Low molecular weight heparin (dalteparin) is equally effective as unfractionated heparin in reducing coagulation activity and perfusion abnormalities during the early treatment of pulmonary embolism.

Little is known about the differences between unfractionated heparin (UFH) and low molecular weight heparin (LMWH) with regard to their effects on coagulation activity during treatment for pulmonary embolism. The objective of this study was to compare UFH and LMWH (dalteparin) in the early treatment of pulmonary embolism in terms of control of coagulation markers and perfusion abnormalities. Thirty-seven patients with acute pulmonary embolism were randomized to receive intravenous UFH or subcutaneous dalteparin, each accompanied by acenocoumarol. Daily blood samples were obtained for the measurement of thrombin generation (fragments 1 and 2 [F1+2], thrombin-antithrombin (TAT) complexes and fibrin monomers [FMs]) and fibrinolysis (d-dimer concentrations and clot-lysis times). Ventilation-perfusion scintigraphies were performed, and with the data they yielded, percentage of vascular obstruction scores (PVOs) were calculated on days 0 and 5. The international normalized ratio was within the therapeutic range in both groups on day 3. F1+2 and TAT complexes rapidly normalized, without differences between the groups (P =.5 and.4, respectively). FM levels did not decrease and, in fact, showed an increase in the UFH group from day 3 on (P <.05 between groups). d-Dimer levels decreased over time, with no differences between groups (P =.6). Clot-lysis times were shorter in the UFH group (P <.05). PVOs on days 0 and 5 were not different (P =.5 and.8, respectively), but the decrease in PVOs over time was greater in the dalteparin group (P =.04). These results show that dalteparin is at least as effective as UFH in reducing coagulation activity and perfusion abnormalities in the early treatment of pulmonary embolism.

Usefulness of a semiquantitative D-dimer test for the exclusion of deep venous thrombosis in outpatients.

PURPOSE: The D-dimer test is used commonly in diagnostic strategies to reduce the need for ultrasonography in patients suspected of having deep venous thrombosis. We studied several clinical and laboratory variables that might limit the accuracy of a semiquantitative D-dimer test. SUBJECTS AND METHODS: In this retrospective cohort study, 704 outpatients suspected of having deep venous thrombosis underwent a semiquantitative D-dimer test and ultrasonography. The performance of the D-dimer test was calculated in patients using anticoagulants (n =61), patients with previous thrombosis (n =127), and patients with malignancy (n =47), including 39 patients with more than one of these characteristics. The 508 remaining patients were considered to be the reference group. RESULTS: A total of 254 patients (36%) had evidence of deep venous thrombosis. The D-dimer test had a sensitivity of 99% (174/176; 95% confidence interval [CI]: 96% to 100%) and a negative predictive value of 98% (98/100; 95% CI: 93% to 100%) in the reference group. The sensitivity of the D-dimer test in patients using oral anticoagulants was 75% (6/8; 95% CI: 35% to 97%; P =0.01 compared with the reference group). Test sensitivity was 96% (51/53; 95% CI: 87% to 100%) in patients with previous thrombosis, and 100% (29/29; 95% CI: 88% to 100%) in patients with cancer. However, 553 (79%) of all patients, including 43 of the cancer patients (91%), had an abnormal D-dimer test. CONCLUSION: The semiquantitative D-dimer test in this study has a high sensitivity and negative predictive value in the exclusion of deep venous thrombosis, except perhaps among patients using oral anticoagulants. D-dimer tests in patients with cancer and in patients over 70 years old may not be worthwhile, because the tests are usually positive.

Malignant fibrous histiocytoma in the abdominal soft tissues of a child: a case report.

An 18-month-old female presented with an abdominal tumor mass which on morphological, immunohistological and ultrastructural examination was found to be a malignant fibrous histiocytoma. This soft tissue sarcoma is rarely encountered in childhood. Treatment in this case consisted of surgical tumor debulking with pre- and post-operative chemotherapy. The child is well and free of detectable tumor at 23 months after diagnosis.

Small bowel infarction associated with pancreatic glucagonoma.

An 88 year old woman presented comatose, hypothermic and hyperglycaemic. She died soon after admission and at autopsy recent small bowel infarction was found. The superior mesenteric artery was encased in a dense pancreatic mass and there was marked luminal narrowing of the vessel. Histology revealed a pancreatic glucagonoma which had metastasized to colonic submucosa and serosa. Glucagonoma is a rare tumour and this presentation of small bowel infarction associated with pancreatic glucagonoma would appear to be a unique event.

Fibronectin and laminin in the early human placenta.

The distribution of fibronectin and laminin was investigated in early intrauterine and ectopic tubal pregnancy using a standard immunoperoxidase technique on paraffin-embedded tissues. Localization of both fibronectin and laminin appeared identical in intrauterine and in ectopic pregnancy. Fibronectin was demonstrated in chorionic villous stroma, in the distal cytotrophoblast cell columns, in infiltrating mononuclear extravillous trophoblast and in endovascular trophoblast. Villous trophoblast and multinucleate interstitial trophoblast did not label. Extracellular fibronectin was demonstrated amidst sheets of infiltrating extravillous trophoblast. Laminin distribution was similar to that described for fibronectin but laminin was also present in the basement membrane of villous cytotrophoblast. Both fibronectin and laminin showed a pericellular distribution around decidual stromal cells. This study demonstrates further heterogeneity of human trophoblast populations. The presence of fibronectin in infiltrating extravillous trophoblast, endovascular trophoblast and in the distal columns may enhance trophoblast adhesion to maternal tissues and facilitate trophoblast migration.

Proteinase and proteinase inhibitor localization in the human placenta.

