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Biomedical subjects

J Ring

Publications and source records attributed to J Ring.

At least 37 records · Page 2Linked to original sources
PubMed1995

Association between the renin angiotensin system and anaphylaxis.

Patients with hymenoptera venom anaphylaxis before immunotherapy (n = 50) showed significantly lower renin, angiotensinogen, angiotensin I and angiotensin II as compared to healthy non-allergic controls (n = 25) (p < 0.05). A significant inverse correlation between the severity of clinical symptoms and the plasma levels of renin, angiotensinogen, angiotensin I and angiotensin II was found: the lower the levels the more severe the clinical symptoms. Hymenoptera venom allergic patients with repeated anaphylactic reactions during hyposensitizatin did not tolerate the sting of a living insect (n = 6). Sting provocation with a living insect induced clinical symptoms of anaphylaxis in all of the 6 patients. Renin, angiotensinogen, angiotensin I and II remained significantly lower in these patients as compared to healthy non-allergic controls. Likewise, no stimulation of the renin angiotensin system occurred during the anaphylactic reaction. The values of angiotensin II were similar or lower than the values before the anaphylactic reaction. In contrast, patients with successful immunotherapy (n = 27) who tolerated the sting of a living insect, renin, angiotensin I and II were significantly higher than in patients without immunotherapy. After immunotherapy, the values for renin, ANG I and ANG II were similar to the values found in healthy non-allergic controls. Patients with a history of hymenoptera venom anaphylaxis (n = 22) showed significantly lower ANG II concentrations in their leukocytes as compared to healthy non-allergic controls (n = 24). Successful immunotherapy induced a significant 9-fold increase in ANG II as compared to patients without immunotherapy. These findings suggest a possible role of the renin angiotensin system in hymenoptera venom anaphylaxis.

Adolescent↗
PubMed1995

[Anaphylaxis caused by latex contamination from the wrapper of the cannula plaster].

A patient with pronounced latex allergy was admitted to hospital because of suspected drug allergy. He developed an anaphylactic reaction manifesting with skin reactions and difficulties in breathing immediately after an intravenous cannula was applied, although the doctor was wearing latex-free gloves. The envelope of the plaster with which the cannula was fixed was found to be the source of the latex responsible for the anaphylactic reaction. Latex contact with the skin was due either to latex contamination of the doctor's hands when opening the envelope or to the plaster itself. The case report demonstrates the difficulties arising both from the clinical reaction pattern of type I reactions to latex and from strict avoidance of latex-containing products and points out the necessity of latex declaration.

Adult↗
PubMed1995

A reduction in allergen-induced Fc epsilon R2/CD23 expression on peripheral B cells correlates with successful hyposensitization in grass pollinosis.

BACKGROUND: The cellular basis for the mechanism of specific hyposensitization is still unclear. OBJECTIVE: We prospectively studied the effect of immunotherapy on allergen-induced proliferation and Fc epsilon R2/CD23 expression of lymphocytes. METHODS: Mononuclear cells prepared from the peripheral blood of 22 patients with grass pollen (GP) allergy before, during, and after a preseasonal immunotherapy period with GP were stimulated with GP or control antigens. Tritiated thymidine uptake and percentage of CD23+ B cells were determined daily during days 6 to 8 and compared with lymphocyte responsiveness of 11 only symptomatically treated atopic patients and 14 nonatopic individuals. RESULTS: GP-induced lymphocyte proliferative response of both hyposensitized and symptomatically treated GP-allergic patients decreased markedly before the pollen season and rose again after seasonal allergen exposure, whereas a long-lived decrease in GP-induced Fc epsilon R2/CD23+ B cells was only observed in GP-treated patients. Alterations in Fc epsilon R2/CD23 expression were closely related to changes in symptoms and medication requirement during the following pollen season. In contrast, immunotherapy had no effect on Fc epsilon R2/CD23 expression of B cells without stimulation or on B cells cultured in the presence of control antigens. CONCLUSION: Because Fc epsilon R2/CD23 expression on B cells is antagonistically regulated by the cytokines interleukin-4 and interferon-gamma, the decrease of allergen-induced Fc epsilon R2/CD23+ B cells indicates an altered cytokine secretion pattern of the allergen-specific T lymphocytes with a predominance of interferon-gamma.

