VILLOUS OBSERVATION IN PIH CASES HISTOPATHOLOGICAL CHANGES MILD SEVERE CYTOTROPHOBLASTIC PROLIFERATION 72% 28% SYNCYTIAL KNOTS 64% 36% BASEMENT MEMBRANE THICKENING 30% 26% MEDIAL HYPERTROPHY 38% 30% FIBRINOID NECROSIS
28% 24% OLD INFARCTS 36% 44%
Other nonspecific features include intimal proliferation, duplication and/or fragmentation of the internal elastic lamina, a sparse perivascular inflammatory infiltrate, and fibrinoid necrosis
of the intima.
The number of areas of fibrinoid necrosis
in PIH group (11.83/100 villi) was also found to be increased than in control group (3.73/100 villi) [Fig-2A].
Light microscopy of fibrillary GN is variable, but glomerular capillary wall thickening, mesangial matrix expansion, and hypercellularity are the common histologic abnormalities. Crescent formation occurs in about 20% of the cases, most of which are fibrous crescents with little activity. Extensive crescent formation and fibrinoid necrosis
are uncommon findings in fibrillary GN.
In some cases of abruptio placenta fibrinoid necrosis
occurs, which are small collection of structureless, eosinophilic, homogeneous material within the villi, usually 3% at term normally but increase in abruptio placenta.
Caption: Figure 3: (a) Hematoxylin and eosin staining of skin biopsy samples revealing leukocytoclastic vasculitis with extensive fibrinoid necrosis
within dermal capillaries, magnification = 200 x.
Arrow indicates fibrinoid necrosis
. *P < 0.05; **P < 0.01; ***P < 0.001.
((a) Hematoxylin y Eosin 10X, (b) Trichrome 10X), associated with vascular changes in interlobular arteries: fibrinoid necrosis
of the intima with fragmentation of erythrocytes, ((c) Tricromico 20X) and mucoid expansion of the intima with luminal obliteration, and ((d) haematoxylin and eosin 10X).
Renal biopsy was done on the 4th hospital day and showed an acute necrotizing and crescentic glomerulonephritis, with ten of fourteen glomeruli showing cellular crescents, often in association with areas of fibrinoid necrosis
(Figures 1(a) and 1(b)).
The neoplastic cells exhibited an angiocentric growth pattern, as well as angiodestruction with mural fibrinoid necrosis
and hemorrhage (Figure 5).
(5,27-31) The morphologic features include placental infarcts, decidual arteriopathy with foamy histiocytes, fibrinoid necrosis
, retroplacental hemorrhage (abruption clinically), accelerated (advanced) villous maturation with distal villous hypoplasia, and lack of physiologic remodeling of the spiral arterioles (Figures 13 and 14).
There was no fibrinoid necrosis
, leukocytoclasia or giant cells in the examined biopsy specimen.