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Biomedical subjects

Henry G Watson

Publications and source records attributed to Henry G Watson.

9 recordsLinked to original sources
PubMed2006

Effect of hypobaric hypoxia, simulating conditions during long-haul air travel, on coagulation, fibrinolysis, platelet function, and endothelial activation.

CONTEXT: The link between long-haul air travel and venous thromboembolism is the subject of continuing debate. It remains unclear whether the reduced cabin pressure and oxygen tension in the airplane cabin create an increased risk compared with seated immobility at ground level. OBJECTIVE: To determine whether hypobaric hypoxia, which may be encountered during air travel, activates hemostasis. DESIGN, SETTING, AND PARTICIPANTS: A single-blind, crossover study, performed in a hypobaric chamber, to assess the effect of an 8-hour seated exposure to hypobaric hypoxia on hemostasis in 73 healthy volunteers, which was conducted in the United Kingdom from September 2003 to November 2005. Participants were screened for factor V Leiden G1691A and prothrombin G20210A mutation and were excluded if they tested positive. Blood was drawn before and after exposure to assess activation of hemostasis. INTERVENTIONS: Individuals were exposed alternately (> or =1 week apart) to hypobaric hypoxia, similar to the conditions of reduced cabin pressure during commercial air travel (equivalent to atmospheric pressure at an altitude of 2438 m), and normobaric normoxia (control condition; equivalent to atmospheric conditions at ground level, circa 70 m above sea level). MAIN OUTCOME MEASURES: Comparative changes in markers of coagulation activation, fibrinolysis, platelet activation, and endothelial cell activation. RESULTS: Changes were observed in some hemostatic markers during the normobaric exposure, attributed to prolonged sitting and circadian variation. However, there were no significant differences between the changes in the hypobaric and the normobaric exposures. For example, the median difference in change between the hypobaric and normobaric exposure was 0 ng/mL for thrombin-antithrombin complex (95% CI, -0.30 to 0.30 ng/mL); -0.02 [corrected] nmol/L for prothrombin fragment 1 + 2 (95% CI, -0.03 to 0.01 nmol/L); 1.38 ng/mL for D-dimer (95% CI, -3.63 to 9.72 ng/mL); and -2.00% for endogenous thrombin potential (95% CI, -4.00% to 1.00%). CONCLUSION: Our findings do not support the hypothesis that hypobaric hypoxia, of the degree that might be encountered during long-haul air travel, is associated with prothrombotic alterations in the hemostatic system in healthy individuals at low risk of venous thromboembolism.

Adolescent↗
PubMed2006

A critical appraisal of the use of recombinant factor VIIa in acquired bleeding conditions.

Recombinant activated factor VII (rVIIa) was initially used for the treatment of inhibitors in patients with haemophilia. However, its localised mode of action at sites of damage to the vessel combined with dramatic clinical observations in exsanguinating patients have resulted in huge interest in its use as a global haemostatic agent. Although it appears safe, with no obvious excess of thrombotic events, its use in assorted acquired bleeding disorders, especially those associated with the development of complex coagulopathies, such as in the post-trauma state, has proved to be less dramatic than hoped.

Blood Coagulation Disorders↗
PubMed2005

Travel and thrombosis.

The available evidence suggests an association between long distance travel and the development of venous thromboembolism. The main problem for travellers and physicians is the interpretation of the evidence and its translation into appropriate advice on the risk and the prevention of thrombosis. Most available data relate to air travel. Thrombosis risk is greater following journeys of more than 8 h and those at greatest risk are travellers with a history of venous thromboembolism or risk factors. Based on the best evidence available the risk of symptomatic venous thromboembolism after flights of more than 12 h is 0.5%. It is likely that stasis plays a major role in the aetiology of travel related thrombosis. The evidence for hypobaric hypoxia induced coagulation activation requires confirmation. There is evidence that compression stockings and low molecular weight heparin prevent asymptomatic deep vein thrombosis (DVT) but clinical DVT has been observed in long distance flyers in spite of prophylaxis with aspirin and stockings.

Humans↗
PubMed2004

Low-dose oral vitamin K therapy for the management of asymptomatic patients with elevated international normalized ratios: a brief review.

Asymptomatic elevation of the international normalized ratio (INR) is a common problem associated with hemorrhage. Evidence from randomized controlled trials supports the use of low-dose oral vitamin K therapy as a treatment that promptly reduces the INR. Vitamin K given orally is more effective than subcutaneous vitamin K injection, and as effective as intravenous administration when INR values are compared 24 hours after administration. A 1.0-mg vitamin K dose is likely most appropriate for patients with INR values between 4.5 and 10. The fear of over-correction of the INR has limited the widespread use of vitamin K; however, our review suggests that this occurs infrequently when small doses are administered orally.

Administration, Oral↗
PubMed2004

The impact of HIV on mortality rates in the complete UK haemophilia population.

OBJECTIVE: To estimate the effect of HIV-1 infection on subsequent mortality in a complete population. DESIGN: Prospective cohort study. SUBJECTS: A total of 7250 haemophilic males were registered in the UK Haemophilia Centre Doctors' Organisation database, 1977-1998. Most were infected with hepatitis C virus. In the early 1980s, 1246 were infected with HIV-1 from contaminated clotting factor concentrate. The main outcome measure was the date of death. RESULTS: During 1977-1984 annual mortality in severely haemophilic males was 0.9%. For those with HIV, annual mortality increased progressively from 1985 reaching over 10% during 1993-1996 before falling to 5% in 1997-1999, whereas without HIV it remained approximately 0.9% throughout 1985-1999. For moderately/mildly haemophilic males the annual mortality was 0.4% during 1977-1984. Without HIV it remained approximately 0.4% throughout 1985-1999, but with HIV it was similar to that in severe haemophilia with HIV. Survival was strongly related to age at HIV infection. The large temporal changes in mortality with HIV were largely accounted for by HIV-related conditions. Without HIV annual liver disease mortality remained below 0.2% throughout 1985-1999, but with HIV it was 0.2% during 1985-1990, 0.8% during 1991-1996, and 0.8% during 1997-1999. CONCLUSION: These data provide a direct estimate of the effect of HIV-1 infection on subsequent mortality in a population with a high prevalence of hepatitis C. From approximately 3 years after HIV infection, large, progressive increases in mortality were seen. From 1997, after the introduction of effective treatment, substantial reductions occurred, although mortality from liver disease remained high.

Adolescent↗