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Scheda a cura di Marco Chilosi (GYM)
FASCIN
Impiego
nella diagnostica istopatologica
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- Dermatopatologia
Am J Dermatopathol 2001 Apr;23(2):104-11- "Juvenile" xanthogranuloma: an
immunophenotypic study with a reappraisal of histogenesis.
Kraus MD, Haley JC, Ruiz R, Essary L, Moran CA, Fletcher CD.
Department of Pathology, Washington University Medical Center, St. Louis,
Missouri 63110, USA.kraus@path.wustl.edu
The non-Langerhans histiocytoses, a nosologic category to which juvenile
xanthogranuoma (JXG) belongs, represent a heterogenous collection of
disorders related to the monocyte/macrophage lineage. The dermal dendrocyte
was previously proposed as the cell of origin for JXG on the basis of Factor
XIIIa reactivity, a suggestion that does not fully explain the occasional
xanthogranulomatous proliferations localizing exclusively to extracutaneous
sites. This study applies a panel of recently developed immunohistochemical
markers to JXGs and relates the phenotype of this process to new concepts of
monocyte/dendritic cell ontogeny. Twenty-seven JXG, ten dermatofibromas (DF),
and ten age-matched normal skin specimens were stained using standard
immunohistochemistry methods, and all JXGs were fascin+ and CD68+, although
26 of 27 were reactive for HLA-DR, 25 of 27 for Factor XIIIa, 25 of 27 for
LCA, 21of 27 for CD4, and 8 of 27 for polyclonal s100. Six of those eight
polyclonal S100+ cases were also reactive for monoclonal S100. None of those
cases was reactive for CD1a, CD3, CD21, CD34, or CD35. Eight of ten
dermatofibromas were FXIIIa+; all were negative for HLA-DR, LCA, CD4, and
polyclonal s100. In controls, fascin+ dendritic cells were present but did
not stain for Factor XIIIa, S100, or CD4. Based on the morphologic and
phenotypic overlap of the lesional cells in JXGs and plasmacytoid monocytes,
it would appear that the plasmacytoid monocyte might be considered the
putative normal counterpart of the major cellular population of JXGs, a
proposal that helps explain the extra-cutaneous, visceral, and soft tissue
location that have been reported for occasional cases of JXG. We would also
conclude that neither Factor XIIIa-nor S100+ results should preclude the
diagnosis of JXG, and find that reactivity for CD4 and LCA may be used to
distinguish JXG from DF when the latter is heavily lipidized or the former
is not.
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