and anti-neutrophil cytoplasmic antibody (ANCA) was negative. Thrombophilia screening test results were as follows: erythrocyte sedimentation rate: 8 mm/h; C-reactive protein: 2.2 mg/L and anti-dsDNA: 8.4 IU/mL; LA: 1.1 R; anti-CL antibodies of IgM isotype: 0.9 MPL·U/mL; IgG isotype: 0.9 GPL·U/mL; anti-phosphatidylserine antibodies of IgM isotype: 1.7 MPL·U/mL; IgG isotype: 1.7 GPL·U/mL; IgA isotype: 1.2 RU·U/mL; anti-
In this case report, we present a patient who had arterial thrombosis and splenic infarct, also found to be heterozygous for prothrombin G20210A mutation and seropositive for anti-
Anti-phospholipid antibodies may predispose to thrombosis in venous and arterial circulation, as well as microcirculation in the absence of a defined anti-phospholipid antibody syndrome. However, not all aPL antibodies are thrombogenic, and transient increases in serum aPL antibodies have been reported during several infections [
Drug-induced lupus anticoagulant (DILA) is a well-known entity with heterogeneous features and various laboratory findings as well as related clinical complications. Despite the drugs associated with LAs are pharmaceutically not similar and heterogeneous group, one of the hypotheses that may explain the associations is disruption of the cell membrane. Drugs’ pharmacologic action by perturbing cell membranes may decrease action potentials and propagation of charge that may facilitate adhesion of antigens, for example,
Prothrombin G20210A mutation may contribute to a state of hypercoagulability, but not particularly with arterial thrombosis including acute ischemic stroke or transient ischemic attack [
Cantharidin has been used since ancient times as an aphrodisiac due to its effect of perceiving sexual arousal. Poisoning usually results after aphrodisiac ingestion [
We propose that cantharidin exerts its thrombotic effects via two possible major mechanisms. The first is its direct toxic effect on endothelial cells, which was reflected to previous reports as mucosal erosions and nephropathy [
In conclusion, to our knowledge this is the first case report about thrombotic events after ingestion of cantharidin in a patient with anti-
The authors declare that they have no conflicts of interest.