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H W Altmann

Publications and source records attributed to H W Altmann.

At least 19 recordsLinked to original sources
PubMed1995

[Hepatocellular nodular hyperplasias, adenomas and carcinomas].

Nodular hyperplasias ("hyperplasiomas") are new formations whose development as a required and regulated response can be traced either to compensatory reactions to the loss of cells (regeneration in a narrow sense) and to decreased cellular performance, or to primary growth impulses. Included in this group are: the "macroregenerative nodules" after extensive cell losses; solitary nodules of uncertain etiology; and the minute foci of "micronodular transformation" whose origin can be traced to a particular disturbance of the hepatic blood supply. The so-called "adenomatous hyperplasias" of the cirrhotic liver that have a tendency towards carcinomatous change are not included in this group and are perhaps better considered as "hyperplasiogenic adenomas". The so-called "focal nodular hyperplasia" too, it must be stressed, should be separated from the simple hyperplasias, for it is more closely related to the adenomas, but represents a new formation of limited growth potential. Morphologically it is conspicuously subdivided by multiple connective tissue bands and scars, but it is above all characterized by metaplastically derived neoductuli, and hence it is appropriately designated as a "combined nodule". Among the true uninodular adenomas there are several variants differing in their morphology,--the so-called "atypical" or "intermediate" forms, that can give rise to carcinomas. The hepatocellular carcinoma, that may arise in a variety of ways, presents multiple cytological and histological variants, but only the so-called "fibrolamellar carcinoma" presents also a clinical peculiarity. "Hepatoblastomas" differ from the common hepatocellular carcinomas by their origin in early childhood from immature early precursor cells and, in the later phases of life, from redifferentiated cells that can even give rise to mesenchymal elements. There is no evidence of the existence of particular pluripotential stem cells.

Adenoma↗
PubMed1994

Hepatic neoformations.

The aim of the paper is an accurate histologic description and illustration of those liver lesions that are usually summarized under the heading of "hepatic tumors and related subjects". For in some cases it may be unclear or at least controversial, whether the individual lesion is indeed an autonomous neoplasia or a malformation, regeneration or hyperplasia, the indifferent master term of neoformation is introduced, based on the fact that all of them are characterized by a cellular multiplication. According to common definitory practice the survey distinguishes between mesenchymal (angiomatous and non angiomatous) and epithelial neoformations. Among the latter hepatocellular and cholangiocellular types are distinguished, the criterium for differentiation being a phenomenological one, which is by no means identical with a histogenetical statement. The definition of subgroups mostly adheres to current nomenclatory usage; only occasionally--in the group of endothelial tumors--a novel term is employed, in view of brevity and coordination with the overall system of neoformations.

Epithelium↗
PubMed1992

Epithelial and mixed hepatoblastoma in the adult. Histological observations and general considerations.

Two instances of hepatoblastoma in adults are reported, with one case representing a purely epithelial, the other a mixed epithelio-mesenchymal variant. The purely epithelial tumour, consisting entirely of so-called fetal elements, was present in the liver of a 35-year-old woman without any other hepatic changes, whereas the mixed tumour developed in the coarsely nodular liver of a 73-year-old man with a currently inactive cirrhosis. Besides the epithelial component, this case held predominantly indifferent spindle-shaped and histiocytic mesenchymal cells which frequently gave rise to osteoid and to bony trabeculae, and on occasion also to vascular structures, biliary ducts and even to groups of hepatocytes. The cytological and histological picture of both cases is comparable even in its details to that seen in the hepatoblastomas of early childhood. This concordance should be insisted upon as a diagnostic pre-condition if a mixed tumour in the adult, consisting of several components, is to be accepted as a hepatoblastoma. This similarity also enables us to recognize the purely epithelial variant of the hepatoblastoma in the older patient as belonging to this tumour category, and to separate it from other hepatic carcinomas. It is suggested that in these tumours the pluripotent cells, or the cells that have again become pluripotent, are derived from differentiated hepatocytes; no evidence in favour of the existence of a particular cellular subpopulation or of "stem cells" has been found.

Adult↗
PubMed1992

[Tertiary gummatous syphilis of the liver--an unexpected disease today. Report of two cases].

