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W Saeger

Publications and source records attributed to W Saeger.

At least 181 records · Page 10Linked to original sources
PubMed1978

Feminizing adrenocortical tumor. Histological and ultrastructural study.

A case of a feminizing adrenocortical tumor associated with Cushing's syndrome in a 29 year old male is presented. The ultrastructural features are compared with adrenal tumors secreting aldosterone, glucocorticoids of androgens. As in adrenal carcinomas, this tumor demonstrates nuclear pleomorphism with enlarged nucleoli and nuclear pseudoinclusions. The cytoplasmic organelles show some parallels between feminizing and androgen-secreting adrenal tumors. Different types of mitochondria occur with varying amounts of smooth endoplasmic reticulum. Numerous microbodies are present. Histological and ultrastructural signs indicating probably malignancy are discussed and it is noted that most of the feminizing adrenal tumors are carcinomata. Neither local recurrence nor distant metastases have yet been detected in this case, two years after excision of the tumor.

Adenoma↗
PubMed1978

[Morphological classification of pituitary adenomas and its value for clinical diagnosis].

Pituitary adenomas should be classified not only by their tinctorial affinities but also by their degree of differentiation. Then useful correlation to the clinical data can be obtained; On this principle our own collection of 299 tumors was classified in undifferentiated acidophilic, highly differentiated acidophilic GH cell-, highly differentiated acidophilic prolactin cell-adenomas, in undifferentiated mucoid cell-, highly differentiated mucoid ACTH cell-, highly differentiated mucoid TSH cell-adenomas, in chromophobic adenomas of small cell type and of large cell type, and in oncocytic adenomas. 95% of the cases with acromegaly based on undifferentiated acidophilic or highly differentiated GH cell adenomas. All patients with hypothalamic-hypophyseal Cushing's syndrome or Nelson's syndrome had undifferentiated mucoid cell adenomas or highly differentiated ACTH cell adenomas. In cases with hyperprolactinemia prolactin cell adenomas or chromophobic adenomas of large cell type with ultrastructurally demonstrated very highly developed rough endoplasmic reticulum or endocrinologically inactive chromophobic adenomas of small cell type were found. In the latter cases the prolactin is probably produced not by the tumor but by the surrounding tumor-free pituitary tissue.

Acromegaly↗
PubMed1977

[Eosinophilic granulomatosis: a case report on a rarely found disease of the hypereosinophilic syndrome (author's transl)].

This ia a case report on a eosinophilic granulomatosis. This disease falls nunder the hypereosinophilic syndrome as well as the eosinophilic leukemia, the disseminated eosinophilic collagenosis, and the endocarditis fibroplastica parietalis Löffler. These diseases are characterized by cardiovascular, pulmonary, abdominal and cerebral symptoms. An increased number of eosinophilic granulocytes constitutes the obligatory hematologic feature. Eosinophilic infiltration and vasculitis especially of the small vessels in heart, lung, liver, spleen, lymphnodes, and cerebrum are typical pathological findings. The eosinophilic granulomatosis shows in addition extravascular granulomas with abundant eosinophilic granulocytes. It is assumed that the hypereosinophilic disorders result from the same basic disease. We would suggest to described this basic disease as allergic eosinophilic collagenosis. This term implies both the supposed etiology and the histologic localisation of the disorder.

Adult↗
PubMed1977

[Classification and pathogenesis of pituitary adenomas in humans and animal experiments].

