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Biomedical subjects

B Przybilla

Publications and source records attributed to B Przybilla.

At least 73 records · Page 4Linked to original sources
PubMed1997

Some alterations of the leucocyte beta2-adrenoceptor/cAMP-system in patients with seasonal allergic rhinoconjunctivitis are related to disease activity.

BACKGROUND: Disturbances of beta2-adrenoceptors are discussed as a pathogenic factor in atopic diseases. METHODS: In this study the expression and function of beta2-adrenoceptors on peripheral blood leucocytes (PBL) of seven atopic patients with seasonal rhinoconjunctivitis and their seven healthy controls was evaluated in relation to disease activity. Earlier reported data during pollen season were now compared with data obtained from the same subjects after their allergic symptoms had subsided. RESULTS: The variables that had indicated a beta2-adrenoceptor subsensitivity in the patients during pollen season returned to control values, i.e. the reduced beta2-adrenoceptor affinity, the reduced beta2-adrenoceptor sensitivity, the reduced increase of intracellular cyclic adenosine monophosphate (cAMP) content upon stimulation with isoproterenol, and the reduced cAMP plasma concentration (values no longer significantly different from those of controls). However, the variable that had suggested an increase in activity of the cAMP degrading enzyme phosphodiesterase (PDE), i.e. the reduced basal intracellular cAMP content of the patients, remained reduced after the pollen season (4.9 +/- 1.1 pmol/10(6) cells in patients vs 8.2 +/- 0.9 pmol/10(6) cells in controls: P<0.05). There were no significant differences in beta2-adrenoceptor density between patients and controls at both investigations. CONCLUSIONS: Atopic seasonal rhinoconjunctivitis is associated with various alterations in the PBL beta2-adrenoceptor/cAMP system that depend on disease activity. The reversible beta2-adrenoceptor subsensitivity is likely to be a consequence of the disease, whereas the irreversibly decreased basal intracellular cAMP content, suggested an elevated PDE activity, might be a basic trait of atopy.

Adult↗
PubMed1997

Malignant melanoma and levodopa: is there a relationship? Two new cases and a review of the literature.

The incidence of malignant melanoma (MM) is rising. Besides UV radiation, other factors may contribute to this. We describe two patients in whom MM developed during treatment with levodopa. Levodopa has been implicated as an agent that could enhance the development of MM. However, review of the literature does not provide evidence of a definite relationship between treatment with levodopa and the development of MM. Despite this, it is suggested that patients treated with levodopa, particularly those with a history of MM, be observed carefully for changes in or development of new pigmented lesions.

Aged↗
PubMed1996

Evaluation of the phototoxic properties of some hypolipidemics in vitro: fenofibrate exhibits a prominent phototoxic potential in the UVA and UVB region.

As some fibric acid derivatives have been reported to exhibit photosensitizing effects in vivo, the antilipemic drugs fenofibrate, bezafibrate, clofibrate, and gemfibrozil were tested for their phototoxic potential in vitro by a photohemolysis test using human erythrocytes and different irradiation sources. In this system only fenofibrate revealed strong phototoxic properties, which were dependent both on the drug concentration and the irradiation doses. Above a surface dose of 40 J/cm2 UVA of an UVA (320-400 nm)-rich irradiation source or 1.6 J/cm2 UVB/0.8 J/cm2 UVA of an UVB (280-320 nm)-rich irradiation source human red blood cells were completely photohemolysed in the presence of fenofibrate. Bezafibrate- and gemfibrozil-induced photohemolysis remained beneath 10%, and clofibrate showed no phototoxicity at all. As the phototoxic potential of fenofibrate lies in the UVB and UVA range, this might be of relevance with regard to clinical photosensitivity.

Bezafibrate↗
PubMed1996

Interaction of ultraviolet-B-rich and ultraviolet-A-rich radiation in ketoprofen-induced photohemolysis.

Interactions between different wavelengths can cause inhibition or enhancement of various biological reactions. We evaluated in vitro the effect of UVB-rich irradiation on UVA-induced phototoxicity. Suspensions of human erythrocytes were incubated with ketoprofen, a phototoxic nonsteroidal anti-inflammatory drug. These samples were exposed to 0, 20, 40, 80, 160 or 320 mJ/cm2 UVB followed by irradiation with 0 or 6 J/cm2 UVA. Photo-induced hemolysis was calculated as a percentage of complete hemolysis. Ketoprofen-dependent hemolysis due to UVA alone was 63% (median). UVB did not induce ketoprofen-dependent photohemolysis at doses < 80 mJ/cm2. Exposure to UVB at all doses enhanced significantly (P < 0.01) UVA-induced ketoprofen-dependent hemolysis in samples from 9 of 15 donors. However, with erythrocytes from the other 6 donors, 20 or 40 mJ/cm2 UVB reduced the median of UVA-induced photohemolysis by 69% (P < 0.05) or 47% (not significant), respectively. Co-incubation of samples with ascorbic acid resulted in a profound inhibition of ketoprofen-dependent photohemolysis. These results indicate that the effect of low UVB doses on UVA-induced phototoxicity depends on individual, yet unknown characteristics of the target cells.

