The data indicate that increased beta-endorphin in psoriatic skin might affect both substance P-mediated neurogenic inflammation and transmission of sensory stimuli due to local antinociceptive effects of this opioid. The differences in the neurogenic response in type I and II psoriasis may be related to the degradation of substance P and beta-endorphin by neutral proteinases in the lesional skin.
Summary
Serum beta‐endorphin was quantified by radioimmunoassay in 71 patients with psoriasis vulgaris, other chronic inflammatory skin diseases with T‐cell infiltrates [atopic dermatitis (n=25), and systemic sclerosis (n=34)], and 100 healthy subjects. The neuropeptide was found to be markedly (P<0.001) increased in patients with psoriasis (14.4 pg/ml), atopic dermatitis (9.2 pg/ml) and systemic sclerosis (9.8 pg/ml) compared with normal controls (6.1 pg/ml). The highest values of β‐endorphin were found in patients with actively spreading plaque psoriasis (17.3 pg/ml), whereas lesion‐free patients showed a reduction in neuropeptide concentration (10.2 pg/ml), The levels were much higher in patients with widespread psoriatic lesions (>60% body surface; 16.2 pg/ml), which lasted longer than 3 months (15.8 pg/ml), whereas neither the presence of stress nor itching correlated with the serum peptide concentration.
Our data suggest that β‐endorphin is produced in psoriatic lesions by inflammatory cells, rather than the increased levels being the result of activation of the pituitary‐adrenal axis by chronic stress. The generation of neuropeptide in psoriatic lesions and its antinociceptive effect on the peripheral sensory nerves might explain why pruritus is a relatively rare phenomenon in psoriasis.
Objective: To determine the increase in healing rate of venous ulcer in patients receiving a micronised purified flavonoid fraction (MPFF) as supplementation to standard local care. Design: A randomised, open, controlled, multicentre study. Setting: Departments of Dermatology and University Outpatients Clinics. Patients: One hundred and forty patients with chronic venous insufficiency and venous ulcers. Intervention: Patients received standard compressive therapy plus external treatment alone or 2 tablets of MPFF daily in addition to the above treatment for 24 weeks. Main outcome measure: Healing of ulcers and their reduction in size after 24 weeks of treatment. Results: The percentage of patients whose ulcers healed completely was found to be markedly higher in those receiving MPFF in addition to standard external and compressive treatment than in those treated with conventional therapy alone (46.5% vs 27.5%; p<0.05, OR = 2.3, 95% CI 1.1–4.6). Ulcers with diameters <3 cm were cured in 71% of patients in the MPFF group and in 50% of patients in the control group, whereas ulcers between 3 and 6 cm in diameter were cured in 60% and 32% of patients ( p<0.05), respectively. The mean reduction in ulcer size was also found to be greater in patients treated with MPFF (80%) than in the control group (65%) ( p<0.05). The cost-effectiveness ratio (cost per healed ulcer) in the MPFF group was €1026.2 compared with €1871.8 in the control group. Conclusions: These results indicate that MPFF significantly improves the cure rate in patients with chronic venous insufficiency.
Human neutrophil elastase was found, by indirect immunofluorescence using rabbit anti-elastase anti-serum, to be bound to basement membrane of psoriatic plaques in vivo. The enzyme was also identified inside the migrating neutrophils in the reticular dermis and dermal papillae, as well as outside the cells in micro-abscesses in psoriatic skin. In vitro incubation of normal skin with human neutrophil elastase resulted in the destruction of hemidesmosomes and separation of the epidermis from the dermis above localizations of bullous pemphigoid antigen. These findings are direct evidence that human neutrophil elastase could play a role in psoriasis in in vivo destruction of the epidermal-dermal junction.
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