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Biomedical subjects

K Neuber

Publications and source records attributed to K Neuber.

At least 19 recordsLinked to original sources

Indoor air pollution by lindane and DDT indicated by head hair samples of children.

The use of the pesticides DDT and lindane as wood preservatives causes indoor air contamination and subsequently exposure of the occupants of these rooms. As hair acts as a passive sampler for air contaminants, we tested pesticide concentrations in hair measured by the GC/MS technique. A comparison of the DDT and lindane concentrations in hair samples of 193 pre-school children from a rural area around Rostock with information concerning their home environments showed that this is a suitable method for screening purposes.

Air Pollution, Indoor

[Painful ischemia of the extremities with T-cell lymphoma].

Two years after the diagnosis of Sézary syndrome, a 50-year old female patient experienced attacks of painful ischemia of both hands and feet, leading to acral necrosis. Another 59-year old patient presented with severe pain in his feet, secondary to ischemia. This was the first symptom of a T-cell-chronic lymphocytic leukemia. Similar cases have only occasionally been described. The relationship between acral ischemia and T-cell-lymphoma is not clear but is discussed in this article.

Chlorambucil

Heterogeneity of chemosensitivity of metastatic cutaneous melanoma.

Advanced melanoma has a poor prognosis and chemotherapy provides little benefit for most patients. This may be related to heterogeneity of chemosensitivity as well as frequent constitutive resistance to individual cytotoxic drugs. We have therefore examined the heterogeneity of chemosensitivity in metastatic cutaneous melanoma specimens using an ex vivo ATP-based chemosensitivity assay (ATP-TCA). Melanoma deposits (n=55) in skin or lymph node were tested using the ATP-TCA, performed in three separate laboratories. Analysis of the data collected (based on an arbitrary sensitivity index < 300) shows considerable heterogeneity of chemosensitivity. The most active single cytotoxic agents in the assay were identified as cisplatin, treosulfan, paclitaxel, vinblastine, gemcitabine and mitoxantrone. There was also a limited direct inhibition of melanoma cell growth by interferon-alpha2b, although this agent is known to have a number of indirect biological antitumor effects. Exposure of tumor cells to combinations of drugs at the concentrations tested as single agents showed the most active combinations to be treosulfan+gemcitabine, cisplatin+paclitaxel and vinblastine+paclitaxel. There was considerable heterogeneity of chemosensitivity: some tumors responded well to one agent or combination, while others showed no response to this and instead responded to one of the alternatives tested. Occasional highly resistant tumors showed no response to any of the single agents or combinations tested. The degree of heterogeneity observed suggests that the ATP-TCA could be used to select patients who might benefit from specific chemotherapeutic agents alone or in combination. This provides the rationale for future randomized controlled trials of ATP-TCA-directed chemotherapy versus physician's choice to determine whether assay-directed chemotherapy can improve patient response and survival.

Adenosine Triphosphate

Treosulfan is an effective alkylating cytostatic for malignant melanoma in vitro and in vivo.

The therapy of metastatic malignant melanoma is limited by poor responses and short overall survival. Thus it remains an important issue to identify and test potential new drugs in this disease. This study was performed to examine the effects of the bifunctional alkylating cytostatic treosulfan in vitro. Using an in vitro microplate ATP bioluminescence tumour chemosensitivity assay (ATP-TCA) five highly chemoresistant melanoma cell lines and melanoma cells freshly isolated from metastases surgically resected from stage IV melanoma patients (n = 10) were incubated with treosulfan. Three cell lines and eight of the 10 tested tumour cells isolated from melanoma metasteses showed tumour growth inhibition >50% after incubation with treosulfan. Therefore, 14 patients with rapidly progressing stage IV malignant melanoma who had been pretreated with at least one standard chemotherapy regimen received treosulfan. In this population of patients with highly refractory advanced melanoma, one complete remission (7.1%), two partial remissions (14.3%) and three cases of stable disease (21.4%) were observed. The median survival time for all the patients measured from the beginning of treosulfan treatment was 9 months, and the median overall survival was 17 months. Except for two patients who developed grade 3 leucopenia, only moderate side effects were observed. Therefore, we conclude that treosulfan was well tolerated in this small series of patients and seems to be a promising alkylating cytostatic for the treatment of metastatic melanoma. Further studies are warranted to test these findings.