Pituitary adenomas should be classified by the grade of differentiation in undifferentiated (acidophil or mucoid cell type) and in highly differentiated types. Corresponding to their structural identify, the latter are separated into GH cell-, prolactin cell-, TSH cell-, or ACTH cell-adenomas. Chromophobe adenomas which are nearly ungranulated tumors, were divided into small cell- and large cell-adenomas and into oncocytic adenomas. Undifferentiated acidophil and GH cell-adenomas mostly induce an acromegaly. Undifferentiated mucoid and ACTH cell-tumors result exclusively in a hyperfunction of ACTH. The morphological correlate of a hyperprolactinemia is variable. Chromophobe adenomas of small cell type and oncocytic adenomas are on the whole endocrinologically inactive. Studies of the paraadenomatous adenohypophysis let us assume that prolactin cell- and ACTH cell-adenomas develop from hyperplasias of the specific cells. In animal experiments, pituitary adenomas can be classified into highly differentiated (prolactin cell-, TSH cell-, or ACTH cell-adenomas) and also into undifferentiated adenomas. The highly differentiated ones develop hyperplasiogenic and are monohormonally active. They are on the whole structurally identical with the human adenomas. The undifferentiated ones are the consequence of a process of dedifferentiation. They show in part a plurihormonal activity.

Acromegaly↗
PubMed1977

[Simultaneous occurrence of primary hyperparathyroidism and pituitary Cushing's syndrome (author's transl)].

A case of primary hyperparathyroidism and coincidental Cushing's syndrome of hypothalamic-hypophyseal origin is reported. The hyperparathyroidism was based on an adenoma of the parathyroid glands and produced a severe hypercalcaemia (4.5 mmol/l) and calcinosis of kidneys and lungs. The Cushing's syndrome was caused by a hyperplasiogenic ACTH cell-adenoma of the pituitary which had induced a regulative hyperplasia of the ACTH-dependent zones of the adrenal cortex. The ultrastructure of the zona fasciculata and reticularis showed a conspicuous activation of the steroid hormone-producing organelles. The two endocrine diseases added together in skeleton, heart, duodenum, and pancreas. As a sign of hyperparathyroidism the osteoclastic absorption of the bone was strongly increased, whereas the bone formation was reduced due to the hypercortisolism. The pancreas showed a severe acute recurrence of chronic pancreatitis which was induced by a parathyrotoxic crisis. This was the immediate cause of death.

Adenoma↗
PubMed1977

[Morphology of the paraadenomatous adenohypophysis. A contribution to the pathogenesis of pituitary adenomas (author's transl)].

98 biopsies of the paraadenomatous adenohypophysis in acromegaly, galactorrhea combined acromegaly, isolated galactorrhea, hypothalamic-hypopphysial Cushing's disease. Nelson's syndrome, and in nonfunctional adenomas were studied by light microscopic methods in order to find evidence for a possible hyperplasiogenic origin of the different types of adenomas. It was hoped that the numerical relations and structures of hypophysial cells might provide significant information. Nodular ACTH cell-hyperplasia was found frequently apart from ACTH cell-tumors in Cushing's disease and Nelson's syndrome and on this basis we suggest that the adenomas in both diseases arise from hyperplasia. During their further development these adenomas seem to become autonomous, since the number of paraadenomatous ACTH cells decreased in bigger tumors. Some of the cases with isolated galactorrhea showed hyperplasia of acidophil and chromophobe cells in the paraadenomatous adenohypophysis. It can thus be assumed that porlactin cell-tumors also develop from prolactin cell-hyperplasia. Both the adenomas and the nonfunctional tumors in acromegaly seem to grow autonomously from the beginning, since paraadenomatous hyperplasia is seldom seen.

Acromegaly↗
PubMed1976

Selective removal of hypersecreting pituitary adenomas? An analysis of endocrine function, operative and microscopical findings in 101 cases.

