Plasma cells are not considered to have phagocytic properties. However, intracellular deposition of iron in plasma cells has been reported in the literature. [1-4] Here, a case of iron deposition in plasma cells in a reactive infiltrate in the skin is reported.
Report of a patient
A pilonidal sinus was excised in a 21-year-old man. The patient was otherwise healthy. Laboratory investigations revealed an elevation of LDH (270 mg/dl). Iron studies were within normal ranges. There was no history of any internal malignancy or of any medication intake.
On histology, a sinus tract with suppurative inflammation associated with extensive fibrosis was seen and a superficial and deep dense infiltrate of lymphocytes, neutrophils, histiocytes and plasma cells was accompanying. Extravasated erythrocytes and hemosiderophages were present, too. No PAS positive structures were found.
At high magnification, a large number of plasma cells contained hemosiderin granules in their cytoplasm. The hemosiderin was better seen with Prussian blue stain (Figs. 1 and 2). Immunohistochemistry with CD 138 highlighted the plasma cells seen to contain intracellular deposition of hemosiderin (Figs. 3 and 4).
Figs. 1 and 2
Prussian blue stain showing in blue the hemosiderin granules inside the plasma cells.
Figs. 3 and 4
CD 138 staining of plasma cells. Inside the plasma cells hemosiderin granules are seen in brown.
The presence of iron in plasma cells is an unusual and often incidental finding and little is known to explain it.  Plasma cell iron has been noted in patients with iron overload, in patients with hematological disorders such as dysgammaglobulinemia, acute myeloid leukemia, acute lymphoid leukemia, myeloma, megaloblastic anemia, and in alcoholics with liver cirrhosis. [2,3] In the most recent case published in the literature,  the pictures of the bone marrow aspirate stained with Prussian blue show the same features as demonstrated in the case of our own (Figs. 5 and 6).
The mechanism of incorporation of iron into plasma cells is unknown, but it has been found ultrastructurally to be located in membrane bound lysosomal vesicles.  The iron within plasma cells is considered to derive from hemosiderin. The histopathological findings shown here also seem to indicate that brown-colored hemosiderin is incorporated into plasma cells. Hemosiderin is a degradation product of hemoglobin of senescent erythrocytes. Usually, senescent erythrocytes are removed from the circulation by macrophages in the bone marrow and spleen or there is intravascular hemolysis followed by phagocytosis of the end products. Erythrophagocytosis has been reported for polymorphonuclear neutrophils and monocytes of peripheral blood as well as for macrophages of bone marrow in a variety of conditions, such as acute leukemia. Erythrocytes engulfed by leukocytes also have been observed in cases of transfusion reaction, erythroblastosis fetalis, paroxysmal cold hemoglobinuria, acquired hemolytic anemia, and in various infections.
Butterworth et al. reported a case of plasma cell leukemia in which erythrophagocytosis by cells of the plasma cell series occurred. According to the authors, their observation suggested that under certain circumstances plasma cells may retain or acquire the phagocytic properties of their reticulum cell line.  Al-Bagdali et al. observed plasma cells with numerous prolongations suggestive of motility and phagocytic activity to be randomly distributed in the medullary cords of lymph nodes of sheep. Their irregular perinuclear zones contained granular material of similar density to that of rough endoplasmic reticulum, and some showed morphological evidence of various phases of erythrophagocytosis. The phagocyted erythrocytes appeared smaller than usual. Most plasma cells contained also Russel bodies in the cisternae of their rough endoplasmic reticulum, and some of the Russel bodies showed fuzzy borders and were separated from the endoplasmic reticulum by a halo of uniform width.  Wirt et al. told of a phagocytic plasma cell myeloma in a 40-year-old man who had presented himself with Coombs-negative hemolytic anemia, hepatosplenomegaly, lytic bone lesions, lambda light chain monoclonal gammopathy, and infiltration of the bone marrow by plasma cells, 10% of which demonstrated phagocytosis of erythroid cells. Electron microscopy demonstrated myeloma cells with prominent cytoplasmic microfilaments and erythroid cells in intracytoplasmic vacuoles.  Raubenheimer et al. studied 10 cases of multiple myeloma and observed erythrophagocytosis as an ultrastructural finding.  Hom observed phagocytic plasma cells and Russell bodies in a patient diagnosed with monoclonal gammopathy of undetermined significance.  Kanoh and Fujii reviewed 17 cases of the phagocytic multiple myeloma, and suggested that erythrophagocytosis by myeloma cells may be responsible for the hemolytic anemia in multiple myeloma. 
These reports indicate that especially neoplastic plasma cells may acquire phagocytic properties. The patient presented here, however, had no signs or symptoms of a monoclonal gammopathy. The iron-containing plasma cells were found in an infiltrate reactive to a ruptured pilonidal sinus. In the vicinity of plasma cells containing hemosiderin, numerous extravasated erythrocytes were found. It may be, that phagocytic properties of plasma cells are not only a sign of malignancy but develop in a certain environment, e.g., one with an overload of erythrocytes and their degradation products.
Figs. 5 and 6
Iron stain of a bone marrow aspirate with plasma cells containing hemosiderin granules. (Reproduced from: Gruszecki et al, 2002 .)
This article reports on the incidental finding of iron deposition in the cytoplasm of plasma cells which are not known to have phagocytic properties. Occasionally, plasma cell iron has been reported in the literature. To our knowledge, this finding was never described in a reactive infiltrate in the skin.
Juliana Jung, M.D., is a pathologist at Hospital Erasto Gaertner, Curitiba, Brazil. This article was reviewed by Almut Böer-Auer, M.D., and Masoud Asgari, M.D. Contact corresponding author via email: firstname.lastname@example.org .
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