Acute lymphocytic leukemia with prominent azurophilic granulation and punctate acidic nonspecific esterase and phosphatase activity.

Cytochemical, ultrastructural, and terminal deoxynucleotidyl transferase determinations in three cases of acute lymphocytic leukemia with azurophilic granules and punctate alpha-naphthyl acetate esterase (ANAE), alpha-naphthyl butyrate esterase (ANBE), and acid phosphatase (AP) activities further described a cytochemical and morphologic variant of acute lymphocytic leukemia. The ANAE, ANBE, and AP activities appeared specially localized within cytoplasmic granules. Electron microscopy substantiated a prominence of membrane-bound dense-core cytoplasmic granules.

Immunologic phenotype in 30 patients with diffuse large-cell lymphoma.

Frozen sections of 30 diffuse large-cell ("histiocytic") lymphomas that had arisen in both nodal and extranodal sites were stained with immunoglobulin light-chain and heavy-chain reagents, with nonoclonal antibodies to THAT HAD ARISEN IN BOTH NODAL AND EXTRANODAL SITES WERE STAINED WITH IMMUNOGLOBULIN LIGHT-CHAIN AND HEAVY-CHAIN REAGENTS, WITH MONOCLONAL ANTIBODIES TO T and B-cell antigens, and with an esterase marker for macrophages. Fourteen lymphomas expressed immunoglobulin light chains and were shown to be monoclonal; F(ab')2 fragments were sometimes necessary to demonstrate their monoclonal nature. Mu (IgM) was the most frequently expressed heavy chain, but in many patients other heavy chains were found.

Azathioprine-induced pure red blood cell aplasia.

Pure RBC aplasia developed in two renal transplant recipients who were receiving long-term azathioprine therapy. With substitution of cyclophosphamide therapy for azathioprine, erythroid hyperplasia and reticulocytosis developed at three weeks in one patient and at three months in the other. Selective erythroid toxic reaction is a potential problem that must be considered when anemia develops in patients receiving long-term azathioprine therapy.

Graft-vs-host reaction.

Observations surrounding the clinical manifestations and pathological studies of a neonate who died at 9 weeks of age, indicate that distinctive cutaneous, histopathologic, and ultrastructural findings occur when graft-vs-host reaction (GVHR) complicates combined immune deficiency syndrome (CIDS). The prominence and specificity of the epidermal lesions, particularly a necrotic cell that occurs in association with satellite lymphocytes ("satellite cell necrosis" (SCN)), lead us to recommend that a cutaneous biopsy be performed to facilitate an early definitive diagnosis. Dermatologists can recognize GVHR at the bedside and establish the diagnosis with the pathological findings obtained from the skin biopsy.

Graft-versus-host reaction (GVHR). A case report suggesting GVHR occurred as a result of maternofetal cell transfer.

A female infant with combined immune deficiency syndrome exhibited graft-versus-host reaction (GVHR) clinically during the nine weeks of her life. Pathologically, the first clue for GVHR was the lymphohistiocytic dermal and epidermal infiltrate with single cell necrobiosis seen on a skin biopsy specimen at 6 weeks of age. Two days before death, she received irradiated (3,500 rads) whole blood and plasma with specific antibodies against mother's lymphocytes, which was the first introduction of an allogenic hematopoietic substance.