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Erythroblastopenia is a condition of an abnormally low number of erythroblasts, a type of red blood cell. Transient erythroblastopenia of childhood (TEC) occurs in healthy children and eventually goes away. The blood test results from 64 patients with TEC were reviewed to determine whether there was also a reduction in neutrophils, a type of white blood cell. Mild neutropenia, low neutrophil count, was found in half of the patients with TEC. The cause of TEC is not known, but four cases appeared simultaneously in Australia in an area where TEC had not previously been seen. A local toxin or bacterial infection may have been the precipitating factor. A Japanese boy taking strong antibiotics developed TEC, along with a decrease in granulocytes, a type of white cells that contain granules. The wide range of blood abnormalities found in patients with TEC should be considered when making a diagnosis.

• Pediatric residents are required to care for a group of children over a period of time. For many, this "continuity" experience is in a hospital outpatient department that may or may not provide primary care. We applied a measure of primary care to the Primary Care Clinic, the continuity clinic at The Johns Hopkins Hospital, Baltimore, Md, and found that it compared favorably with private pediatric practices in the Baltimore area, providing significantly more "principal care" (93% vs 84.5% of encounters), and to the Harriet Lane Home walk-in clinic, where only 51% of encounters were "principal care." The Primary Care Clinic scored higher on a primary care index, a measure of the extent to which the facility serves as a primary care source for patients, suggesting that hospital-based training can provide residents with an opportunity to provide primary care.(AJDC. 1989;143:809-812)

A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11 q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and κ light chain genes as well as the gene for the βchain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for κ light chain, interferon-γ(IFN-γ), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic κ light chain was detected. The presence of nuclear factor κB (NFκB), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line produced IFN-γ, a T-lymphocyte-associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-γby the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.

Purpose: Little experience exists with the use of arsenic trioxide in the treatment of recurrent, all-trans retinoic acid (ATRA)-resistant, acute promyelocytic leukemia (APL). The authors report a patient with multiply recurrent APL treated with arsenic trioxide (As2O3), which was administered as recommended in the protocol from the People's Republic of China. The results of this treatment and its toxicity are discussed. The available literature on arsenic therapy is reviewed.