A 53-year-old man developed delayed-onset neutropenia 6 weeks after completing first-line therapy with rituximab, cyclophosphamide, mitoxantrone, vincristine, and prednisone for high-grade B-cell lymphoma. Bone marrow biopsy demonstrated hypercellular marrow with normal maturation. He also developed interstitial pneumonitis, an adverse event associated with rituximab use. Infiltrates of T cells were found in the patient's lungs. For the next 6 months, the patient required subcutaneous granulocyte colony-stimulating factor 300 mug twice/week to maintain a granulocyte count above 1000 cells/mm3. He also received oral antibiotics for mouth sores and thrush. Based on the existing evidence, monitoring blood counts for as long as 8 weeks after rituximab therapy may be advisable, although the literature reports that neutropenia can develop up to 1 year after treatment. The development of a registry and uniform testing may help uncover the cause of this delayed-onset neutropenia.

Serums from six patients with progressive idiopathic acute or chronic polyneuropathy possessed a cytolytic activity against transformed mouse cholinergic or noncholinergic neuroblasts but not against transformed rat astrocytes. This activity was not qualitatively nor quantitatively present in serums from normal controls or from patients with a variety of other motor system disorders and other neurologic disorders. Fluorescein conjugated goat antihuman IgG and IgM monospecific immunoglubulins were used to characterize further the cytotoxic activity from patient serums and these studies suggested the presence of immunoglobulin G (IgG) and immunoglobulin M (IgM) directed against a cell surface neuroblastoma antigen. Cold reactive immunoglobulins of the IgG and IgM type were present in the serums of all six patients. A bioassay is described that may be helpful in evaluating other patients with progressive idiopathic polyneuropathies.

Posttransfusion purpura (PTP) (platelet count 5000/microliter) was diagnosed in a female patient (never transfused, gravida IV, para IV) 1 week after transfusion for hysterectomy in 1978. She did not respond to pooled random-donor platelets but recovered following a single plasma exchange. Her platelets were PlA1 negative, and her plasma contained potent anti-PlA1. In 1986, her sister (never transfused, gravida III, para III) developed PTP (platelet counts 5-15,000/microliter) following surgery-associated transfusion. She did not respond to pooled random-donor platelets. Platelet-associated IgG was markedly elevated (5365) molecules/platelet; normal, less than 660); her plasma contained a potent platelet antibody with anti-PlA1 specificity. Her platelets were subsequently shown to be PlA1 negative. The platelet count did not rise above 30,000 per microliter, despite 3 days of high-dose methylprednisolone sodium succinate and 2 weeks of prednisone (80 mg/day). Later, her platelet count increased and remained normal after steroids were discontinued. The two sisters proved to be HLA-identical, and each possessed one haplotype carrying the DR3 marker, which has been implicated as a risk factor in neonatal alloimmune thrombocytopenia associated with anti-PlA1.

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