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Kaposi's sarcoma (KS) is a low grade malignant neoplasm which shows invasive growth and often occurs in immunosuppressed patients with the Acquired Immune Deficiency Syndrome (AIDS; epidemic KS). It is also found in elderly men where it is usually limited to the skin (classic KS). The present study investigated the chemotaxis and invasive migration of epidemic KS cells in vitro and compared them to cells grown from classic KS lesions and to fibroblasts. Epidemic KS cells demonstrated invasive migration through reconstituted basement membrane (Matrigel) as well as through interstitial connective tissue (collagen 1) in early passages, whereas fibroblasts did not invade either barrier. Epidemic KS cells in late passages did not show any invasive migration. Following pretreatment with tumour necrosis factor α (TNF-α) there was no enhanced migration through the Matrigel and collagen I for epidemic KS cells, whereas classic KS cells showed an increased migration through the type I collagen barrier. [ABSTRACT FROM AUTHOR]

Thirty-seven men (36 homosexual or bisexual and one heterosexual) with epidemic Kaposi's sarcoma and underlying HIV infection were followed up over a period of up to 32 months. Fourteen patients (38%) died, with a median survival time of 72 months after the diagnosis of AIDS. Seventeen patients (46%) presented with one or more opportunistic infections, mostly Pneumocystis carinii pneumonia. Eighteen patients (49%) had lymphadenopathy syndrome according to the definition of the CDC. Using the Laubenstein-classification of Kaposi's sarcoma, all patients either remained stable or deteriorated, improvement was never observed. Absolute T4 lymphocyte counts and the T4/T8 ratio were not related to the disease stage. With the onset of B symptoms (systemic symptoms), however, the absolute T4 numbers and the T4/T8 ratio markedly decreased. Delayed type hypersensitivity also showed no relationship to the clinical stages of Kaposi's sarcoma. Thus, the clinical progression of Kaposi's sarcoma lesions seems to be largely independent of the immunological parameters investigated. However, the onset of B symptoms was observed to be related to changes in immune status. [ABSTRACT FROM AUTHOR]

We have quantified Langerhans cells (LC) in cryosections of normal human skin and lesional skin from patients with atopic eczema and psoriasis vulgaris using six different methods. The results from the different methods varied considerably and were sometimes contradictory, for example when LC numbers in psoriatic skin were compared with those in normal skin. Thus, in addition to the staining technique used and the selection of the dendritic cell type to be counted, the enumeration method used can also influence the quantitation of LC in normal and pathological skin. [ABSTRACT FROM AUTHOR]

A patient with a 12-year history of a relapsing bullous dermatosis is presented. Unusual clinical features included urticarial erythema, conspicuous mottled hyper- and depigmentation, lichenification and ichthyosiform hyperkeratosis. Serum immunoglobulin E levels were elevated. Histological examination showing deposits of amyloid in the uppermost dermis confirmed the diagnosis of bullous amyloidosis. Ultrastructurally, blister formation occurred at the level of the lamina lucida. The amyloid did not react with a panel of antibodies directed against amyloid fibril proteins. No underlying systemic disease was found. The bullous eruption responded to prednisolone therapy. [ABSTRACT FROM AUTHOR]

In a retrospective study of 503 well-documented cases of primary malignant melanoma (stage I) clinical criteria were analysed for their prognostic relevance. The maximum elevation (in mm) of the tumour was found to be the most important single prognostic factor. There was a close association with tumour thickness, measured histologically by the method of Breslow (correlation coefficient = 0.73). A combination of elevation and three additional clinical criteria (site, nodule- or lesion-diameter, and surface defects such as erosion, ulceration or bleeding) allowed a further improvement in prognostic accuracy. This clinical classification into low-risk and high-risk melanomas was as effective as the use of tumour thickness measured histologically, and can therefore be used for the preoperative planning of treatment. [ABSTRACT FROM AUTHOR]

