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EOSINOPHILIA AS TRIGGER FACTOR FOR DEEP VEIN THROMBOSIS AND PULMONARY EMBOLIA IN A PACIENT WITH THROMBOPHILIA

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Introduction. Pulmonary infiltrate and eosinophilia represent a heterogenous group of diseases causes by extrinsic or intrinsic factors. Extrinsic factors represented by medication or infectious agents (parasites, fungi, mycobacteria) may trigger an eosinophilic immune response. We report the case of a 53 years old male patient with pulmonary infiltrate and eosinophilia secondary to Toxocariasis infection who was diagnosed with deep vein thrombosis and pulmonary embolism one month later from the diagnosis of pneumonia. Further investigations demonstrated a hypercoagulable state. Case presentation. On March 2015 a 53 years old male came to my office because of a very intense pain on the left posterior thorax which increased by deeply breathing. Physical exam was in normal range, but chest computer tomography without contrast done in emergency showed pulmonary infiltrate at the base of the left lung with pleuritic reaction. Blood tests showed white blood cells at the upper range with eosinophilia (21.75%, 2,050/mc) and inflammatory syndrome. Investigations for eosinophilia showed a positive Western blot test for Toxocara canis so the patient began the treatment with Albendazolum 800 mg/day for three weeks with positive response. One month later the patient visited us for a pain on the right calf. The ultrasound Doppler vein confirmed the diagnosis of deep vein thrombosis and the chest Computer Tomography with contrast substance described mild right pulmonary embolism. The patient started the anticoagulant treatment. Thrombophilia tests were done, MTHFR A1298C gene and PAI1 675 were positive. Discussions. Helminthic infections are associated with eosinophilia. Helminths who migrate to the viscera as like as Toxocara canis could produce high eosinophilic response. Our questions was if eosinophilia was responsible for the patient thrombosis or was it only the trigger factor? As two genetic tests for thrombophilia (MTHFR A1298C gene and PAI1 675) were positive we considered deep vein thrombosis and pulmonary embolism in the context of hypercoagulable states. Conclusion. This case highlights the implication of eosinophilia as trigger factor for vein thrombosis and pulmonary embolism.
Title: EOSINOPHILIA AS TRIGGER FACTOR FOR DEEP VEIN THROMBOSIS AND PULMONARY EMBOLIA IN A PACIENT WITH THROMBOPHILIA
Description:
Introduction.
Pulmonary infiltrate and eosinophilia represent a heterogenous group of diseases causes by extrinsic or intrinsic factors.
Extrinsic factors represented by medication or infectious agents (parasites, fungi, mycobacteria) may trigger an eosinophilic immune response.
We report the case of a 53 years old male patient with pulmonary infiltrate and eosinophilia secondary to Toxocariasis infection who was diagnosed with deep vein thrombosis and pulmonary embolism one month later from the diagnosis of pneumonia.
Further investigations demonstrated a hypercoagulable state.
Case presentation.
On March 2015 a 53 years old male came to my office because of a very intense pain on the left posterior thorax which increased by deeply breathing.
Physical exam was in normal range, but chest computer tomography without contrast done in emergency showed pulmonary infiltrate at the base of the left lung with pleuritic reaction.
Blood tests showed white blood cells at the upper range with eosinophilia (21.
75%, 2,050/mc) and inflammatory syndrome.
Investigations for eosinophilia showed a positive Western blot test for Toxocara canis so the patient began the treatment with Albendazolum 800 mg/day for three weeks with positive response.
One month later the patient visited us for a pain on the right calf.
The ultrasound Doppler vein confirmed the diagnosis of deep vein thrombosis and the chest Computer Tomography with contrast substance described mild right pulmonary embolism.
The patient started the anticoagulant treatment.
Thrombophilia tests were done, MTHFR A1298C gene and PAI1 675 were positive.
Discussions.
Helminthic infections are associated with eosinophilia.
Helminths who migrate to the viscera as like as Toxocara canis could produce high eosinophilic response.
Our questions was if eosinophilia was responsible for the patient thrombosis or was it only the trigger factor? As two genetic tests for thrombophilia (MTHFR A1298C gene and PAI1 675) were positive we considered deep vein thrombosis and pulmonary embolism in the context of hypercoagulable states.
Conclusion.
This case highlights the implication of eosinophilia as trigger factor for vein thrombosis and pulmonary embolism.

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