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Biomedical subjects

W Glinski

Publications and source records attributed to W Glinski.

At least 19 recordsLinked to original sources
PubMed2001

[Effectiveness of a micronized purified flavonoid fraction (MPFF) in the healing process of lower limb ulcers. An open multicentre study, controlled and randomized].

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. METHODS 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.

Aged↗
PubMed1999

Mast cells in developing subepidermal bullous diseases: emphasis on tryptase, chymase and protease inhibitors.

The possible involvement of mast cell tryptase and chymase in subepidermal bullous diseases was studied enzyme-histochemically in specimens from erythematous and vesicular skin and from non-involved skin of patients with dermatitis herpetiformis, bullous pemphigoid, erythema multiforme, infective bullous eruption and linear IgA dermatosis. Patients with pemphigus were biopsied for comparison. The immunoreactivity of chymase inhibitors, alpha1-proteinase inhibitor (alpha1-PI) and alpha1-antichymotrypsin (alpha1-AC), in mast cells was demonstrated using the sequential double staining method. Tryptase-positive mast cells were unchanged or only slightly increased in number in erythematous lesions and slightly decreased in blistering skin compared with healthy-looking skin. Only occasionally were mast cells seen in apparent contact with the basement membrane zone. Chymase-positive mast cells and the chymase/tryptase ratio steadily decreased during the development of the lesions in each subepidermal bullous disease. The percentage of alpha1-PI+ and/or alpha1-AC+ mast cells increased simultaneously, which could explain the disappearance of chymase activity. Similar results were obtained regardless of the bullous disease. The results were also similar in pemphigus, which is an intraepidermal bullous disease. In conclusion, these results show significant alterations in mast cell chymase and protease inhibitors in a range of different bullous diseases, suggesting mast cell involvement. The apparent inactivation of chymase could be due to the action of chymase inhibitors detected in numerous mast cells. However, these alterations probably reflect general inflammation rather than a specific reaction in a certain bullous disease.

Adolescent↗
PubMed1995

Excessive costimulation of CD3-dependent lymphocyte response by extracellular matrix proteins in severe widespread psoriasis.

Costimulation of anti-CD3-triggered proliferative T-cell responses by type I and type IV collagen and fibronectin was studied in 25 patients with psoriasis and 12 healthy subjects. The stimulation index of anti-CD3-mediated responses in the presence of type I collagen was about half that in the controls. Although the CD3-dependent proliferative response of psoriatic lymphocytes in patients with active widespread plaque psoriasis was reduced by about 50%, costimulatory responses induced by type IV collagen and fibronectin were found to be enhanced in relation to the controls. The degree of costimulation by type IV collagen and fibronectin was related to disease severity. The highest values of the stimulation index were found in patients with a PASI greater than 24, skin involvement of more than 40% of body surface area, and a duration of psoriatic lesions of more than 3 months. The results indicated that in active widespread plaque psoriasis subpopulations of T cells bearing receptors for some extracellular matrix proteins were increased in the peripheral blood. A factor responsible for this phenomenon may be trafficking of T cells through the basement membrane zone of psoriatic lesions, which presumably causes modification of T cell immunological responsiveness after recirculation.

Adult↗
PubMed1995

Modulation of CD3-dependent lymphocyte proliferation by extracellular matrix proteins in atopic dermatitis.

Patients with atopic dermatitis were found to have an about 7-fold increased spontaneous proliferative response of peripheral blood lymphocytes and an about 4-fold elevation of CD3-dependent lymphocyte transformation as compared to normal controls. The CD3-dependent lymphocyte response in patients with severe atopic dermatitis lesions was increased to a lower degree than in those with mild skin lesions. Despite a highly increased CD3-dependent lymphocyte response, the extracellular matrix proteins could induce further co-stimulation of lymphocytes in patients with atopic dermatitis, similar to that in normal controls. However, co-activation by type IV collagen was markedly increased in patients with severe lesions, whereas co-stimulations by both type I collagen and fibronectin were decreased in patients with mild lesions. This finding reflects presumably the changes in lymphocyte subpopulations and their activities related to the recirculation of these cells through the active skin lesions and to the contact of T cells with extracellular matrix proteins. The percentage of CD26-positive lymphocytes was also significantly (p < 0.05) increased in patients with severe atopic dermatitis. These data indicate that helper T cells are excessively activated in atopic dermatitis and that the function of beta-1-integrin receptors underlying the extracellular matrix protein-mediated co-activation of CD3-dependent lymphocyte responses is modified by disease severity.