Vitamin A and several other retinoids were added to fibroblast cultures in order to study possible alterations in biochemical properties and cellular responsiveness. The proliferation of cells was inhibited as the concentration of retinoids increased from 10-9 to 10-5 mol/l. Synthesis of non-collagenous proteins and production of both type I and type III collagen were decreased. The onset of type III collagen synthesis by tendon fibroblasts in culture was delayed. Furthermore, the chemotactic response of fibroblasts to fibroblast-conditioned medium was markedly reduced in the presence of retinoids (10-6 to 10-12 mol/l). [ABSTRACT FROM AUTHOR]

Axillary skin biopsies from fifteen patients with axillary hyperhidrosis who had received long-term treatment with aqueous aluminium chloride solution were examined histologically. The apocrine glands were normal, but the eccrine glands showed conspicuous morphological changes of varying severity. These included vacuolization of the secretory epithelium, dilatation of eccrine acini with atrophy of secretory cells, and accumulation of PAS-positive, diastase-resistant material in the dilated lumen of the secretory coils. The histological changes correlated in most patients with decreased secretion of sweat. We conclude that long-term blockage of the distal acrosyringium due to aluminium salts may lead to functional and structural degeneration of the eccrine acini. [ABSTRACT FROM AUTHOR]

In 4 cases of allergic vasculitis circulating immune complexes (IC) were demonstrated. Spontaneous and histamine induced vascular changes were studied by immunofluorescence microscopy. The early events in IC vasculitis were investigated at the ultrastructural level by immunoelectronmicroscopy using the peroxidase-antiperoxidase multistep technique. Our findings support the concept that human IC vasculitis is triggered by the deposition of circulating IC in the walls of postcapillary venules between endothelial cells, pericytes and the layers of the basal lamina. Tissue destruction is only secondary due to local complement activation and the release of lysosomal enzymes from chemotactically attracted leukocytes. [ABSTRACT FROM AUTHOR]

A new apparatus consisting of a 200 W super pressure mercury lamp and a flexible light guide with a liquid hght-conducting core is presented. Its transmission for UVA irradiation is mare than threefold as compared to conventional quartz fibre optic bundles. The light guide is capable of transmitting density levels exceeding 1 W/cm2. UVA and UVB are transmitted. By inserting a filter platelet (WG 345) into the light guide the UVB is cut off. The output of the unfiltered guide is 700 mW (3570 mW/cm2), of the filtered guide 400 mW (2040 mW/cm2), centered mainly at 366 nm. The light apparatus proved useful for several dermatological applications. It replaces in many respects conventional Kromayer lamps, especially because the flexible light guide, which is 160 cm long and weighs only 210 g, can be brought into direct contact with the skin. Results of determining the minimal erythema dose (MED), of phototesting (8-MOP photoallergy, persistent light reactor, erythropoietic protoporphyria) and of photochemotherapy are given. [ABSTRACT FROM AUTHOR]

Seven ³H-TdR-labelled early psoriatic lesions were quantitatively evaluated after serial sectioning and autoradiography. Epidermal thickness was measured planimetrically, whereas labelled cells as well as the number of nuclei present in the dermis were counted. Marked differences in the number of labelled cells as well as in their grain density were observed. These differences correlated with the density of the dermal infiltrate. It is concluded that psoriatic epidermal hyperplasia possibly develops as a response to antecedent and persisting events in the dermis. [ABSTRACT FROM AUTHOR]

Single psoriatic lesions were analysed planimetrically and autoradiographically after ³H-thymidine labelling. The results indicate maximum alterations of epidermis and papillary body in the centre of a lesion. Epidermal volume values are elevated at the periphery while the papillary body is still normal. After stripping, the proliferative activity of the peripheral epidermis increases in proportion to epidermal volume, while no stimulatory effect can be exerted in the centre of a lesion. Comparison of several lesions reveals large differences for volume values and between single rete pegs for ³H-thymidine labelling. The role of an epidermal defect in evoking the changes is discussed. [ABSTRACT FROM AUTHOR]

Numerous drugs have been recommended for the treatment of systemic sclerosis, but without any significant effect on the fibrotic stage of this disorder. Because recombinant gamma-interferon (gamma-IFN) is a potent and selective inhibitor of fibroblast proliferation and collagen production by human dermal fibroblasts in vitro, we assessed the effects of gamma-IFN treatment on the skin and on pulmonary function in patients with systemic sclerosis. Fourteen patients entered the study, and nine completed the 12-month trial. Fifty micrograms/day of gamma-IFN was administered subcutaneously 3 days per week. At the end of the 12-month treatment period a significant improvement was observed in total skin score, and blood gas analysis showed a significant increase in Pa O2 during therapy with gamma-interferon. Other clinical parameters (dysphagia, Raynaud's phenomenon, cardiac involvement) were not altered significantly. No serious adverse effects were noted. These results suggest a beneficial effect of gamma-IFN on the cutaneous fibrotic abnormalities and on lung fibrosis in systemic sclerosis.

