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INTERESTING IMAGE
Year : 2021  |  Volume : 36  |  Issue : 2  |  Page : 203-204  

Paraneoplastic hyperfibrinolysis: detection of occult prostate cancer with 18F-fluorodeoxyglucose positron emission tomography-computed tomography


Department of Nuclear Medicine and PET-CT, Apollo Gleneagles Hospital, Kolkata, West Bengal, India

Date of Submission21-Aug-2020
Date of Decision28-Aug-2020
Date of Acceptance29-Aug-2020
Date of Web Publication21-Jun-2021

Correspondence Address:
Dr. Punit Sharma
Department of Nuclear Medicine and PET/CT, Apollo Gleneagles Hospital, 58, Canal Circular Road, Kolkata - 700 054, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnm.IJNM_195_20

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   Abstract 


Hyperfibrinolysis caused by abnormal over-activation of the fibrinolytic system can be associated with occult cancer. We present an interesting case of a 48-year-old man with paraneoplastic hyperfibrinolysis, where 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography (PET-CT) was able to detect occult prostate-specific antigen-negative metastatic prostate cancer as the underlying etiology. This shows that while 18F-FDG PET-CT has overall poor sensitivity for prostate cancer, it can be useful in certain clinical situations.

Keywords: 18F-fluorodeoxyglucose, hyperfibrinolysis, hypofibrinogenemia, positron emission tomography-computed tomography, prostate cancer


How to cite this article:
Sharma P. Paraneoplastic hyperfibrinolysis: detection of occult prostate cancer with 18F-fluorodeoxyglucose positron emission tomography-computed tomography. Indian J Nucl Med 2021;36:203-4

How to cite this URL:
Sharma P. Paraneoplastic hyperfibrinolysis: detection of occult prostate cancer with 18F-fluorodeoxyglucose positron emission tomography-computed tomography. Indian J Nucl Med [serial online] 2021 [cited 2021 Jul 27];36:203-4. Available from: https://www.ijnm.in/text.asp?2021/36/2/203/318871



A 48-year-old man presented at our hospital with sudden onset multifocal muscle pains and cutaneous ecchymosis. There was no history of trauma. He had known comorbidities of hypertension and chronic kidney disease (Stage III). He was on a renal diet with fluid restriction, was not on dialysis and antiplatelet. Physical examination revealed tender lumpy swellings in the thighs, back, and shoulders, along with few cutaneous ecchymosis. Ultrasound examination showed multiple intramuscular hematomas. Blood examination revealed moderate anemia (hemoglobin: 8.3 g/dL, normal 12.0–15.0), moderate thrombocytopenia (82,000/μl, normal 1.5–4.0 lacs), raised serum creatinine (2.1 mg/dL, normal 0.6–1.1), and raised serum lactate dehydrogenase (380 IU/L, normal 140–280). Coagulation studies showed prolonged thrombin time (27 s, normal 14–19), with normal prothrombin time (PT) (14.0 s, normal 14.2) and activated thromboplastin time (APTT) (36 s, normal 30–40), low fibrinogen (96 mg/dL, normal 200–400), raised D-dimer (450 ng/ml, normal <250), and fibrin degradation product (48 mg/L, normal <10). Liver function tests were normal. With suspicion of paraneoplastic coagulopathy, multiple tumor markers were assayed. Prostate-specific antigen (PSA) was normal (2.6 ng/mL, normal <4), while carcinoembryonic antigen, cancer antigen-19.9, α-fetoprotein, and β-human chorionic gonadotropin were all normal. A noncontrast 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography (PET-CT) was then performed to localize occult malignancy if any [Figure 1]a, [Figure 1]b, [Figure 1]c, [Figure 1]d, [Figure 1]e, [Figure 1]f, [Figure 1]g. Maximum intensity projection whole-body PET image (a) showed multiple foci of increased 18F-FDG uptake in the body (broken arrows, arrows). On transaxial CT (b) and PET-CT (c) images of the pelvis focal 18F-FDG uptake was seen in the peripheral zone of prostate (bold arrow, SUV max 5.8), raising suspicion of primary prostatic malignancy. Also noted were extensive skeletal sclerotic lesions, including in the pelvic bones (d and e), showing increased 18F-FDG uptake (broken arrows; SUV max 6.5). Some 18F-FDG-avid pelvic nodes were also seen. Many hematomas were seen in the muscles. One in the right rectus femoris muscle is seen in coronal (f) and sagittal (g) PET-CT images of the thigh with peripheral increased 18F-FDG uptake (arrow, SUV max 4.6), suggesting organizing hematoma. Based on PET-CT findings a diagnosis of metastatic prostate cancer was made. Transrectal ultrasound-guided biopsy from the prostate was performed which showed high-grade adenocarcinoma (Gleason score 5 + 4). The patient was then managed with fresh frozen plasma transfusion, hormonal therapy, and spinal palliative radiotherapy. The patient improved clinically and was discharged in stable condition. He was doing fine till follow-up at 4 months.
Figure 1: Maximum intensity projection whole-body positron emission tomography image (a) showed multiple foci of increased 18F-fluorodeoxyglucose uptake in the bones (broken arrows) and muscles (arrows). Transaxial computed tomography (b) and positron emission tomography-computed tomography (c) images of the pelvis showed focal 18F-fluorodeoxyglucose uptake in the right postero-lateral peripheral zone of prostate (bold arrow). Transaxial computed technology (d) and positron emission tomography-computed tomography (e) images also showed 18F-fluorodeoxyglucose-avid extensive skeletal sclerotic lesions in the pelvic bones (broken arrows). Coronal (f) and sagittal (g) positron emission tomography-computed tomography images of thigh showing organizing hematoma in the right rectus femoris muscle with peripheral 18F-fluorodeoxyglucose uptake (arrow)

