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Biomedical subjects

L R Marshall

Publications and source records attributed to L R Marshall.

At least 19 recordsLinked to original sources
PubMed2000

Neutralisation of the clotting activity of Australian snake venoms by snake plasma.

Plasmas from Pseudonaja textilis and Notechis scutatus were tested in vitro for their ability to neutralise the procoagulant activity, in human plasma, of nine elapid venoms. Pseudonaja textilis plasma inhibited the procoagulant activity of all Pseudonaja species and in one taipan (Oxyuranus scutellatus). However there was no inhibitory activity against any from the Notechis species. Plasma from Notechis scutatus exhibited no inhibitory activity against any Notechis species, including self, only weak inhibition against the Pseudonaja species and, again, total inhibition of Oxyuranus scutellatus. Thus, protection of a species from the effects of its own venom does not appear to be universal.

Animals↗
PubMed1999

Platelet indices during normal pregnancy and pre-eclampsia.

Platelet count and mean platelet volume (MPV) were estimated in 349 normal pregnancies at various gestational stages, and in 30 cases of pre-eclampsia. A probability plot was constructed from these data using discriminant analysis of MPV versus platelet count for the pre-eclamptic versus normal pregnancies. The sensitivity for pre-eclampsia was 90% (27/30) and the specificity was 83.3%. This plot may be of use in confirming risk of pre-eclampsia.

Blood Platelets↗
PubMed1995

Elevated mid-trimester hCG and maternal lupus anticoagulant.

An association is described between women with lupus anticoagulant and abnormal prenatal serum screening results. Three cases of positive second-trimester serum screening for Down syndrome, with karyotypically normal fetuses, in women demonstrated to have lupus anticoagulant are presented. Serum screening positivity was principally due to a disproportionately elevated maternal serum human chorionic gonadotrophin (hCG) level. In each case, early, severe intrauterine growth restriction was documented, with only one fetus surviving the neonatal period. As maternal lupus anticoagulant may have a profoundly adverse effect on the course of pregnancy, we suggest that an elevated hCG level on prenatal screening prompt consideration of maternal lupus anticoagulant testing if ultrasonography demonstrates an otherwise normal singleton gestation and the fetal karyotype is normal.

Adult↗
PubMed1995

Antenatal diagnosis and management of fetomaternal alloimmune thrombocytopenia.

Fetomaternal alloimmune thrombocytopenia (FMAT) arises from maternal-fetal platelet antigen incompatibility, which stimulates the production of maternal immunoglobulin G (IgG) platelet-specific antibody. Transplacental passage of this antibody results in fetal platelet destruction and consequent thrombocytopenia. Sequelae of thrombocytopenia may be observed in both the fetus and neonate with intracranial hemorrhage occurring in approximately 10 to 30% of affected infants. No antenatal universal screening test is currently available to detect the 50% of cases occurring in the first pregnancy. The recurrence rate in subsequent pregnancies is 75 to 85%, with a tendency to increasing disease severity. Paternal platelet genotyping is recommended to assist in risk counseling following an affected pregnancy. Prenatal therapeutic strategies are aimed at elevating the fetal platelet count in affected pregnancies and thus decreasing hemorrhagic sequelae. The most effective treatment regimen is uncertain, but encouraging results are reported with the use of maternal intravenous gamma globulin. We report our experience in the antenatal diagnosis and management of FMAT.

Adult↗
PubMed1994

Prediction of neonatal alloimmune thrombocytopenia using PCR.

Neonatal alloimmune thrombocytopenia (NAIT) is a potentially fatal condition and in the majority of cases is associated with maternal antibodies to the HPA-1a (PLA1) haplotype. Early diagnosis in utero can enhance survival rates. The application of DNA genomic analysis and PCR technology for the determination of the HPA-1a/HPA-1b (PLA1/PLA2) locus is described and applied in a family study where the fetus was diagnosed to have NAIT. This rapid technique differentiated between the 3 haplotypes HPA-1a/HPA-1a, HPA-1b/HPA-1b and HPA-1a/HPA-1b using the polymorphism at base 196 of the GPIIIa gene. This is the first Australian report on the establishment of this technology for platelet genotype typing and the application in the diagnosis of NAIT. This technique can be performed on DNA extracted from any nucleated cells and avoids the difficulty of requiring fetal platelets for serological typing when NAIT is suspected. The PCR technique of genomic DNA analysis has an important application in the prediction and management of this potentially severe condition.

Adult↗
PubMed1993

A fatal case of necrotizing enterocolitis in a neonate with polyagglutination of red blood cells.

An infant of 30 weeks gestation developed necrotizing enterocolitis (NEC) 8 days after birth and died 2 days later after a fulminating course. During her illness she received two blood transfusions, both of which produced sub-optimal rises in her haemoglobin and were associated with evidence of haemolysis. Retrospective analysis demonstrated T antigen (Tk) polyagglutination of the infant's red blood cells and donor plasma. Although bacterial cultures were negative throughout the course of the illness in this case, T antigen exposure is associated with certain anaerobic infections and with severity of NEC. Infants with NEC should be regularly screened for T antigen exposure and if this test is positive, plasma (immunoglobulin) containing infusions should be avoided.

Blood Component Transfusion↗
PubMed1993

Detection of lupus anticoagulant--an Australian perspective.

