[A case of desmoplastic malignant mesothelioma].

A 43-year-old man was admitted to Nara Medical University Hospital because of right-sided chest pain. Computed tomographic examination revealed a right pleural effusion and diffuse pleural thickening. Malignant mesothelioma was diagnosed from the results of a percutaneous pleural biopsy, and the patient then underwent right pleuro-pneumonectomy. The resected specimen was examined by light and electron microscopy, which revealed scattered sarcoma-like malignant cells with some epithelial differentiation, in abundant extracellular collagen with storiform derangement. Therefore, desmoplastic malignant mesothelioma (mixed type) was diagnosed. This is a rare histological subgroup of malignant mesotheliomas. The patient died 2 months after the operation, due to multiple and rapidly growing metastases. After lung tissue was dissolved, ferruginous (asbestos) bodies were counted, and the results were consistent with occupational exposure to asbestos (413 asbestos bodies per 5 g of lung tissue).

Impaired high-shear-stress-induced platelet aggregation in patients with chronic renal failure undergoing haemodialysis.

We investigated shear-induced platelet aggregation (SIPA) in 30 patients with chronic renal failure (CRF) undergoing haemodialysis. 26 patients showed a significant decrease in SIPA at high shear stress but no change in SIPA at low shear stress. The former reaction reflects the interaction between plasma von Willebrand factor (vWF) and its platelet receptors, glycoprotein (GP) Ib-IX and IIb/IIIa complex, whereas the latter is assumed to involve the binding of plasma fibrinogen to GP IIb/IIIa complex. These SIPA profiles in CRF patients after haemodialysis showed almost no change compared to those before haemodialysis. The ratio of ristocetin cofactor/vWF antigen in plasma was slightly lower in CRF patients than in controls (P < 0.01). However, the level of GPIb antigen in the platelets of these patients was significantly reduced (42.1 +/- 20.3% of normal platelets), with partial destruction of GPIb antigen. The number of vWF receptors on the GPIb molecule was quantitated using the GPIb-binding protein alboaggregin-B (AL-B), purified from the snake venom of Trimeresurus albolabris. AL-B bound to GPIb at a total of 48,760 +/- 9944 molecules per normal platelet and a Kd of 85.44 +/- 15.70 nM at saturation. In contrast, binding in CRF platelets was 22,980 +/- 6395 molecules per platelet and Kd was 50.08 +/- 13.83 nM. Taking these results together, we conclude that the impaired SIPA found in CRF patients is due to both abnormalities in plasma vWF and in its platelet GPIb receptor.