A 36-year-old male football player with no significant past medical history recently diagnosed with unprovoked deep venous thrombosis of the lower limb, presented with acute right-sided hemiplegia, hemi-sensory loss, facial upper motor neuron lesion and expressive aphasia. Prior to the presentation, the patient had a history of undocumented fever, but no reported history of chest pain, shortness of breath, weight loss, night sweating, drug abuse, alcohol consumption or family history of similar presentation. With the aid of the above information, the computed tomography (CT) of the brain showed multiple bilateral occipital and frontoparietal areas of hypodensities more on the left cerebral hemisphere. The transthoracic echocardiogram revealed left ventricular ejection fraction of 60%, the presence of masses attached to mitral and aortic valves needed to be evaluated further by tranesophageal echocardiogram (TEE). The TEE showed multiple highly mobile, irregular shape masses attached to right and left coronary cusps of the aortic valve, largest mass measuring 20 × 18 mm2 with eccentric severe aortic regurgitation, no associated abscess or fistula, similar echogenicity mass attached to anterior mitral valve measures 7 × 4 mm2, and posterior mitral valve mass measures 5 × 3 mm2, and there was mild mitral regurgitation and no intracardiac shunt ( and ()). Magnetic resonance imaging (MRI) of the brain ( and ()) revealed multifocal diffusion restrictions involving bilateral high frontal and left thalamus, bilateral occipital lobes, and bilateral cerebellar hemispheres, with no significant mass effect. Forty-eight hours of follow-up CT of the brain confirmed the presence of hemorrhagic transformation. Clinically, the patient showed improvement in the expressive aphasia and the right-sided hemiplegia during the first week of admission. The patient was clinically stable throughout his hospitalization course. The follow-up investigations of all the tests performed on the patient leads to the following conclusions: (1) all blood cultures were negative; (2) Brucella titer and serology for Q fever were negative; (3) markers for tumors came back positive (CA-125 102 U/mL, CA19-9 5247 U/mL, CEA 13.6 U/mL); (4) thrombophilic evaluation, including anti-nuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), antiphospholipid antibodies (cardiolipin IgG and IgM), Factor-V Leiden mutation, homocysteine, Protein-S, Protein-C and Antithrombin-III levels, was unremarkable; and (5) CT scan of chest, abdomen and pelvis unveiled the presence of hypovascular hepatic mass having dimensions of 7.8 × 5.7 × 6.4 cm3, which invaded the right portal vein as well as the right hepatic duct with multiple porta hepatis and retroperitoneal lymphadenopathies, thereby leading to an alarming stage of cholangiocarcinoma (). On a similar note, the peripheral right lung showed lesion with central cavitation probably infarction or metastasis, in addition to the presence of bilateral hypodense renal cervical lesions. The patient underwent ultrasound-guided liver biopsy showed well-differentiated adeno-carcinoma, consistent with the diagnosis of cholangiocarcinoma ( and ()).\nThe follow-up transthoracic echocardiogram after 10 days of admission showed the presence of a small calcified aortic valve mass, which measures 6 × 4 mm2, mild aortic and mitral regurgitation and no evidence of mitral valve mass ( and ()). At this stage, upon his and his family request, the patient was transferred to an oncology center in the United States, where he was recommended for palliative treatment. Unfortunately, 6 months later, the patient died.
A 73-year-old Japanese woman experienced light-headedness and dementia of unknown cause for 6 months. She had had diabetes for 20 years and had a history of surgical excision of breast cancer and laparoscopic cholecystectomy 10 and 20 years before, respectively. Her neurological disturbance had advanced, and she sought treatment at Kansai Medical University Kori Hospital.\nAt the first medical examination, no abnormalities were detected by brain computed tomography (CT) scan. However, 1 month after the consultation, the patient experienced general hypotonia with progressive dementia and was hospitalized. At the time of admission, her blood coagulation tests were as follows (normal range in parentheses): platelets 6.8 × 104/μl (14–34 × 104/μl), fibrinogen 74.0 mg/dl (180–355 mg/dl), D-dimer 101.6 μg/ml (0–0.9 μg/ml), prothrombin time 81.2% (75–130%) and activated partial thromboplastin time 27.9 s (23–35 s). Her serum albumin had decreased to 1.8 g/dl (3.8–5.0 mg/dl), and γ-GTP had increased to 172 U/l (8–45 U/l). The serum CA19-9 level was 376,100 U/ml (<37 U/ml), and the CA15-3 level was 124 U/ml (<27 U/ml), both of which were significantly increased. Upper abdominal CT scan revealed a large ill-defined mass in the periphery of the right liver lobe and multiple ischemic lesions in the spleen. Because of her poor condition, further examination of the liver mass was impossible. Cerebral magnetic resonance imaging showed multi-regional hypointense areas in the hemisphere of her right cortex, which were compatible with acute cerebral infarction. Cardiac ultrasound showed abnormal movements in the mitral and aortic valves.\nDespite continuous anticoagulant therapy, her consciousness deteriorated and she died 3 months after the hospitalization due to multiple organ failure. The postmortem examination was performed 8 h after her death. The main object of the autopsy was to elucidate the pathological cause of the cerebral infarction.