Lymphocytes from healthy human donors were used as a model system for studying the combined effect of 8-methoxypsoralen (8-MOP) plus UVA. Two hours after oral administration of therapeutic doses of the drug enough 8-MOP was taken up in vivo by the circulating peripheral lymphocytes to cause significant inhibition of phytohaemagglutinin induced lymphocyte proliferation when the cells were exposed in vitro to UVA irradiation. The inhibition of proliferation as monitored by a reduced 3H-thymidine incorporation into cellular DNA was shown to be UVA-dose dependent. Control cultures of 8-MOP containing lymphocytes which were not UVA irradiated showed normal blast transformation. In lymphocytes obtained from the same donors prior to 8-MOP intake, PHA-induced lymphocyte transformation was not impaired by UVA irradiation. In 8-MOP containing lymphocytes exposed repeatedly to UVA during the 72 h culture period a cumulative effect of irradiation could be observed. A varying sensitivity towards 8-MOP plus UVA was noted when the cells were irradiated at different times after PHA stimulation. The cells were most vulnerable to UVA irradiation during the DNA-synthesis phase of the proliferating lymphocytes. The results suggest that dermal inflammatory infiltrates containing locally proliferating lymphocytes are influenced by systemic photochemotherapy since UVA penetrates well into the dermis.

Four patients are described, two with histologically proven multiple foci of bowenoid lesions, one patient with bowenoid lesions and Bowen's disease, and one patient with two keratoacanthomas, most of the lesions occurring in non sun-exposed but photochemically treated areas of the body. These patients had received long-term PUVA treatment for their psoriasis. Two patients had a history of arsenic intake. The possible relationship of these epidermal lesions to light treatment is discussed.

In order to elucidate the pathogenesis of the skin lesions in 'benign gonococcal sepsis' direct immunofluorescence of an early macular lesion and routine histopathology of a mature papulopustular lesion in a patient with septic gonococcal dermatitis have been performed. Histopathology of the mature skin lesion revelaed a pattenr of 'allergic vasculitis'. Direct immunofluorescence showed exclusively deposits of C3 around and within the capillaries and in the basement membrane zone. No specific IgG, IgM, IgA or C4 deposits could be demonstrated. This, together with serological findings and reports from the literature, suggests an important pathogenetic function for complement, activated through the alternative pathway by means of gonococcal endotoxic lipopolysaccharide, in the pathogenesis of the skin lesions in benign gonococcal sepsis.

Histochemical and electron microscopic studies were carried out on the newborn mouse model of the staphylococcal scalded skin syndrome to investigate the mechanism of action of the staphylococcal epidermolytic toxin that causes it. Histochemical studies showed that an intra-epidermal split develops below the subcorneal zone which is rich in catabolic enzymes (the so-called esterase-acid phosphatase-rich band). However, histochemical alterations in the enzyme pattern could not be demonstrated. The earliest change revealed by electron microscopy was a widening of the intercellular space, with the formation of microvilli at the level between the stratum spinosum and stratum granulosum where the split later occurs. A clearing of the peripheral cytoplasm along the cell membranes was also revealed. In pre-split areas, adhesion between cell membranes of adjacent cells seems to be lost; desmosomes continue to hold the cells together but the split develops when these are broken by mechanical pressure. Later, damaged cell membranes may be seen. Extracellular keratinosomes remain unchanged. Although these findings do not agree with the already divergent results of other studies, they help support the findings of all groups that cases of the Lyell syndrome produced by staphylococci do not occur through necrolysis; it is therefore inappropriate to continue applying the term 'toxic epidermal necrolysis' to such cases.