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Aims: To compare the expression of the cell adhesion molecules intercellular adhesion molecule-1 (ICAM-1), ELAM-1 (E-selectin), and vascular cell adhesion molecule-1 (VCAM-1) in cutaneous leucocytoclastic and lymphocytic vasculitis., Methods: Immunohistochemical analysis was performed on early lesional skin biopsy specimens of leucocytoclastic vasculitis (n = 14), lymphocytic vasculitis (n = 10), non-lesional skin (n = 12), and normal skin (n = 5). A standard immunoperoxidase technique was used to detect expression of ICAM-1, E-selectin, VCAM-1, and the cell markers CD11a, CD11b, CD11c, von Willebrand factor, CD3, CD68, and neutrophil elastase (NP57)., Results: Basal keratinocyte intercellular adhesion molecule-1 was expressed in eight (80%) cases of lymphocytic and in only one (7%) case of leucocytoclastic vasculitis, and not in non-lesional skin or control biopsy specimens from normal subjects. E-selectin was expressed on vascular endothelium in eight (57%) cases of leucocytoclastic and in seven (70%) cases of lymphocytic vasculitis. Endothelial vascular cell adhesion molecule-1 expression was seen in three (21%) biopsy specimens of leucocytoclastic and five (50%) of lymphocytic vasculitis. There were increased numbers of cells in the dermal infiltrate stained for NP57, CD11b, and CD11c in leucocytoclastic compared with lymphocytic vasculitis (p < 0.001, p = 0.013, p = 0.009, respectively); immunoreactive positive cells for CD3 and CD11a were increased in lymphocytic compared with leucocytoclastic vasculitis (p < 0.001, p = 0.011, respectively)., Conclusions: These observations indicate that upregulation of adhesion molecule expression occurs in both leucocytoclastic and lymphocytic vasculitis. The different patterns of adhesion molecule expression in the two groups of vasculitis may reflect differences in the local release of cytokines. In particular, detection of intercellular adhesion molecule-1 expression by keratinocytes in lymphocytic vasculitis is consistent with an active role for mediators derived from T lymphocytes in the pathogenesis of the lesion.

The development of naevus spilus-like hyperpigmentation at sites of resolving plaques of psoriasis has been reported previously. Although the mechanism is not understood, PUVA therapy has been implicated in most cases. We report an additional case in which lentigines, confined to sites of resolving psoriasis, occurred following oral PUVA. We also describe similar clinical features in two patients who had not received PUVA, which strengthens the observation that this treatment is not a prerequisite for development of this unusual pattern of pigmentation.

A controlled double-blind study of oral zinc supplementation was performed in twenty-five patients with chronic plaque psoriasis over twelve weeks to assess changes in both psoriasis (using the psoriasis area and severity index) and neutrophil zinc content. There were no statistically significant differences in the psoriasis area and severity index during the trial between the placebo- and zinc-treated group, nor in the zinc levels. There was therefore no evidence of a benefit from zinc supplementation in patients with this disease.

The case of a 71-year-old woman is reported, who neglected a chronic venous ulcer, and presented to the orthopaedic surgeons with a pathological fracture of her tibia due to an invasive squamous cell carcinoma arising from the ulcer. Malignant degeneration of venous ulcers is fortunately rare. However, this case emphasizes the need for regular assessment of long-standing venous ulcers, and illustrates that they may present as an acute emergency to other specialities.

Rhabdomyosarcoma is an uncommon tumour that may present at a wide variety of different sites. We report a 4-year-old girl who developed an embryonal rhabdomyosarcoma arising in the left pinna which was clinically indistinguishable from a lymphangioma. The case illustrates that this neoplasm can be easily misdiagnosed because of its variable morphology. Early recognition is important as successful treatment is now possible with a combination of chemotherapy, surgery and/or radiotherapy.

The follow up of a case of the carcinoid syndrome complicated by scleroderma is reported, in which progress of the disease may have been halted by treatment with a combination of cyproheptadine, parachlorophenylalanine and prednisolone. Impairment of tryptophan and 5-hydroxytryptamine (serotonin) metabolism appears central to the development of skin fibrosis in the carcinoid syndrome and may be indicative of important mechanisms in the pathogenesis of idiopathic scleroderma.

Cutaneous vasculitis is frequently located on the lower limbs. We describe a patient who developed palpable purpura affecting the penis as the presenting sign of more widespread lesions of Henoch-Schönlein purpura.

Infectious mononucleosis is rarely associated with skin lesions. A 23-year-old woman with acute infectious mononucleosis who presented with moderately severe erythema multiforme is reported. The role of steroids in the management of this condition is briefly discussed.

We have reviewed the histopathological features of 11 patients with pustular drug eruptions. Two main histological patterns were seen. Eight cases revealed features of toxic pustuloderma with the presence of spongiform intraepidermal pustules in association with papillary oedema and a mixed inflammatory cell infiltrate around upper dermal blood vessels. Pustules were present at different levels within the epidermis. The other three cases exhibited leucocytoclastic vasculitis with neutrophil collections both below and within the epidermis. One case showed continuity between the subepidermal and intra-epidermal pustules. These findings suggest a dynamic process in which neutrophils collect around upper dermal blood vessels and are then eliminated via the overyling epidermis. The presence of extravasated red blood cells within the intra-epidermal pustules indicates that this process is passive rather than the result of specific chemotaxis or cell migration.

