A case of renal abscess mimicking metastatic lesion in a patient with lung carcinosarcoma.

Renal abscesses require prompt diagnosis and appropriate intervention, as they can be life-threatening. However, diagnosis based solely on clinical findings is often challenging. We present the case of a 69-year-old woman with left renal masses on follow-up computed tomography (CT) after surgery for pT2aN0M0 lung carcinosarcoma. The masses were localized only in the left kidney without suspected metastatic lesions at other sites. The patient was referred to our department for further evaluation and treatment under a diagnosis of suspected metastatic lung carcinosarcoma of the left kidney. On enhanced CT, the left renal masses, the largest of which had a diameter of 40×36 mm had thick irregular walls gradually enhanced by the contrast media and an internal low-attenuation area. The masses showed heterogeneous signal intensity with a pseudocapsule on T2-weighted magnetic resonance imaging. Clinical symptoms such as fever or costovertebral angle tenderness were absent, and blood and urine tests were not sufficiently inflammatory to suggest a renal abscess. Histopathological findings on CT-guided renal biopsy revealed only inflammatory tissue and no tumor cells. However, because lung carcinosarcoma metastatic nodules could not be ruled out, laparoscopic left nephrectomy was performed for a definitive diagnosis and curative intent. The pathological diagnosis was renal abscess without malignant lesions. Here, we present a case of renal abscess mimicking metastatic lesions in a patient with lung carcinosarcoma. Accurately differentiating renal abscesses from metastatic renal tumors before treatment is often difficult. Renal abscess diagnosis should be considered through a comprehensive evaluation of the clinical findings of individual cases.

Estimation of Microvascular Dysfunction by Using 13N-Ammonia Positron Emission Tomography with Quantitative Myocardial Blood Flow Analysis in Chronic Coronary Syndrome.

BACKGROUND: Although coronary artery disease (CAD) is characterized by epicardial atherosclerosis and microvascular disease, the importance of evaluating microvascular dysfunction has not been sufficiently recognized in clinical practice. We estimated microvascular disease severity by assessing hyperemic microvascular resistance (MVR), as determined by absolute quantification of myocardial blood flow (MBF) with 13N-ammonia positron emission tomography-myocardial perfusion imaging (PET-MPI). METHODS: We retrospectively collected data for 23 CAD patients who underwent both stress/rest PET-MPI and invasive coronary angiography (CAG) with fractional flow reserve (FFR) measurement. Among 30 vessels for which FFR measurement was performed, 13 had a low FFR (FFR ≤0.75). For each patient, myocardial segments of a standard 17-segment model were assigned to the stenotic myocardial area perfused by the FFR-measured vessel and a reference normal-perfusion area based on PET-MPI and the coronary distribution on CAG. Hyperemic MVR was calculated by using the formula, hyperemic MVR = hyperemic mean blood pressure × FFR/hyperemic MBF of the stenotic vessel. RESULTS: A strong negative correlation was observed between hyperemic MVR and hyperemic MBF in the reference normal-perfusion area (R = -0.758, P<0.001). CONCLUSION: Microvascular disease severity in chronic CAD can be estimated by hyperemic MBF of the normal-perfusion area with 13N-ammonia PET-MPI.

Peripheral Coronary Artery Circulatory Dysfunction in Remote Stage Kawasaki Disease Patients Detected by Adenosine Stress 13N-Ammonia Myocardial Perfusion Positron Emission Tomography.

Coronary peripheral circulatory disturbances in the remote stage of Kawasaki disease have been reported. In this study, of the 50 patients in the remote stage of Kawasaki disease who underwent coronary perfusion evaluation using adenosine-loaded 13N-ammonia positron emission tomography, 28 patients who did not have stenosis of ≥75% in the left coronary artery underwent an evaluation for myocardial flow reserve (MFR) of the left anterior descending artery (LAD) and left circumflex artery (LCx). Clinical findings were compared between patients with normal (≥2.0) and abnormal (<2.0) MFRs. In the group with an abnormal MFR in the LAD, the responsiveness of the coronary vascular resistance to adenosine stress decreased even in the LCx (3.50 ± 1.23 vs. 2.39 ± 0.25, p = 0.0100). In the group with an abnormal MFR in the LCx, the responsiveness of the coronary vascular resistance in the LAD also decreased (3.27 ± 1.39 vs. 2.03 ± 0.25, p = 0.0105), and the age of onset of Kawasaki disease tended to be younger in the group with abnormal MFR in the LAD and LCx. We found that the peripheral coronary circulation was extensively impaired in the remote stage of Kawasaki disease, suggesting that an early onset of Kawasaki disease may affect the peripheral coronary circulation in later years.

Efficacy and safety of gemcitabine plus S-1 in pancreatic cancer: a pooled analysis of individual patient data.

BACKGROUND: Three randomised trials (GEST, JACCRO PC-01, and GEMSAP) were conducted to evaluate the efficacy of gemcitabine plus S-1 (GS) vs gemcitabine alone in patients with advanced pancreatic cancer (PC). In this pooled analysis, the efficacy and safety of GS vs gemcitabine were evaluated. METHODS: Additional follow-up was conducted and survival data were updated in each study. A total of 770 patients (gemcitabine 389; GS 381) were included in the pooled analysis. The efficacy and safety data were analysed according to disease extent: locally advanced PC (LAPC) or metastatic PC (MPC). RESULTS: There were 738 (95.8%) overall survival events. In patients with LAPC (n=193), the median survival was 11.83 months for gemcitabine and 16.41 months for GS (hazard ratio (HR)=0.708; 95% confidence intervals (CI), 0.527-0.951; P=0.0220). In patients with MPC (n=577), the median survival was 8.02 months for gemcitabine and 9.43 months for GS (HR=0.872; 95% CI, 0.738-1.032; P=0.1102). The rate of grade 3/4 toxicity (rash and thrombocytopenia in LAPC; rash, diarrhoea, vomiting, and neutropaenia in MPC) was significantly higher for GS than for gemcitabine. CONCLUSIONS: Gemcitabine plus S-1 is a viable treatment alternative to gemcitabine, which is one of the standard treatments in patients with LAPC.

Myocardial T2 Mapping in Patients With Hypertrophic Cardiomyopathy.

OBJECTIVE: The aim of this study was to evaluate the usefulness of T2 mapping for detecting myocardial injuries in patients with hypertrophic cardiomyopathy (HCM). METHODS: Twenty-one HCM patients and 7 healthy volunteers were examined. The T2 values were measured at hyperintense areas (high-T2 areas) identified with T2 mapping, at late gadolinium enhancement (LGE) areas, and in nullified myocardium of the HCM patients. The associations between T2 values and laboratory data or LGE areas were assessed. RESULTS: High-T2 areas had significantly greater T2 values than LGE areas (P < 0.05) and nullified areas (P < 0.01) of HCM and normal myocardium (P < 0.01). The presence of high-T2 areas was associated with an increase in troponin T levels (P = 0.02), and T2 values correlated with the levels of brain natriuretic peptide (P = 0.036, r = 0.86). CONCLUSIONS: T2 mapping identified myocardial injuries suggested by the laboratory data in HCM.