The detection of lupus anticoagulant is important in laboratory evaluation of patients with thrombotic tendencies. The aim of this workshop was to assess the effectiveness of Australian laboratories in detecting these antibodies and assess the tests used. Fourteen laboratories took part in the exercise, held as a Workshop of the National Meeting of Australian Medical Laboratory Scientists in 1990. Seven unknown plasmas were distributed for testing prior to the meeting. While 100% correctly identified 3 strong inhibitors and a moderate strength inhibitor, the detection rate for specific individual tests varied from 38-100%. The detection rate for 2 weak inhibitors varied from 0-50%. Of the most commonly performed tests the least sensitive was the dilute Russell's viper venom time and the most sensitive was the tissue thromboplastin inhibition test, however, the degree of sensitivity seemed dependent on the source of thromboplastin. In some laboratories the Kaolin clotting time, with variations, was more sensitive. All participants correctly identified a factor VIII inhibitor as not of the lupus type. The false positive detection rate was 0%. All but one of the participating laboratories used 2 or more phospholipid dependent tests for the analysis of lupus anticoagulant (LA) which is in keeping with current international guidelines.

Australia↗
PubMed1989

Australian snake venoms and their in vitro effect on human platelets.

Thrombocytopenia is generally not associated with cases of envenomation by Australian snakes, however the clinical evidence is conflicting. The in vitro effect of these venoms upon platelets had hitherto not been studied. This study systematically examines the effect on human fresh and fixed platelets of twenty Australian snake venoms, nineteen elapid and an hydrophiid; for comparision four crotalid venoms from the Americas and S.E. Asia were also included. Electron micrographs were taken of platelets after exposure to some of the venoms. Results demonstrated that all venoms except the hydrophiid venom caused fresh platelets to irreversibly aggregate directly, and this was associated with degranulation as evidenced by electron microscopy (EM). Response to all venoms by fixed platelets was less marked and also suggests, that metabolically, active platelets are necessary for the venoms to exert their maximal effect. The hydrophiid venom's action on fresh platelets was unique, as a plasma co-factor was required before aggregation could be induced. Crotalid and hydrophiid venoms were more active against platelets than the elapid venoms. Nevertheless, platelet aggregation and degranulation in the presence of elapid venoms suggests that a platelet response in vitro may be a significant factor in the "defibrination syndrome" induced in humans by Australian snakes.

Australia↗
PubMed1986

Plasma cofactors necessary for Enhydrina schistosa (beaked sea snake) venom to induce platelet aggregation.

A study of the effect of the venom of the beaked sea snake (Enhydrina schistosa) was undertaken on platelet aggregation. It was found that platelet aggregation and the release reaction occurred in the presence of both venom and plasma but, not with the venom alone. No effect was observed with fixed platelets distinguishing the effect of the venom from that of platelet aggregation with ristocetin or botrocetin and indicating metabolic dependence. Studies to elucidate the plasma factor required for platelet aggregation under the release reaction indicated dependence on the presence of both Factor II and calcium ions. This venom may prove to be a useful laboratory reagent in coagulation studies because of the Factor II and calcium dependence.

Animals↗
PubMed1984

Cross-reactivity of bardick snake venom with death adder antivenom.

A case of a young man who was bitten by a bardick snake (Notechis curtus) and who, apart from marked local swelling, had neither signs of coagulopathy nor neurological symptoms, is reported. The bardick snake venom taken from the site of the bite reacted strongly with the death adder antivenom in the snake venom detection kit, but did not react with the Notechis antivenom. This anomalous reactivity was confirmed when dried bardick snake venom was used. In-vitro observations of the bardick snake venom showed that it had anticoagulant properties similar to those of death adder venom, and was not procoagulant as are the venoms of other snakes of the Notechis genus. The clinical importance of these findings is discussed.

Adolescent↗
PubMed1983

Coagulant and anticoagulant actions of Australian snake venoms.

A systematic study was made of the action on the plasma coagulation system of 20 Australian and Papuan Elapid and Hydrophiid snake venoms and compared with 4 Crotalid venoms and 1 Viper. The majority of Australian venoms were shown to be prothrombin activators with variable dependence on the presence of factor V phospholipid and calcium. None of these venoms had strong thrombin like activity in contrast to the Crotalid venoms which were powerfully thrombin like. The Crotalid venoms were also strongly fibrinolytic unlike the Elapid venoms which showed no or minimal evidence of fibrinolytic activity. Four Elapid venoms and 2 Crotalid venoms showed anticoagulant activity which contained neither antithrombin nor fibrinogenolytic activity and may act upon the prothrombin complex.

Animals↗
PubMed1981

Passovoy factor deficiency in five Western Australian kindreds.

Passovoy factor deficiency, a coagulation abnormality affecting the intrinsic coagulation system, was discovered in 5 Western Australian kindreds. The defect is inherited as an autosomal dominant and is associated with a clinical bleeding tendency characterized by easy bruising and undue blood loss following trauma such as dental extraction and tonsillectomy. Fresh frozen plasma appears to provide effective prophylaxis during surgery. The activated partial thromboplastin time (APTT) shows a prolongation which, in most patients, is of relatively slight degree, and this may be the reason for the paucity of reports in the literature. The discovery of 5 kindreds carrying the defect suggests that it may be relatively common in the Australian community and that care should be taken to identify and follow up minor grades of abnormality of the APTT where individuals suspected of having an inherited bleeding tendency are screened. A sample from one case was distributed, with a clinical history, to participants in the Royal College of Pathologists of Australasia 1980 Quality Assurance Programme in Haematology. Approximately one-third of 175 participants failed to detect the definite abnormality present.

Australia↗