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| Chronic Villitis |
| Etiology • Approximately 5% associated with viral infections such as CMV or parvovirus B19, listeria or other organisms • Vast majority are non-specific or of unknown etiology |
| Pathogenesis • In cases caused by organisms the infection reaches the placenta via the maternal circulation • The organisms breach the villi and involve the stroma with a fetal inflammatory response • In non-specific villitis the cells first accumulate in the intervillous space ("intervillositis") and then cross into the villus stroma • These cells are maternal CD3+ T cells. • Other studies suggest that cells within the villus may be either fetal or maternal in origin., |
| Epidemiology • Between 5-10% of consecutive pregnancies • Recurrent if not infectious • Associated with intrauterine growth retardation and poor pregnancy outcome |
| General Gross Description • May have pale granular appearance to villi • Usually normal |
| General Microscopic Description • Mononuclear inflammation in the intervillus space • Erosion of the trophoblast and trophoblast necrosis resulting in an irregular villus outline • Agglutination of the villi • Mononuclear inflammation within the villus stroma • Plasma cells and lymphocytes as well as inclusions may be seen in viral infections • Eventual destruction of the fetal circulation with hemosiderin deposition • End result is avascular villus |
| Clinical Correlation • Recurrent (non-infectious variety) • Associated with intrauterine growth retardation • May also be associated with pregnancy induced hypertension |
| References • Benirschke K, Kaufmann P. Pathology of the human placenta, 3rd ed. New York: Springer-Verlag, 1995, pp. 596-601. |
| Chronic Villitis |
| Synopsis by: Melinda Sanders M.D. (T88220M43000)[381] |
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