Claudin-18 Immunohistochemical Staining Facilitates the Identification of Metastatic Carcinoma of Gastric or Pancreatic Origin in Effusion Specimens.

Determining the primary origin of a malignant effusion remains a common challenge for cytopathologists. Although immunohistochemical (IHC) markers are available for most primary sites, ideal IHC markers for metastatic gastric adenocarcinoma and pancreatic ductal adenocarcinoma are lacking, and related interpretation is often hindered by mesothelial cells. We recently revealed that claudin-18 IHC staining is useful for identifying the stomach and pancreas as the primary sites of metastatic adenocarcinoma. Thus, we assessed the use of claudin-18 IHC staining in 111 cell blocks obtained from various metastatic cancers and specimens negative for malignancy. Positive membranous claudin-18 staining was noted in all 10 (100%) metastatic pancreatic ductal adenocarcinomas, 9 (90%) of 10 gastric adenocarcinomas, and 1 (9%) of 11 nonmucinous lung adenocarcinomas. The cases of metastatic mucinous carcinomas of lung origin (1 case) and ovarian origin (1 case) were also positive for claudin-18. The other remaining 89 cases showed variable cytoplasmic staining on some cells (73 cases) or complete absence of staining (16 cases). After normalization to the tumor frequency, the sensitivity and specificity for identifying the stomach or pancreas as primary tumor sites in ascites were 95% (confidence interval: 0.83-0.99) and 99% (confidence interval: 0.94-1), respectively. In conclusion, membranous claudin-18 staining is a useful marker for metastatic gastric adenocarcinoma and pancreatic ductal adenocarcinoma in effusion specimens.

Reduced global longitudinal strain as a marker for early detection of Fabry cardiomyopathy.

AIMS: Fabry cardiomyopathy (FC) is characterized by progressive left ventricular hypertrophy (LVH). Conventional echocardiography is not sensitive in detecting preclinical FC before the development of LVH. We aim to investigate whether myocardial deformation analysis is useful to detect preclinical FC before LVH. METHODS AND RESULTS: One hundred and sixty patients carrying mutated gene were prospectively enrolled, including 86 patients without LVH and 74 patients with LVH. Another 33 healthy individuals were also included for comparison. Standard transthoracic two-dimensional, Doppler, tissue Doppler echocardiography and deformation analysis were performed. The mean age of the overall 193 subjects was 48 ± 15 years, with 51% men. Fabry patients with LVH were older, more often to be men. They also had the worst diastolic function as evidenced by the largest left atrium, lowest E/A, and highest E/e' ratio. The global longitudinal strain (GLS) deteriorated with the development of LVH (control vs. LVH- patients vs. LVH+ patients = -21.2 ± 2.7 vs. -19.0 ± 2.9 vs. -16.5 ± 4.2%, P < 0.001). Despite similar LV systolic, diastolic function, and LV mass, LVH- Fabry patients still had a reduced GLS as well as regional longitudinal strains at mid-to-apical, anterior, and inferolateral wall when compared to healthy subjects. The basal longitudinal strain was consistently worse in male patients than in female patients, irrespective of LVH. CONCLUSION: Reduced GLS could be a marker of early FC before the development of LVH.