Altered expression of angiogenesis and lymphangiogenesis markers in the uninvolved skin of plaque-type psoriasis.

BACKGROUND: Vascular alterations are significant events in the pathomechanism of psoriasis. A disorder in the mechanisms regulating skin angiogenesis and lymphangiogenesis could participate in the pathogenesis of the disease. OBJECTIVES: To quantify differences in the expression of angiogenesis and lymphangiogenesis growth factors, receptors, coreceptors as well as their antagonists in the uninvolved skin of patients with psoriasis compared with the skin of nonpsoriatic volunteers. METHODS: Skin biopsies were collected from the involved skin of 13 patients with untreated plaque-type psoriasis, from their nonlesional skin at distance from the lesions and from the skin of 16 healthy volunteers. The mRNA steady-state level of keratins 10, 14 and 16, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), vimentin, collagen I and IV, proliferating cell nuclear antigen, the various splice variants of vascular endothelial growth factor, VEGF-A, VEGF-C and VEGF-D, their receptors VEGFR1, VEGFR2 and VEGFR3, neuropilin (NRP)-1 and its soluble forms, NRP-2, semaphorin 3A and prox-1, was measured by reverse transcription-polymerase chain reaction. Immunohistochemistry was performed for Ki-67, von Willebrand factor and D2-40. Blood and lymphatic vessel density, area and distance from epidermis were estimated by morphological analysis coupled to an original computer-assisted method of quantification. RESULTS: Skin from healthy volunteers and nonlesional skin from patients with psoriasis displayed similar histological, morphometric and proliferative features. However, a significant overexpression of VEGFR3, the VEGF-A isoform VEGF121, soluble 12 NRP-1 and GAPDH was observed in the nonlesional psoriatic skin as compared with that of normal volunteers. CONCLUSIONS: These data point to significant differences in the blood and lymphatic vascular transcriptome between the clinically normal-appearing skin of patients with psoriasis and the skin of volunteers without psoriasis.

[Biological therapy of inflammatory diseases]. / Le traitement biologique des maladies inflammatoires à médiation immune. Le cas de la dermatologie et de la rhumatologie.

The pathophysiology and the treatment of diseases with clinical presentation so different as rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and psoriasis vulgaris have been revolutionized by the discovery of common pro-inflammatory effector mechanisms involving TNF-alpha and by the use of targeted therapies, the anti-TNF-alpha antibodies. In the past 10 years, our experience has helped several hundreds of patients who were treated with novel drugs, years before they became routinely available. In parallel tools of metrology were developped that can now be applied to the routine patient. Lastly, clinical research on these new drugs has also generated derived research works allowing the university hospital to satisfactorilly fullfil its specific missions.

[Psoriasis and psoriatic arthritis]. / Psoriasis et arthrite psoriasique.

Psoriasis is a frequent multifactorial chronic skin disease that can lead to a decreased quality of life. Some patients also present arthritis. Those two complex inflammatory diseases share some of their characteristics, but several clinical manifestations can be distinguished in each of them. In addition to classical medications (constituted of topical treatments, methotrexate, ciclosporin and retinoids for cutaneous psoriasis and non steroidal anti-inflammatory drugs or methotrexate for psoriatic arthritis), they are the target of a new generation of therapies: the biologics.

[Place of ivermectin in the treatment of scabies]. / Comment je traite ... la gale par l'ivermectine.

Ivermectin is the first oral treatment available for scabies. It is however not licensed for use in Belgium. In this article, we review its mechanism of action, its preferential indications among which crusted scabies and institutional outbreaks, its contra-indications and its advantages in comparison with topical treatments.

[Non bullous impetigo: streptococcal or staphylococcal?]. / Impétigo non bulleux: streptococcique ou staphylococcique?

Non bullous impetigo is very common among the pediatric population. It is caused by bacteria. For twenty years, Staphylococcus aureus has been the most frequently isolated organism (present in 80 % of non bullous impetigo lesions, it is the only pathogen cultured in 50 % of patients). The group A beta-haemolytic streptococcus is at the moment isolated alone in 3% of lesions and in association with S. Aureus in 30 % of patients. An epidemiologic change seems to have occurred. Until the early 1980s, group A beta-haemolytic streptococcus was indeed the most predominant etiologic agent causing non bullous impetigo. Unfortunately, the rate of resistance among staphylococci responsible of non bullous impetigo is increasing. As serious complications can follow this skin infection, an appropriate treatment is necessary combining local care, topical antibiotics and sometimes adjunction of systemic antibiotics.

[Medication of the month. Tazarotene 0.05%-0.1% (Zorac)]. / Le médicament du mois. Tazarotène 0.05%-0.1% (Zorac).

Since April 28th, a new topical retinoid is available in Belgium: tazarotene (Zorac) gel (Pierre Fabre). It exists at two concentrations: 0.05% or 0.1%. It is the first receptor-selective topical retinoid. It is indicated in the treatment of plaque-type psoriasis. In the USA, tazarotene is also licensed for use in the treatment of acne and several studies show its efficacy for the treatment of other skin diseases like photodamage and ichthyoses.