Absence Of Plasma Cells Research Articles

Histiocytic Necrotizing Lymphadenitis (Kikuchi's Disease)

Histiocytic necrotizing lymphandenitis (HNL), or Kikuchi's disease, is a newly recognized disease of unknown origin that causes cervical lymphadenitis, usually in young women. Initially described in Japan, cases of HNL are being reported in the United States and other western countries with increasing frequency. Symptoms of HNL include tender cervical adenopathy, fever, weight loss, and night sweats. Laboratory studies reveal leukopenia with relative granulocytopenia and lymphocytosis. Lymph node biopsy reveals areas with frank cellular necrosis, karyorrhexis, and absence of plasma cells. The histologic features of HNL are distinctive but can be confused with those of lymphoma. We describe two cases of HNL and present recommendations for diagnosis and treatment.

Cellular composition of human fetal bone marrow. Histologic study in methacrylate sections.

The cellular composition of the human marrow was studied in thin sections of undecalcified bone 24 fetuses aged from 11 to 22 weeks of gestation, embedded in methacrylate and stained by the Giemsa method. This procedure provides much better cellular detail than the decalcified bone sections embedded in paraffin used in previous studies. Hemopoiesis is already present at the 11th week of gestation in the long bones of the extremities. The cellularity of their marrow increases during the 4th month and is abundant in the months thereafter. Its composition is similar to that of adults but differs by the presence of a large number of stromal cells and by the absence of plasma cells and lymph follicles in the fetal marrow. Differential counts for blood-forming cells and stromal elements are given for the initial period of marrow development.

Fatal myocarditis associated with ECHO virus, type 22, infection in a child with apparent immunological deficiency

A 14-month-old boy succumbed to fulminating myocarditis. ECHO virus, type 22, was recovered in high titer from the myocardium, and in lower titer from pericardial fluid, liver, and lung. The diagnosis of congenital agammaglobulinemia was supported at autopsy by the absence of plasma cells, abnormal organization of lymphoid tissue, and absence of immunoglobulins in all tissues examined by fluorescent antibody techniques. This is believed to be the first isolation of an ECHO virus from the heart. Fatal virus infection in a child with non-lymphopenic agammaglobulinemia, with the exception of hepatitis, appears to be a very rare event.

AGAMMAGLOBULINEMIA: THE FUNDAMENTAL DEFECT.

Addition of phytohemagglutinin and of streptolysin S to in vitro cultures of leukocytes of normal and agammaglobulinemic subjects resulted in mitosis of lymphocytes and their differentiation to plasma cells. In contrast, specific antigens induced mitosis and differentiation of lymphocytes of normal but not of agammaglobulinemic donors. The data suggest that the absence of plasma cells in agammaglobulinemia is not in itself responsible for failure of antibody production, but is rather the morphologic concomitant of the primary defect (failure of antibody production on exposure to antigenic stimulus).

Multiple Serum Protein Deficiencies in Congenital and Acquired Agammaglobulinemia

Three forms of agammaglobulinemia have been described: (1) the physiologic or transient form in infancy, (2) a congenital inherited form occurring in males, and (3) an acquired form occurring in both sexes and associated with the onset of infections in adolescents or adults. The congenital and acquired forms are due to absence of plasma cells in the tissues; these cells appear to be the sight of synthesis of gamma globulin. Using an immunochemical technique it was demonstrated that at least two plasma proteins besides gamma globulin are absent or markedly diminished in congenital and acquired agammaglobulinemia. These proteins appear to belong to the group of beta globulins. A previous finding was confirmed—that in patients with agammaglobulinemia the deficiency of gamma globulin is often not complete.