Walters Haney (policeclick1)

HCC in non-CE and four-CE except in equilibrium phase (r = 0.42, 0.44, 0.35, and 0.33; all P less then .05), and very strong correlations for liver in all phases (r = 0.86, 0.83, 0.85, 0.87, and 0.84; all P less then .05). Those correlation coefficients were significantly higher for liver for each phase (all P less then .05). FVFDECT did not differ significantly across scan phases regarding HCC or liver (P = .076 and 0.56). Bland-Altman analysis showed fixed bias in all phases between non- and four-CE FVFDECT in HCC and liver.As compared with liver, correlations between FVF measured by DECT-based MMD and FF measured by CSI were weak in HCC in all phases. FVF is reproducible across all scan phases in HCC and liver. The MMD algorithm requires modification for HCC fat quantification given the heterogeneous components of HCC. Simultaneous occurrence of anti-glomerular basement membrane (anti-GBM) disease and thin basement membrane nephropathy (TBMN), both of which invade the type IV collagen subunits, is very rare. Here, we present the case of a 20-year-old male patient diagnosed with both anti-GBM disease and TBMN upon presenting dyspnea and hemoptysis. No laboratory abnormalities, except arterial hypoxemia (PaO275.4 mmHg) and microscopic hematuria, were present. Chest computed tomography revealed bilateral infiltrations in the lower lung fields; thus, administration of empirical antibiotics was initiated. Gross hemoptysis persisted nonetheless, and bronchoscopy revealed diffuse pulmonary hemorrhage with no endobronchial lesions. Broncho-alveolar lavage excluded bacterial pneumonia, tuberculosis, and fungal infection. Enzyme-linked immunosorbent assay of his serum was positive for anti-GBM antibody (95.1 U/mL). Human leukocyte antigen (HLA) test was positive for both HLA-DR15/-DR04. Other than diffuse thinning of the GBM (a research is needed to elucidate the pathogenesis and long-term outcome of the comorbidity of these 2 diseases. When a cancer patient presents with ST-segment elevation on an electrocardiogram (ECG), several causes including acute myocardial infarction (MI) should be considered. Myocardial metastasis is one of the rare causes of ST-segment elevation in cancer patients and its clinical silence makes it difficult to diagnose. A 78-year-old man with lung cancer presented to the emergency room for chest pain. ECG revealed ST-segment elevation in inferior and lateral leads. After emergent coronary angiography, percutaneous coronary intervention (PCI) on proximal right coronary artery was performed. Even 7 days after PCI, ST-segment elevation in inferior and lateral leads still existed. Cardiac markers continued to be within the normal range. We found evidence of metastasis of lung cancer on the inferolateral wall of the myocardium by trans thoracic echocardiogram and positron emission tomography (PET)/computed tomography (CT). We diagnosed myocardial metastasis as the cause of ST-segment elevation in the patient. Myocardial metastasis is one of the differential diagnosis of ST-segment elevation in cancer patients. Periodic ECG is necessary for lung cancer patients and rapid cardiac work-up is recommended when ST-segment elevation is newly discovered. Myocardial metastasis is one of the differential diagnosis of ST-segment elevation in cancer patients. Periodic ECG is necessary for lung cancer patients and rapid cardiac work-up is recommended when ST-segment elevation is newly discovered. Nowadays, myelin oligodendrocyte glycoprotein (MOG)-antibody-associated disease (MOGAD) is regarded as an independent inflammatory demyelinating disease. Here, we report a rare case of unilateral cerebral cortical encephalitis (CCE) with positive anti-MOG antibodies. A 19-year-old woman was admitted to our hospital owing to acute onset fever and headache. Four days later, she experienced a focal seizure that