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.

Aims-To compare the expression of the cell adhesion molecules intercellular adhesion molecule-I (ICAM-1), ELAM-1 (E-selectin), and vascular cell adhesion molecule-i (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-i 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-i 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-i expression by keratinocytes in lymphocytic vasculitis is consistent with an active role for mediators derived from T lymphocytes in the pathogenesis of the lesion.

Vibration white finger or hand-arm vibration syndrome is the episodic blanching of the fingers in response to cold occurring in those who work with hand held vibrating tools. Clinically the condition differs from primary Raynaud's phenomenon as persistent paraesthesiae and pain are common in the hands and arms and these occur independently from the ‘white attacks’. Symptoms can become severe enough to warrant a change of occupation. Industrial compensation may be awarded for vibration white finger but, at present, no simple or reliable objective diagnostic test is available. Calcitonin gene-related peptide (CGRP) is a neuropeptide with powerful vasodilator properties. A deficiency of immunoreactive CGRP nerve fibres has been previously demonstrated in the digital cutaneous microvasculature of patients with primary and secondary Raynaud's phenomenon with the distribution and quantity of other types of nerve fibres not being significantly altered. To determine if the innervation of the cutaneous microvasculature in vibration white finger was also abnormal skin biopsy samples from the fingers of 15 patients with vibration white finger, six healthy age matched controls who worked with vibrating machinery and 26 healthy age matched controls who were heavy manual workers without exposure to vibrating machinery were examined by immunohistochemistry. To try to correlate any histological abnormalities with clinical neurological deficit sensory nerve conduction studies have so far been performed in six patients with vibration white finger. There was a significant reduction in both the number of CGRP and protein gene product 9.5 (PGP) immunoreactive nerve fibres in the digital cutaneous biopsies from the patients with vibration white finger when compared to the biopsies from the heavy manual workers and the healthy workers exposed to vibration. The pattern of the loss of CGRP immunoreactive nerve fibres was similar to that described previously in Raynaud's phenomenon and may account for the episodic vasospasm seen in both conditions. PGP is a constitutive protein of all nerves therefore the reduced PGP immunostaining indicates generalized structural neuronal damage which could account for the persistent pain and paraesthesiae characteristic of vibration white finger. The nerve conduction studies revealed sensory nerve action potentials within the low range of normal in five patients with vibration white finger and mild median nerve compression in the remaining patient implying that the neuronal damage in the patients with vibration white finger is confined mainly to the small unmyelinated nerve fibres. The immunohistochemical findings may provide the basis for a diagnostic test for vibration white finger.

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