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Biomedical subjects

J Meynadier

Publications and source records attributed to J Meynadier.

At least 163 records · Page 9Linked to original sources
PubMed1978

[The pathogenesis of psoriasis : realities and hypotheses (author's transl)].

Our pathogenic pattern, may be summarised in 7 propositions : - psoriasis is a proliferative disease of the epidermis. - the increased mitotic activity is related to imbalance of cyclic nucleotides and of prostaglandins. - this imbalance may be explained by abnormalities of the membranes of the keratinocytes. - this alteration in cell membranes results from immunological phenomena located in psoriatic epidermis. - the disturbance of immunity with production of auto-antibodies may be related to a deficiency in a sub-population of thymus-dependent lymphocytes. - this cyclic deficiency could be due to a viral agent whose penetration and persistence in the body would be dependent upon multiple genetic factors. - numerous external factors may act upon the various steps of this pathogenic chain, to worsen a pre-existent imbalance and precipitate the development of the lesions.

Antibodies, Antinuclear↗
PubMed1978

[Sézary's syndrome (author's transl)].

The syndrome described in 1938 by Sézary and Bouvrain is characterized by a possibly hyperpigmented erythroderma with oedema and infiltration of the skin, palmo-plantar keratoderma, diffuse alopecia and large lymphadenopathies. The cutaneous histopathology frequently shows a dermal mononuclear infiltrate with, sometimes, epidermal microabcesses. But none of these signs is actually specific for the Sézary syndrom, the only criteria of which is the presence of circulating Sézary cells with their folded, cerebriform nucleus demonstrated by electron microscopy. The Sezary cell is to date clearly identified as a T lymphocyte but membrane markers and Tcell fonction studies could elicite abnormal and poor reactive T cell. In order to assert the Sézary Syndrome it is stated by the authors that the erythroderma must be associated with more than 10% of Sézary cells in peripheral blood. This feature is needed to differentiate the Sézary syndrome from the erythrodermic form of mycosis fondoïdes in which the abnormal T cell proliferation is mainly located in the skin. The relationship with the T cell chronic lymphatic leukemia and the main treatments of the Sezary syndrome are discussed.

Dermatitis, Exfoliative↗
PubMed1978

Immunologic aspects of psoriasis. III. Fc-gamma-receptor bearing mononuclear cells in peripheral blood.

An anti-IgG activity has previously been reported at the cellular level in patients with psoriasis. This activity was demonstrated by the so-called 'rheumatoid' rosette test. In the present work the nature of 'rheumatoid' rosette-forming cells was studied in comparison with other EA rosette techniques. The use of purified cell populations showed that the lymphocytes participating in the 'rheumatoid' rosette phenomenon were lacking conventional T and B cell membrane markers, and were thus referred to as null cells. Such mononuclear cells bearing a receptor for the Fc part of IgG were able to act as killer cells to IgG-coated target cells. The cytotoxic activity was mainly restricted to a small proportion of lymphocytes forming 'rheumatoid' rosettes which had a high avidity for EA complexes. Such cytotoxicity could contribute to the aetiology of lesions in psoriasis.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1978

[In vitro study of cellular immunity in atopic and in contact eczema (author's transl)].

Peripheral blood lymphocytes from 20 atopic dermatitis patients, 10 contact dermatitis and 50 healthy subjects were studied by the following methods: E rosettes, active E rosettes anti-HTLA serum (T cells), surface immunoglobulins (B cells), Ea rosettes (Fc-gamma-receptor bearing cells) stimulation by PHA, ConA, PWM. In contact dermatitis the results only indicated significantly low percentages of active E rosettes (whereas E rosette, HTLA, surface immunoglobulins, Ea rosettes are normal) and a poor response to PHA and ConA. In atopic dermatitis the presence of a T cell defect was assessed by low percentages of E rosettes. However normal results obtained with an anti-HTLA serum indicated that this T cell defect was not quantitative but could be due to intrinsic lymphocyte abnormalities or serum factors. Moreover the percentage of B cells was significantly increased. The stimulation index was lower after ConA than after PHA stimulation. This could be in favor of a T suppressor cell impairment. The place of this T cell defect in atopic dermatitis and the possible correlations with the Sczentivanyi's theory are discussed.

