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Biomedical subjects

Samuel Machin

Publications and source records attributed to Samuel Machin.

5 recordsLinked to original sources
PubMed2006

Prophylaxis of venous thromboembolism during early inpatient rehabilitation after acquired brain injury: how guidelines change management.

PURPOSE: To establish guidelines for prophylaxis of venous thromboembolism (VTE) in younger adults undergoing early inpatient rehabilitation following acquired brain injury (ABI). METHOD: A two-phase (phase 1: retrospective; phase 2: prospective) observational study was carried out involving patients admitted to an inpatient neurological rehabilitation unit during a 40-month period. In phase 1, VTE prophylaxis was prescribed on an ad hoc basis. In phase 2, prophylaxis was considered in accordance with guidelines agreed locally. The prescribing behaviour in each phase of the study was compared using a VTE risk stratification tool based on expert opinion and a review of the literature. RESULTS: Data were obtained on 94 patients in phase 1 and 23 patients in phase 2. During phase 1, the prophylactic prescribing behaviour of the referring hospitals and our unit after admission were similar ( p = 0.13). In phase 2, our prescribing behaviour had changed compared with that of the referring hospitals, with a significant increase in the proportion of patients on appropriate treatment ( p = 0.01) and a decrease in the numbers under-treated ( p = 0.002). We were also significantly less likely to under-treat ( p = 0.005) and more likely to over-treat ( p = 0.004) after admission during phase 2 compared with phase 1, whilst practice was variable in patients at moderate risk. CONCLUSIONS: Guidelines modify behaviour. They must stratify risk, particularly to avoid inconsistencies in the management of patients at moderate risk. There is a need to establish national guidelines for VTE prophylaxis during early inpatient rehabilitation after ABI; these guidelines should include a risk stratification tool.

Adolescent↗
PubMed2006

Successful management of pregnancy in women with a history of thrombotic thrombocytopaenic purpura.

Pregnancy is an initiating event for acute thrombotic thrombocytopaenic purpura (TTP). There is a high risk of relapse during pregnancy and of foetal morbidity. We describe five cases with successful maternal and foetal outcomes in patients with a history of TTP. Cases 1 and 2 presented with TTP in their first pregnancy and had second-trimester foetal losses. Case 3 had four TTP relapses and soon after achievement of clinical remission became pregnant. Case 4 presented with TTP and left-sided stroke in pregnancy. ADAMTS-13 activity was less than 5% at presentation in four patients and prior to therapy during pregnancy in cases 1-4. Case 5, who had a single acute episode of TTP and became pregnant 6 years later, had normal ADAMTS-13 activity throughout pregnancy. Only case 3 had evidence of an inhibitor on mixing studies. All five patients underwent close haematological and obstetric monitoring and continued low-dose aspirin throughout pregnancy. Patients 1-4 had regular plasma exchange and received low molecular weight heparin during pregnancy. Patient 4 also received rituximab during the third trimester with no observed maternal or neonatal toxicity. Live healthy infants were delivered in all five cases in the third trimester. These findings suggest that successful pregnancy outcome is achievable in patients with a history of TTP and that patients with severely reduced ADAMTS-13 activity at the onset of pregnancy, necessitates regular plasma exchange during pregnancy.

ADAM Proteins↗
PubMed2002

The expression of prion protein by endothelial cells: a source of the plasma form of prion protein?

The neuronal prion protein (PrPC) is also expressed within peripheral tissues including human blood. The majority of blood PrPC is found within the plasma fraction. We hypothesized that the vascular endothelium could be a source of this PrPC. Reverse transcription polymerase chain reaction demonstrated that both human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1) expressed PrPC mRNA. Flow cytometry confirmed PrPC expression on HMEC-1s and HUVECs (120900 +/- 15058 and 58327 +/- 4577 molecules PrPC/cell respectively), with no upregulation following cellular activation. Confocal immunofluorescence microscopy confirmed that HMEC-1s and HUVECs were positive for PrPC on the plasma membrane. Time-resolved dissociation-enhanced fluoroimmunoassay (DELFIA) analysis of cell culture medium demonstrated a slow constitutive release of soluble PrPC not associated with activation. In contrast to von Willebrand factor antigen, PrPC plasma levels in vivo decrease following desmopressin therapy in patients with von Willebrand disease. Measurement of PrPC plasma levels in patients with varying blood counts demonstrated no association between cell count and PrPC concentration. However, there was a higher level of PrPC in plasma from patients with end-stage renal failure. In conclusion, endothelial cells of both macrovascular and microvascular origin expressed high levels of PrPC which can be constitutively released into the cell culture medium.

Blood Cell Count↗