Digital Public Defence: Christian Qvigstad
MD Christian Qvigstad at Institute of Clinical Medicine will be defending the thesis Age-related health and comorbidities in haemophilia for the degree of PhD (Philosophiae Doctor).
The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Digital Trial Lecture - time and place
- First opponent: Professor Michael Makris, Royal Hallamshire Hospital, Sheffield, United Kingdom
- Second opponent: Professor John-Bjarne Hansen, UiT - The Arctic University of Norway, Tromsø
- Third member and chair of the evaluation committee: Professor II Ingebjørg Seljeflot,
Institute of Clinical Medicine, University of Oslo
Chair of defence
Professor Emeritus Frank Brosstad, University of Oslo
Professor II Pål André Holme, Institute of Clinical Medicine, University of Oslo
Until around 1960, haemophilia was a disease experienced only by young people. The reason was that few survived past adolescence as it proved impossible to prevent fatal haemorrhages. In this period, when haemophilia caused death before old age, comorbidities were a secondary concern. With the advent of factor replacement treatment, however, life expectancy for people with haemophilia (PWH) is now approaching that of the general male population.
For the first time, we now have a large ageing haemophilia population. However, as the number of ageing PWH increases, so does the number of age-related diseases and comorbidities. These are now a primary concern, causing new clinical challenges.
In this thesis, we have investigated comorbid conditions in more than 500 PWH in Europe. As all data were obtained from an observational study, we have discussed associations discerned from cross-sectional data. We examined risk factors for chronic liver disease (CLD) and we discussed possible ways to limit macroscopic haematuria and possible adverse effects of bleeding episodes.
We documented that the main risk factors for CLD were hepatitis C virus (HCV), human immunodeficiency virus (HIV), and diabetes. Furthermore, we showed that the same risk factors were responsible for the CLD deteriorating. On a brighter note, we discussed and recommended new promising treatments, in particular direct-acting antivirals, specifically targeted at combating HCV, the most significant risk factor for CLD.
We documented that frequent prophylaxis with coagulation factor concentrates appeared to limit haematuria and argued that this was likely due to frequent prophylaxis ensuring factor levels above a critical threshold. Furthermore, we showed that macroscopic haematuria seemed to be a risk factor for hypertension, but only when a family history of hypertension
was present. We discussed why this may be plausible and pointed to recent empirical
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