Adolescent↗
PubMed1995

Increased concentration of beta-endorphin in the sera of patients with severe atopic dermatitis.

Serum beta-endorphin was measured by radioimmunoassay in 25 patients with atopic dermatitis and 100 healthy subjects. The neuropeptide was found to be markedly (p < 0.001) increased in patients with atopic dermatitis (9.2 +/- 3.4 pg/ml) as compared to normal controls (6.1 +/- 1.5 pg/ml). A correlation between increased serum beta-endorphin concentration and some clinical parameters of the disease has been found. The statistically significant elevation of beta-endorphin was found in patients with widespread atopic dermatitis lesions involving more than 20% of the skin surface (11.1 +/- 3.6 pg/ml), a high disease severity score (10.7 +/- 3.7 pg/ml), and previous bronchial asthma symptoms (11.6 +/- 3.1 pg/ml). A possible explanation of increased beta-endorphin is either its generation in atopic dermatitis lesions by inflammatory cells or activation of pituitary-adrenal axis by psychoneural factors in the mechanism of chronic stress.

Adolescent↗
PubMed1994

Increased concentration of beta-endorphin in sera of patients with psoriasis and other inflammatory dermatoses.

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 beta-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 beta-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.

Acute Disease↗
PubMed1994

Neuropeptides in psoriasis: possible role of beta-endorphin in the pathomechanism of the disease.

BACKGROUND: An increased concentration of neuropeptides in psoriatic lesional skin may be responsible for alterations in the neurogenic erythematous response and transmission of stimuli through sensory nerve fibers (sensation of pruritus). METHODS: Increasing doses of capsaicin from 0.125 to 4 micrograms/cm2 were applied to nonlesional psoriatic skin to establish the minimal dose that induced the substance P-mediated neurogenic response in 30 patients with psoriasis. Plasma beta-endorphin was quantitated in 71 psoriatics by radioimmunoassay using NEN 1251-RIA kit. RESULTS: The mean beta-endorphin concentration was increased about 2-fold compared to normals, whereas doses of capsaicin needed to induce erythema were higher (1-4 micrograms/cm2) in psoriatics (mainly in patients with type II psoriasis) than in healthy subjects (0.125-0.25 microgram/cm2). CONCLUSIONS: 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.

Capsaicin↗
PubMed1991

Decreased specific anti-elastase activity in the uninvolved skin of patients with psoriasis.

Inhibitory activities against elastase, chymotrypsin and trypsin were studied in the fluid from experimentally developed suction blisters in the uninvolved skin of patients with psoriasis. These activities determined by spectrophotometry of specific synthetic low molecular weight substrates were compared with respective antiproteinase activities in sera of 32 patients with psoriatic lesions, ten patients in remission, and ten healthy volunteers. A marked reduction (29.2%) in the specific elastase inhibitory activity of blister fluid was found in patients with psoriasis when compared with normal subjects (p less than 0.05), since neither chymotrypsin nor trypsin inhibitory activities were altered. This reduction was despite about a 30% increase in the elastase inhibitory activity in the sera of these patients, which was related presumably to their increased activity of alpha 1-proteinase inhibitor, the main serum antiserine proteinase inhibitor. A decreased blister fluid:serum elastase inhibition ratio was shown in a large majority of patients with psoriasis, even in symptomless patients. The deficiency in specific elastase inhibitory activity of suction blister fluid was predominantly associated with early onset of psoriasis, guttate lesions and inactive lesions, skin involvement less than 20% of body surface, duration of relapse shorter than 2 months, and frequent relapses. These data indicate that the uninvolved skin of patients with psoriasis contains low concentrations of specific elastase tissue inhibitor, which deficiency might result in an excessive in vivo hydrolytic activity of neutrophil elastase released from migrating cells in the psoriatic skin.

Adult↗
PubMed1991

Ultrastructural changes of the skin induced by human leukocyte elastase and cathepsin G.

Human neutrophil elastase and cathepsin G at a concentration of 10(-6) M were found to attack various substrates when normal skin biopsy specimens were incubated at 37 degrees C for 1 h with either of these enzymes. Elastase damaged primarily hemidesmosomes, leading to the epidermal cleavage from the dermis, whereas cathepsin G damaged the membrane structures. Both these neutral proteinases were highly specific to basal lamina of blood vessels. This indicates that neutrophil elastase and neutrophil cathepsin G may play different roles in various skin diseases related to enhanced activity and infiltration of neutrophils.

