Zentralblatt fur allgemeine Pathologie u. pathologische Anatomie最新文献

The role played by LDL cholesterol in pathogenesis of atherosclerosis is described, with particular reference being made to the risk factor of hypercholesterolaemia. An account is given of the molecular mechanisms of lipid infiltration, and conclusions are drawn of prophylaxis and therapy of atherosclerosis.

Accumulating mainly experimental evidence from research of the last 3 decades shows that many types of arterial wall injury can accelerate and intensify the development of atherosclerosis in arteries exposed to chronic hyperlipemia by increasing the permeability of their endothelium for plasma lipoproteins, proteins and several types of smooth muscle mitogens (including soluble platelet-derived growth factor). Of the numerous artery-injuring agents studied experimentally today only those that can be proven to operate in humans at concentrations and durations of action that injure animal arteries can be accepted as capable of playing a role in human atherogenesis. Seven such groups of agents can be recognized at present: blood turbulence, hypertension, certain viruses, metabolic disturbances (including hyperlipemia), certain immune insults, exogenous chemicals, and obstruction of adventitial lymphatics. Most of the above agents cause various degenerative changes in individual endothelial cells or open interendothelial junctions, and they seem to promote the penetration of plasma macromolecules into the wall in 3 different ways: directly through the altered endothelial cytoplasm, through opened interendothelial junctions or through transport in the cytoplasm of immigrating monocytes. None of the commonly occurring injury agents produce complete endothelial denudation of wide areas of the arterial cylinders. New findings from the transmission electron microscopic study of step-serial sections of human arteries obtained under conditions minimizing artificial endothelial loss indicate that endothelial denudation accompanied by platelet adherence and aggregation does not occur over early myoproliferative lesions but occasionally develops over small areas of advanced plaques with mostly necrotic or damaged caps and is, therefore, not an initiating event but a late complication of atherosclerosis. Light microscopic serial section studies of human thrombosed vessels in several centers reveal that thrombogenesis in most human atherosclerotic arteries is initiated by a severe structural injury of the cap of advanced plaques that leads to a microscopic break of the plaque surface through which some blood can enter the plaque interior before it is sealed by a thrombus.

The histological inhomogeneity of colorectal adenocarcinomas has hardly been systematically investigated up to now. Currently, however, this awareness is gaining in importance, e.g. within the framework of grading measures, for analysis of immunohistochemical results or for interpretation of flowcytometric data. Thus, 100 colon carcinomas each were semiquantitatively investigated on four different sites in terms of either homogeneous or inhomogeneous expression of histological, cytological and immunohistochemical (CEA, UEA I) criteria. Although all carcinomas contained tubular structures, there was no intraindividual uniformity but considerable inhomogeneity on the part of histological as well as cytological features. Quantitative and qualitative positivity of CEA and UEA I too, varied markedly. Our results lead to the conclusion that the phenotypic inhomogeneity of colorectal carcinoma is at least partially attributable to genetic tumor cell instability. In spite of this, there might be a trend to intra-individual localisation-related tumor cell differentiation, because several parameters showed significant differences between luminal and deep carcinoma regions.

The paper describes an unusual case of two adenomatoid tumours in one patient. The first tumour was diagnosed in a hysterectomy specimen, when the patient was 39 years old. A wedge-shaped fragment was intraoperatively obtained from the left ovary. An adenomatoid tumour of the left ovary was diagnosed two years later. Multiple talc granulomas, inclusion cysts, and adhesions were found in close proximity to the tumour. It seems from this observation and from the reviewed literature that talc crystals as well as repair and inflammatory processes should be taken into account as initiating factors in the development of ovarian adenomatoid tumours in patients with susceptibility to such tumours.

Cholesterol and cholesteryl esters play an active role in the metabolism of intimal cells which are involved in the arteriosclerotic process (macrophages derived from monocytes and smooth muscle cells). LDL is the main carrier protein of both lipids and enters the vessel wall to become retained. Macrophages in cell culture have been shown to internalise LDL in an irregular fashion, if LDL is modified by oxidation, by formation of complexes with proteoglycans, malondialdehyde, etc. The development of foam cells in the intima may be interpreted in this way. Lipid-laden smooth muscle cells appear as well. Importance must be attributed to the processes of lysosomal hydrolysis of cholesteryl esters and subsequent re-esterification and hydrolysis of these lipids in cytoplasma. The free cholesterol delivered in this way may be transported by a carrier protein to the cell surface, taken up by the cholesterol acceptor HDL, and removed from the vessel wall. Phospholipids and apo E take part in this cholesterol reverse transport. But the ability of arterial tissue to release cholesterol is limited. Extracellular precipitations of cholesterol occur in the lipid accumulations which are sclerogenic. In advanced ulcerated arteriosclerosis they are the source of cholesterol crystal embolization. Cholesteryl esters extruded in the extracellular space by lysis of foam cells are taken up by monocyte-derived macrophages after interaction with albumin or fibronectin which function as opsonins.

Occurrence of mature and immature chorionic villi was morphometrically analysed in 30 human placentae of children born on term. The following results were obtained from a method specially developed for surface determination of villus cross-section: The surface of mature villi (end or absorption villi) in children born on term with low birth weight was much smaller than that of immature villi. Total surfaces of mature and immature villi were almost equal in size as of the 25th percentile of child weight. The importance is underlined of a "transitional" class between hypotrophic and eutrophic children born on term, and a pattern of results is suggested.

The structures of normal ductal and ductular epithelium were compared with cytological peculiarities of pancreas carcinoma. This provided the basis on which to propose histogenetic classification of exocrine pancreas carcinoma. Most of the pancreas carcinomas are adenocarcinomas and originate from small lateral ductules. Preneoplastic ductal alterations, such as proliferation of ductal epithelium, adenomatous dysplasia, and light-cell transformation, may be topographically distinguished from ductular changes, including centroacinic hyperplasia, oncocytic transformation, microglandular metaplasia, ductulo-acinic metaplasia, hepatocellular metaplasia, and peri-insular metaplasia. The close correlations that exist between ductular and acinic cells may be summarised under the cover term of terminal ductulo-acinic intercalated duct complex. Dysplasia is generally accompanied by decline in neutral glycosaminoglycans and occurrence of unsubstituted sialomucin of the embryonic type.

The surface of coronary arteries is subjected to pronounced changes in all stages of atherogenesis. Structural and functional re-arrangements within the endothelial cell monolayer reflect one or another degree of manifestation of defensive or adaptative reactions in the course of pathogenesis. The formation of crater-like defects and monocyte adhesions is a constant and characteristic feature of initial stages of atherosclerosis. Focal formation of microthrombi can be observed in initial stages of atherogenesis. Endothelium impairment and its regeneration occur at all stages of atherogenesis. Macrophages of monocyte origin play a key role in the formation of foam cells.

Atherosclerotic involvement of 1,106 coronary arterial trees was investigated by means of gross inspection, light microscopy, and the method of successive observations of similar topographic sites placed in sequence according to age, sex, cause of death, and anatomic branching pattern. The results obtained, based on strict adherence to routine autopsy protocols, were compared with control studies, which demonstrated that such strict adherence had constrained us to overlook the following aspects: a) existence of particular anatomic branching patterns, such as those of atherogenic character and/or involved in onset of myocardial ischemia; b) development of obstructive plaques in coronary branch vessels; c) presence of obstructive lesions in vessels which supply the conduction system; d) the obstructive character of platelet and fibrin microemboli and thrombi which showered the intramyocardial vessels; e) accurate identification, classification, and grading of atherosclerotic lesions with the aid of routine autopsy protocols, which was not possible in our material.