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Hyperfibrinolysis is characterized by abnormal over-activation of the fibrinolytic system, thereby causing excessive degradation of coagulation factors, including fibrinogen and bleeding.[1] It can be a paraneoplastic disorder, most commonly associated with prostate cancer and promyelocytic leukemia.[2],[3] In that setting, hyperfibrinolysis is caused by the production of urokinase-type plasminogen activator and tissue-type plasminogen activator by tumor cells. Furthermore, some tumor cells can overexpress urokinase plasminogen activator receptor on the cell membrane, which favors over activation of the fibrinolytic cascade.[4] In prostate cancer disseminated intravascular coagulation is the most frequent coagulation disorder (30%–40%), whereas primary hyperfibrinolysis is rare (0.4%–1.6%).[5] These two entities can be differentiated by normal PT and APTT in the latter. While PSA is a sensitive marker for prostate cancer, a subset of patients can have normal PSA values even with high-grade cancers, as was seen in the present case. Such cancers are commonly hormone-refractory and have a poorer prognosis.[6] While 18F-FDG PET-CT has overall low sensitivity for prostate cancer,[7] it continues to be useful in certain clinical scenarios.[8],[9] In the present case, 18F-FDG PET-CT was able to detect the occult PSA negative metastatic prostate cancer as the underlying etiology for acquired hyperfibrinolysis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Kolev K, Longstaff C. Bleeding related to disturbed fibrinolysis. Br J Haematol 2016;175:12-23.  Back to cited text no. 1
    
2.
Sacco E, Pinto F, Sasso F, Racioppi M, Gulino G, Volpe A, et al. Paraneoplastic syndromes in patients with urological malignancies. Urol Int 2009;83:1-11.  Back to cited text no. 2
    
3.
Meijers JC, Oudijk EJ, Mosnier LO, Bos R, Bouma BN, Nieuwenhuis HK, et al. Reduced activity of TAFI (thrombin-activatable fibrinolysis inhibitor) in acute promyelocytic leukaemia. Br J Haematol 2000;108:518-23.  Back to cited text no. 3
    
4.
Falanga A, Marccheti M. Oncology. In: O'Shaughnessy D, Makris M, Lillicrap D, editors. Practical Haemostasis and Thrombosis. Oxford: Blackwell Scientific Publications; 2005. p. 195-6.  Back to cited text no. 4
    
5.
Smith JA Jr., Soloway MS, Young MJ. Complications of advanced prostate cancer. Urology 1999;54:8-14.  Back to cited text no. 5
    
6.
Yang DD, Mahal BA, Sweeney C, Trinh Q, Feng FY, Nguyen PL. Identification of low prostate-specific antigen, high Gleason prostate cancer as a unique hormone-resistant entity with poor survival: A contemporary analysis of 640,000 patients. J Clin Oncol 2017;35:S5080.  Back to cited text no. 6
    
7.
Salminen E, Hogg A, Binns D, Frydenberg M, Hicks R. Investigations with FDG-PET scanning in prostate cancer show limited value for clinical practice. Acta Oncol 2002;41:425-9.  Back to cited text no. 7
    
8.
Jadvar H. Is there use for FDG-PET in prostate cancer? Semin Nucl Med 2016;46:502-6.  Back to cited text no. 8
    
9.
Sharma P, Karunanithi S, Singh Dhull V, Jain S, Bal C, Kumar R. Prostate cancer with lytic bone metastases: 18F-fluorodeoxyglucose positron emission tomography-computed tomography for diagnosis and monitoring response to medical castration therapy. Indian J Nucl Med 2013;28:178-9.  Back to cited text no. 9
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