Cathepsin G↗
PubMed1991

Neurogenic inflammation induced by capsaicin in patients with psoriasis.

Increasing doses of capsaicin were applied topically to the forearm skin of 30 patients with psoriasis, 16 patients with systemic scleroderma and 16 healthy volunteers. Only one-third of the patients with psoriasis responded with neurogenic inflammation to capsaicin doses of 0.125 and 0.25 microgram/cm2 in contrast to 81% of scleroderma patients and all the normal controls, who showed a positive cutaneous reaction. Higher doses of capsaicin (0.5-4 micrograms/cm2) were required to induce erythema and flare in patients with late-onset psoriasis (after 21 years of age) as well as in patients with more than 40% of skin surface involved with psoriatic lesion.

Administration, Cutaneous↗
PubMed1990

Basement membrane zone as a target for human neutrophil elastase in psoriasis.

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.

Basement Membrane↗
PubMed1989

Two subpopulations of patients with early and late onset of psoriasis differ regarding alpha 1-proteinase inhibitor activity.

Two subpopulations of patients with psoriasis were identified when activity of alpha 1-proteinase inhibitor was analysed according to the patient's age at onset of the disease. Patients with early onset had more active lesions, high incidence of familial psoriasis, and reduced alpha 1-proteinase inhibitor during flare similar to that activity in remission. In contrast, alpha 1-proteinase activity increased significantly during flare in patients with late onset (above 21 yrs of age) in response to the inflammatory process in the psoriatic skin.

Adolescent↗
PubMed1988

Leukotriene B4 enhances adherence of human polymorphonuclear leukocytes to dermal microvascular endothelial cells in vitro.

Adherence of polymorphonuclear leukocytes (PMNs) to endothelial cells (ECs) is a crucial step in the diapedesis of inflammatory cells to the site of inflammation. We have demonstrated that leukotriene B4 (LTB4), a metabolite of the arachidonic acid cascade, and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) significantly enhance the binding of human PMNs to selected populations of human dermal microvascular endothelial cells (MECs) in vitro. MECs were isolated from the vascular-rich portion of foreskins of newborns. MECs were grown in Iscove's modified Dulbecco's media with 2% prepartum serum and 8% newborn calf serum on 1% gelatin-coated plastic dishes. PMNs isolated from five human donors were added to the culture dishes for varying time intervals (usually 30 min) in the presence and absence of the chemotactic stimuli LTB4 and FMLP. Addition of PMNs to MECs in the absence of chemotactic stimuli results in "baseline" binding to the MEC monolayer. About one in every 150 ECs binds more than five PMNs. These selected ECs are randomly distributed throughout the monolayer. LTB4 from 10(-10) to 10(-7) M increases the number of MECs which selectively bind PMNs by 260% at 10(-7) M. FMLP also increases adherence in qualitatively and quantitatively similar fashion. These data support a role for LTB4 in the mediation of adherence of neutrophils to dermal MECs. In contrast to other endothelial cells from the large blood vessels, such as from umbilical veins or calf thoracic aortae, PMNs bind only to selected MECs in culture, even when stimulated with LTB4 or FMLP.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion↗
PubMed1987

Reduced expression of surface receptors for synthetic N-formylated chemotactic oligopeptides by stimulated peripheral blood neutrophils in psoriasis.

