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In 23 patients with psoriatic arthritis and 9 patients with psoriasis without joint involvement, we took bone biopsies from the iliac crest. Histomorphometrical investigations showed that the volume density of the bone was not decreased in either group of patients, but we found a high rate of turnover remodelling. An elevated rate of bone turnover is regarded as the characteristic principle of "psoriatic osteopathy", which--more exactly--should be called "latent osteopathy". Deficiency of vitamin D is discussed as a possible etiological factor.

In the morning urine of 24 patients with psoriasis and that of 24 patients with psoriatic arthritis, we determined the excretion of hydroxyproline (mg HP/mumol crea), after preceding diet low in collagen. Surprisingly, psoriatic patients without articular involvement showed a significantly higher excretion of HP than those with psoriatic arthritis. Further differentiation revealed that there were no clear-cut correlations between the amount of HP excretion and the activity of the articular process; we proved, however, that the amount of HP excretion was definitely related to the activity of the skin eruptions in both groups of patients. We discuss whether an osteopathy pathogenetically associated with the skin disease (irrespective of synovitis in psoriatic arthritis) may possibly be responsible for these results.

In an open clinical trial on stationary psoriatic plaques, we compared the effects of shortime occlusive (SO) dressing (24h) and prolonged occlusion (PO: 5-28 days). IN SO, Weinstein's index decreased from 7.3 +/- 1.7 to 3.3 +/- 1.8 (n = 21), in PO from 6.5 +/- 1.1 to 3.7 +/- 1.7 (n = 15). The results were even better in cases with optimal PO dressing (decrease from 6.8 +/- 1.4 to 2.5 +/- 0.9). The most important side effects were itching and exsudation with ensuing smell. In only one of the cases did the side effects cause a drop-out after 5 days. Regarding stationary psoriatic plaques on the extensor sides of the lower legs and forearms. We recommend continuous occlusive dressing for 8-10 days--either as an alternative mode of therapy, or as an intermediate regimen.

Seborrheic keratoses were investigated by means of histo- and biochemical techniques in order to define the epidermal differentiation and proliferation of this most common epithelial tumor in adults. The following markers have been used in our study: cytokeratins, epidermal proteins binding zinc, insulin receptors, tissue plasminogen activator (tPA), as well as calmodulin (immunohistochemical and quantitative evaluation). Immunohistochemical investigation of seborrheic keratoses revealed a decreased tPA expression; their epidermal concentration of calmodulin was doubled. The differentiation markers failed to show any significant deviation from normal skin. Thus, seborrheic keratoses are associated with normal epidermal differentiation in spite of morphogenic alterations. Pathogenetically, we have to consider epidermaldermal interactions.

The Ro/SSA antigen-antibody system is of great importance with regard to the cutaneous manifestations and the photosensitivity of patients suffering from lupus erythematosus (LE). On account of in vitro investigations on cultured fibroblasts taken from psoriatic skin, we evaluated both the effect of UVA/PUVA irradiation and that of the metabolic activity of cells on this antigen-antibody system. We found that UVA irradiation is able to demask Ro/SSA. Thus it becomes accessible so subsequent antibody binding, which can be seen as nuclear fluorescence positive for IgM. Incubation of vital cells with these autoantibodies and subsequent irradiation resulted in a high degree of cytoplasmic fluorescence (IgG, IgM) in part of the fibroblasts exposed to UVA. Regarding the clinical application of light protective agents in LE patients with antibodies to Ro/SSA, UVA light--aside from UVB--should be taken into consideration.

Subepidermal immune deposits containing IgG and C3 by 9 patients suffering from SLE were exposed to extreme excess of antigens in order to solubilize tissue-bound immune complexes. Sections of 4 micron were incubated at room temperature either with calf thymus DNA (0.3-30 mg/ml) or with human gamma-globulin (HGG) (1.6-16 mg/ml). The sections thus pretreated were compared with "native" samples by means of direct immunofluorescence technique. Only HGG resulted in drastic removal of IgG deposits along the dermoepidermal junction. DNA proved to be ineffective; deposits of C3 remained uninfluenced. Our results are discussed in the light of the composition of the subepidermal immune complex in SLE.

Serum concentrations of AFP have been determined in patients suffering from systemic lupus erythematosus (SLE) or other "collagenoses" using fluorescence ELISA adapted to the chamber analytical technique. 20% of the SLE patients showed elevated AFP levels (range 30-233 ng/ml), some of them repeatedly. Only 2 of the 14 patients without SLE had AFP levels above 30 ng/ml (37 resp. 40 ng/ml). In SLE sera there was a significant correlation of raised AFP to higher anti-dsDNA antibody concentrations (Mann-Whitney U-test: p = 0.042). The mean dosage of azathioprin and prednisone in patients with SLE did not significantly differ from the non-SLE group. We discuss the possible reactivation of AFP synthesis on account of SLE itself.

We studied the influence of neutral solvents on epidermal lectin binding in normal and lesional psoriatic skin. 1% solution of Tween 80 or Triton X-100 had no effect on the binding of the following lectins: PHA, ConA, and LCA. The HPA staining of the str. spinosum in normal skin, however, was completely removed by neutral solvents. In psoriatic skin, str. spinosum staining with HPA was resistant. Our results are discussed in the light of an altered keratinocyte maturation in psoriasis.

Frozen sections from psoriatic lesions were investigated regarding their reactivity with endothelial markers (UEA I, EEA I, LTA, Con A, factor VIII-related antigen). We compared the findings obtained with those of both uninvolved psoriatic skin and normal skin. Although all lectins showed altered epidermal binding in comparison to the controls, the endothelial lectin binding as well as the expression of factor VIII-related antigen were the same in both psoriatric lesions and controls. Our findings argue for (1) intact dimorphic genetic control of ABH expression in both epidermal and endothelial cells, (2) altered epidermal differentiation of lesional psoriatric skin, and (3) secondary vascular alterations.