Adenosine Triphosphate

Expression of complement regulator proteins in primary and metastatic malignant melanoma.

The expression of complement regulatory antigens C3b/C4b receptor, (CD35) membrane cofactor protein (CD46), decay accelerating factor (CD55), and homologous restriction factor 20 (CD59) was determined immunohistochemically on ten primary malignant melanomas, 16 metastatic lesions, and ten melanocytic nevi. All of the melanocytic nevi and 9/10 primary melanomas showed both expression of CD46 and CD59. In one primary melanoma lacking CD46, expression of CD35 could be detected. In metastatic melanoma, 9/16 metastases were CD46+/CD59+, two were CD46-/CD59+, one CD46+/CD59-, and four CD46-/CD59-. Additionally, CD55 could be detected in two CD46+/CD59+ metastases, and CD35 in one. Expression or lack of complement regulatory antigens did not correlate with the expression of GD2, GD3, HMB-45 or S-100. In conclusion, some cases of metastatic melanoma show loss of normal expression of complement regulatory proteins. This might have implications on the immune response or the efficacy of immune therapy in malignant melanoma.

Adolescent

Risk and outcome in metastatic malignant melanoma patients receiving DTIC, cisplatin, BCNU and tamoxifen followed by immunotherapy with interleukin 2 and interferon alpha2a.

Combined chemo-/immunotherapy has shown high objective response rates and a significant though small proportion of long-term complete responders in metastatic malignant melanoma. The purpose of this study was to determine response rates, freedom from treatment failure (FFTF) and overall survival in patients with advanced metastatic malignant melanoma treated with combined chemo-/immunotherapy, and to determine the value of a prognostic model for prediction of treatment outcome, FFTF and survival. Sixty-nine patients with metastatic malignant melanoma received combined chemo-/immunotherapy consisting of up to four cycles of DTIC (220 mg m(-2) i.v. days 1-3), cisplatin (35 mg m(-2) i.v. days 1-3), BCNU (150 mg m(-2) i.v. day 1, cycles 1 and 3 only) and tamoxifen (20 mg orally, daily). Two cycles of chemotherapy were followed by 6 weeks of outpatient immunotherapy with combined interleukin 2 (20 x 10(6) IU m(-2) days 3-5, weeks 1 and 4; 5 x 10(6) IU m(-2) days 1, 3, 5, weeks 2, 3, 5, 6) and interferon-alpha (6 x 10(6) IU m(-2) s.c. day 1, weeks 1 and 4; days 1, 3, 5, weeks 2, 3, 5, 6). All patients were evaluated on an intention-to-treat basis. Of 69 patients entered in the study, seven achieved complete remissions and 20 reached partial remissions with an objective response rate of 39% (95% confidence interval 28-52%). Median survival was 11 months, median FFTF was 5 months. Seven patients achieved ongoing long-term remissions, with maximum survival of 58 + months, and maximum FFTF of 58 + months. By Kaplan-Meier survival analysis and two-proportional Cox regression analysis, pretreatment performance status and serum lactic dehydrogenase were statistically significant and independent predictors of survival; risk groups could be defined as (a) the absence of both or (b) the presence of either one or both of these risk factors. Whereas survival and response were significantly influenced by patient risk, no influence could be demonstrated for FFTF. This combined outpatient chemo-/immunotherapy is feasible and results in objective response rates and survival similar to earlier trials. Pretreatment risk, as defined by serum lactate dehydrogenase (LDH) and performance status, has a significant impact on treatment outcome and patient survival.

Adult

Effects of recombinant human soluble interleukin-4 receptor on interleukin-4/staphylococcal enterotoxin B-stimulated peripheral mononuclear cells from patients with atopic eczema.

