Histological and
immunohistochemical study of granuloma annulare and subcutaneous
granuloma annulare in children.
J Cutan Pathol. 2007 May;34 (5):392-6.
BACKGROUND: The
aim of this study was to investigate the histological and
immunohistochemical features of granuloma annulare (GA) in comparison
to deep granuloma annulare (DGA) and granulomatous dermatoses (GDs).
METHODS: Our material comprised 13 GA, 8 DGA and 1 atypical granuloma
annulare (AGA) in a child with primary immunodeficiency, 10 cases of
nonspecific GDs and 1 case of sarcoidosis with cutaneous involvement.
The immunohistochemical streptavidin-biotin-Horseradish peroxidase (HRP)
analysis was performed on paraffin sections for the detection of
CD68/KP-1, CD68/anti-human CD68 clone PGM1 (PGM1), lysozyme, S-100
protein, CD1a, CD3, CD20/L-26, CD4 and CD8. RESULTS: All 13 GA were
characterized by typical palisading and interstitial granulomas. In 6
cases, the lesion extended to the subcutaneous fat, while a
considerable perivascular lymphocytic infiltrate without any signs of
vasculitis was observed in 10 cases. The DGA were located to the deep
dermis and subcutaneous fat, showing palisading granulomas with
central necrobiosis. Immunohistochemistry revealed a broad intense
expression of CD68/PGM1 in the histiocytic population in all cases, a
constant but fainter detection of CD68/KP-1 and a variable one
of lysozyme. T-cell markers (CD3, CD4 and CD8) were mainly detected in
the perivascular lymphocytic infiltrate of GA and DGA, with CD4+ T
lymphocytes predominating over CD8+ in GA and DGA, while CD8+ T
lymphocytes was the predominant population in AGA. CONCLUSIONS:
CD68/PGM1 is a sensitive and reliable histiocytic marker in confirming
the histiocytic nature of equivocal GA and DGA, but the histiocytic
immunoprofile is of no particular usefulness in differentiating GA
from other GD.
Granuloma annulare--a genetic disorder that sustain an incomplete
foreign-body granuloma reaction.
Med
Hypotheses. 2006;67(4):876-8. Epub 2006 Jul 14.
Granuloma
annulare (GA) is a common dermatosis characterized by an annular
arrangement of erythematous papules, plaques, rarely nodules or
patches. It is a type of non-infectious granuloma with unknown
etiology. Hypothesis. The immune reaction always begins with the
foreign-body granuloma formation. However, if during the process the
antigen is recognized as too small the immune reaction stops the
granuloma development. In the case of GA the dysfunctional control
mechanism continues to sustain the granulomatous formation. Because
the target does not exist anymore, the initiated process starts the
"search" for a new target (circular spreading). Different histological
and clinical presentations depends on which gene of the control
mechanism is dysfunctional, while the distribution depends on the type
of antigen and its distribution at the start of the immune reaction.
The disappearance of GA after biopsy, that occurs in some cases, could
be attributable to the specific defective gene involved (the biopsy
can disrupt only some type of GA). So, new therapies for solitary GA
formations could be directed to the disruption and creation of a new
and healthy immune response from the point of disruption. A
comparative analysis of the gene expression of GA and the foreign-body
granuloma in the same patient, and GA among different patients could
clarify which genes are involved in granulomatous formations. The
cells affected by those genetic defects are probably histiocytes and
lymphocytes (both always present in GA). Because of some similarity,
necrobiosis lipoidica could also be a specific type of GA.