Adolescent↗
PubMed1996

Phototoxicity of non-steroidal anti-inflammatory drugs: in vitro studies with visible light.

Photosensitivity reactions due to non-steroidal anti-inflammatory drugs (NSAID) are well-known side-effects of these agents and are usually attributed to ultraviolet (UV) radiation. Eight NSAID (carprofen, diclofenac, ibuprofen, ketoprofen, naproxen, piroxicam, phenylbutazone, tiaprofenic acid) were assessed in a photohemolysis test for phototoxic effects in the visible light range. For the studies an experimental visible light lamp was used, emitting 5% UVA at most. To control for UVA-induced effects, additional samples were exposed to appropriate UVA doses from an UVA source and as well to the visible light lamp while being covered by a GG 400 or GG 420 filter. Photo-induced hemolysis was found after exposure to the visible light lamp with carprofen, ketoprofen, naproxen, piroxicam, phenylbutazone or tiaprofenic acid; diclofenac or ibuprofen did not cause photohemolysis. Control irradiation with UVA induced minor hemolysis only with carprofen, ketoprofen and tiaprofenic acid. When the samples were exposed to the filtered visible light lamp, using the GG 400 filter, photohemolysis was found with carprofen, naproxen and phenylbutazone and, using the GG 420 filter, with carprofen and phenylbutazone. Phototoxic effects induced by visible light may be of importance with regard to clinical photosensitization.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Change of skin roughness due to lowering air humidity in climate chamber.

Rough skin ("dry skin") is characteristic of atopy and thought to be a pre-stage of atopic eczema. Atopic eczema frequently deteriorates in winter, which may be related to low air humidity during the heating period. We have assessed skin roughness before and after decreasing air humidity to 30% in a climatic chamber. Replicas of clinically non-inflamed and not scaling skin from 10 patients with atopic eczema and 10 controls were taken before and after lowering air humidity for 3 h and were analyzed for the roughness parameters Ra, RZ(DIN) and RZ(ISO). After exposure to low air humidity there was a significant increase of RZ(DIN) from 61.5 microns to 66.9 microns (p < 0.05) and of RZ(ISO) from 63.8 microns to 66.4 microns (p < 0.05) in patients with atopic eczema, whereas no significant change occurred in controls. Development of skin roughness over 3 h under natural indoor environmental conditions did not indicate spontaneous variations. These quantitative data show that a short period of exposure to low air humidity increases skin roughness and may particularly influence the condition of patients with atopic eczema.

Adult↗
PubMed1996

IgE antibodies to Hymenoptera venoms in the serum are common in the general population and are related to indications of atopy.

Determination of Hymenoptera venom (HV)-specific serum IgE antibodies is a useful diagnostic method in patients with systemic anaphylactic reaction (SAR) to Hymenoptera stings. In a general population cohort, we determined the prevalence of SAR and HV-specific IgE antibodies and assessed parameters associated with the latter. A total of 277 voluntarily participating inhabitants of rural Bavaria (Germany) (232 adults, mean age 38.0 years; 45 children, mean age 8.4 years) were investigated for a history of atopic disease or SAR to insect stings; in 258 of these, total IgE and specific IgE antibodies to HV (Apis mellifera, Vespula vulgaris/germanica) and four common aeroallergens (birch pollen, grass pollen, house-dust mite, and cat dander) in the serum were determined. Nine (3.3%) subjects reported SAR to insect stings. In 27.1% of the sera, specific IgE antibodies to HV were found, to bee venom in 24.8%, and to wasp venom in 8.5% (P < 0.0001). Of those exhibiting HV-specific IgE, 7.1% reported SAR to insect stings. A personal history of atopic disease (hay fever, asthma, or atopic eczema) was present in 16.7%, specific IgE to common aeroallergens was found in 32.6%, and total IgE > 100 kU/l was found in 22.5%. Specific serum IgE to HV was significantly associated with male sex (female vs. male, OR = 0.47; CI 0.25-0.86), young age (children vs. adults, OR = 2.80; CI 1.25-6.28), a history of SAR to insect stings (OR = 4.16; CI 1.15-15.03), total sIgE > 100 kU/l (OR = 3.88; CI 1.98-7.60), and specific IgE antibodies to three of the four aeroallergens (grass pollen, OR = 7.24 CI 3.66-14.38; birch pollen, OR = 3.67 CI 1.54-8.81; and house-dust mite, OR = 4.61 CI 2.08-10.32). It is concluded that immunologic sensitization to HV is common in the general population and is associated with atopy-related humoral IgE hyperresponsiveness.

