[Expression of CD44 and isoforms v4, v5, v6, v7, v10--new prognostic parameters in ductal pancreatic carcinoma?]. / Expression von CD44 und seiner Isoformen v4, v5, v6, v7, v10--neue prognostische Parameter beim duktalen Pankreascarcinom?

UNLABELLED: Prognostically relevant factors based on the histological assessment of the resected pancreas are known. However, additional parameters, such as biological staging of the intrinsic malignant potentiality of the tumor, would be useful. There has been no uniform finding of a relationship between CD44 variant expression and tumor progression. METHOD: We assessed the expression pattern and prognostic impact of CD44 standard and CD44 isoforms v4, v5, v6, v7 and v10 in 40 ductal pancreatic carcinomas by immunochemistry on paraffin-embedded tumor material in patients after tumor resection. At the time of the investigation neither histomorphological parameters nor the survival time were known. RESULTS: There was no correlation between the histomorphological parameter and the expression of CD44 splice variants. CD44 splice variants v4-v10 were almost only expressed in tumor tissue. In ductal pancreatic carcinoma, patients with an overexpression of CD44 splice variants had a worse prognosis. However, because of the small number of cases this was statistically not significant. CONCLUSION: CD44 splice variants may have an influence on prognosis in ductal pancreatic carcinoma. However, further investigation on a larger number of patients is necessary to confirm these results.

[Melkersson-Rosenthal syndrome. 2: Diagnosis, differential diagnosis, course, prognosis, neuropathology, therapy]. / Melkersson-Rosenthal-Syndrom. Teil 2: Diagnose (Forts.), Differentialdiagnose, Verlauf, Prognose, Neuropathologie, Therapie.

The diagnosis of Melkersson-Rosenthal syndrome (MRS) is rarely established, mainly because abortive cases are common. The principal symptoms are recurrent circumscribed swelling mostly of the orofacial region, peripheral facial paralysis and lingua plicata, which is nowadays no longer regarded as pathognostic. The syndrome is defined best as general disorder respectively "recurrent edematous granulomatosis" with specific pathoclisis to "angioneurotic intermittent edemas". The--non obligatory--classical histological finding is cheilitis granulomatosa. Etiopathogenesis, clinic, symptomatology and therapy are dealt with. Disorders of the function of the salivary glands, vegetative marginal symptoms, extrafacial intermittent edemas, cranial nerve syndromes and mostly mild peripheral neural and/or CNS syndromes along with psychiatric disorders are communicated. Atypical constellations of symptoms, differential diagnosis and neuropathological results are discussed. Finally neurovegetative, pathophysiological and phylogenetic aspects as well as therapeutic principles are mentioned.

[Neurological-psychiatrical and muscular manifestations of vasculitis nodosa (author's transl)]. / Die neurologisch-psychiatrischen und muskulären Manifestationen der Vasculitis nodosa.

A general review on vasculitis nodosa of report in literature since the work of Strammler 1958 is given. The neurological and psychiatric manifestations of the disease are completely dealt with, whereas dermatological, ophthalmological and otological aspects are brieftly mentioned. Varieties of diffuse and localized cerebral, as well as peripheral syndromes are described. The neuropathological findings are also discussed extensively.

[Erythematodes and nervous system (author's transl)]. / Erythematodes und Nervensystem.

Lupus erythematodes is related to the vegetative nervous system in Raynaud's disease, the butterfly distribution in the face, the involvement of the lateral part of the eyebrows (Hertoghe) and in cerebral attacks. Involvement of peripheral and central animal nervous systems is common and produces primary and secondary syndromes. Prominent are polymyositis or lupus-myopathy, in the brain mainly functional psychoses, epileptiform attacks, and a variety of focal, often very massive, signs. There are very clear differences from the neurologic signs of dermatomyositis, less so from arteritis nodosa and even less from progressive sclerodermia. Peripheral neurologic syndromes in lupus erythematosus are less common and more subtle than in arteritis nodosa. Bio-electric parameters of the petitmal-trias have been found. The relative absence of collagenoses from the spinal cord is also noticed in lupus erythematosus. Signs of involvement here appear to be limited and often subacute. Differential diagnosis has to consider many neurologic diseases, a special problem when MS is simulated just as in sclerodermia. Since cerbral attacks appear early in about 5%, the use of anticonvulsive drugs, particularly of the hydantoin group, provides special problems. Signs of myasthenia demand further attention. The neuropathologic changes are known in essential points and can obviously hardly be mistaken for inflammatory processes due to other causes. Certain basic facts appear to apply to other collagenoses. All 4 "grand" or "classic" collagen diseases are very similar and have much in common, but also show more or less definite differences. This is true for their clinical and anatomical appearance and last but not least to their neurologic aspects. The "roof-concept" of Collagenosis" is once more proved to be justified. As far as is known today the autonomic system plays a decisive and obligatory role only is sclerodermia. This syndrome is also the only one which contains the odd phenomenon of atrophy of which the best-known form is facial hemia-atrophy.