| 1. |
- Nilsson, Mats, 1954-
(författare)
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Cobalamin communication in Sweden 1990 – 2000 : views, knowledge and practice among Swedish physicians
- 2005
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Cobalamin (vitamin B12) is one of several essential micronutrients needed by the human organism. Other important micronutritients, which interplay with vitamin B12, are folate and iron. During the last ten years, the attention has been drawn to different forms of neurological disorders supposed to be caused by vitamin B12 deficiency. Vitamin B12 deficiency states are common among elderly patients in primary health care and sometimes in hospital care, especially in geriatric practice. This is a study to define the cobalamin treatment traditions, among Swedish physicians in the period 1990 – 2000. The period was distinguished by an intense debate on the issue by the physicians, an increase of cobalamin consumption, and a shift from parenteral therapy towards oral high-dose therapy. It had been known that symptoms of cobalamin deficiency could start in the nervous system. This knowledge was reinforced by the application of homocysteine and methyl-malonic acid (MMA) in deficiency diagnosis. Introduction of homocysteine and MMA in deficiency diagnosis changed the view on deficiency prevalence, by identifying persons at risk to develop B12 deficiency prior to established symptoms. In this study, Swedish physicians are regarded mainly as receivers of communication about the markers homocysteine and MMA, and deficiency states of cobalamin and folate. The main senders were scientists from North America, Norway, Denmark, and Sweden. This study sets the senders and the receivers of cobalamin communication on a collegial level and quantifies and evaluates the feed-back from the receivers. The receivers, gen¬eral practitioners and geriatricians, appeared to be familiar with old knowledge and frontier concepts in the field. Thus, it is suggested that the increase of B12 prescriptions in Sweden 1990 – 2000 reflected an increased awareness of B12-associated clinical problems among the physicians managing the majority of deficiency patients, although a possible overconsumption of pharmaceutical drugs must be kept in mind.
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| 2. |
- Nilsson, Mats, et al.
(författare)
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Medical intelligence in Sweden. Vitamin B12 : oral compared with parenteral?
- 2005
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Ingår i: Postgraduate medical journal. - : Oxford University Press (OUP). - 0032-5473 .- 1469-0756. ; 81:953, s. 191-193
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Sweden is the only country in which oral high dose vitamin B12 has gained widespread use in the treatment of deficiency states. OBJECTIVE: The aim of the study was to describe prescribing patterns and sales statistics of vitamin B12 tablets and injections in Sweden 1990-2000.Design, setting, and sources: Official statistics of cobalamin prescriptions and sales were used. RESULTS: The use of vitamin B12 increased in Sweden 1990-2000, mainly because of an increase in the use of oral high dose vitamin B12 therapy. The experience, in statistical terms a "total investigation", comprised 1,000,000 patient years for tablets and 750,000 patient years for injections. During 2000, 13% of residents aged 70 and over were treated with vitamin B12, two of three with the tablet preparation. Most patients in Sweden requiring vitamin B12 therapy have transferred from parenteral to oral high dose vitamin B12 since 1964, when the oral preparation was introduced. CONCLUSION: The findings suggest that many patients in other post-industrial societies may also be suitable for oral vitamin B12 treatment.
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| 3. |
- Westman, Bo, et al.
(författare)
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Effects on skeletal muscle glutathione status of ischemia and reperfusion following abdominal aortic aneurysm surgery.
- 2006
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Ingår i: Annals of Vascular Surgery. - : Elsevier BV. - 0890-5096 .- 1615-5947. ; 20:1, s. 99-105
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Tidskriftsartikel (refereegranskat)abstract
- Glutathione (GSH) is an important endogenous scavenger against reactive oxygen species. Elective abdominal surgery without ischemia and reperfusion leads to decreased muscle GSH concentrations 4-72 hr postoperatively without altering GSH redox status. In the present study, we investigated to what extent muscle GSH status was affected during and following elective abdominal aortic aneurysm repair. From patients (n = 10) undergoing abdominal aortic repair, thigh muscle specimens were taken preoperatively, at maximal ischemia, and at 10 min and 4, 24, and 48 hr of reperfusion. Specimens were analyzed for GSH, amino acids, and energy-rich compounds. At maximal ischemia, phosphocreatine decreased by 37% (p < 0.05) and lactate and creatine increased by 274% and 57% (p < 0.001 and 0.05), respectively, indicating ischemia during the clamping of aorta. Adenosine triphosphate, on the other hand, remained unaltered during the entire study period. Total GSH (tGSH) decreased by 46% at 24 hr and by 43% at 48 hr of reperfusion (p < 0.001), while reduced GSH decreased by 48% at 24 hr and by 44% at 48 hr (p < 0.001). The redox status (GSH/tGSH) of GSH and oxidized GSH remained unaltered. Among the constituent amino acids of GSH, glycine and cysteine remained unaltered while glutamine and glutamate decreased by 55% and 55%, respectively (p < 0.001). Abdominal aortic aneurysm repair induces metabolic alterations characteristic for ischemia. The antioxidative capacity in terms of muscle levels of GSH was decreased. However, the oxidative stress during reperfusion did not change GSH status more than what has been reported following abdominal surgery without ischemia and reperfusion. The results indicate that the oxidative stress elicited by elective abdominal aortic aneurysm repair is outbalanced by a compensated GSH metabolism not giving rise to an increased amount of oxidized GSH or an altered GSH redox status.
