Publications
348 results found
Laffan MA, Manning R, 1996, The influence of factor VIII on measurement of activated protein C resistance, BLOOD COAGULATION & FIBRINOLYSIS, Vol: 7, Pages: 761-765, ISSN: 0957-5235
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- Citations: 68
Hay CRM, Lozier JN, Lee CA, et al., 1996, Safety profile of porcine factor VIII and its use as hospital and home-therapy for patients with haemophilia-A and inhibitors: The results of an international survey, THROMBOSIS AND HAEMOSTASIS, Vol: 75, Pages: 25-29, ISSN: 0340-6245
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- Citations: 78
Ireland H, Thompson E, Lane DA, 1996, Gene Mutations in 21 Unrelated Cases of Phenotypic Heterozygous Protein C Deficiency and Thrombosis, Thrombosis and Haemostasis, Vol: 76, Pages: 0867-0873, ISSN: 0340-6245
<jats:title>Summary</jats:title><jats:p>Mutations have been identified in the protein C gene in 21 patients with venous thromboembolism and phenotypic heterozygous protein C deficiency. In 20 probands, single mutations were the only abnormalities identified by sequencing all coding regions, intron exon boundaries and the promoter region back to -1540. In one proband 2 mutations were identified and in another family 2 mutations were identified (but not both in the proband). Of the 23 mutations, 18 resulted in predicted amino acid substitutions, 3 were mutations resulting in stop codons, one was a mutation within a consensus splice sequence and another a 9 base pair insertion within exon 5 (this region within exon 5 is proposed as a deletion/insertion hot spot). A novel polymorphism was also, uniquely, identified in the propeptide region of the molecule (Pro-21 Pro; CCT to CCC) in a kindred from Hong Kong. Cosegregation of the protein C gene mutation with protein C deficiency could be determined in 13 families. In a further family, phenotypic protein C deficiency and the genetic mutation cosegregated in only 4/5 members.</jats:p><jats:p>The first thrombotic incident occurred in the probands between the ages of 11 and 59 years and 12 individuals suffered recurrent thrombosis. Thrombosis occurred in at least one other family member in 9/21 families, but in 2 of these it was inconsistently associated with protein C deficiency. An independent genetic risk factor, factor V Arg506Gln (FV Leiden) was identified in 2 probands (and 3 family members) and in 4 protein C deficient members of a third family but not in the proband. The results suggest that in the majority of probands with thrombosis and phenotypic protein C deficiency, a single protein C gene mutation is associated with thrombosis. However, it is also possible that additional unknown genetic risk factors contribute to the thrombotic risk. An added, acquired, risk factor leads to thromb
Hay CRM, Lozier JN, Lee CA, et al., 1996, Safety Profile of Porcine Factor VIII and Its Use as Hospital and Home-Therapy for Patients with Haemophilia-A and Inhibitors: the Results of An International Survey, Thrombosis and Haemostasis, Vol: 75, Pages: 025-029, ISSN: 0340-6245
<jats:title>Summary</jats:title><jats:p>A multicentre retrospective survey was conducted to re-assess the use of porcine factor VIII (HYATE:C), its side effects and the selection of patients for regular or home-therapy. 15,152,000 units of HYATE:C were used by 154 patients. The median inhibitor cross-reactivity to porcine VIIIC of 137 patients was 15%, 27% of patients lacking cross-reactivity. An absent, intermediate or brisk specific antiporcine anamnestic response was observed in 29, 40 and 31% of patients respectively. Seven patients were treated on-demand as home-therapy for a median 6.2, range 1.5-13 years. 23 further patients were treated regularly in hospital for a median of 3, range 2-7 years. This group used 8,319,000 U of porcine VIIIC for 2,000 bleeding episodes.</jats:p><jats:p>The incidence of transfusion reactions was 0.001%, 0.64% and 2.3%, for domiciliary infusions, infusions in multiply treated inpatients, and unselected in-patient infusions, respectively. The risk of reactions was dose-related. A post-infusion fall in platelet count was common, but usually transient and clinically insignificant. This was also dose-related (r = -0.64, p = 0.002). Marked reductions in platelet count were occasionally seen, usually with intensive replacement therapy. The relative lack of side effects observed amongst patients treated at home is attributable to the low, median 33 U/kg, dose used by this group.</jats:p><jats:p>A subgroup of inhibitor patients, identifiable by their absent or modest anamnestic response to porcine factor VIII may be treated regularly and safely with this product in small doses, over a period of years.</jats:p>