The binding of five different lectins by normal as well as psoriatic lesional epidermis was investigated with regard to its dependence on the pH value. As we studied the reactions within the pH range of 3.0 to 9.66, we obtained the following results: lectin binding almost independent from pH (FITC-Con A, -PHA, HPA), fluorescence intensity dependent on pH (TRITC-Con A, FITC-LCA, -GCA), binding pattern dependent on pH (FITC-LCA, GCA). In contrast to normal epidermis, there was no pH dependence of the FITC-GCA binding pattern in psoriatic lesional epidermis.

Dermal nevocytic nevi (NN) were histochemically studied with the help of FITC-conjugated lectins as well as antisera against keratin and plasminogen activators of the urokinase type. 3 out of 18 NN showed interpenetrating nevus cells in atrophic parts of the epidermis. These cells revealed strong lectin reactivity both with Con A (cytoplasmatic binding) and WGA/RCA II (membraneous binding). In addition we found membraneous reaction with anti-urokinase, whereas there was no anti-keratin staining. Our findings suggest active transepidermal elimination of nevus cells in dermal nevocytic nevi.

Serum concentrations of alpha 1-fetoprotein (AFP) during PUVA treatment have been analyzed in 12 patients suffering from severe psoriasis or psoriatic arthritis. The results have been compared with AFP levels in psoriatics without PUVA treatment (group II), patients with psoriatic arthritis treated with methotrexate (group III), as well as dermatological patients without psoriasis (group IV). All groups revealed AFP levels below 25 ng/ml. Although a slight raise of AFP could be observed during PUVA therapy (p less than 0.005), we assume that AFP detection cannot be regarded as a marker of potential PUVA side-effects in psoriasis.

Using 11 different kinds of lectins, we histochemically studied 18 dermal nevocytic nevi (NCN). The investigation included both unfixed frozen sections and pretreated sections fixed with acetone (pretreatment: chloroform/methanol, Triton X-100, neuraminidase). In this way, we hoped to get some information both on the expression of surface glycoconjugates and the chemical nature of the sites of lectin binding. Our results argue for an abundance of glucosyl, mannosyl, galactosyl, and N-acetyl galactosamine residues on the surface of nevus cells. In comparison to keratinocytes, we found a greater sensitivity to chloroform/methanol, which suggests a relative increase of glycolipids. Dermal NCN showed heterogenic lectin binding: The highest intensity was seen in the marginal nevus cells, the lowest in the central cells of epidermal nests. Dermal cells showed a moderate binding intensity. Epidermal cells lying above the NCN disclosed some modifications of their lectin binding pattern. In contrast to normal epidermis, basal keratinocytes failed to bind LCA; suprabasal cells showed cytoplasmic staining. In some NCN, we observed an intensive perinuclear staining of the upper keratinocytes with granular ConA. Our results suggest (1) a modified lectin binding pattern of nevus cells depending on their microenvironment, as well as (2) a distinctly altered lectin binding of keratinocytes in the adjacent epidermis.

PUVA effects on frozen sections of human epidermis were investigated (20 micrograms 8-methoxypsoralen/ml; UVA wavelength 365 +/- 5 nm; radiation dose between 2 X 10(2) and 2 X 10(2) J/m2). The quality of the glycocalyx was characterized by lectins labeled with FITC (HPA, PHA, LCA, PNA, SBA, RCA, GCA I, UEA I). Serum antibodies of bullous pemphigoid (BP) served as membrane markers for the basement membrane. Fixed BP antibodies were detected by FITC-antihuman IgG. The fluorescence intensity was markedly decreased at a dose of 2 X 10(5) J/m2; 2 X 10(4) J/m2 were less effective. At 2 X 10(3) J/m2, there was nearly no alteration of the fluorescence intensity observed. Changes were seen in the case of BP antibodies and lectins, except UEA I. The relatively high intensity (radiation dose) and the effects immediately observable suggest direct membrane alterations by PUVA in vitro.

The aim of our study was the characterization of epidermal lectin binding pattern in psoriatic vs. non-psoriatic skin in order to reveal possible alterations of the glycocalyx composition of psoriatic keratinocytes. We used fluoroisothiocyanate-labeled lectins of Canavalia ensiformis (ConA), Phaseolus vulgaris (PHA), Lens culinaris (LCA), and Helix pomatia (HPA). The binding pattern of psoriatic (involved and non-lesional) skin did not differ from the control samples in ConA, PHA, and LCA. In psoriasis, there was a prominent HPA binding to the dermo-epidermal junction and to a lesser degree, intercellular epidermal near the uppermost cell layers. In seborrheic keratosis, in contrast, there was no fluorescence of the dermo-epidermal junction or the first layers of the epidermis. The most pronounced binding was observed perinuclear in the upper epidermis. The results are discussed in the light of an altered keratinocyte maturation in psoriasis.

We investigated the effects of anti-psoriatic therapy with dithranol (1/20-1%) in salicylic acid (0.5%) in white petrolatum on lesional skin. FITC-labeled lectins and pemphigus vulgaris antibodies (PV) served as analytical means to study the glycocalyx. Antibodies of bullous pemphigoid (BP) were used as basal membrane markers. Nuclear antigens were recorded according to the binding of speckled, anti-nuclear antibodies (ANA) as well as antibodies to dsDNA. With some lectins, dithranol therapy resulted in pronounced fluorescence of the lower parts of the basal cells. ConA was fixed by the basal cell layer. To a lesser degree, ANA were fixed by nuclei of keratinocytes. PV antibodies were not fixed at all.