The aim of this study of 101 pre- and postoperatively controlled hypersecreting pituitary adenomas (80 acromegalies, 15 Cushing's diseases, 6 Nelson's syndromes) was to establish in what cases a selective adenoma extirpation by the transnasal route is possible and advisable. In primary operations on acromegalics with small and medium size tumours 92% were postoperatively GH normal. Eighty five per cent of these had intact pituitary function. The results with larger tumours were worse (72%). During a control period of 1.5-5.5 years a renewed elevation of GH levels was observed in three cases, all in the first year, but never after clearly selective adenomectomy. These results, and the anterior lobe biopsies, which showed no GH cell hyperplasia, favour selective adenoma extirpation. In contrast to acromegaly, nodular ACTH cell hyperplasia in the anterior lobe was found in most cases of Cushing's disease, and therefore complete hypophysectomy was performed. The cortisol levels became either normal or, in most cases, lower than normal. A selective operation was performed on 6 Nelson tumors. The ACTH values became normal in about 50% of the patients but there was a tendency towards recurrence. Our experiences with Cushing's disease and Nelson's syndrome lead us to recommend total hypophysectomy.

Acromegaly↗
PubMed1976

[Definition and differential diagnosis of chromophobe pituitary adenomas: light and electron microscopic studies].

INTRODUCTION: Chromophobe adenomas have been defined by the absence of secretory granules in them. But this definition has become doubtful since a granulation could be electron microscopically demonstrated. Hence we studied a collection of more than 100 surgically removed pituitary adenomas in order to find precise morphological criteria for the differential diagnosis of chromophobe adenomas, specially from the sparsely granulated chromophilic tumors. Furthermore we tried to find relations between the amount and type of granulation of the tumor cells and the clinical endocrine hyperfunction. MATERIAL AND METHODS: 108 unselected pituitary tumors were studied by light and electron microscopic methods. For histology the tissue was fixed in Helly's fluid or in buffered formalin. The paraffin wax sections were stained with haematoxylin-eosin, PAS, gallocyanin-chrome alum, carmoisine L-orange G-wool green, Herlant's tetrachrome method, and performic acid-alcian blue-PAS-orange G. For electron microscopy small pieces of the tumor were fixed in buffered glutaraldehyde, postfixed in osmium tetroxide, and embedded in epon 812. Sections were stained with toluidine blue for light microscopy. Thin sections were stained with uranyl acetate and lead citrate. Electron microscopical pictures with a primary magnification of 4000 were semi-quantitatively judged for the content and the extent of rough endoplasmic reticulum, Golgi complexes, secretory granules, lysosomes, and mitochondria by a grading with 6 degrees. Results. With special stains and the electron microscope 46 adenomas could be identified which consisted only of slightly granulated or agranular cells but not of densely granulated cells. These were defined as chromophobe adenomas. Oncocytic adenomas were regarded as another tumor type and were not included. One half of the chromophobe adenomas showed ultrastructurally well developed protein-synthesizing organellas. The diameter of the secretory granules amounts up to 500 mum. One quarter had many autolysosomes or lipid droplets. On the other hand, 18 adenomas of our collection exhibited moderate acidophilic granulation with only a few denser or fully granulated cells. These were designated as sparsely granulated acidophilic adenomas. They were rich in organelles. 89% of them showed a well developed rough endoplasmic reticulum and large Golgi complexes as signs of high endocrine activity. The secretory granules had diameters between 200 and 600 upsilonm. The autolysosomes were for the most part small and rare. The 20 fully granulated acidophilic adenomas could be easily recognized and are not discussed in this paper. The sparsely granulated mucoid cell-adenomas were easily identified by a positive PAS-reaction. DISCUSSION: From our studies we conclude that chromophobe adenomas exhibit only sparse granulation and no denser or fully granulated tumor cell...

Adenoma↗
PubMed1975

[Comparative light and electron microscopic studies of oncocytic pituitary adenomas (author's transl)].