Receptors for synthetic N-formylated chemotactic peptides on peripheral blood neutrophils were studied by the binding of fluorescein-labeled hexapeptide (N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys) to the cells in vitro at the range of concentrations 0.01-100 nM. Mean fluorescence of neutrophils was quantitated by a flow cytometry using FACS III. Comparison was made between 27 patients with psoriasis vulgaris and 14 normal controls. Various receptor states related to cell activities were induced by different temperatures, by incubation of cells with cytochalasin B and by preincubation with nonlabeled N-formyl-Met-Leu-Phe. This allowed us to distinguish between the specific binding of fluoresceinated hexapeptide to plasma membrane receptor already present (0 degree C), modulation of receptors by peptide and cytochalasin B stimulated degranulation (25 degrees C), and net binding, including internalization of peptide and receptor recycling system (37 degrees C). At peptide concentrations of 1-10 nM, the labeling of neutrophils at 25 degrees C and 37 degrees C, but not at 0 degree C, was found to be about 10-35% lower in psoriatic than in healthy subjects (p less than 0.002). The amount of fluorescein-labeled peptide bound to the cells at 25 degrees C was markedly increased by cytochalasin B, but to a much lower extent in psoriatic patients than in normal controls. Although the number of plasma membrane receptor for chemotactic peptides in the nonstimulated neutrophils was not altered in psoriasis, the receptor up-regulation induced by preincubation of the cells with 1-10 nM of nonlabeled N-formyl-Met-Leu-Phe at 37 degrees C was reduced when measured by subsequent fluoresceinated hexapeptide uptake at 0 degree C. Receptor recycling, as measured by an increase with time (0-30 min) in the binding of chemotactic peptide by neutrophils in which receptors had been down-regulated, was found to be within normal range in patients with psoriasis. These data indicate that nonstimulated, circulating neutrophils have a normal number of chemotactic peptide receptors on the cell surface, but are less able to recruit intracellular receptors to the cell surface. This finding may be related to smaller internal pools or less efficient translocation of these receptors.

Adolescent↗
PubMed1986

Decreased extracellular release of granule enzymes from in vitro-stimulated polymorphonuclear leukocytes in guttate psoriasis.

In vitro degranulation of polymorphonuclear leukocytes, which were stimulated either with synthetic chemotactic peptide (N-formyl-methionyl-leucyl-phenylalanine, FMLP) or with C3b-opsonized zymosan as a promotor of phagocytosis, was studied in 66 patients with psoriasis, 18 lesion-free psoriatics, 18 healthy subjects, and 14 other dermatological disorder controls. Stimulated release of lysozyme (from specific granules and azurophil granules) and beta-glucuronidase (from azurophil granules) in the presence of both FMLP and serum-activated zymosan was markedly reduced in patients with actively spreading guttate psoriatic lesions, in whom relapse of lesions lasted for less than 1 month and papules involved about 13-25% of skin surface. In contrast, stimulated degranulation was within normal range in active plaque psoriasis, stationary plaque psoriasis, symptomless psoriatics, and patients with disseminated eczema. Spontaneous release of lysozyme and beta-glucuronidase (background) was found to be not different in all groups studied; however, patients with active guttate psoriasis had significantly lower total lysozyme activity than those with active and stationary plaque psoriasis as well as psoriatics in the remission. These data are in favor of in vivo activation of neutrophils in active guttate psoriasis by some factors related to the early relapse of the lesions. This results in a possible combination of the following phenomena: (1) in vivo partial degranulation of neutrophils; (2) induction of "unresponsiveness state" of these cells to subsequent in vitro stimulation; and/or (3) migration of highly responsive neutrophils to skin lesions, which leaves in the circulation the subpopulation less reactive to chemotactic and phagocytic stimuli.

Cells, Cultured↗
PubMed1985

In vitro effects of enzymes of polymorphonuclear leukocytes on the antigenicity of stratum corneum.

Anti-stratum corneum (SC) antibodies of human serum bind in vitro to the SC of frozen sections of normal skin of psoriatic patients and of healthy controls. Pretreatment of skin sections with selected dilutions of acid extracts from polymorphonuclear leukocytes (PMN) prior to the incubation with serum containing anti-SC autoantibodies enhances this binding in comparison with binding to untreated sections. Pretreatment of at least some specimens with higher concentrations of the same PMN extracts brings about a reduction in their reactivity with anti-SC autoantibodies. These findings indicate that enzymes of PMN are capable of altering SC antigens by first increasing and then decreasing their reactivity with SC autoantibodies.

Antigens↗
PubMed1985

[Peritoneal dialysis and leukopheresis in psoriasis: indications and contraindications].

Twenty-four patients with severe psoriasis were treated with continuous peritoneal dialysis and ten patients with repeated leukopheresis, with comparable clinical results: about 20%-30% of the patients had complete remission of the lesions during the therapy, about 40% showed spontaneous regression of above 50% of psoriatic lesions, and the remaining patients had some improvement. However, despite partial improvement during treatment, the psoriatic lesions of the patients that were previously unresponsive to any external and internal treatment disappeared within 2-3 weeks, after discontinuation of dialysis or leukopheresis, with the use of anthralin or tar ointments. Peritoneal dialysis and leukopheresis seem to be useful methods of treatment for especially resistent and widespread psoriasis in patients having contraindications to other methods, i.e., PUVA and/or aromatic retinoids.

Female↗