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Biomedical subjects

G D Lowe

Publications and source records attributed to G D Lowe.

At least 271 records · Page 15Linked to original sources

Radio-isotopic joint scans in haemophilic arthritis.

The majority of severe haemophiliacs will develop a crippling arthritis consequent upon recurrent haemarthroses although the pathogenic mechanism remains unclear. We have carried out technetium-99 pertechnetate joint scans in the elbows, knees and ankles of 23 haemophilic patients and compared the isotope uptake of the 15 patients with clinical and radiological evidence of arthritis to that of eight patients without arthritis, to 13 age-matched healthy male controls, and to 10 age-matched males with active rheumatoid arthritis. Isotope uptake into the knee joints was significantly higher in haemophilic arthritis than in controls, haemophiliacs without arthritis, and patients with rheumatoid arthritis [median percentage uptake of administered technetium (Tc) dose X 10(3) in right knee = 9.4, 6.2, 6.4 and 6.6, respectively]: and the differences from haemophilic arthritis were all significant (p less than 0.01, Mann-Whitney U test). Similar differences were seen in the elbows and ankles. Increased Tc uptake correlated strongly with frequency of haemarthrosis, pain, synovitis, range of movement and radiological changes in knees and elbows, but poorly with the lesser changes seen in the ankles. These results would support the theory that haemophilic arthritis amongst the inflammatory arthropathies and that scanning is an appropriate technique for following progression of joint disease.

Ankle Joint↗

Application of an intragenic genomic probe to genetic counselling for haemophilia B in the west of Scotland.

Total ascertainment revealed 28 families with haemophilia B in the west of Scotland (prevalence 1/26 870 males). In 12 of these families more than one person was affected and 26 living obligate carriers were identified and tested. Of these, 42% were heterozygous for a DNA polymorphism recognised by a factor IX genomic probe. No recombination was observed in 11 phase known and four phase unknown informative meioses. Definitive genetic counselling was possible for 14 of 42 females at risk, 11 could not be traced, in 10 the probe was not informative, and in seven paternal absence prevented interpretation. Linkage disequilibrium was apparent for this restriction fragment length polymorphism and haemophilia B in the west of Scotland.

DNA↗

Evaluation of euglobulin methods for the study of blood fibrinolytic activity: results for patients with rheumatoid arthritis and in the postoperative period.

Euglobulin fractionation is a frequently employed pretreatment of plasma for the determination of fibrinolytic activity. The fractionation procedure suffers from possible in vitro artifacts, e.g., variable precipitation of C1-inactivator. This is illustrated by the following two situations. It is shown that increased amounts of C1-inactivator not related to an increased plasma concentration are present in euglobulin fractions in cases of classic rheumatoid arthritis. Similarly, postoperatively, a disproportional increase in C1-inactivator in euglobulin fractions occurs. In both cases, an artificially reduced fibrinolytic activity is recorded due to increased inhibition by C1-inactivator. This is circumvented and recognized by adding sodium flufenamate or C1s-esterase to euglobulin fractions to uniformly eliminate C1-inactivator. Two specific assays for tissue-type plasminogen activator activity in euglobulin fractions (as C1-inactivator-resistant activator activity and a parabolic rate assay on a synthetic substrate) correlate excellently (r = 0.8728; p less than 0.001; n = 108). The first mentioned is corrected for variable endogenous C1-inactivator; the latter assay is found to be insensitive to inhibition by C1-inactivator. It is concluded that with euglobulin methods a misinterpretation of blood fibrinolytic activity is possible in rheumatoid arthritis patients. In the postoperative period, the fibrinolytic shutdown concerns tissue-type plasminogen activator activity; the pattern of the shutdown can be misjudged in using traditional euglobulin methods.

Abdomen↗

The effect of fibrinolytic stimulation by stanozolol on postoperative pulmonary complications.

Platelet aggregation in the lungs is common following abdominal surgery and may contribute to postoperative hypoxaemia. The hypothesis that an anabolic steroid, stanozolol, by preventing fibrinolytic shutdown, would prevent postoperative hypoxaemia was tested. Fifty patients undergoing abdominal surgery were randomly allocated to receive either placebo or stanozolol. Despite preventing fibrinolytic shutdown in most patients, the use of stanozolol did not influence the extent of postoperative hypoxaemia or the incidence of postoperative pulmonary complications. These results suggest that fibrinolysis does not play a significant part in the pathogenesis of postoperative pulmonary dysfunction.