Standard immunoperoxidase techniques were used to investigate the distribution of the intracellular proteinase cathepsin D, two serine proteinase inhibitors--alpha 1-antitrypsin (alpha 1-AT) and alpha 1-antichymotrypsin (alpha 1-AChy)--and plasma fibrin stabilizing factor XIII (FXIII) in paraffin-embedded tissues from early and late intrauterine pregnancy and ectopic pregnancy. Localization of cathepsin D, alpha 1-AT, and alpha 1-AChy was identical in ectopic and intrauterine gestation: there was labeling of villous syncytiotrophoblast and a proportion of Hofbauer cells but no labeling of villous cytotrophoblast. The majority of interstitial extravillous trophoblast yielded negative results, but alpha 1-AT and alpha 1-AChy were consistently demonstrated in endovascular trophoblast. FXIII was not found in any trophoblast population but was demonstrated in Hofbauer cells, stromal fibroblasts, and interstitial dendritic cells. Granular, extracellular FXIII reactivity was present among sheets of infiltrating extravillous trophoblast in ectopic pregnancy but only occasionally in early intrauterine pregnancy. The results document further the heterogeneity of trophoblast, with the endovascular trophoblast forming an immunophenotypically distinct population. Furthermore, the pattern of extravillous trophoblastic invasion of maternal tissues in ectopic pregnancy appears to differ from intrauterine pregnancy; the poor decidualization of tubal mucosa in ectopic pregnancy may play a role in this variation.

Leucocyte populations in ectopic tubal pregnancy.

Leucocytes at the ectopic implantation site in 10 cases of early tubal pregnancy were characterised with a series of monoclonal antibodies using an indirect immunoperoxidase technique on cryostat sections. Most were HLA-DR positive macrophages, and there were a small number of mature T lymphocytes (UCHT1 and Dako-T1 positive cells). These results were compared with those reported in normal first trimester intrauterine pregnancies, and the contributions of the various leucocyte types to successful implantation at both the ectopic and intrauterine sites were assessed.

The expression of class II MHC gene products by fallopian tube epithelium in pregnancy and throughout the menstrual cycle.

The expression of HLA class II antigens by human fallopian tube epithelium was investigated in ectopic tubal pregnancy, in normal early and full-term intrauterine pregnancy, and during the menstrual cycle. Monoclonal antibodies directed against non-polymorphic (DA6.231, CR3/43, B7/21) and polymorphic (DA6.147, DA6.164, anti-leu-10) determinants of the HLA-D locus were used in a standard indirect immunoperoxidase method on fresh cryostat sections of fallopian tube. In ectopic pregnancy the tube epithelium showed uniform, intense reactivity for DR, DP and DQ. A similar reaction pattern was observed in normal first-trimester pregnancy. At term, most epithelial cells were DR-, DP- and DQ-positive, but a few were DP- and DQ-negative. In fallopian tubes from non-pregnant individuals, a variable number of epithelial cells labelled for DR alpha and DR beta but there was essentially no reactivity for DP or DQ. These results suggest differential regulation of class II MHC gene expression by tube epithelial cells, possibly mediated by hormones and/or a trophoblast product.

Placenta accreta: an immunohistological study of trophoblast populations.

Trophoblast populations in four cases of placenta accreta were characterized using antibodies directed against cell membrane antigens, placental hormonal products and low-molecular-weight cytokeratins in standard immunoperoxidase techniques. The results obtained with antibody to syncytiotrophoblast membrane (rabbit anti-StMPM), antibody to an epithelial membrane antigen (HMFGI) and a cytokeratin marker (CAM 5.2) appeared identical to those reported for normal term placental tissues. Similarly the localization of human placental lactogen (hPL), human chorionic gonadotrophin (hCG) and pregnancy-specific beta 1-glycoprotein (SP1) within trophoblast populations in placenta accreta was identical to their reported distribution in term placenta. However, increased reactivity at the villous-maternal junction was demonstrated with NDOGI, an antibody raised against term syncytiotrophoblast membrane and directed against hyaluronic acid. NDOGI reactivity at this site is normally maximal during early placental development and is virtually absent in the third trimester. The results suggest that placenta accreta does not arise through excessive trophoblast invasiveness or proliferation and the absence of decidua is of more importance in the pathogenesis. Trophoblast may regulate its development at an unfavourable intramyometrial implantation site by the production of hyaluronic acid.

Immunohistochemical characterisation of trophoblast antigens and secretory products in ectopic tubal pregnancy.

Fetal trophoblast populations in ectopic fallopian tube pregnancy have been characterised using immunohistochemical techniques. The distribution of trophoblast membrane antigens, low molecular weight epithelial cytokeratins, epithelial membrane antigen, human chorionic gonadotrophin, human placental lactogen, and pregnancy-specific beta 1-glycoprotein in ectopic tubal pregnancy appears similar to that reported in normal early intrauterine pregnancy. These findings emphasise the potential importance of ectopic pregnancy in the study of human gestation.

The expression of major histocompatibility complex antigens by trophoblast in ectopic tubal pregnancy.

The reactivity of the various trophoblast populations found in ectopic fallopian tube pregnancy with established trophoblast-reactive markers and monoclonal antibodies to MHC antigens has been studied. In ectopic tubal pregnancy fetal trophoblast shows an identical reaction pattern with these antibodies to that seen in intrauterine pregnancy, suggesting that ectopic implantation is not related to an inherent immunological abnormality of fetal trophoblast. However, from this and other studies, it appears that extravillous trophoblast displays an unusual class I MHC antigenic structure. This observation may explain the ability of class I MHC--bearing fetal trophoblast--to survive both in the uterus and at an abnormal implantation site.