The histology and immunopathology of vitiligo.

Twenty-nine Caucasoid patients with 'common' vitiligo were studied. The sera of these patients were tested for autoantibodies. Shave biopsies from uninvolved, marginal and involved areas were studied by DOPA method, direct immunofluorescence tests, indirect immunofluorescence complement fixation technique, Epon embedded tissue for light microscopy and by electron microscopy. All the patients had symmetrical vitiligo apart from one. About 50% of these patients had the onset of their vitiligo before the age of 20 years. The incidence of autoimmune disorders that are commonly associated with vitiligo seemed to be increased. These patients frequently had a positive family history of vitiligo and other autoimmune disorders. The organ specific autoantibodies were also increased in the sera of these patients. There was no significant deposition of immunoglobulins in all areas biopsied apart from the presence of cytoid (colloid/amyloid) bodies. However, in many patients, there was deposition of fibrin in the papillary dermis and at the dermo-epidermal junction of the marginal and involved areas. There was no complement fixing antibody to the melanocytes in the sera of all the patients tested.On light and electron microscopy, inflammatory changes were seen in the skin of these patients, mostly in the marginal areas. This consisted of spongiosis of the epidermis with a mononuclear cell infiltrate. Many of the intraepidermal lymphocytes were found in direct contact with melanocytes and Langerhans cells. The degree of mononuclear cell infiltrate of the dermis did not parallel that seen in the epidermis. Sometimes, there was a massive lymphocytic infiltrate in the epidermis, even forming Pautrier-like micro-abscess, but only a few lymphocytes in the upper dermis. It is suggested that the primary inflammatory reaction occurs in the epidermis where an antigen is present. Langerhans cells were found to be increased in the epidermis-of uninvolved areas of patients with vitiligo compared to that of normal controls. These cells were also increased in the involved depigmented areas. Some of these cells were seen to be in direct contact with lymphocytes. The melanocytes were markedly reduced in the marginal areas and only a few residual cells were found in the involved skin. The melanosomes had the tendency to be singly dispersed in the keratinocytes rather than in membrane bounded complexes. There was no obvious pathological changes in the cutaneous nerves. However, there appeared to be some evidence of regeneration of axons. In a third of the patients intra-epidermal nerves were found in the basal layer. Some of these nerves were adrenergic in type and observed occasionally in direct contact with a secretory melanocyte. Colloid/amyloid bodies were demonstrated in the papillary dermis, by a variety of techniques. They had the tendency to occur in the skin of patients with vitiliqo compared to that of normal controls. These colloid/amyloid bodies had many features that would suggest these bodies were derived from degenerating melanocytes. Three patients with occupational vitiligo due to paratertiary butyl phenol were studied. The findings were similar to that found in idiopathic vitiligo. The light microscopic ultrastructural and immunopathological findings in vitiligo do support the hypothesis that this condition is an 'autoimmune' disorder.