Adult↗

AIDS--again.

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Acquired Immunodeficiency Syndrome↗

Haematocrit in patients attending a hypertension clinic.

In view of recent interest in the relationship of haematocrit and blood viscosity to hypertension and vascular disease, we have analysed retrospectively the relationship of haematocrit to blood pressure, vascular complications and other variables in 2,381 patients referred to the Glasgow Blood Pressure Clinic. Haematocrit correlated negatively with age and systolic pressure in men, and positively with age and systolic pressure in females. Positive correlations were found in both sexes between haematocrit and serum alanine aminotransferase (possibly due to mutual correlation with alcohol); and between haematocrit and overweight (Quetelet Index) but not obesity (Ponderal Index). Increased haematocrit was also associated with cigarette smoking; and with history of angina, myocardial infarction and intermittent claudication in females. No correlation was observed between haematocrit and history of stroke. These findings suggest that prospective studies of haematocrit in hypertensives may be of interest.

Adult↗

Serum oestradiol and ischaemic heart disease--relationship with myocardial infarction but not coronary atheroma or haemostasis.

Elevated oestradiol (E2) levels may be a risk factor for ischaemic heart disease in men, although the mechanisms for the elevation of oestrogen and for its adverse effects remain unclear. We have studied 100 Caucasian males undergoing elective coronary angiography for ischaemic chest pain and measured serum oestradiol, a profile of haemostatic tests, extent of coronary artery disease and evidence of previous myocardial infarction in order to assess any relationships which could explain the effect of elevated serum oestradiol levels. Levels were significantly higher in men with a history of myocardial infarction compared to those without (p less than 0.01), but were unrelated to the extent of coronary disease or to the haemostatic tests. These results suggest that the association of oestradiol with coronary events relates to myocardial infarction, not to atherogenesis, and is not due to any currently measurable alterations of haemostasis. Current beta-adrenoceptor blocker treatment was associated with lower oestradiol and thromboxane B2 concentrations (both, p = 0.06). These incidental findings suggest that further studies of the effects of beta-blockade on oestradiol and thromboxane metabolism are indicated.

Adrenergic beta-Antagonists↗

Abnormal haemostasis and blood viscosity in malignant hypertension.

We have previously shown abnormalities of haemostasis suggestive of intravascular coagulation in patients with malignant hypertension, a condition associated with retinopathy and renal fibrin deposition. To determine whether such abnormalities are specific to malignant hypertension, we have measured several haemostatic and haemorheological variables in 18 patients with malignant hypertension (Group 1), 18 matched healthy controls (Group 2), and 18 patients with non-malignant hypertension (Group 3) matched for renal pathology, blood pressure and serum creatinine with Group 1. Both Groups 1 and 3 had increased mean levels of fibrinogen, factor VIIIc, beta-thromboglobulin, plasma viscosity and blood viscosity (corrected for haematocrit); and decreased mean levels of haematocrit, antithrombin III and platelet count. Mean levels of fast antiplasmin and alpha2-macroglobulin were elevated in Group 1 but not in Group 3. We conclude that most blood abnormalities are not specific to malignant hypertension; are also present in patients with non-malignant hypertension who have similar levels of blood pressure and renal damage; and might result from renal damage as well as promoting further renal damage by enhancing fibrin deposition. However increased levels of fibrinolytic inhibitors in malignant hypertension merit further investigation in relation to removal of renal fibrin.

Adult↗

HTLV-III seropositivity in European haemophiliacs exposed to Factor VIII concentrate imported from the USA.

77 Scottish haemophiliacs and 22 Danish haemophiliacs were serologically tested for antibodies to human T-cell leukaemia virus III (HTLV-III). Since 1979 the Scottish patients had been treated largely with factor VIII concentrate produced in Scotland, whereas all but 2 of the Danish patients had received both locally prepared concentrate and commercial concentrate made from US donor material. 15.6% of Scottish and 59.1% of Danish haemophiliacs were antibody positive (p less than 0.001). None of 11 haemophiliacs not treated in the period 1979-84 was seropositive. 2 (6.7%) of 30 subjects who had been treated with locally produced concentrate only were antibody positive, compared with 23 (39.7%) of 58 subjects who had been treated with commercial concentrate. Among 52 users of both commercially and locally produced factor VIII concentrate, seropositivity was directly correlated with the consumption of commercial concentrate (p less than 0.001) but not locally produced material. These data indicate that European haemophiliacs were exposed to HTLV-III via some factor VIII concentrates obtained from the USA.

