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01.12.2015 | Case report | Ausgabe 1/2015 Open Access

BMC Urology 1/2015

Factor V Leiden mutation triggering four major complications to standard dose cisplatin-chemotherapy for testicular seminoma: a case report

Zeitschrift:
BMC Urology > Ausgabe 1/2015
Autoren:
Klaus-Peter Dieckmann, Petra Anheuser, Ralf Gehrckens, Sven Philip Aries, Raphael Ikogho, Wiebke Hollburg
Wichtige Hinweise

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

KPD conceived the study, wrote the manuscript. PA co-conceived the study, did most of the literature research. RG did most of the radiological examinations, assisted in drafting the manuscript. SPA did the pulmonary examinations, guided particular parts of the clinical management. RI guided particular parts of the clinical management, co-conceived the study. WH did most of the clinical management, assisted in drafting the manuscript. All authors have critically revised and finally approved the manuscript.

Abstract

Background

Major life-threatening complications secondary to cisplatin-based chemotherapy are rare in patients with testicular germ cell tumour (GCT). The incidence of complications increases with dosage of chemotherapy and with a variety of patient-related as well as disease-related conditions. We here report the first case of GCT experiencing as many as four major complications most of which can be explained by the conjunction of several predispositions.

Case presentation

A 48 year old patient with testicular seminoma and bulky retroperitoneal and mediastinal metastases underwent cisplatin based chemotherapy. During the third cycle of chemotherapy, he developed thrombosis of the central venous port device, subtotal splenic infarction, and Bleomycin induced pneumonitis (BIP). Three months after completion of therapy, he was struck by thalamic infarction. Genetic testing then revealed heterozygote mutation of Factor V Leiden (FVL). He received full-dose warfarin anticoagulation treatment and steroid treatment for BIP. 18 months thereafter, the patient is still disease-free, oncologically. Neurological symptoms have disappeared, but pulmonary dysfunction persists with a vital capacity of 50%.

Conclusion

The unique co-incidence of four major complications occurring in this patient were obviously triggered by the genetically determined predisposition of the patient to thrombotic events (FVL). Additionally, several patient-related and disease-related conditions contributed to the unique pattern of complications, i.e. (1) the slightly advanced age (48 years), (2) the prothrombotic condition caused by the disease of cancer, (3) the central venous port device, (4) retroperitoneal bulky metastasis, and (5) cisplatin chemotherapy. Whether or not FVL contributed to the pulmonary fibrosis as well, remains elusive. Practically, in the case of one major vascular complication during cisplatin chemotherapy at standard dose, genetic testing for hereditary thrombophilia should be considered. Thus, precautions for preventing further complications could be initiated.
Literatur
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