Zentralblatt fur allgemeine Pathologie u. pathologische Anatomie最新文献

The 43rd World Health Assembly approved the 10th Revision of the International Classification of Diseases (ICD-10) in May 1990 and recommended its implementation by January 1, 1993. The ICD-10 uses a new alpha-numeric code, which provides sufficient code-numbers for all new entities, included in ICD-10 and for further amendments in the future. The extended tabular list of ICD-10 contains HIV-disease (AIDS) and permits separate coding of HIV-disease resulting in various infections, neoplastic and other diseases, such as HIV-dementia complex. Extensions and rearrangements have been made in other groups of diseases, for instance in the chapter on diseases of the genitourinary system. ICD-10 now permits a clear distinction between glomerular and renal tubulointerstitial diseases. The different groups of glomerular diseases can be further characterized by a fourth-digit subdivision of the code-number according to the histopathological findings. Thus, ICD-10 reflects recent developments in medial science. The scientific and practical impact of ICD-coding on mortality statistics, however, largely depends on the use of precise diagnosis and their proper arrangement on the death certificate by the physician, certifying the death. This permits the underlying cause of death to be clearly identified by the coder. The role of the pathologist in this process is stressed. Exact and internationally unified formulation of the diagnosis will be supported in the future by the on-going project developing an International Nomenclature of Diseases (IND). A few volumes of the IND have already been published in English, others are in preparation.

The author studied the influence of the solvents and of the rinsing fluids on the result of silver impregnation. A titrimetric method is described for the determination of the concentration of formaldehyde solutions.

The cytological findings in fine needle aspiration biopsies of 5 hepatocellular carcinomas and 9 secondary liver tumours were compared with the histological findings in autopsy or surgical material. Definite diagnosis of malignancy was made in all cases. Similarity with liver cells, arrangement of the tumor cells corresponding to the different histological types of hepatocellular carcinoma, and the presence of bile pigment characterize the cytological picture of the hepatocellular carcinoma. Pleomorphic tumour cells and prominent nucleoli are other typical cytological findings. Liver metastasis were correctly typed in nearly all cases by the cytological examinations. The attempt to suggest the primary site is more difficult, but possible in some cases.

Arteriosclerosis is a process over time. It is described with reference to its historical dimension, evolution, aspect of comparative anatomy, and autonomy. The need is emphasized for examining this process in its discontinuity, with a view to realizing the variable nature of causative relationships at different stages of the disease. It is of particular interest to clear up the factors responsible for progression of the arteriosclerotic process. In this context, attention should be focussed at the process of aging and its importance to arteriosclerosis in interaction with exogenous noxae.

Prednisolone was administered to two groups of rats for 2 or 4 weeks, respectively. A third group served for control. Serum glucose and insulin levels were measured, and changes in population size along with alterations in staining density of the intracellular granules in pancreatic B-, A- and D-cells were assessed. Two weeks of prednisolone treatment induced significant increases in the staining density of the intracellular granules of B- and D-cells as well as the population size of A-cells, while significant hyperglucosaemia and hyperinsulinaemia were observed. Four weeks of prednisolone administration induced significant increases in population size of B- and D-cells and significant decrease in the population size of A-cells, while hyperglucosaemia and hyperinsulinaemia were even greater. It is concluded that corticosteroids cause an increase in pancreatic B-cell activity and, eventually A-cell numerical atrophy by altering the glucose metabolism. The changes in activity of D-cells possibly reflect functional adaptation to increased B-cell activity.

Neuropathological findings obtained from a female patient, 49 years of age, with progeria adultorum (Werner's syndrome) are described in this paper. Vascular sclerosis with multiple ischaemic infarctions, cerebral atrophy, and vascular myelopathy were the most strongly pronounced CNS findings. Also recorded were severe lipofuscin depositions from the cortex, dentate nucleus, and olivae as well as amylaceous bodies in the insula of Reil and the hippocampus. Neurofibrillary tangles or plaques were not recordable. The central nervous system proved somewhat comparable to other organs, in that mesenchymal regressive changes were the main features.

Described in this paper are the effects on formalin fixation of 106 human brains autopsied at a large neuropsychiatric hospital. Mass and volume of the brains changed considerably during a 3-week fixation period. On average mass increased by 50 g, volume by 57 ml. Mean brain density decreased during the first week and attained its final value almost at the end of the third week. Most changes seem to happen during the first week. Male and female brains behaved differently. Formulas to predict at autopsy time mass and volume of the brain after 3-week fixation in formalin are presented. Possible interpretations of our findings are discussed and compared with results reported by previous workers on this subject.

Experiments were conducted under various conditions, including hypoxaemia, endothelial damage by means of balloon catheterisation, cholesterol feeding, administration of lipofundin, and obstruction of lymphatic drainage. As a result, damage to endothelial cells along with increase in permeability is considered to be the initial process in the development of arteriosclerosis. This is followed by penetration of plasma, formation of fibrinoid in the subendothelial layer and in the media as well as by a number of cellular phenomena, the latter including adhesion of thrombocytes, penetration of monocytes into the intimal space, and proliferation of smooth muscle cells. Cellular, fibromuscular lesion is, eventually, caused as a result of those processes.

The review deals with two complexes: 1. Role of hepatocytes in the origin and course of general atherosclerosis. 2. The "Perisinusoidal Functional Unit" as pathogenetic factor in atherosclerosis. The central place of hepatocytes in the metabolism of lipoproteins of both exogenous and endogenous origins points to the fact that hepatocytes have a key function in the pathogenesis of atherosclerosis. In order to play their role in the metabolism, lipoproteins have to be capable of reaching the hepatocytes and of getting back from them into the circulation. The requisite for that is the passage of lipoproteins through the sinusoidal wall, i.e. the endothelial sieve. Its structuring is thought to be the cause for both distinct manifestation of atherosclerosis in different species, especially due to exogenous supply of lipids, and increasing risk of atherosclerosis, e.g., by nicotine or certain drugs. The following question might be derived from latest international research: "Is atherosclerosis a liver disease with secondary consequences for the vascular system?"