Hj Houthoff

Glial fibrillary acidic protein in human gliomas.

The presence of GFA protein, an astrocyte specific antigen, was investigated in surgical biopsies of ninety‐five gliomas using an immunoperoxidase detection method. In some cases electron microscopy was added and also in one tumour immunoelectron microscopy. The results were correlated with the histological classification and grading of the tumours. In astrocytomas, the number of GFA positive cells decreased with increasing malignancy. Some malignant oligodendrogliomas surprisingly showed GFA in oligodendroglial and gemistocytic tumour cells. Thus, transition from oligodendroglial into astrocytic tumour cells seems to occur. In the mixed astrocytoma/oligodendrogliomas, theoli godendroglioma areas were negative. Subependymomas were strongly GFA positive, whereas ependymomas and medulloblastomas were negative. The presence or absence of GFA seems to contribute a ‘hard’ criterion for classifying gliomas and may be helpful in grading them according to the degree of malignancy.

Intracranial malignant lymphomas

SummaryFifteen primary intracranial reticulum cell sarcomas and five cases with an additional solitary extracranial tumor mass have been studied. For comparison, seven extracranial malignant non-Hodgkin lymphomas and normal lymphoid tissue were included. The methods used on formalin-fixed paraffin-embedded tissue sections were an immunoperoxidase technique for the demonstration of intracellular immunoglobulins, microglial staining, Gomoris reticulin, methylgreen-pyronin, Giemsa, diastase resistant PAS, Mallorys PTAH and H&E. Electron microscopy was performed in one primary brain tumor.According to histopathologic criteria all tumors could be classified as malignant non-Hodgkin lymphomas, predominantly of the pleomorphic immunocytic or of the immunoblastic type; follicular lymphomas were notably absent. In all cases intracellular immunoglobulins were demonstrable in tumor cells and in a majority of the tumors these were monoclonal. Thus, all malignant lymphomas proved to be of B cell origin with demonstrable cytoplasmic immunoglobulin production. Based on the microglial staining more than half of the malignant lymphomas could also be classified as microgliomas. As a comparable staining was present in non-Hodgkin lymphomas outside the CNS, microglioma characteristics are not associated with intracranial growth.

The mechanisms of blood-brain barrier impairment by hyperosmolar perfusion

SummaryProtein tracer flux from brain microvessels has been studied at intervals of 10 s and 5, 15 and 60 min following hyperosmolar perfusion injury of the blood-brain barrier with 0.6 ml of a 4 M urea solution. In one group of Wistar rats 75 mg horseradish peroxidase (HRP) was given intravenously 10 min before killing as an exogenous protein tracer. In another group endogenous IgG was used as tracer; to enhance serum levels and to facilitate demonstration, the rats were immunized with HRP beforehand, resulting in high titer serum antibodies of IgG class. After perfusion fixation and tracer demonstration in Vibratome sections the localization of the tracer was studied in 1 μm Epon sections and unstained ultrathin sections. The incidence of tracer presence was estimated with quantitative and statistical methods.The results indicate that in this experimental model of blood-brain barrier damage protein tracer extravasation only occurs during the first minutes and thus may be a rapidly reversible phenomenon. The signs of endothelial activation include increased numbers of vesicles and channel-like structures. As the ratio of vesicles with and without tracer remains fairly constant, increased vesicle formation seems to occur randomly in activated endothelial cells and thus does not represent a tracer outflow mechanism by itself. Any qualitative sign of endothelial activation and protein tracer uptake may occur with or without tracer passage into the surrounding brain, actual tracer extravasation thus appearing to be an overflow mechanism in endothelial cells that can be estimated only with quantitative methods. Protein tracer extravasation may occur by random uptake in vesicular or channel-like structures or by cytoplasmic pooling in endothelial cells or cell segments; tracer extravasation through interendothelial junctional areas is not substantiated by our results. Removal of extravasated tracer may occur at least in part by local tracer backflow into the lumina of larger vessles. And finally, the differences in extravasation pathways between HRP and IgG appear to be significant, demonstrating that more than one pathway may be involved and that the predominance of a pathway may at least in part be tracer dependent.

Morphology and origin of arachnoid cysts scanning and transmission electron microscopy of three cases

SummaryThree surgically removed primary arachnoidal cysts were studied with scanning electron microscopy (SEM) and two of the cases with transmission electron microscopy (TEM). The cells lining the cyst cavity had microvilli at the surface, true cilia were absent. In the cytoplasm multivesicular bodies, many pinocytotic vesicles, some large vacuoles and strands of tonofilaments were prominent features. The cells were interconnected by desmosome-like junctions and were interconnected by desmosome-like junctions and were separated from the surrounding tissue by a distinct but sometimes incomplete basal membrane.Based on these findings it is concluded that arachnoid cysts are derived from the outer arachnoid cells (subdural neurothelium), the formation of the cysts being attributable to secretory capacity of the subdural neurothelium.

ETRETINATE (TIGASON) HEPATITIS IN 2 PATIENTS

A histologically confirmed, clinically inapparent and reversible hepatitis occurred in 2 patients (1 psoriasis, 1 basal cell nevus syndrome) within the first months after introduction of etretinate therapy. Causes of hepatitis other than etretinate were not found. Reintroduction of etretinate resulted in reactivation and/or persistence of the hepatitis in both patients. These data strongly suggest that the hepatitis in both patients was caused by etretinate. Later the basal cell nevus syndrome patient was given 13-cis-retinoic acid, which caused no liver test disturbances during a follow-up period of 6 months.