Acquired B antigen associated with infection by Bacillus cereus: in vivo and in vitro transformation of A1 red cells.
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Biomedical subjects
Publications and source records attributed to H Riess.
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Failure of local tumor control is of critical importance in the clinical management of large pelvic tumors. For bulky sarcomas of the pelvis a new treatment strategy could be of importance in the future using preoperative regional hyperthermia combined with systemic chemotherapy. In our case history of a patient with unresectable Ewing sarcoma of the pelvis no tumor response could be observed during multi-drug chemotherapy alone. However, after treatment with regional hyperthermia combined with systemic chemotherapy, the tumor mass became resectable and was separated from the adjacent tissue by a fibrotic pseudocapsule. Histological evaluation of the tumor tissue showed a complete change of the pattern.
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The dose-response relationship in the intravenous immunoglobulin treatment of idiopathic thrombocytopenic purpura was studied in 20 adult patients in a multicenter prospective crossover trial. The rate of response increases from 3 out of 11 (27%) to 6 out of 10 treatment periods (60%) by raising the 7S-IgG dose given on 5 consecutive days from 164.50 +/- 24.55 to 359.65 +/- 58.62 mg/kg body weight. The onset and duration of response as well as the peak platelet count were found to be independent of the doses. A long-term benefit induced by intravenous immunoglobulin treatment could be achieved in 2 out of 14 patients with chronic idiopathic thrombocytopenic purpura.
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Two cases of mania secondary to head injury are reported. Only four well-documented reports of head trauma as a cause of secondary mania were found in an English and foreign literature search, although such a search is made difficult by the paucity of cases meeting modern diagnostic criteria for mania. Previous reviews of the causes of secondary mania have not included head injury, but the two case reports confirm that head injury may be an additional cause. A diagnosis of mania secondary to head trauma should be considered in manic patients with atypical age of onset, absence of previous psychiatric illness, negative family history for bipolar illness, and close temporal proximity of head trauma to subsequent mania.
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In a randomized pilot study we compared the antiplatelet effects of aspirin and BM 13.177 in two groups of 7 patients each undergoing PTCA. As compared with the pretreatment values template bleeding time was prolonged and collagen induced aggregation was inhibited in PRP and WB in all patients. In the course of angiography and PTCA a rise in platelet factor 4 and beta thromboglobulin was observed in both groups, followed by a decrease below the baseline levels. Thromboxane B2 in plasma and serum decreased in the aspirin group but remained unchanged during BM 13.177 treatment. In PRP and WB aggregation induced by U 46 619 was inhibited after ingestion of BM 13.177 but not following ASA. After three months a control coronary angiography was done. There was no difference in regard to the degree of restenosis between both groups. Medication was well tolerated, compliance was good and no side effects were noted.
Unsaturated platelet-activating factor (paf-acether) aggregated thrombocytes of healthy male volunteers like saturated paf-acether. Unsaturated paf-acether released serotonin in the presence of imipramine. Within one minute the release increased depending on the concentrations of unsaturated paf-acether up to 45% of the serotonin. Human thrombocytes synthesized only a small amount of thromboxane B2 (TXB2) after aggregation induced by unsaturated paf-acether. Unsaturated paf-acether prevented the binding of radiolabelled saturated paf-acether to intact washed thrombocytes in the same extent as saturated paf-acether.
Platelet aggregation induced by ADP and collagen was monitored in 25 patients with increased serum levels of triglycerides (7 HLPs type IIb, 14 type IV, 4 type V patients) and compared with a group of 10 normolipidaemic control persons. Platelet aggregation was studied simultaneously in platelet rich plasma (PRP) by both turbidometric and impedance technique and also in whole blood (WB) by the impedance method. Whereas platelet aggregation testing by turbidometry was limited by the optical density of the plasma samples in hypertriglyceridemia, the aggregation process could easily be registered in PRP and WB using the impedance method. Threshold aggregatory concentrations with both agonists were significantly lower for all three groups of HLP.
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Platelet aggregation studies generally are performed in platelet-rich plasma (PRP) by the turbidometric method. The authors compared this technic with the recently introduced impedance aggregometry in PRP and whole blood (WB). In healthy controls there was a good correlation between the two technics when aggregation was induced by ADP or collagen. As compared with PRP, platelets in WB were more sensitive to the aggregating effect of thrombin, ristocetin, and arachidonic acid. Platelet sensitivity to prostacyclin was increased in WB. The anti-platelet effect of a single oral dose of aspirin could be detected for a longer period in WB than in PRP. Platelet aggregation tests in WB from patients with platelet dysfunctions showed the same response pattern to different aggregating agents as in PRP. In contrast to turbidometry, the impedance method in PRP and WB enabled registration of platelet aggregation in a dose-dependent fashion in a sample from a patient with severe hyperlipoproteinemia. It is concluded that platelet aggregation can be studied conveniently with the impedance method in the more physiologic medium of WB. Providing the same information as the well-established turbidometry, the time-sparing impedance method needs less citrated blood. Moreover, our results show an increased sensitivity of the WB system to some aggregating and anti-platelet agents.
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Protein C, a potent anticoagulant, has been detected in large amounts in some prothrombin complex concentrates (PCC). We extended these findings to eight PCC commercially available in West Germany detecting 0.82 to 1.92 plasma equivalent units of protein C antigen (PC:Ag) per unit factor IX. Infusion of PCC in four patients on stable oral anticoagulation resulted in a recovery of 58.6 +/- 10.9%. Estimated from the decrease in plasma levels of PC:Ag half life was 7.9 +/- 0.6 h.
Cytogenetic analysis of bone marrow cells in a 40-year-old man revealed a mosaic of two cell lines during blast crisis: one diploid with typical Ph1 chromosome (46 XY Ph1) and one with hyperdiploidy of 54 chromosomes with double Ph1 chromosome, trisomy 4, 6, 8, 18, 21 and duplication of the sex chromosomes X and Y. Immunological characterization showed common acute lymphoblastic leukemia antigen in 90% of the blasts. In spite of intensive chemotherapy the patient died in a third blast crisis 15 months after the first blast crisis, 3 months after successfully treated central nervous system relapse.
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Seven males with atherosclerotic disease received daily 1.6 g of the thromboxane antagonist BM 13.177 in two separate oral dosages over a period of four days. The drug significantly reduced elevated plasma levels of thromboxane B2, beta-thromboglobulin and platelet factor 4, whereas thromboxane B2 generation was only slightly depressed. BM 13.177 inhibited platelet aggregation by collagen, and to a minor degree the second wave of ADP induced aggregation. Platelet sensitivity to prostacyclin and aggregation by ristocetin were not altered. Bleeding time was prolonged. All effects disappeared within 24 hours after the last application of the drug. No side effects were noted. Thus BM 13.177 appears to be a safe and effective new antiplatelet drug.