H. Ralph Schumacher

Multicentric reticulohistiocytosis: Case report with immunohistochemical analysis and literature review

This report describes the case of a patient with multicentric reticulohistiocytosis. Immunohistochemical analysis revealed prominent markers of monocyte/macrophage origin, as well as the presence of tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-12; the occurrence of the latter in this disease has not previously been reported. Clinical, laboratory, radiographic, and histologic findings in multicentric reticulohistiocytosis are reviewed. In addition, all published cases of multicentric reticulohistiocytosis which included reports of cytokine and immunohistochemical analysis are reviewed, and evidence for a monocyte/macrophage origin and role in disease pathogenesis is provided.

The synovitis of acute gouty arthritis: A Light and electron microscopic study*

Abstract The synovium participates in the inflammatory process of acute gouty arthritis with intense polymorphonuclear leukocyte infiltration, but many chronic inflammatory cells are also seen even during the acute attack. Crystals in the synovial membrane were found in three patients and then only in well defined tophi. Tophus structure was consistent with crystal deposition in a collagen and amorphous matrix with little adjacent inflammatory reaction. Microtophi were superficial and thinly encapsulated, suggesting that crystals from these tophi might easily rupture into the joint space to initiate the inflammatory reaction. Crystals were seen in detached lining cells and other macrophages as well as in polymorphonuclear leukocytes in the synovial fluid. Clinically satisfactory doses of colchicine produced no detectable morphologic changes in microtubules or other structures.

Null cells in peripheral blood of normals and systemic lupus erythematosus

Enriched null cell populations were obtained by fractionating blood mononuclear cells on discontinuous bovine serum albumin gradients. Null cells from 22 normals were compared to those from 14 patients with systemic lupus erythematosus who had various degrees of disease activity and to 8 patients with other autoimmune phenomena. Null cell layer lacked T cells (E rosette forming cells), cells with surface membrane immunoglobulin, cells capable of latex particles phagocytosis or cells capable of binding to IgG-coated human erythrocytes (EA rosette assay). Cells carrying receptors for complement were present. Cells of the null cell layer failed to respond in vitro to mitogens and allogeneic cells but were capable of Ig synthesis upon incubation with pokeweed mitogen. On transmission electron microscopy, null cells had large nucleus, narrow cytoplasm, and short surface processes. Null cells of SLE patients, when compared to normals, were increased in numbers (p < 0.01), and had the capacity to bind to native DNA (p < 0.01). Binding of cells to DNA could not be blocked by prior treatment of cells with anti-Ig antisera. There was a positive correlation between disease activity, null cell numbers, and DNA binding to serum or to the null cells. Defective maturation and/or differentiation of the null cells of SLE into mature cells with expansion of cell clones reactive to native DNA could be important in the pathogenesis of SLE. This could be due to the lack of maturation factors and/or rapid emigration of the precursor null cells from the stem cell compartment to the circulating pool.