Essentials
Delayed‐onset heparin‐induced thrombocytopenia can lead to severe thrombocytopenia in the setting of recent major vascular surgery.Intravenous immunoglobulin (IVIG) can be used as a supplementary treatment when platelet count fails to improve with conventional treatment.When platelet counts are severely low, benefits of using IVIG can outweigh the risks of thromboembolic events.
Delayed onset heparin induced thrombocytopenia (HIT), is characterized by a late nadir due to persistent platelet‐activating IgG antibodies. It typically begins or worsens 5 or more days after heparin is discontinued with complications such as thrombosis up to 3 weeks after exposure to heparin.1–3 In 50% of cases, the platelet count can decrease to very low numbers (<20 000/μL), which is not usual for typical HIT. Here we report 2 cases of post‐operative delayed onset HIT manifesting as severe thrombocytopenia that persisted despite cessation of heparin and initiation of argatroban. Key Clinical Question: Is intravenous immunoglulin beneficial in severe refractory delayed‐onset HIT?
Summary Thirty-five patients with advanced malignant disease have been treated as outpatients with increasing doses (0.1 -00 mcg) of interleukin 2 (IL2) by once daily self-administered subcutaneous (s.c.) injection, 5 days weekly for 8 weeks followed by a 4 week observation period. Systemic side effects were not experienced by patients at the 3 lower doses. Three patients required dose reduciton from 100 mcg daily because of intolerance (fever, rash, lethargy, nausea and vomiting) and one patient was discontinued because of dyspnoea. We observed immunological effects at the 100 mcg dose (but not at the lower doses). These consisted of (a) a modest sustained lymphocytosis, (b) eosinophilia in six (out of nine) patients and (c) a significant rise in IL2-stimulated peripheral blood lymphocyte activated killer (LAK) cell activity in six (out of nine) patients to a mean of 2.0 times pretreatment levels (P<0.01). Two (out of nine) patients with renal cell carcinoma treated with 100 mcg daily had partial responses of duration 4 and 9 months respectively and a further three had disease stabilisation for at least 3 months. Low dose long-term s.c. IL2 is clinically and immunologically active, and in comparison to other IL2 regimens it has minor toxicity and is easy to administer. These characteristics make low dose s.c. IL2 suitable for study in the adjuvant setting.
A retrospective analysis of factors influencing survival in patients with primary lymphoma of bone (PLB) treated at a single institution was performed. The records of 30 eligible patients were evaluated for overall survival (OS) as related to age, sex, stage, International Prognostic Index (IPI) score, number of sites involved and type of treatment. There was a significant difference in OS in patients with IPI scores of low (L) and low intermediate (LI) versus high intermediate (HI) (P = 0.0035), regardless of stage. Sex, age, stage and number of sites did not have a significant influence on OS. There was a statistically significant difference in OS favouring use of combined chemotherapy (with or without rituximab) and radiation compared with either modality alone (P = 0.02). The addition of rituximab resulted in a non-significant trend towards improved OS (P = 0.11). With a median follow up of 49 months, 73% of patients are alive 5 years from diagnosis.
The human BCR-ABL oncogenes encoded by the Philadelphia chromosome (Ph) affect the pathogenesis of diverse types of leukemia and yet are rarely associated with T-lymphoid leukemia. To determine whether BCR-ABL kinases are inefficient in transforming T lymphocytes, BCR-ABL-expressing retroviruses were injected intrathymically into mice. Thymomas that expressed BCR-ABL kinase developed after a relatively long latent period. In most thymomas, deletion of 3' proviral sequences resulted in loss of tk-neo and occasionally caused expression of kinase-active carboxy-terminally truncated BCR-ABL oncoprotein. In contrast, deletion of 3' proviral sequences was not observed in thymomas induced with Abelson murine leukemia virus (A-MuLV). BCR-ABL viruses induced distinct patterns of disease and involved different thymocyte subsets than A-MuLV and Moloney murine leukemia virus (Mo-MuLV). While Mo-MuLV only induced Thy-I' thymomas, v-abl-and BCR-ABL-induced thymomas often contained mixed populations of B220+ and Thy-1+ lymphocytes in the same tumor. In most v-abl and BCR-ABL tumors, Thy-l+ lymphoid cells expressed CD8 and a continuum of CD4 ranging from negative to positive. Conversely, Mo-MuLV thymomas contained distinct populations of CD4+ cells that were either CD8+ or CD8-. A-MuLV-transformed T-lymphoid cells did not express the CD3/T-cell receptor complex, while BCR-ABL tumors were CD3+. Thus, BCR-ABL viruses preferentially induce somewhat more differentiated T lymphocytes than are transformed by A-MuLV. Furthermore, rare B220+ lymphocytes may represent preferred v-abl and BCR-ABL transformation targets in the thymus.
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