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W. Müller and M. Mortillaro

Seit der klassischen Darstellung der Hypophyse durch Romeis (1940) verlagerte die Ära der Lehre von der Neurosekretion (Scharrer, 1954, und Bargmann, 1954) die Bedeutung des Hinterlappens durch deskriptive und experimentelle Untersuchungen vom Hormonproduzenten in zunehmendem Masse zum Hormonstapelort. Mit elektiven Färbmethoden wurden diese Vorstellungen von Hild (1952) und Hild & Zetler (1952) auf das Zwischenhirn-Hypophysensystem des Menschen übertragen. Beide Autoren schildern ein den Säugern prinzipiell ähnliches Verhalten des färberisch darstellbaren Neurosekrets. Sowohl deren Untersuchungen wie die anderer Autoren (Lit. s. Rabl, 1955) beziehen sich fast ausnahmslos auf Sektionsgut aus pathologischen Instituten. Da es sich auch bei unserem Material2 um Hypophysen von kranken Menschen handelt, ist es in keinem der Fälle möglich von einem typischen Normalbild zu sprechen. Ebensowenig ist es möglich manche Befunde auf ein etwa in der Literatur geschildertes Normalbild des Hinterlappens des Menschen bei elektiver Neurosekretdarstellung zu beziehen (vergl. Hild's Kritik – 1. c. – an der

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M. MÜLLER-SCHULZ and K. WIELCKENS

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B. VON SCHÜTZ and M. J. MÜLLER

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M. Kempfle, K.-O. Mosebach and R. Müller

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A. M. Riondel, M. C. Sanz and A. F. Muller

In 1950 Porter & Silber (1950) described a colour reaction between 17,21-dihydroxy-20-keto-steroids and phenylhydrazine. Four years later, the same authors (Silber & Porter, 1954) developed a relatively simple method for the routine clinical estimation of these corticosteroids in human plasma. The procedure involves four steps: (1) extraction with 5 volumes of chloroform, (2) washing with dilute alkali, (3) extraction of an aliquot of the alkali-washed chloroform extract with alcoholic phenylhydrazine-sulfuric acid reagent, and (4) measurement of optical density in micro-cuvettes in the Beckman spectrophotometer after heating the sample to 60° for 30 minutes.

We have shown in a preliminary communication (Muller et al., 1955) a very good agreement between the relatively simple method of Silber & Porter and the more elaborate procedure of Nelson & Samuels (1952), requiring adsorption of the plasma extract on a Florisil column with subsequent elution. Since both techniques employ the phenylhydrazine-sulfuric acid reagent for identification

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Barbara Krautli, J. Müller, A. M. Landolt and F. von Schulthess

Abstract.

In 2 women with known Addison's disease, progressive hyperpigmentation reappeared years after an initial remission under conventional substitution therapy with cortisone. Excessively elevated plasma ACTH concentrations and radiological evidence of sella turcica deformation led to the diagnosis of ACTH-producing adenomas and prompted their removal by transsphenoidal microsurgery.

In one patient, a large Crooke's cell adenoma with extensive extrasellar expansion had caused severe and irreversible bilateral defects of the visual fields and unilateral optic atrophy. Surgical removal of the tumour and radiotherapy brought about a permanent disappearance of the hyperpigmentation, but eventually led to secondary hypothyroidism. In the second patient, the selective removal of a small intrasellar eosinophilic adenoma consisting of ACTH-producing cells did not alleviate the hyperpigmentation and did not lower the plasma ACTH concentration. However, hyperpigmentation regressed markedly within a year of treatment with a higher dose of cortisone.

The rarity of similar cases in the literature seems to indicate that insufficient feedback suppression of ACTH-producing cells in treated Addison's disease does not by itself induce the development of a pituitary adenoma, but might promote the growth of an independently and coincidentally occurring microadenoma, which would have caused Cushing's disease in a person with intact adrenal glands.

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M. Müller-Bardorff, W. Hochheuser, K. Schwarz and P. C. Scriba