Adolescent↗
PubMed1995

Atopy patch test with different vehicles and allergen concentrations: an approach to standardization.

BACKGROUND: In some patients with atopic eczema, eczematous skin lesions can be induced by patch testing with aeroallergens. METHODS: To establish a standardized system for the atopy patch test (APT), 36 patients with atopic eczema, four patients with rhinoconjunctivitis and 10 healthy control subjects were epicutaneously tested with allergen extracts from house dust mite, cat dander, and grass pollen. APTs were performed on nonabraded, uninvolved skin with 1000 and 10,000 protein nitrogen units (PNU)/gm allergen in petrolatum or hydrogel. Reactions were evaluated after 48 and 72 hours and compared with skin prick and specific serum IgE (CAP-RAST; Pharmacia, Uppsala, Sweden). RESULTS: After 48 hours, 57 clear-cut positive reactions with eczematous, often follicle-bound, appearance were diagnosed from a total of 432 test sites. Seventy-two percent of these positive reactions in patients with atopic eczema developed with 10,000 PNU/gm and 28% with 1000 PNU/gm. Sixty-seven percent of reactions were elicited with allergens in petrolatum versus 33% when hydrogel was used as vehicle. Allergen-specific concordances of APT (10,000 PNU/gm, petrolatum) ranged from 0.39 to 0.53 (prick test) and 0.42 to 0.69 (CAP-RAST). In healthy control subjects and patients with rhinoconjunctivitis without atopic eczema, no clear-cut positive APT reaction was seen. CONCLUSIONS: Petrolatum as vehicle and an allergen concentration higher than 1000 PNU/gm may lead to improved APT results on unchanged skin. In the future, the clinical relevance of an IgE-mediated sensitization for eczematous skin lesions may be evaluated by the APT.

Adolescent↗
PubMed1995

Cytokine-mediated effects of peripheral blood mononuclear cells from patients with atopic eczema on keratinocytes (HaCaT) in a new coculture system.

Interactions between keratinocytes and mononuclear cells via cytokines and adhesion molecules are thought to play a crucial part in inflammatory skin diseases. The cytokine-mediated effects of peripheral blood mononuclear cells (PBMC) from patients with atopic eczema (AE) and healthy individuals on keratinocytes (HaCaT) were investigated in vitro. A new coculture model (Transwell system) which consists of a lower and an upper compartment, which are separated by a polycarbonate-treated membrane, was established. 3[H]thymidine incorporation of keratinocytes and lymphocytes, as well as IL-6, IL-8 and IFN-gamma synthesis, were measured. Keratinocyte proliferation was significantly enhanced in the presence of PBMC from patients with AE. In contrast, PBMC from normal donors did not enhance HaCaT cell proliferation when they were cocultured. Lymphocytes from patients with AE showed a significantly enhanced proliferation after coculture with keratinocytes. However, PBMC from normal donors did not proliferate in the presence of HaCaT cells. Keratinocyte supernatants incubated with PBMC from either atopic or normal volunteers induced a suppression of lymphocyte 3[H]thymidine incorporation. In supernatants from cocultures of PBMC from patients with AE and keratinocytes, significantly enhanced amounts of IL-6 and IL-8, compared with normal donor's lymphocytes and HaCaT cells, were measured. No differences in IFN gamma production were observed. When PBMC were cultured without HaCaT cells, supernatants contained equal levels of IL-6, IL-8 and IFN-gamma in normal donors and in patients with AE. Interestingly, HaCaT cells spontaneously secrete measurable amounts of IL-6, IL-8 and IFN-gamma. Blocking experiments with neutralizing antibodies against these interleukins showed a complete inhibition of keratinocyte proliferation when PBMC from normal donors were used whereas the proliferative potency of PBMC supernatants from patients with AE on keratinocytes remained. Our data indicate that (i) PBMC from patients with AE stimulate keratinocyte proliferation via soluble factor(s) that are different from IL-6, IL-8 and IFN-gamma; (ii) probably, HaCaT cells spontaneously produce lymphocyte/monocyte inhibitory soluble factors and IL-6, IL-8 as well as IFN-gamma; and (iii) secretion and/or activity of keratinocyte-derived inhibitory mediators is regulated via cytokines of PBMC infiltrating inflammatory skin.

