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Biomedical subjects

J F Merlen

Publications and source records attributed to J F Merlen.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

[Klippel-Trenaunay, syndrome or disease].

Two cases which were clinically typical of the Klippel Trenaunay syndrome and in which the integrity of the deep venous system demonstrated by phlebography form the basis for the author's discussion of the various theories and classifications which have been put forward up to now. The authors favour Schobinger's opinion, according to which three varieties of the Klippel Trenaunay syndrome are recognised. Malan's anatomoclinical classification has been adopted : this permits the grouping together of the numerous variations possible in this type of dysplasia.

Adult↗
PubMedDate not supplied

[Klippel-Trenaunay syndrome of the upper extremity. Apropos of 2 cases].

The authors report a case of Klippel-Trenaunay syndrome in the upper limb of a 27 years old migrant manual worker. This very typical case due to agenesis of the humeral vein is used as a basis for a discussion of the theories of Servelle on the pathogenesis of this syndrome.

Abnormalities, Multiple↗
PubMedDate not supplied

[Postphlebitic disease, stasis microangiopathy].

The terminology of this is incorrect, but hallowed by usage; it is an old thrombosis of the deep veins, and therefore part of the venous zone; it terminates distally in the zone of the terminal circulatory units, that is, at a microangiopathy of interstitial and lymphatic venous stasis, and the interstitium is involved. There is a polyangiopathy, all the vascular systems being involved, and there is a panangiopathy, every coat of the wall being damaged. The hydraulics of the blood, tissular liquids and lymph are progressively and permanently thrown into disorder; losses of head, pressure surges, choking and failure of the pumps, obliteration of the valvular canal all follow one another and tractage occurs. Microangiopathies of stasis are not only situated in the skin, the aponevrotic spaces and the vascular walls, but are situated also in the distribution "networks" which affect the flow-conditions and the interstitial restraint from which the treatment indications derive.

Blood Viscosity↗
PubMedDate not supplied

[Pigmentation and venous stasis].

Local pigmentations can occur in the course of venous diseases and are said to be secondary to venous stasis and due to blood pigment. Most often, the pigment is haemosiderin and more rarely melenin pigments. Haemosiderin is a result of dermal biligenesis of extravasated red blood cells, the erythrodiapedesis being due to alterations in the vessel wall. Melanin pigments remain a mystery. Meaanoid may stimulate dermal melanocytes more than the true melanocytes of neural origin which have migrated to the epidermis. Above all, the problem is dominated by stasis and its microvascular and tissue consequences. The pigmentation is part of the "microangiopathy of stasis", as are the pigmentations occurring after therapeutic sclerosis.

Capillaries↗
PubMedDate not supplied

[Acrocyanosis: certain paradoxes, its pathogenesis].

First described by Crocq (1896) the clinical pattern of acrocyanosis is well known and its diagnosis is easy but acrocyanosis is a nosological frame with multiple aspects and a constitutional basis of microvasculotissular dysregulation. Acrocyanosis is made of capillarovenular hypotonia and stasis with a large and permanent opening of arteriovenous glomic anastomosis.

Adolescent↗