In atopic eczema both in local inflammatory reactions and in peripheral blood high interleukin (IL) 4: interferon-gamma (IFN-gamma) production ratios have been demonstrated, indicating predominance of TH2 cell subsets resulting in increased IL-4 production and high serum IgE. The in vitro immunomodulatory effects of recombinant human soluble IL-4 receptor (rsIL-4R) on IL-4-stimulated lymphocyte proliferation, IgE and IFN-gamma production were studied in peripheral blood mononuclear cells from 10 patients with atopic eczema and seven healthy donors. In addition to control cultures (without any stimulus) and cultures with simultaneous application of rsIL-4R and IL-4, time-kinetic experiments were performed. We further investigated the influence of rsIL-4R on IL-4 production in staphylococcal enterotoxin B (SEB) stimulated peripheral blood mononuclear cells. Early addition of rsIL-4R to IL-4-stimulated peripheral blood mononuclear cells resulted in an increase in IFN-gamma production and in suppression of IL-4 induced proliferation and IgE secretion. Unexpectedly, rsIL-4R in combination with SEB exhibited an IL-4 protective effect with a significant increase in detectable IL-4 in the culture supernatants. The present data support the assumption that rsIL-4R might be a promising new immunomodulatory substance in the treatment of atopic eczema.

Adolescent

Determinants of lung volume in spontaneously breathing preterm infants.

To study the effects of apneic pauses, sighs, and breathing patterns on functional residual capacity (FRC), we measured FRC repeatedly in 48 healthy preterm infants (weight at study 2,042 +/- 316 g [mean +/- SD], postconceptional age 36.6 +/- 2.0 wk), during unsedated sleep using a modified heliox/nitrogen washout technique. Breathing movements and pulse oximeter saturation (SpO2) were recorded throughout and recordings analyzed for the presence of regular and nonregular breathing pattern, apneic pauses, sighs, and desaturations (SpO2 < 90%) during the last 2 min prior to each FRC measurement. FRC was lower during nonregular than during regular breathing pattern (23.3 +/- 7.2 ml/kg versus 26.9 +/- 7.8 ml/kg, p < 0.02); however, this apparent effect of breathing pattern disappeared after controlling the data for apneic pauses. Apneic pauses resulted in a significant decrease in FRC: mean FRC was 20.0 +/- 6.8 ml/kg if measured within 2 min of an apneic pause, 26.0 +/- 6.9 ml/kg if measured after a sigh (p < 0.001), and 24.0 +/- 7.7 ml/kg if there had been neither a sigh nor an apneic pause (p < 0.05). The interval between the apneic pause and the FRC measurement had no effect on FRC. There was an inverse correlation between FRC and the speed with which SpO2 fell during desaturation (r = -O.5, p < 0.03). Apneic pauses resulted in a persistent reduction in FRC in these preterm infants. Sighs appeared to restore FRC. The significant relationship between FRC and the speed of desaturation found in this study underscores the importance of endogenous or exogenous strategies that help to increase FRC, such as sighs or the application of continuous positive airway pressure, for the stability of oxygenation in preterm infants who have difficulty maintaining their oxygenation.

Female

B-cell chronic lymphocytic leukemia associated with high serum IGE levels and pruriginous skin lesions: successful therapy with IFN-alpha 2b after failure on IFN-gamma.

BACKGROUND: Chronic lymphocytic leukemia of the B-cell type (B-CLL) associated with highly elevated serum IgE levels and skin involvement has rarely been observed. Furthermore, not much is known about therapeutic strategies in such diseases. OBJECTIVE: We describe a 56-year-old male patient with a 5-year history of chronic and relapsing pruritic skin lesions as well as recurrent Staphylococcus aureus infections of the skin. RESULTS: Histologically, a lymphocytic and eosinophilic skin infiltrate was seen. Laboratory analysis revealed lymphocytosis (46.5%), eosinophilia (11.9%) as well as markedly elevated serum IgE levels (140,000 IU/ml). Immunohistology showed dermal B cells with intracytoplasmic IgE. Bone marrow biopsy showed a diffuse infiltrate of small lymphoplasmacytic lymphocytes. Over 80% of blood and bone marrow lymphocytes were CD5 +, CD19 +, CD20 +, CD23 + and CD38 +. Based on these findings, the diagnosis of B-CLL was made. The strong pruritus was resistant to antihistamines and steroids. Therefore, a trial with interferon (IFN) gamma 50 micrograms s.c. daily was started in order to suppress elevated serum IgE but failed. After 1.5 million units s.c. of IFN-alpha 2b every second day for 2 weeks, pruritus and serum IgE levels diminished markedly (48,000 IU/ml). Skin lesions, pruritus as well as skin infection and serum IgE level improved under continuing IFN-alpha 2b therapy for 2 years. CONCLUSION: In cases with suspected hyper-IgE syndrome, hematological neoplasias have to be excluded. The results argue for a benefical effect of IFN-alpha 2b in suppressing IgE production and symptoms of pruritus in an early-stage B-CLL.

