PubMed · 14137401
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R COLLE. 1964-01-15. [CLINICAL CASE].. https://pubmed.ncbi.nlm.nih.gov/14137401/
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PURPOSE: Molecular approaches as supplements to cytological examination of malignant ascites may play an important role in the clinical management of cancer patients. HLA-G is a potential tumor-associated marker and that one of its isoforms, HLA-G5, produces a secretory protein. This study is to assess the clinical utility of secreted HLA-G levels in differential diagnosis of malignant ascites. EXPERIMENTAL DESIGN: We used ELISA to assess whether secretory HLA-G (sHLA-G) could serve as a marker of malignant ascites in ovarian and breast carcinomas, which represent the most common malignant tumors causing ascites in women. RESULTS: On the basis of immunohistochemistry, 45 (61%) of 74 ovarian serous carcinomas and 22 (25%) invasive ductal carcinomas of the breast demonstrated HLA-G immunoreactivity ranging from 2 to 100% of the tumor cells. HLA-G staining was not detected in a wide variety of normal tissues, including ovarian surface epithelium and normal breast tissue. Revese transcription-PCR demonstrated the presence of HLA-G5 isoform in all of the tumor samples expressing HLA-G. ELISA was performed to measure the sHLA-G in 42 malignant and 18 benign ascites supernatants. sHLA-G levels were significantly higher in malignant ascites than in benign controls (P < 0.001). We found that the area under the receiver-operating characteristic curve for sHLA-G was 0.95 for malignant versus benign ascites specimens. At 100% specificity, the highest sensitivity to detect malignant ascites was 78% (95% confidence interval, 68-88%) at a cutoff of 13 ng/ml. CONCLUSIONS: Our findings suggest that measurement of sHLA-G is a useful molecular adjunct to cytology in the differential diagnosis of malignant versus benign ascites.
Pathological blood platelet activation promotes thrombosis in cancer patients, but the specific substances involved are still under investigation. Tumor exudates have been described to contain lysophosphatidic acid (LPA), a known platelet-activating substance, and the concentration of mediators present in malignant ascites are constantly equilibrated with the concentration in plasma. We hypothesized that the ascites of cancer patients might activate platelets, and that this may be caused by LPA. Indeed, ascites samples from 15 different patients with cancer induced shape change and an increase of cytosolic Ca2+ of isolated platelets; both responses were cross-desensitized by lysophosphatidic acid (LPA), but not by other platelet stimuli. Moreover shape change, Ca2+ mobilization and aggregation induced by ascites could be completely blocked by pretreatment of platelets with specific LPA-receptor antagonists. Phospholipids were extracted from ascites, separated by thin layer chromatography, and individual fractions were tested for activity on platelets. The platelet activating substance co-migrated with LPA, whereas other fractions were inactive. Notably, ascites induced through LPA-receptor activation platelet aggregation in whole blood. Our results suggest that LPA plays an essential role in the pathological platelet activation in cancer patients. We propose that LPA receptor antagonists could be effective in blocking cancer-associated platelet activation and thus preventing thrombosis.
UNLABELLED: A case of chronic eosinophilic ascites with onset in early infancy is described. An intensive diagnostic work-up ruled out other known causes of ascites in childhood. The final diagnosis was made at 2 years of age when a large number of eosinophils was detected in the ascitic fluid. The outcome was complicated by an ex vacuo intraperitoneal haemorrhage. Steroids were able to control the disease only after complete aspiration (1600 ml) of the ascitic fluid. On discontinuation of treatment, peritoneal inflammation recurred indicating steroid-dependency. CONCLUSION: eosinophilic ascites, a very rare disorder in children, should be considered in the differential diagnosis of even very young children presenting with ascites.