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Biomedical subjects

J P Isbister

Publications and source records attributed to J P Isbister.

At least 19 recordsLinked to original sources
PubMed1995

Activated protein c resistance (APC) and inherited factor V (FV) mis-sense mutation in patients with venous and arterial thrombosis in a haematology clinic.

BACKGROUND: Inherited factor V (FV) mis-sense point mutation has recently been identified as a major cause of familial venous thrombosis. The incidence of this congenital haemostatic disorder in Australia is unknown. AIM: To examine the incidence of this congenital defect in patients with thrombosis attending a haematology clinic. METHODS: Individuals investigated or treated for venous and arterial thrombosis over a four month period, as well as those who were on anticoagulant for valvular replacement or arrhythmia were studied for the presence of FV mis-sense point mutation, FV Q506 (G to A at nucleotide position 1691) by a polymerase chain reaction based test, and activated protein C (APC) resistance using an APTT based coagulation assay. RESULTS: Forty-five patients with venous thromboembolism (VTE), 20 patients with coronary artery disease and 25 patients with valvular replacement or arrhythmia who were on anticoagulant were examined. The frequency of FV mis-sense point mutation in these three groups was 26.7%, 15% and 4% respectively. In this study, patients with FV Q506 were of a younger age and had a higher incidence of extensive thrombosis or recurrence as compared to those with the normal factor V gene. This mutation was found in a diverse group of people (four of the 12 patients were of non-European origin). Nearly 50% of these patients had other risk factors for VTE. The number of patients with a family history of VTE was similar for those with the FV mutation and the normal FV. CONCLUSION: This study confirms the high incidence of FV Q506 mutation in patients with VTE reported overseas. Several clinical features, i.e. young age of onset of VTE, high recurrence rate, diverse ethnic background and importance of associated risk factors are highlighted. The findings in this study also raise the possibility that this mutation may be a risk factor for arterial thrombosis. Large studies are required to substantiate these findings.

Adult↗
PubMed1994

Haematological parameters. What to order and why.

With the enormous range of laboratory investigations available from a modern haematology laboratory it is not surprising that a clinician may at times feel 'at sea' when finding a way through the diagnostic process. It is hoped that this 'haematological map' will help the busy clinician.

Algorithms↗
PubMed1989

CFU-GM inhibitors in neutropenia.

Peripheral blood lymphocytes from 20 patients with neutropenia not consistent with aplastic anaemia were tested for their ability to inhibit the proliferation of normal granulopoietic precursor cells (CFU-GM) in agar culture. Two patients, both with features of an autoimmune disorder, had lymphocytes which were more inhibitory than normal lymphocytes to both normal and their own CFU-GM. Two other patients had lymphocytes which were more inhibitory than normal lymphocytes to either their own CFU-GM or normal CFU-GM but not both. Eight patients had lymphocytes which were significantly less inhibitory than normal lymphocytes to either normal or their own CFU-GM, but only one showed this feature against both normal and their own CFU-GM. One patient had a highly potent plasma inhibitor of CFU-GM--this patient had received multiple transfusions and had a leucocyte antibody of a broad specificity. No clinical or haematological features were common to any of these groups of patients which reflects the heterogeneity of patients studied and stresses the importance of controls.

Adolescent↗
PubMed1987

Detection of a multidrug resistant phenotype in acute non-lymphoblastic leukaemia.

Most adult patients with acute non-lymphoblastic leukaemia (ANLL) relapse with drug resistance. Overexpression of a plasma membrane protein, P-glycoprotein, correlates with multidrug resistance in human and animal cell lines. We have detected a multidrug resistance phenotype in two patients with drug resistant ANLL by an immunocytochemical assay using a monoclonal antibody to P-glycoprotein. Sequential analysis of peripheral blood samples from both patients showed a progressive increase in both the intensity of staining and the proportion of leukaemic cells that bound antibody as the disease progressed. The assay is simple, and may have prognostic and therapeutic implications.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1987

The contracted plasma volume syndromes (relative polycythaemias) and their haemorheological significance.