Epidermal antinuclear antibody (ANA) staining was noted during routine direct immunofluorescence (DIF) of skin biopsies from 22 cases at St John's Dermatology Centre over a 2-year period. We have reviewed the clinical, serological and immunopathological features of these patients. They comprised 13 cases of lupus erythematosus (LE), 3 dermatomyositis, 1 morphoea, 1 systemic sclerosis, 1 CREST syndrome, 1 mixed connective tissue disorder and 1 probable cutaneous sarcoidosis. Five (38.4%) patients with LE had moderate to severe oral mucosal involvement. Epidermal nuclear staining (ENS) was seen following IgG deposition in 21 cases and IgA in only 1 case. Complement C3 staining was an additional feature in 1 patient. Circulating ANA was absent in 7 cases at the time of biopsy, confirming that this pattern of staining does not occur as a result of tissue contamination during processing. The presence of ENS by DIF corroborates a diagnosis of a connective tissue disorder, and our results suggest that it may also be associated with oral involvement in L.E.

We describe the clinical, histological and immunopathological features of four female patients with the bullous eruption of systemic lupus erythematosus (bullous SLE). Three patients had circulating anti-basement membrane zone (BMZ) antibodies, and Western blot analysis in two cases revealed binding to type VII collagen. Immunoelectron microscopy in one of these patients demonstrated deposition of antibody in the lamina densa and sublamina densa regions, thus sharing immunopathological features with epidermolysis bullosa acquisita (EBA). The vesiculobullous lesions developed 8 months to 6 years after the initial symptoms of SLE, and cleared promptly with dapsone treatment.

A 46-year-old woman with the Dowling-Meara variant of epidermolysis bullosa simplex (DM-EBS) presented with worsening recurrent, pruritic, circinate crops of clear and haemorrhagic herpetiform blisters affecting her trunk and limbs. Electron microscopy showed tonofilament aggregation and an intra-epidermal level of blister formation confirming a diagnosis of DM-EBS rather than an acquired immunobullous disorder. Antihistamines failed to control the intense pruritus, but dapsone (up to 150 mg daily) was beneficial. Mutations of basal cell keratin genes (K14 and K5) are thought to be of aetiopathological significance in this form of epidermolysis bullosa, but the underlying cellular mechanisms responsible for the clinical deterioration and severe itching in this adult patient are not yet clear.

Seven patients with nodular prurigo, five patients with lichenified eczema and seven control volunteers were studied immunohistochemically using antisera to the pan-neuronal marker protein gene product 9.5 (PGP), and the neuropeptides calcitonin gene-related peptide (CGRP), substance P (SP), tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP) and the C-flanking region of neuropeptide Y (C-PON). PGP-, CGRP- and SP-immunoreactivities were also evaluated using image analysis quantification, and the data compared by statistical analysis. No significant changes were noted in the lichenified skin of patients with chronic eczema, compared with the control groups. In contrast, a significant increase in PGP immunoreactive nerve fibers was seen in lesional skin of all nodular prurigo cases studied, when compared with non-lesional skin from the same patient or from control subjects (P < 0.001). In one case massive neural hyperplasia was also identified. Staining for CGRP and SP showed a large increase of immunoreactive nerves in lesional skin of nodular prurigo patients, which closely paralleled that of PGP. Staining with VIP, C-PON and TH was similar in both lesional and non-lesional skin. These results indicate that neural changes in nodular prurigo are associated with an increase of sensory neuropeptides, which could be related to the intense pruritus which accompanies nodular prurigo. The absence of significant changes in lichenified skin suggests that the increase in CGRP- and SP-immunoreactive nerve fibres is a characteristic feature of nodular prurigo and may be important in its pathogenesis.

We have studied four patients from two families and obtained the clinical data from four other affected family members who demonstrated the coexistence of multiple cylindromas and trichoepitheliomas. An autosomal dominant pattern of inheritance with variable penetrance was exhibited in both families, with a female to male ratio of 3:1. The clinical and pathological features of this rare association are discussed.

We report the case of a 54-year-old female who was found to have adenocarcinoma of the gall bladder 2 years after the onset of yellow discolouration and deformity of all 20 nails. She also exhibited a past history of chronic sinusitis and mild bronchiectasis. As the tumour was inoperable, palliative surgery was performed. This case adds further support to a possible association between malignancy and the yellow nail syndrome (YNS).

A female patient with disfiguring lupus erythematosus profundus (LEP) from the age of 13 years was found to have an isolated partial C4 deficiency, with reduced levels of both allotypes, C4A and C4B. A genetic basis for the hypocomplementaemia was confirmed by a family study of complement and HLA types which revealed heterozygous null alleles for C4A and C4B in the proband. Marked improvement in her cutaneous lesions occurred with thalidomide.