Flow Cytometry

Preferential expression of T-cell receptor V beta-chains in atopic eczema.

Chronic skin colonization with Staphylococcus aureus is a characteristic feature of atopic eczema, and about 60% of S. aureus strains isolated from the skin of patients with atopic eczema secrete enterotoxins. T-cell stimulation by staphylococcal enterotoxins is restricted to the V beta-chain of the T-cell receptor. Therefore, the expression of different V beta-chains (V beta 3, 5 a,b,c, 6, 8, 12) on peripheral blood T-cells (CD4+) from patients with atopic eczema was measured by flowcytometry before and after stimulation with staphylococcal enterotoxin B. Lymphocytes from healthy donors served as controls. Additionally, the expression of V beta-chains in normal skin and in lesional skin of patients with atopic eczema was determined by immunofluorescence histology. In atopic eczema, higher numbers of CD4+ T-cells expressed V beta 3, V beta 8 and V beta 12 compared to the control group. No correlation between S. aureus enterotoxin B-stimulated V beta-expression and HLA-haplotypes was found. In lesional skin of patients with atopic eczema most of the infiltrating T-cells were V beta 3+, whereas in normal skin only very few T-cell receptor-expressing cells were detected. To evaluate the significance of these T-cell clones for allergic inflammation, T-cells from patients with atopic eczema and normal donors were stimulated with monoclonal antibodies against V beta 3, 5(c) and 8. Afterwards, the proliferative response of lymphocytes as well as IL-5 and IFN gamma synthesis were measured. T-cells from patients with atopic eczema showed a significantly higher proliferation and IL-5 secretion than normal donors after stimulation with monoclonal antibodies against V beta 3 and V beta 8. In contrast, the monoclonal antibodies directed to V beta 5(c) induced a markedly elevated proliferation and IFN gamma production of normal lymphocytes compared to patients with atopic eczema. Our results suggest a preferential expression of certain V beta-subgroups during inflammation in atopic eczema; this may be explained by a selective stimulation of TH2-cells via S. aureus-derived enterotoxins.

Cells, Cultured

Stage-dependent expression of CD7, CD45RO, CD45RA and CD25 on CD4-positive peripheral blood T-lymphocytes in cutaneous T-cell lymphoma.

Flow cytometric analysis of T-cell surface markers in peripheral blood has revealed abnormal patterns in patients with cutaneous T-cell lymphomas (CTCL). Here we investigated CD7, CD25, CD45RO and CD45RA expression on CD4+ T-lymphocytes in patients with CTCL stage I/II and III/IV and in patients with severe inflammatory skin diseases (ISD), as well as in healthy controls. Only late stage CTCL (III/IV) showed a lymphocytosis with a distinct surface marker pattern: CD3+, CD4+, CD8-, CD7-, CD45RO+, CD45RA-. Early stage CTCL (I/II) showed normal lymphocyte counts, a normal T-helper cell expression of CD7, CD45RO and CD45RA, and a slightly increased percentage of CD4+ CD25+ lymphocytes, which was also found in ISD. It is concluded that flow cytometric analysis of the above T-cell surface markers may be useful in the diagnosis of patients with late stage CTCL. However it does not allow us to distinguish patients with early stage CTCL from patients with ISD or controls.

Aged

Effects of Pityrosporum ovale on proliferation, immunoglobulin (IgA, G, M) synthesis and cytokine (IL-2, IL-10, IFN gamma) production of peripheral blood mononuclear cells from patients with seborrhoeic dermatitis.