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| 4. |
- Westman, Bo
(författare)
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Studies of ischemia and reperfusion in muscle and liver on glutathione and amino acid metabolism in man
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Oxidative stress increases the formation of reactive oxygen species (ROS), which can induce damage and breakdown of enzymes and lipoproteins. This leads to impaired cellular function and ultimately to death of cells and eventually organ failure. ROS are thought to be responsible for the damage during reperfusion following ischemia. ROS are counteracted by scavengers (anti-oxidants) among which glutathione is one of the most important. Glutathione and oxidative stress during ischemia and reperfusion have been extensively investigated in animal models earlier. However, the relevance for human physiology especially during disease is not clear. The aim of the present studies was to characterise glutathione and amino acid metabolism in human skeletal muscle and liver during ischemia and reperfusion using surgical interventions as potential human models. In the first study abdominal aneurysm surgery with an ischemia time of about 65 minutes was used. Biopsies from the thigh muscle were obtained before ischemia, at maximal ischemia and after 10 min, 4, 24 and 48 hours of reperfusion. In a second study aorto bi-femoral surgery patients were studied because of the longer ischemia times up to 120 minutes with this procedure. Biopsies from both legs were obtained before ischemia, at maximal ischemia and at 10 min. and 24 h of reperfusion. In the third study knee replacement surgery was used as a model since the obtained ischemia is more complete than in the first 2 studies and because no severe metabolic stress due to abdominal surgery is present in this model. Muscle biopsies were taken before ischemia, at maximal ischemia and 24 h into reperfusion. In the last study the effect of ischemia and reperfusion on human liver was studied during liver resection surgery. In this study biopsies were obtained before ischemia, at maximal ischemia and at 5, 10, 15, 20, 25 and 30 minutes of reperfusion. Results from the first two studies show that both reduced and total glutathione are decreased at 24 and 48 hours of reperfusion. No changes were observed at maximal ischemia or in oxidised glutathione at any point. The changes were however very similar to those previously obtained in muscle following abdominal surgery without ischemia to the muscle. And therefore the observed changes are mainly due to the surgical trauma. In the knee surgery model reduced and total glutathione were also only decreased after 24h of reperfusion. However in this model a complete ischemia is obtained without the metabolic stress of abdominal surgery. The decrease here is therefore more likely to be due to ischemia and reperfusion in combination with a minor surgical trauma. Ischemia of the human liver had no effect on glutathione levels at all. Changes in amino acid levels during reperfusion were very similar as those seen in skeletal muscle following surgery without ischemia reperfusion. However the changes in amino acids seen at maximal ischemia are specific for the ischemia. Alanine is increased and glutamate decreased most likely to remove pyruvate to maintain the flux in the glycolysis. The branched chain amino acids behave differently in liver and muscle during maximal ischemia with and increase in liver and a slight decrease in muscle. Glutamate is decreased at ischemia in both muscle and liver, and decreases in reperfusion in muscle, while an increase is seen in liver at reperfusion. Glutamine is not affected by ischemia but decreases in muscle and increases in liver at reperfusion. In conclusion, ischemia times of up to 120 minutes for skeletal muscle and about 30 minutes for liver do not affect glutathione levels in humans. During early reperfusion phase in the liver no changes are seeneither. In skeletal muscle at 1 to 2 days after reperfusion decreases in glutathione can be observed which seem to a large extend to be caused by the surgical stress rather then the ischemic insult. However in a human model with minimal surgical stress also a decrease is observed suggesting a contribution of the IR. Amino acids are used during the ischemia to maintain the energy status of both skeletal muscle and liver in humans.
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