Today the luetic hepatitis and gummata of liver are very rare manifestations of a tertiary syphilis because of the antibiotic therapy. Therefore a luetic involvement of liver is a most unexpected and at first mostly misinterpreted finding. In the both represented cases foci in the liver were present, which were suspicious for a metastasizing malignoma and set off the search for an unknown primary tumor. In liver biopsies no malignant process was seen, but necroses with a granulomatous reaction at the border were found which were classifiable definitively only after serological investigations as gummata of liver. Especially by the presence of an additionally reactive hepatitis in the remaining liver parenchyma, possibly with some sarcoid-like granulomas, a tertiary gummatous syphilis should be taken into consideration. The regression of gummata in sonography and computertomography as well as the return to normal of the laboratory findings are important parameters in the follow-up to confirm the diagnosis under antibiotic therapy. The described cases stress the importance that even today the tertiary lues should be taken into consideration by liver foci of unknown origin and should be excluded serologically.

Biopsy↗
PubMed1990

Some histological remarks on the fibrolamellar carcinoma of the liver.

Investigations on five fibrolamellar carcinomas of the liver suggest that this tumor originates from purely epithelial proliferations, while the ensuing fibrous growth leading to lamellar formations is but a secondary event. Nevertheless, progressing fibrosis has a considerable influence on cell shape as the surrounded cell complexes are quasi immured, and their supply and transport procedures impaired. Its influence further evokes a compensatory increase of mitochondria so that, in advanced cases, these cells may be mistaken for genuine oncocytes, although the appraisal of an oncocytic tumor is not confirmed. At this point only, increased amount of fibrinogen-containing (endoplasmic) vacuoles and PAS positive globuli are interpreted as phenomena of cellular retention, and so is the accumulation of unexcretable copper. Ultimately, this fibrous incarceration will cause cell death, destruction and depletion resulting in abundant scarring especially in the center of the focus, without, however, signalling any close relationship with focal nodular hyperplasia. Excess fiber formation exerts a proliferation-inhibiting effect resulting in slower growth and consequently, in the more favorable prognosis of this tumor of distinctive and well-characterized morphology.

Adenoma↗
PubMed1990

[Not Available].

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History, Modern 1601-↗
PubMed1985

[Not Available].

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History, Ancient↗
PubMed1977

[The structure of the nucleolus during the inhibition of RNA-and protein synthesis (author's transl)].

In cells treated with antimetabolites to inhibit RNA- and protein synthesis, electron microscopic studies reveal structural alterations of the nucleolus. The morphological appearance of the nucleolus differs depending of the inhibitor used. If transcription is prevented, segregation of nucleolar components is observed. Inhibition of processing of newly synthesized RNA results in a degranulation and an increase in the amount of nucleolar fibrils. A disturbance of the release of nucleolar ribonucleoproteins into the cytoplasm leads to an enlargement and a hypergranulation of the nucleolus. On the other hand interruption of translation of mRNAs has no immediate effect on the appearance of the nucleolar structure. Only after longer treatment of the cells with the translation inhibitor the nucleolus shrinks and becomes degranulated. The use of inhibitors with clearly defined mechanisms of action in a morphological study should make it possible to interpret similar nucleolar alterations seen in cancer cells and virus-infected cells on a molecular biological basis.

Animals↗
PubMed1977

[Iron containing nuclear inclusions in human pigmentary cirrhosis (author's transl)].

In human pigmentary cirrhosis nuclear (pseudo-)inclusions of cytoplasmic material, containing less or more degenerated and therefore faintly stained hemosiderin granules, are to be observed. But sometimes there are also finely fibrillar or granular proteinaceous materials, stainable by the Prussian-blue reaction, lying between the chromatin-strands or occupying the whole nucleus and displacing the chromatin to the nuclear envelope (margination of chromatin). Such uncoloured substances may condense into homogeneous masses and nearly hexagonal (0r related) crystals with a diameter up to 14 micron and a yellow-brownish colour, giving a strongly positive PERL's reaction. In contrast to the preceding stages intranuclear crystals of this kind have been observed in one case only. After destruction of the nuclear envelope and the marginated chromatin the crystals are lying free in the cytoplasm and later on, the cytoplasm being destroyed too, they may be ingested by von Kupffer cells. All the iron containing crystals, to be found in the cytoplasm, derive from former intranuclear inclusions. The intranuclear deposits of iron containing protein are interpreted as ferritin-aggregates. It is supposed that ferritin molecules, built up in the cytoplasm, do enter the nucleus via the pores of the nuclear envelope. Such an event not only signalizes a cytopathologic reaction but in turn may give rise to such additional cytopathologic lesions as cell shrinking and cell death.

Aged↗