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.