Abstract
Authors describe human schistosomal granuloma in late chronic phase, from the morphological and evolutionary viewpoints. The study was based on a histological analysis of two fragments obtained from a surgical biopsy of peritoneum and large intestine of a 42-year-old patient, with a pseudotumoral form mimicking a peritoneal carcinomatosis associated to the schistosomiasis hepatointestinal form. Two hundred and three granulomas were identified in the pseudotumor and 27 in the intestinal biopsy, with similar morphological features, most in the late chronic phase, in fibrotic healing. A new structural classification was suggested for granulomas: zone 1 (internal), 2 (intermediate) and 3 (external). Regarding granuloma as a whole, we may conclude that fibrosis is likely to be controlled by different and independent mechanisms in the three zones of the granuloma. Lamellar fibrosis in zone 3 seems to be controlled by matrix mesenchymal cells (fibroblasts and myoepithelial cells) and by inflammatory exudate cells (lymphocytes, plasmocytes, neutrophils, eosinophils). Annular fibrosis in zone 2, comprising a dense fibrous connective tissue, with few cells in the advanced phase, would be controlled by epithelioid cells involving zone 1 in recent granulomas. In zone 1, replacing periovular necrosis, an initialy loose and tracery connective neoformation, housing stellate cells or with fusiform nuclei, a dense paucicellular nodular connective tissue emerges, probably induced by fibroblasts. In several granulomas, one of the zones is missing and granuloma is represented by two of them: Z3 and Z2, Z3 and Z1 or Z2 and Z1 and, ultimately, by a scar.
Highlights
Authors describe human schistosomal granuloma in late chronic phase, from the morphological and evolutionary viewpoints
It is generally the longest and the less stained both by hematoxylin and eosin (HE) and by special staining such as Gomori trichrome and picrosirius. It frequently houses the embryonated egg or its shell, whether or not surrounded by an eosinophilic amorphous area of necrosis, and by a thin fibrillar substance, mixed with few starry cells resembling fibroblasts or by cells with fusiform nuclei and macrophages (Figures 1A and 1B). This amorphous eosinophilic material, seen in the early evolutive phase of the acute phase of schistosomiasis around the egg, known as Hoeppli phenomenon, contains egg antigens, host immunoglobulins[12] and fibronectin with a high molecular weight produced by fibroblasts and by other mesenchymal cells[13,14]
Examining a large number of granulomas in the peritoneum and in the serosa and external muscular tissue of the large intestine (27), in the same individual, E.F.C., 42 years old, from Belo Horizonte (MG), with a tumor or pseudotumoral form of schistosomiasis mansoni, provided a favorable view of the morphology of granulomas in their several evolutive phases in humans. Both in the peritoneum and in the large intestines (LI), granulomas were in several evolutive phases, which indicates an active long-lasting disease, probably lasting for years and modulated, with egg deposition at different stages
Summary
Authors describe human schistosomal granuloma in late chronic phase, from the morphological and evolutionary viewpoints. Annular fibrosis in zone 2, comprising a dense fibrous connective tissue, with few cells in the advanced phase, would be controlled by epithelioid cells involving zone 1 in recent granulomas. Granulomas are nodular formations in which exudate cells are displayed in particular arrangements to the inflammatory focus, forming structures with peculiar aspects and architecture which frequently allow to diagnose the disease even without finding its causal agent. Macrophages and their derivatives (remarkably epithelioid and giants cells) and lymphoid cells and their derivatives ( plasma cells) comprise the required cells. Recent studies have indicated that IL-13 receptor α2 (IL-13 R α2) secreted by TCD4+ cells type 2 is the main mediator for granulomatous response and for hepatic fibrosis, which are two fundamental lesions in schistosomiasis[3]
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