Bleeding cerebral neoplasms with symptomatic hematoma.

AIM: This article discusses the role of intracranial tumors in the etiology of spontaneous intracerebral hematomas, compared to other causes such as hypertension, aneurysm, arteriovenous malformation (AVM) or cavernoma. An analysis of cerebral tumors, with a particular oncological emphasis on intrinsic bleeding during growth and resulting in symptomatic hematoma, is presented. METHODS: We analyzed 110 cases of intracranial tumor with symptomatic bleeding, accounting for 1.5% of 7373 intracranial neoplasms and 4.4% of 2514 intracerebral hematomas, surgically treated at the Department of Neurosurgery in Verona, from 1968 to 2000. The bleeding tumors comprised 36 (33%) glioblastomas, 23 (21%) metastases, 14 (13%) anaplastic gliomas, 13 (12%) low-grade gliomas, 13 (12%) meningiomas, 5 (5%) adenomas, 2 (2%) hemangioblastomas, 2 (2%) melanomas, 1 (1%) neuroblastoma and 1 (1%) pinealoblastoma. RESULTS: Analysis of the data of the 110 cases of tumors with symptomatic hematoma showed that there was a statistically significant correlation between the incidence of bleeding and histological groups according to the World Health Organization classification. A clinical study of these cases indicates that hematoma onset is more frequent in anaplastic gliomas (93%) and meningiomas (62%) than in other pathologies (p=0.008); meningiomas are prevalent on the left side (92%) (p=0.000); favorable bleeding factors correlate with meningioma (62%), (p=0.009). The postoperative short-term results following hematoma evacuation and tumor removal were significantly influenced only by patient age (p=0.000) and preoperative clinical condition (p=0.000). CONCLUSION: The analysis of our study population shows that the tumoral etiology of intracerebral hematomas is by no means negligible, accounting for 4.4% of 2514 hematomas operated on, and emphasizes the fact that not all bleeding neoplasms are malignant. Out of a total of 110 hemorrhagic tumors 23 (21%) were benign and 6 (5%) low-grade. The tumoral origin of cerebral hematoma is not always correctly diagnosed by non-contrast-enhanced CT and angiography, and therefore, in the presence of a hematoma with an "atypical" appearance, it is advisable to complete the diagnostic investigations with contrast-enhanced CT or MRI for the purposes of better planning surgical evacuation of hematoma and tumor removal, bearing in mind the high incidence of bleeding in benign and low-grade tumors as well as the optimal short and long-term results obtained with surgery.

Bronchoalveolar neutrophilia during late asthmatic reactions induced by toluene diisocyanate.

The mechanism by which late asthmatic reactions are induced by toluene diisocyanate (TDI), a low molecular weight chemical that causes occupational asthma in exposed subjects, is unknown. We investigated whether early and late asthmatic reactions induced by TDI are associated with changes in airway responsiveness to methacholine and airway inflammation as determined by bronchoalveolar lavage. We measured FEV1 before and at regular intervals after exposure to TDI, and performed dose-response curves to methacholine and bronchoalveolar lavage at 8 h after TDI in a group of 6 subjects with late asthmatic reactions and in 6 subjects with only early asthmatic reactions. The same procedure was followed 2 h after TDI in a group of 6 subjects with previously documented late asthmatic reactions and in a group of 6 subjects without any previously documented asthmatic reaction after TDI. In subjects with late asthmatic reactions, neutrophils were increased at both 2 and 8 h, and eosinophils and airway responsiveness were increased only at 8 h. By contrast, neutrophils, eosinophils and airway responsiveness were not increased at 8 h after TDI in subjects with an early asthmatic reaction or at 2 h after TDI in normal control subjects. These results suggest that late asthmatic reactions to TDI, and the associated increase in airway responsiveness, may be caused by airway inflammation.