PubMed · 10912010
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J Proust. 1999. [Immunologic aging].. https://pubmed.ncbi.nlm.nih.gov/10912010/
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BACKGROUND: Previous reports of laparoscopic cholecystectomy (LC) in patients with biliary pancreatitis suggested increased operative difficulty, high rates of conversion, and greater morbidity and mortality. METHODS: Between 1990 and 1997, LC was performed for biliary pancreatitis in 63 patients (Group I) and for other causes in 829 patients (Group II). RESULTS: Patients with biliary pancreatitis were significantly older (median age 57 vs 50 years, p = 0.009), with greater co-morbidity (ASA III/IV 24% vs 11%, p = 0.008). The groups were comparable with respect to the frequency of previous abdominal operations, acute inflammation of the gallbladder, and the frequency of bile duct calculi detected by intraoperative cholangiography. Moderate to severe adhesions involving the gallbladder were significantly more frequent in patients with biliary pancreatitis (46% vs 29%, p = 0.004). No significant differences were observed between the two groups with respect to intraoperative (1.5% Group I vs 6.0% Group II, p = 0.109) or postoperative complications (10% vs 8%, p = 0.426), conversion rate (0 vs 2.7%, p = 0.181), or duration of operation (median 92 vs 85 min, p = 0.33). CONCLUSION: Despite increased age and co-morbidity and more frequent adhesions, our data showed no evidence that intraoperative or postoperative complications were more frequent in patients with biliary pancreatitis than in other patients undergoing LC.
Wilms tumor gene product WT1 and proteinase 3 are overexpressed antigens in acute myeloid leukemia (AML), against which cytotoxic T lymphocytes can be elicited in vitro and in murine models. We performed this study to investigate whether WT1- and proteinase 3-specific CD8 T cells spontaneously occur in AML patients. T cells recognizing HLA-A2.1-binding epitopes from WT1 or proteinase 3 could be detected ex vivo in 5 of 15 HLA-A2-positive AML patients by interferon-gamma (IFN-gamma) ELISPOT assay and flow cytometry for intracellular IFN-gamma and in 3 additional patients by flow cytometry only. T cells producing IFN-gamma in response to proteinase 3 were further characterized in one patient by 4-color flow cytometry, identifying them as CD3(+)CD8(+)CD45RA(+) CCR7(-) T cells, resembling cytotoxic effector T cells. In line with this phenotype, most of the WT1- and proteinase-reactive T cells were granzyme B(+). These results provide for the first time evidence for spontaneous T-cell reactivity against defined antigens in AML patients. These data therefore support the immunogenicity of WT1 and proteinase 3 in acute leukemia patients and the potential usefulness of these antigens for leukemia vaccines.
Acute thrombocytopenia is a recognized complication of treatment with GPIIb/IIIa inhibitors whose cause is not yet known. We studied 9 patients who developed severe thrombocytopenia (platelets less than 25 x 10(9)/L) within several hours of treatment with the GPIIb/IIIa inhibitors tirofiban (4 patients) and eptifibatide (5 patients). In each patient, acute-phase serum contained a high titer (range, 1:80-1:20 000) IgG antibody that reacted with the glycoprotein IIb/IIIa complex only in the presence of the drug used in treatment. Four patients had been previously treated with the same drug, but 5 had no known prior exposure. Pretreatment serum samples from 2 of the latter patients contained drug-dependent antibodies similar to those identified after treatment. No tirofiban- or eptifibatide-dependent antibodies were found in any of 100 randomly selected healthy blood donors, and only 2 of 23 patients receiving tirofiban or eptifibatide who did not experience significant thrombocytopenia had extremely weak (titer, 1:2) tirofiban-dependent antibodies. In preliminary studies, evidence was obtained that the 9 antibodies recognize multiple target epitopes on GPIIb/IIIa complexed with the inhibitor to which the patient was sensitive, indicating that they cannot all be specific for the drug-binding site. The findings indicate that acute thrombocytopenia after the administration of tirofiban or eptifibatide can be caused by drug-dependent antibodies that are "naturally occurring" or are induced by prior exposure to drug. These antibodies may be human analogs of mouse monoclonal antibodies that recognize ligand-induced binding sites (LIBS) induced in the GPIIb/IIIa heterodimer when it reacts with a ligand-mimetic drug.