Antibodies, Monoclonal↗
PubMed1995

Decreased monocyte interleukin-1 beta production in atopic eczema.

It has been suggested that in atopic eczema (AE) a reduced lymphocyte response to T-cell mitogens in vitro is secondary to altered production of cytokines or inflammatory mediators. We investigated, in parallel, the mitogen-induced T-cell proliferation, monocyte interleukin-1 beta (IL-1 beta) production, and prostaglandin E2 (PGE2) production of monocytes and of peripheral blood mononuclear cells (PBMC) in AE patients and non-atopic controls. After stimulation with concanavalin A (Con A) PBMC of AE patients showed a significantly reduced proliferative response compared with the controls. The monocyte production of IL-1 beta after stimulation with lipopolysaccharide (LPS) was significantly decreased in AE. No differences between AE patients and controls were observed with regard to the PGE2 production of PBMC after stimulation with Con A or the monocyte release of PGE2 after LPS stimulation. Because IL-1 plays a central role in the activation of T-cell proliferation, the decreased monocyte IL-1 beta production may provide a plausible explanation for the reduced mitogen response of T cells in AE.

Adolescent↗
PubMed1995

Acanthosis nigricans: a marker for hyperinsulinemia.

A 12-year-old girl developed acanthosis nigricans due to increased levels of serum insulin. Hyperinsulinemia has been recognized as the underlying cause in most cases of acanthosis nigricans. In this paper we outline a typical clinical case with special regard to the proposed pathogenesis.

Acanthosis Nigricans↗
PubMed1995

Origin of angiotensin in human leukocytes.

The capability of human leukocytes to synthesize angiotensin peptides was studied. Leukocytes which were prepared from heparinized blood by sedimentation in dextran were incubated for 0, 1, 2, 4, 6, 8, and 24 h at 37 degrees C with the 3H-labeled amino acid isoleucine. At the various time points the washed cells were extracted with 0.1 M acetic acid. The extracts contained radioactive material which eluted from a Bio Sil TSK 125 gel filtration column in the low-molecular-weight range with the same retention time as synthetic angiotensin I (ANG I) or angiotensin II (ANG II). The extracted radioactive material also bound to anti-ANG I and anti-ANG II antibodies. However, excess of unlabeled synthetic ANG I or ANG II failed to displace the bound radioactivity. Rechromatography of the radioactive material which eluted in the low molecular weight fractions of the gel filtration column could be characterized as non-incorporated 3H-isoleucine on a reversed phase C18 column with an acetonitrile gradient. These findings demonstrate the lack of an angiotensin-generating pathway in human leukocytes. Further studies are necessary to determine the origin of angiotensin peptides in human leukocytes.

Adult↗
PubMed1995

Elevated serum levels of soluble adhesion molecules ICAM-1 and ELAM-1 in patients with severe atopic eczema and influence of UVA1 treatment.

BACKGROUND: ICAM-1 is known to be strongly expressed on keratinocytes in lesional atopic eczema correlating with the degree of inflammation. ELAM-1 was found to be expressed on dermal vascular endothelium in lesional atopic eczematous skin. OBJECTIVE: The present study was performed to investigate whether elevated serum levels of soluble forms of these molecules are detectable in patients with severe atopic eczema and whether these parameters could be useful markers for disease activity. METHODS: Serum levels of soluble ICAM-1 (sICAM-1) and ELAM-1 (sELAM-1) were measured by ELISA in 18 patients with severe atopic eczema before and after UVA1 therapy. RESULTS: Before onset of treatment, serum sICAM-1 (565 +/- 99 ng/ml) and sELAM-1 (89.7 +/- 29.9 ng/ml) levels were significantly (p < 0.001) elevated compared to 22 healthy control persons (296 +/- 46 and 48.8 +/- 22.7 ng/ml). After achievement of significant clinical improvement after 3 weeks of UVA1 therapy, there was neither a decrease in serum sICAM-1 nor in sELAM-1 levels. The posttherapeutic serum sICAM-1 and sELAM-1 values remained elevated (p < 0.001) above the normal range. CONCLUSION: Based on these data we suggest that (1) serum sICAM-1 and sELAM-1 are elevated in patients with severe atopic eczema, (2) sICAM-1 does not decrease together with reduction of ICAM-1-positive keratinocytes in atopic eczema following clinical improvement and might therefore be mainly of a different origin, i.e. leukocytes/endothelial cells, and that (3) sICAM-1 and sELAM-1 seem not to be suitable markers of actual disease activity in severe atopic eczema.