Adolescent↗
PubMed1995

[Intraoperative anaphylaxis due to natural latex in a 3-year-old boy].

A nearly three-year-old boy with a genitourinary malformation, which had already been operated on several times, developed generalized urticaria, facial swelling and bronchospasm within 15 minutes of the induction of anaesthesia. The signs quickly responded to the administration of methylprednisolone (32 mg), clemastine (10 mg) and ranitidine (25 mg). There was a twofold positive immediate reaction in the prick test to natural rubber latex (white and brown), and specific IgE was demonstrated against the latex (2.58 kU/l). On the other hand, prick tests with perioperatively administered drugs and an oral provocation test with an antibiotic administered in the perioperative period were negative. The history of itching caused by an indwelling bladder catheter, vesicles on the lips after sucking on a rubber dummy and the described findings on examination both point to the natural rubber latex as the responsible allergen. No complications occurred three months later during a surgical intervention under administration of steroids and H1- and H2-receptor antagonists, as well as avoidance of materials made of natural rubber latex.

Anaphylaxis↗
PubMed1995

Multiple superficial basal cell carcinomas (basalomatosis) following cobalt irradiation.

Basalomatosis is an uncommon skin condition characterized by the occurrence of multiple basal cell carcinomas. Many cases reported in the literature have been attributed to arsenic treatment in psoriasis patients. We report a patient with basalomatosis caused by cobalt-60 (60Co) irradiation. A 55-year-old farmer developed 43 basal cell carcinomas 20 years after treatment of an immunoblastoma with 60Co irradiation. All the tumours were located within the radiation fields. Other possible causes of basalomatosis, such as arsenic intoxication and basal cell naevus syndrome, were excluded. The patient's multiple superficial basal cell carcinomas probably represent a late adverse effect of the 60Co irradiation.

Basal Cell Carcinoma↗
PubMed1995

Tryptase and histamine release due to a sting challenge in bee venom allergic patients treated successfully or unsuccessfully with hyposensitization.

BACKGROUND: Hyposensitization with been venom leads to full protection in most, but not all patients with IgE-mediated systemic reactions to bee stings. OBJECTIVE: To determine the relationship of clinical reactivity to the release of mediators and to changes of antibody concentrations in the peripheral circulation at a bee sting challenge test. METHODS: Blood was sampled before (1 min) and at 15, 60 and 180 min after a sting challenge from 19 patients on hyposensitization. Of these six still reacted and 13 were protected. Histamine, mast cell tryptase, bee venom-specific IgE and IgG in the serum, and histamine release from peripheral blood leucocytes (PBL) upon exposure to bee venom were determined. RESULTS: Tryptase above the detection level was found only at 15 (60) min in 4/6 (1/6) patients who reacted. After the sting challenge there was a significant increase of the histamine levels in patients who reacted at 15 min (P < 0.05) and in patients who did react at 60 and 180 min (P < 0.01). The total histamine content of PBL was significantly decreased after 15 and 60 min in patients who reacted (P < 0.01) and in those that did not (P < 0.05). Bee venom-induced histamine release was significantly reduced in patients reacting and those that did not at 15 min (P < 0.05), and was significantly decreased in reactors also at 60 and 180 min (P < 0.05/0.01). Specific IgG antibodies showed a minor decrease (P < 0.05) after the sting challenge in both groups, whereas specific IgE did not change significantly. CONCLUSION: These results indicate that bee venom anaphylaxis is associated with the release of mediators from both mast cells as well as basophils. Successful hyposensitization does not induce a state of immunological non-reactivity, but rather alters the magnitude and the pattern of mediator release.

Adult↗
PubMed1995

Frequency and activity of IgE-secreting peripheral blood B-cells in atopic eczema.

Increased immunoglobulin (Ig) E-levels are frequently found in the sera of patients with atopic eczema. To further understand the mechanisms underlying this increase of IgE, like enlarged number of IgE-producing cells, enhanced activity of IgE-producing cells or altered IgE metabolism, we analyzed the frequency and activity of IgE-producing B-lymphocytes within peripheral blood mononuclear cells of patients with atopic eczema. By use of a sensitive solid phase enzyme-linked immunospot assay (ELISPOT), IgE-secreting cells could be visualized within peripheral blood mononuclear cells of 14 individuals (12 patients with atopic eczema, one patient with impetigo contagiosa, one patient with allergic contact dermatitis) at a frequency of 10-1,120 IgE-secreting cells/10(5) B-lymphocytes. The number of IgE-secreting cells was markedly correlated with the corresponding serum IgE-level (r = 0.97). Secretory activity was also reflected by in vitro IgE production, which was assessed in parallel 7-day cultures and found to be related with actual serum IgE-levels. The enhanced serum IgE-levels in patients with atopic eczema seem to result primarily from an increased number of circulating IgE-secreting B-cells, which may also be found, however, in patients with elevated serum IgE-levels, showing different skin diseases.

Adolescent↗