In a collection of 108 surgically removed, light and electron microscopically studied pituitary tumors, 19 adenomas (17.6%) could be found of which oncocytic tumor cells constituted more than 50%. These showed histologically, in conformity with the criteria of oncocytes, a fairly broad cytoplasm with finely granular or, in part, finely vacuolar structures and distinct cell membranes. The nuclei were predominantly round and moderately rich in chromatin but also in part, pyknotic. In paraffin-embedded sections the tumors could not be distinguished with certainty from chromophobe or moderately granulated acidophil adenomas. In plastic-embedded sections they could be identified by the typical filmy and finely granular feature of the cytoplasm which was distinctly different from conglomerations of secretory granules. Ultrastructurally they were characterized by many densely packed mitochondria. These were, in part, hydropically swollen. Furthermore, 5 tumors exhibited increased hormone-synthesizing organelles, 2 of which induced an acromegaly. Probably the oncocytic pituitary adenomas are secondarily transformed chromophobe or moderately chromophil tumors which must be regarded as independent, for the most part endocrinologically inactive pituitary tumors. In addition to these purely or almost purely oncocytic tumors further 12 adenomas (11.1%) with oncocytic parts constituting between 10 and 50% of the tissue were in our collection. Of these, 5 were moderately or distinctly acidophil adenomas with clinical symptoms of acromegaly; 2 were, for the most part, mucoid cell adenomas with Nelson's syndrome.

Acromegaly↗
PubMed1975

[Light and electron microscopic studies for classification of pituitary adenomas (author's transl)].

85 surgically removed pituitary adenomas were studied by light and electron microscopical and in part immunohistochemical methods. The tumors were histogically classified and reexamined by the ultrastructure. Histochemically the adenomas could be differentiated in acidophil adenomas (1. group, 41%), mucoid cell adenomas (2. group, 6%), and chromophobe adenomas (3. group, 37%) whereas oncocytic adenomas (4. group, 16%) could be identified only in plastic-embedded sections. About half of the acidophil adenomas were highly differentiated and showed structures which correspond to those of normal STH cells (subgroup 1.1). 1 adenoma consisted of cells of prolactin type (subgroup 1.2). The other acidophil adenomas were differentiated to a lower degree and showed no resemblance to the structures of normal acidophil cells. The 5 mucoid cell adenomas were proved to be with all methods highly differentiated adenomas of ACTH-cell type (subgroup 2.1). TSH-cell adenomas (subgroup 2.2) and lower differentiated mucoid cell adenomas (subgroup 2.0) were lacking in our collection. More than one third of the chromophobe adenomas showed well developed endoplasmic reticulum and Golgi complexes. The other had little and small organellas that resemblances to immature stem cells were evident. The oncocytic adenomas were identified in plastic-embedded sections by their fine-granular structures which were based ultrastructurally not on small secretory granules but on closely arranged mitochondrias.

Adenoma↗
PubMed1975

[Pituitary adenomas of patients with galactorrhea. Light and electron microscopic studies (author's transl)].

A collection of 108 surgically removed pituitary adenomas was studied by histologic, immunohistochemical and electron microscopical methods. It included 7 predominantly chromophobe adenomas of patients whose clinical symptoms consisted of a pure galactorrhea. Ultrastructurally, 4 of these adenomas contained little endoplasmic reticulum so that an endocrine activity of the tumors could not be assumed. These cases represented inactive adenomas which probably led to a disturbance of the secretion of prolactin-inhibiting factor by suprasellar extension resulting in stimulation of the non-tumorous adenohypophysis and secondary hyperprolactinemia. Another 3 adenomas consisted of cells that showed histologic and immunocytochemical reactions of the same kind as normal prolactin cells. Electron microscopically, these adenoma cells exhibited a very well developed rough-surfaced endoplasmic reticulum, dilatation of the Golgi complexes, sparsely arranged pleomorphic secretory granules, an increased number of microtubules, and interdigitating microvilli formed by the cell membrane. These features resembled closely the characteristics of stimulated non-tumorous prolactin cells during lactation, and thus could be termed "prolactin cell adenomas". These tumors surely caused a hyperprolactinemia through their own hormone production. In addition 3 other adenomas were present which showed the same light and electron microscopic structures as the prolactin cell adenomas but did not cause galactorrhea. From the findings in these cases we assume that the tumors effected neither a clinically peculiar hyperprolactinemia nor produced an endocrinologically inactive polypeptide.

Adenoma, Chromophobe↗