ABSTRACT
The histopathological differentiation of the pseudoneoplastic lesions from the tumors of the central nervous system (CNS) is not easy in a proportion of cases and the risk of diagnostic misinterpretation in biopsies of the CNS remains relatively high. Here we discuss selected CNS lesions, which can be easily mistaken for a tumor, particularly in the absence of relevant clinical and neuroradiological data - gliosis, tumefactive demyelination, radionecrosis and focal cortical dysplasia. With the exception of the recently available IDH1 immunohistochemistry, there is a lack of simple and reliable histochemical or molecular markers which could facilitate this differential diagnosis. To avoid a diagnostic error, pathologists have to rely on careful microscopic analysis along with its correlation with clinical data and neuroradiological findings.
Subject(s)
Central Nervous System Diseases/pathology , Central Nervous System Neoplasms/pathology , Central Nervous System Diseases/diagnosis , Central Nervous System Neoplasms/diagnosis , Demyelinating Diseases/diagnosis , Demyelinating Diseases/pathology , Diagnosis, Differential , Gliosis/diagnosis , Gliosis/pathology , Humans , Radiation Injuries/diagnosis , Radiation Injuries/pathologyABSTRACT
Chronic sojourn in hypoxic environment results in the structural remodeling of peripheral pulmonary arteries and pulmonary hypertension. We hypothesize that the pathogenesis of changes in pulmonary vascular structure is related to the increase of radical production induced by lung tissue hypoxia. Hypoxia primes alveolar macrophages to produce more hydrogen peroxide. Furthermore, the increased release of oxygen radicals by other hypoxic lung cells cannot be excluded. Several recent reports demonstrate the oxidant damage of lungs exposed to chronic hypoxia. The production of nitric oxide is high in animals with hypoxic pulmonary hypertension and the serum concentration of nitrotyrosine (radical product of nitric oxide and superoxide interaction) is also increased in chronically hypoxic rats. Antioxidants were shown to be effective in the prevention of hypoxia induced pulmonary hypertension. We suppose that the mechanism by which the radicals stimulate of the vascular remodeling is due to their effect on the metabolism of vascular wall matrix proteins. Non-enzymatic protein alterations and/or activation of collagenolytic matrix metalloproteinases may also participate. The presence of low-molecular weight cleavage products of matrix proteins stimulates the mesenchymal proliferation in the wall of distal pulmonary arteries. Thickened and less compliant peripheral pulmonary vasculature is then more resistant to the blood flow and the hypoxic pulmonary hypertension is developed.