Adult↗
PubMed1995

Pityrosporum ovale extracts increase interleukin-4, interleukin-10 and IgE synthesis in patients with atopic eczema.

Evidence for a possible role of the lipophilic yeast Pityrosporum ovale in the pathophysiology of atopic eczema has been found both in laboratory and therapeutical studies. Positive type I prick test reactions to P. ovale correlate with the intensity of eczematous skin lesions in the head and neck regions of patients with atopic eczema. Furthermore, antifungal treatment has been shown to be helpful in atopic eczema. In the present study the effect of P. ovale on IgE synthesis and cytokine production (IL-2, IFN gamma, IL-4, IL-10) was investigated in patients with atopic eczema, in vitro. Eight patients with atopic eczema were studied; of these, 5 patients had specific IgE antibodies against P. ovale, as determined by fluoroimmunoassay (RAST). The control group consisted of 5 healthy non-atopic, P. ovale IgE-antibody-negative volunteers. Freshly isolated peripheral blood mononuclear cells (PBMC) were incubated in the presence of different antigen concentrations (0.01, 0.1, 1.0, 10 micrograms/l x 10(6) cells) of P. ovale. IgE contents in the cell culture supematants were significantly elevated in RAST(+) patients with atopic eczema (p < 0.05), compared with RAST(-) atopic eczema patients and healthy volunteers. Coincubation of P. ovale-stimulated PBMC with IL-4 (50 U/l/ 1 x 10(6) cells) resulted in a significantly higher IgE synthesis only in the RAST(+) atopic eczema patients. Additionally, incubation of PBMC from RAST(+) patients with atopic eczema led to an elevated synthesis of the TH2 related cytokines IL-4 and IL-10. Within the atopic eczema group, two subgroups differed markedly in their response to P. ovale antigen stimulation with a good correlation to the presence of specific IgE in serum and in vitro IL-4 and IL-10 production. The data support the assumption that P. ovale antigens might play a role in skin inflammation in at least a subgroup of patients with atopic eczema characterized by the presence of specific IgE antibodies to P. ovale.

Adult↗
PubMed1995

Low dose versus medium dose UV-A1 treatment in severe atopic eczema.

Twenty-two patients with severe atopic eczema were included in a therapy study with UV-A1 (wavelengths > 340 nm) treatment. The patients were divided into two dose groups, each consisting of 11 patients. One group received 10 J/cm2 and the other 50 J/cm2 five times a week for 3 consecutive weeks. No topical or systemical steroids or antihistamines were allowed. Using the SCORAD index as a measure of disease activity before onset of therapy and after 10 and 15 treatments, we observed a significant improvement in both dose groups after 15 treatments (10 J/cm2: p < 0.05, 50 J/cm2: p < 0.005). After 10 treatments only the improvement in the 50 J/cm2 group was significant (p < 0.005); the difference between the two dose groups was significant (p < 0.05). The clinical efficacy of treatment was reflected neither by a decrease of serum IgE nor by a decrease of elevated serum levels of soluble adhesion molecules sICAM-1 and sELAM-1 in the two dose groups. In contrast, a marked but not significant decrease of serum ECP could be observed in the 50 J/cm2 group only. We conclude from these and other published data that although 10 J/cm2 UV-A1 has a limited effect on patients with severe atopic eczema, higher doses are of higher efficiency in the treatment of this condition.

Adult↗