Relative polycythaemia is a general term which includes patients with a normal red cell mass but a contraction of the plasma volume as the cause for the polycythaemia. The relative polycythaemias can broadly be divided into two groups. Firstly, relative polycythaemia may be due to a primary loss of plasma volume due to dehydration, capillary leak or hypo-oncotic pressure. Secondly, relative polycythaemia may be due to a primary contraction of the vascular compartment (i.e. reduced venous compliance). It is this second group which is the least understood and is analysed in detail in this review. In general, this group of polycythaemias is secondary to exogenous or endogenous stress and is mediated via the sympathetic nervous system. Hypoxia, smoking, neurological disorders, myocardial infarction and acute psychological stress have all been demonstrated as possible factors. In many cases of chronic stress polycythaemias aetiological factors may be identified, whereas in others the term idiopathic is probably appropriate. There appears to be a relationship between the idiopathic stress polycythaemias, hypertension and psychological stress. Other patients may have primarily a disorder of blood volume control involving the autonomic nervous system and its receptors. The haemorheological significance of relative polycythaemia and its management are discussed. Treatment is generally dictated by the underlying cause. In stress polycythaemias the stimulus should be removed as far as possible. However, in some patients with chronic idiopathic stress polycythaemia, regular venesection may be required to maintain the venous haematocrit at an appropriate level.

Blood Viscosity↗
PubMed1987

Iron deficiency. Misunderstood, misdiagnosed and mistreated.

Iron deficiency is a common medical problem that may present in a variety of ways to the general practitioner or the specialist. An understanding of iron physiology is relevant to diagnosis and treatment of iron deficiency. Human iron metabolism is a system based on conservation. For this reason, the most common cause of iron deficiency is loss of the normal conservation of iron and this usually means blood loss. The important implication is that the search for the cause of iron deficiency will usually focus on the gastrointestinal tract in males and non-pregnant, non-menstruating females. Iron deficiency is commonly misdiagnosed. The usual error is misinterpretation of the laboratory features of the anaemia of chronic disease. The serum iron is low, but the iron binding capacity is normal and ferritin is normal or high. There are problems and exceptions involved in interpretation of iron indices. Treatment of iron deficiency requires an understanding of iron absorption and the ability of the marrow to respond. In most circumstances, iron deficiency will respond to adequate doses of oral iron; however, there are a few situations when oral iron is unsuitable and parenteral iron is required. An inadequate response to iron may indicate inadequate supply of iron to the bone marrow (e.g. malabsorption, non-compliance) or failure of the marrow to respond (e.g. concomitant folate deficiency). Pregnancy is a special situation in which conservation of iron is overcome by fetal iron requirements and in which application of the knowledge of iron physiology should be applied to prevent and treat iron deficiency.

Acute-Phase Reaction↗
PubMed1985

The heparin induced thrombosis--thrombocytopenia syndrome (H.I.T.T.S.): a review.

Thrombocytopenia and thrombosis occurring as a direct consequence of heparin therapy are being recognized with increasing frequency in recent years. Current conceptions of the pathophysiology of this syndrome are explained, together with the mechanisms leading to the clinical features. The clinical spectrum of H.I.T.T.S. is widening, but there are diagnostic problems arising from a lack of awareness of the syndrome by some practising clinicians. Many laboratory methods for detecting H.I.T.T.S. have been used, but particular attention should be given to the method of platelet aggregometry. Finally, problems encountered in diagnosis and management of this condition are discussed.

Aged↗
PubMed1984

CFU-C inhibitors in aplastic anaemia.

Peripheral blood lymphocytes from 15 patients with marrow aplasia were tested for their ability to inhibit the proliferation of normal granulopoietic precursor cells (CFU-C) in agar culture, relative to the inhibitory effect of normal lymphocytes studied in parallel. Eight of the 15 patients with marrow aplasia had lymphocytes which were significantly less inhibitory to normal CFU-C than controls whereas 3 patients had lymphocytes which were significantly more inhibitory. Two further patients who had recovered from marrow aplasia were also studied. The effect of patient's plasma and normal plasma on normal CFU-C proliferation was also studied and in 1 case a potent inhibitor of granulopoiesis was demonstrated. In 9 cases CFU-C could be cultured from patient's marrow, and parallel studies examining the effects of lymphocytes or plasma on patient's CFU-C were performed in these. All 9 patients had low numbers of marrow CFU-C. In none of the 9 marrow samples tested was inhibition by patient lymphocytes significantly greater than normal controls. The results highlight the heterogeneity inherent in the study of aplastic states and serve to underline the importance of controls. In only a minority of cases (20%) was lymphocyte suppression of normal granulopoiesis by lymphocytes from patients with aplastic anaemia significantly greater than normal lymphocyte suppression.

Adolescent↗