Adolescent↗
PubMed1978

In vitro immunological studies in atopic and contact dermatitis.

Serum immunoglobulins, five lymphocyte markers and three mitogen assays were used in an investigation of 20 patients with atopic dermatitis. A slight impairment of the cell-mediated immunity was detected. Ten patients suffering from contact dermatitis had sub-normal lymphocyte reactivity.

Adolescent↗
PubMed1978

[Oral treatment of severe psoriasis with a new aromatic retinoid (Ro 10-9359) (author's transl)].

The aromatic retinoic acid derivative Ro 10-9359 was administered orally to 25 severe psoriatic patients (14 with generalized plaques, 7 erythrodermic, 4 pustular). The initial dose was 25 mg/20 kg body weight daily for 4 weeks; afterwards the same posology was given every other day during several months (Max : 18 months). Excellent results were obtained in 16 patients (64 p. 100) particularly in severe erythrodermic and pustular psoriasis. However, under follow-up therapy relapses sometimes occurred leading to temporary resumption of initial posology. The most important side effects are cheilitis, palmoplantar scaling with thinning of the skin, hyperhidrosis and diffuse hair loss. A slight increase of transaminases and of alkaline phosphatases was found in a few patients. The Ro 10-9359 compound is a very useful new therapy of severe psoriasis.

Administration, Oral↗
PubMed1976

Immunological aspects of psoriasis. I. Immunoglobulins and anti-IgG factors.

Sixty patients with psoriasis have been studied for quantitative estimation of serum immunoglobulin A, G and M (60 cases), immunoglobulin E (43 cases), salivary immunoglobulin A (28 cases) and anti-IgG factors in the serum (40 cases). All the data have been statistically compared to a large control group (300 subjects). The results show an increase of the serum IgG and IgA means, an increase of salivary IgA which is correlated with the serum IgA, an increase of IgE levels in some patients and the presence of anti-IgG activity in the serum of 45% of patients with psoriasis. All these findings are statistically significant when compared to controls. These data could be in favour of auto-immune processes in psoriasis.

Adult↗
PubMed1976

Immunological aspects of psoriasis. II. Dissociated impairment of thymus-dependent lymphocytes.

We have investigated lymphocyte subpopulations (six different markers) and T cell functions (mitogen responses and serum thymic factor determination) in twenty patients with psoriasis compared with thirty-five healthy subjects. Normal results were found for B cell markers, but significantly lower numbers of T cells were assessed by E-rosettes and anti HTLA serum. Mitogen responses were significantly higher in psoriasis than in normal subjects of the same age. These findings could be in favour of a T cell subpopulation defect involved in an auto-immune pathogenesis of psoriasis.

Adolescent↗
PubMed1976

[The biochemistry of psoriasis].

Numerous general metabolic systems are disturbed in association with psoriasis: the frequency of diabetes mellitus and of hyperuricaemia, lipid disturbances and a decrease in folates as a result of their excessive consumption by the skin. Cutaneous metabolism is also altered. Numerous compounds are formed in excess from glucose: amino acids, fatty acids and sterols, lactic acid--the formation of which persists in the corneal layer, ribose and ribulose--synthesised as a result of glucose-6-phosphate-dehydrogenase hyperactivity (role of the increased catabolism of dehydro-epi-androsterone) and uronic acids. The accumulation of glycogen is probably due to excessive synthesis and impaired breakdown. These abnormalities may exist to a lesser extent in healthy skin. In the corneal layer there are lipid vacuoles visible under the electron microscope. Lipogenesis is increased. The same may apply to lipolysis (blood NEFA are increased). Esterification of cholesterol is decreased. The utilisation of ATP by cell membranes is probably diminished (low ATP ase activity). The absence of formation of keratohyaline is due to persistence of the repression which normally prevents it in the mucus body. Renewal of collagen appears increased. The synthesis of DNA is increased in the lesions and neighbouring areas. It is possible that these various abnormalities are dependent upon modifications in the regulator systems of cyclic AMP and GMP, variations in which are however discussed.

Adenosine Triphosphatases↗