The aetiology of seborrhoeic dermatitis (SD) is still unknown. An increased number of Pityrosposurm ovale in lesional skin of patients with SD has been suggested to play a crucial role in the pathogenesis of the disease since double-blind trials with antifungal drugs (e.g. ketoconazole) have shown that these agents result in a significantly reduced disease intensity. The frequent association of HIV infection and SD may be due to a suppressed cell-mediated immunity. In order to characterize the role of the humoral and cellular immune response in patients with SD the effects of a P. ovale extract on the proliferation of, and interleukin-2 (IL-2), IL-10 by an interferon-gamma (IFN gamma) production, and immunoglobulin (IgA, IgG, IgM) synthesis by peripheral blood mononuclear cells (PBMC) from patients with SD were studied in vitro. Healthy volunteers served as controls. PBMC from normal donors responded with a significantly increased proliferation to P. ovale antigen, whereas cells from patients with SD did not. Additionally, IL-2 and IFN gamma production by PBMC from patients with SD was markedly depressed compared with normal cells after stimulation with P. ovale. However, stimulation of PBMC from SD patients with P. ovale antigen induced significantly increased IL-10 synthesis. IgA, IgG and IgM synthesis was significantly increased in cultures of PBMC from patients with SD whether the cells were antigen-stimulated or not. Our results support the assumption that strong skin colonization with P. ovale in SD is due to an altered cellular immunity, which may be induced by increased IL-10 secretion.

Antigens, Fungal

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

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

Arterial oxygen saturation in infants at risk of sudden death: influence of sleeping position.

To study the possible influence of sleeping position on arterial oxygen saturation, measured by pulse oximetry (SpO2), 7-h overnight recordings of breathing movements and ECG were performed in 43 infants (median age 2.4 months, range 0.2-11 months) at increased risk of sudden infant death syndrome (SIDS). Infants were randomly allocated to start sleeping either in their usual sleeping position or in the opposite position. After 3.5 h, all infants were gently turned over. Thus, each infant served as their own control. Recordings were analysed for sleep time, baseline SpO2 (only during regular breathing), and the number and duration of desaturations (a decrease in SpO2 to < or = 80%). In the prone position, a significantly higher proportion of time was spent asleep (median 79% versus 70%; p < 0.05). Median baseline SpO2 was 98.8% (91.7-100%) in the prone and 99.0% (92.0-100%) in the supine position (ns). A total of 191 desaturations were found in 29 recordings; 96 in the prone and 95 in the supine position (ns). One infant subsequently died of SIDS while sleeping in the prone position. He had a relatively high number of desaturations (n = 12) which all occurred in the prone position. These results confirm earlier studies which could not find a significant influence of sleeping position on baseline oxygenation. The occurrence of desaturations in the prone position only in the infant who subsequently died requires further investigation.

Electrocardiography

Responsiveness of peripheral blood mononuclear cells from normal and atopic donors to microbial superantigens.

Patients with atopic dermatitis (AD) are frequently colonized with Staphylococcus aureus strains secreting exotoxins such as the staphylococcal enterotoxin B (SEB) and A (SEA). Nonetheless the role of SEB and SEA in AD is yet unknown. We analyzed the responsiveness of peripheral blood mononuclear cells (PBMCs) and isolated T cells from donors with AD and from normal donors to SEB and SEA. PBMCs as well as T cells from normal donors showed a significantly enhanced proliferation after stimulation with enterotoxin B, whereas the 3H-thymidine uptake of the T lymphocytes from patients with AD was markedly suppressed. Furthermore, we show that IFN-gamma mRNA and protein and mRNA for both chains of IL-12 (p35 and p40) are produced in human PBMCs from normal donors upon stimulation with SEB and SEA. In contrast to normal donors T cells from donors with AD predominantly express mRNA for IL-4, IL-5, and only diminished levels for IFN-gamma and IL-12 upon stimulation with SEB and SEA. Furthermore, in contrast to normal donors, PBMCs from donors with AD spontaneously produce high levels of IgE and express increased levels of CD23, the low-affinity receptor for IgE. Nonetheless, the superantigens by themselves, from 0.1 fg up to 1 microgram/10(6) cells, induced neither IgE secretion nor CD23 expression on PBMCs. Moreover, the addition of superantigens to IL-4-treated PBMC cultures diminished or totally suppressed the IL-4-induced IgE synthesis and CD23 expression. No differences were observed between PBMCs from normal donors of donors with AD. Both PBMCs isolated from normal and atopic donors produced high levels of soluble IL-4-receptor (up to 210 +/- 90 pg/ml). Addition of soluble IL-4-receptor to PBMC cultures downregulated the IL-4-induced IgE synthesis and CD23 expression in unstimulated as well as in SEB-stimulated PBMCs from normal donors and donors with AD. Our results suggest that superantigen-producing staphylococcal strains on the skin of patients with AD may modulate and/or amplify allergic inflammation.

Base Sequence

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