DARBY SC, EWART DW, GIANGRANDE PLF, et al., 1995, MORTALITY BEFORE AND AFTER HIV-INFECTION IN THE COMPLETE UK POPULATION OF HEMOPHILIACS, NATURE, Vol: 377, Pages: 79-82, ISSN: 0028-0836
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- Citations: 103
Tuddenham EG, Laffan M, 1995, Purified factor VIII., BMJ, Vol: 311, Pages: 465-466, ISSN: 0959-8138
TUDDENHAM EGD, LAFFAN M, 1995, PURIFIED FACTOR-VIII - THEORETICAL ADVANTAGES, BUT AT A COST, BRITISH MEDICAL JOURNAL, Vol: 311, Pages: 465-466, ISSN: 0959-8138
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- Citations: 5
ATHANASSIOU P, MCHALE J, DIKEOU S, et al., 1995, BUERGERS-DISEASE AND PROTEIN-S DEFICIENCY - SUCCESSFUL TREATMENT WITH PROSTACYCLIN, CLINICAL AND EXPERIMENTAL RHEUMATOLOGY, Vol: 13, Pages: 371-375, ISSN: 0392-856X
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- Citations: 14
KAYANO H, DYER MJS, ZANI VJ, et al., 1994, ABERRANT REARRANGEMENTS WITHIN THE IMMUNOGLOBULIN HEAVY-CHAIN LOCUS IN HAIRY-CELL LEUKEMIA, 4th International Workshop on Hairy Cell Leukemia, Publisher: HARWOOD ACAD PUBL GMBH, Pages: 41-47, ISSN: 1042-8194
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- Citations: 14
LAFFAN MA, CHITOLIE A, OWENS D, et al., 1993, ACQUIRED ANTI FACTOR-VIII INHIBITORS FOLLOWING PREGNANCY - A REPORT OF 2 CASES RESPONDING TO TREATMENT, CLINICAL AND LABORATORY HAEMATOLOGY, Vol: 15, Pages: 195-202, ISSN: 0141-9854
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- Citations: 1
LAFFAN M, LUZZATTO L, 1992, ANOMALOUS REARRANGEMENTS OF THE IMMUNOGLOBULIN HEAVY-CHAIN GENES IN HUMAN LEUKEMIAS SUPPORT THE LOOP-OUT MECHANISM OF CLASS SWITCH, JOURNAL OF CLINICAL INVESTIGATION, Vol: 90, Pages: 2299-2303, ISSN: 0021-9738
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- Citations: 12
BRITOBABAPULLE V, CRAWFORD A, KHOKHAR T, et al., 1991, TRANSLOCATIONS T(14,18) AND T(8,14) WITH REARRANGED BCL-2 AND C-MYC IN A CASE PRESENTING AS B-ALL (L3), LEUKEMIA, Vol: 5, Pages: 83-87, ISSN: 0887-6924
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- Citations: 41
SINGH AK, LAFFAN M, ERIDANI S, et al., 1991, REARRANGEMENT OF T-CELL RECEPTOR (DELTA, GAMMA AND BETA) GENES AND ITS SIGNIFICANCE IN T-CELL CHRONIC LEUKEMIAS, LEUKEMIA & LYMPHOMA, Vol: 4, Pages: 17-25, ISSN: 1042-8194
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- Citations: 1
MARSH JCW, HARHALAKIS N, DOWDING C, et al., 1989, RECURRENT GRAFT FAILURE FOLLOWING SYNGENEIC BONE-MARROW TRANSPLANTATION FOR APLASTIC-ANEMIA, BONE MARROW TRANSPLANTATION, Vol: 4, Pages: 581-585, ISSN: 0268-3369
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- Citations: 12
FORONI L, LAFFAN M, BOEHM T, et al., 1989, REARRANGEMENT OF THE T-CELL RECEPTOR DELTA-GENES IN HUMAN T-CELL LEUKEMIAS, BLOOD, Vol: 73, Pages: 559-565, ISSN: 0006-4971
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- Citations: 53
GANLY PS, LAFFAN MA, OWEN I, et al., 1988, AUTO-ANTI-JKA IN EVANS SYNDROME WITH NEGATIVE DIRECT ANTIGLOBULIN-TEST, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 69, Pages: 537-539, ISSN: 0007-1048
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- Citations: 17
GANLY PS, ISAACS JD, LAFFAN MA, et al., 1987, ACQUIRED FACTOR-VIII INHIBITOR ASSOCIATED WITH LUNG ABSCESS, BRITISH MEDICAL JOURNAL, Vol: 295, Pages: 811-811, ISSN: 0959-8138
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- Citations: 3
LAFFAN MA, TALAVERA JG, CATOVSKY D, 1986, HYPERCALCEMIA IN T-CELL ACUTE LYMPHOBLASTIC-LEUKEMIA - REPORT OF 2 CASES, JOURNAL OF CLINICAL PATHOLOGY, Vol: 39, Pages: 1143-1146, ISSN: 0021-9746
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- Citations: 6
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