Adolescent↗

AIDS and hepatitis B.

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Acquired Immunodeficiency Syndrome↗

The effects of acute smoking on platelet behaviour, fibrinolysis and haemorheology in habitual smokers.

There is an increased frequency of arterial thrombosis in cigarette smokers. The changes in blood coagulation seen in these subjects have been studied by many workers but results have not always been in agreement. We wished to study the effects of acute smoking on platelet behaviour, fibrinolysis and haemorheology in ten habitual smokers, and to compare these results with non-smoking controls. Results show that the smoking group had higher plasma fibrinogen (p less than 0.04), lower plasminogen (p less than 0.02) and plasminogen activator (p less than 0.05), and higher plasma viscosity (p less than 0.003). The changes seen in cigarette smokers after smoking three cigarettes were an increase in the rate of platelet aggregation to ADP (p less than 0.02), an increase in alpha 2M, (p less than 0.02), and factor VIII RAG (p less than 0.05). Plasma viscosity was decreased (p less than 0.02) as was red cell deformability (p less than 0.02). We confirm an increased tendency to hypercoagulability in smokers compared to controls which becomes more pronounced immediately after smoking three cigarettes.

Adult↗

A double-blind trial of intramuscular stanozolol in the prevention of postoperative deep vein thrombosis following elective abdominal surgery.

Fibrinolytic shutdown may be important in the development of postoperative deep vein thrombosis (DVT). We have previously shown that stanozolol 50 mg, given intramuscularly 24 hr before surgery, prevents the decrease in plasminogen activator activity (PA) seen on the first postoperative day in patients at high risk of DVT. To investigate the role of fibrinolytic shutdown in causation of DVT, sixty patients were randomized in a double-blind controlled trial to receive stanozolol or placebo intramuscularly, and DVT was detected by leg scanning and confirmed by venography. Scan positive DVT occurred in 11 of 31 placebo patients (35%) and 12 of 29 who received stanozolol (41%). A significant decrease in PA was confirmed in the placebo group, while stanozolol caused a significant increase in PA on the first postoperative day. Patients in either group who did not develop DVT showed minimal changes in PA. We conclude that prevention of fibrinolytic shutdown by this regimen of stanozolol does not prevent postoperative DVT, and that further studies are required to clarify the relationship of postoperative fibrinolysis and DVT.

Abdomen↗

Response of femoral venous oxygen tension to graduated pressure stockings--possible relationship to deep vein thrombosis.

Venous oxygen tension (pO2) was measured in discrete samples of blood obtained through the femoral vein of cardiac catheterisation patients before, during and after application of sustained external graduated pressure in the form of compression stockings (T. E. D. Kendall). There was a significant reduction (p less than 0.05) of pO2 from the baseline value both 30 sec and one minute after the application of the pressure stockings. Thereafter, the pO2 rose to baseline values. Two minutes after the stockings were removed there was again a significant reduction (p less than 0.05) of pO2 from the baseline value. We suggest that the decrease in venous pO2 on application of external pressure may be a reflection of washing out of stagnant hypoxic blood from the venous valve pockets, which may be related to the formation of deep vein thrombosis (DVT).

Blood Gas Analysis↗

A comparison of spontaneous platelet aggregation in whole blood with platelet rich plasma: additional evidence for the role of ADP.

ADP, generated from red blood cells is believed to be responsible for the spontaneous aggregation of platelets in whole blood. This notion is based mainly on the use of enzymes which remove ADP. We have studied spontaneous platelet aggregation in whole blood and autologous platelet rich plasma obtained from 12 healthy male and female volunteers. Platelet aggregation was quantitated by measuring the fall in the number of single platelets counted using a whole blood platelet counter (Ultra Flo 100). In a rotating tube model, the mean fall in the number of platelets due to spontaneous aggregation was 56% in whole blood but, only 3% in platelet rich plasma prepared from the same blood samples. Spontaneous platelet aggregation in whole blood was unaffected by apyrase grade I, but was reduced to 15% by apyrase grade II, to 38% by creatine phosphokinase/creatine phosphate and to 9% by pyruvate kinase/phosphoenolpyruvate. The results of this study provide additional evidence that ADP generated in whole blood triggers the spontaneous aggregation of platelets.

Adenosine Diphosphate↗